Cardiovascular Notes - All in One File

Week
1
A&P
CardioVascular Medicine Notes
Heart Anatomy

Heart Anatomy:
• Location:
o Snugly enclosed within the middle mediastinum (medial cavity of thorax)
§ Contains the heart, pericardium, vessels to & from the heart & lungs, trachea & oesophagus.
§ M.Mediastinum – located in the inferior mediastinum (lower than the sterna angle)
o Extends obliquely from 2nd rib à 5th intercostals space.
o Anterior to Vertebrae
o Posterior to Sternum
o Flanked by 2 lungs
o Rests on the diaphragm
o 2/3 of its mass lies to the LHS of the midsternal line.

• The Pericardium: (Coverings of the Heart)
o A double-walled sac
o contains a film of lubricating serous fluid
o 2 Layers of Pericardium:
§ Fibrous Pericardium:
• Tough, dense connective tissue
• Protects the heart
• Anchors it to surrounding structures
• Prevents overfilling of the heart – if fluid builds up in the pericardial cavity, it can
inhibit effective pumping. (Cardiac Tamponade)
§ Serous Pericardium: (one continuous sheet with ‘2 layers’)
• Parietal Layer – Lines the internal surface of the fibrous pericardium
• Visceral Layer – (aka Epicardium) Lines the external heart surface

• Layers of the Heart Wall:
o Epicardium:
§ Visceral layer of serous pericardium
o Myocardium:
§ Muscle of the heart
§ The layer that ‘contracts’
o Endocardium:
§ Lines the chambers of the heart
§ Prevents clotting of blood within the heart
§ Forms a barrier between the O2 hungry myocardium and the blood. (blood is supplied via the
coronary system)
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• Fibrous Skeleton of the Heart:
o The network of connective tissue fibres (collagen & elastin) within the myocardium
o Anchors the cardiac muscle fibres.
o Reinforces the myocardium
o 2 Parts:
§ Septums:
• Flat sheets separating atriums, ventricles & left and right sides of the heart.
• Electrically isolates the left & right sides of the heart (conn. Tissue = non-conductive)
o Important for cardiac cycle
• (interatrial septum/atrioventricular septum/interventricular septum)
§ Rings:
• Rings around great vessel entrances & valves
• stop stretching under pressure

• Chambers & Associated Great Vessels:
o 2 Atrias (superior): [Atrium = Entryway]
§ Thin-walled Receiving Chambers
§ On the back & superior aspect of heart.
§ Each have a small, protruding appendage called Auricles – increase atrial volume.
§ Septal Area
• Connective tissue dividing L & R atria. (Site of Foetal Shunt Foramen ovale)
§ Right Atrium:
• Smooth internal posterior wall
o Where veins drain into (either from body/lungs)
• Ridged internal anterior wall – due to muscle bundles called Pectinate Muscles.
• Blood enters via 3 veins:
o Superior Vena Cava
o Inferior Vena Cava
o Coronary Sinus (collects blood draining from the myocardium)
§ Left Atrium:
• Smooth internal post. & ante. walls.
• Blood enters via:
o The 4 pulmonary veins (O2 blood) [Pulmonos = Lung]

o 2 Ventricles (inferior): [Vent = Underside]
§ Thick, muscular Discharging Chambers
§ The ‘pumps’ of the heart
§ Trabeculae Carnea [crossbars of flesh] line the internal walls
§ Papillary Muscles play a role in valve function.
§ Right Ventricle:
• Most of heart’s Anterior Surface
• Thinner – responsible for the Pulmonary Circulation – Via Pulmonary Trunk
§ Left Ventricle:
• Thicker – it is responsible for the Systemic Circulation – Via Aorta
• Most of the heart’s PosteroInferior Survface

• Landmarks of the Heart:
o Coronary Sulcus (Atrioventricular Groove):
§ Encircles the junction between the Atria & Ventricles like a ‘Crown’ (Corona).
§ Cradles the Coronary Arteries (R&L), Coronary Sinus, & Great Cardiac Vein
o Anterior Interventricular Sulcus:
§ Cradles the Anterior Interventricular Artery
§ Separates the right & left Ventricles anteriorly
§ Continues as the posterior Interventricular Sulcus.
o Posterior Interventricular Sulcus:
§ Continuation of the Anterior Interventricular Sulcus
§ Separates the right & left Ventricles posteriorly

Pathway of Blood Through the Heart:
• The systemic and pulmonary circuits:
o The right side of the heart pumps blood through the pulmonary circuit (to the lungs and back to the
left side of the heart).
§ Blood flowing through the pulmonary circuit gains oxygen and loses carbon dioxide,
indicated by the color change from blue to red.
o The left side of the heart pumps blood via the systemic circuit to all body tissues and back to the
right side of the heart.
§ Blood flowing through the systemic circuit loses oxygen and picks up carbon dioxide (red to
blue color change)

Coronary Circulation:
• The myocardium’s own blood supply
• The shortest circulation in the body
• Arteries lie in epicardium – prevents the contractions inhibiting bloodflow
• There is a lot of variation among different people.
• Arterial Supply:
o Encircle the heart in the coronary sulcus
o Aorta à Left & Right coronary arteries
§ Left Coronary Artery à 2 Branches:
• 1. Anterior InterVentricular Artery (aka. Left Anterior Descending Artery ...or LAD).
o Follows the Anterior InterVentricular Sulcus
o Supplies blood to InterVentricular Septum & Anterior walls of both
Ventricles.
• 2. Circumflex Artery
o Follows the Coronary Sulcus (aka. AtrioVentricular Groove)
o Supplies the Left Atrium & Posterior walls of the Left Ventricle
§ Right Coronary Artery à 2 (‘T-junction) Branches:
• 1. Marginal Artery:
o Serves the Myocardium Lateral RHS of Heart
• 2. Posterior Interventricular Artery:
o Supplies posterior ventricular walls
o Anastomoses with the Anterior Interventricular Artery
• Venous Drainage:
o Venous blood – collected by the Cardiac Veins:
§ Great Cardiac Vein (in Anterior InterVentricular Sulcus)
§ Middle Cardiac Vein (in Posterior InterVentricular Sulcus)
§ Small Cardiac Vein (along Right inferior Margin)
o - Which empties into the Right Atrium.

Heart Valves:
• Ensure unidirectional flow of blood through the heart.
• 2x AtrioVentricular (AV) (Cuspid) Valves:
o Located at the 2 Atial-Ventricular junctions
o Prevent backflow into the Atria during Contraction of Ventricles
o Attached to each valve flap are chordae tendinae (tendonous cords) “heart strings”
§ Anchor the cusps to the Papillary Muscles protruding from ventricular walls.
• Papillary muscles contract before the ventricle to take up the slack in the chordae
tendinae.
• Prevent inversion of valves under ventricular contraction.
o Right AV Valve:
§ The “Tricuspid Valve”
§ 3 flexible ‘cusps’ (flaps of endocardium + Conn. Tissue)
o Left AV Valve:
§ The “Mitral Valve” or “Biscupid Valve”
§ (resembles the 2-sided bishop’s miter [hat])

• 2x SemiLunar (SL) Valves:
o Guard the bases of the large arteries issuing from the Ventricles.
o Each consists of 3 pocket-like cusps resembling a crescent moon (semilunar = half moon)
o Open under Ventricular Pressure
o Pulmonary Valve:
§ Between Right Ventricle & Pulmonary Trunk
o Aortic Valve:
§ Between Left Ventricle & Aorta


Valve Sounds:
• 1. “Lubb”:
o Sound of a Cuspid Valve closing
• 2. “Dupp”:
o Sound of a Semilunar Valve Closing

• Where to Listen:


Basic Anatomy & Physiology:
Cardiovascular
Heart Anatomy:
Location:
o Snugly enclosed within the middle mediastinum (medial cavity of thorax). Contains:
Heart
Pericardium
Great Vessels
Trachea
Esophagus.
The Pericardium: (Coverings of the Heart)

o A double-walled lubricating sac
o 2 Layers of Pericardium:
Fibrous Pericardium:
Tough, dense connective tissue
Protects the heart
Anchors it to surrounding structures
Serous Pericardium: (one continuous sheet with ‘2 layers’)
Parietal Layer – Lines the internal surface of the fibrous pericardium
Visceral Layer – (aka Epicardium) Lines the external heart surface
Layers of the Heart Wall:

o Epicardium:
Visceral layer of the serous pericardium
o Myocardium:
Muscle of the heart
o Endocardium:
Endothelium lining the chambers of the heart
Prevents clotting of blood within the heart
Forms a barrier between the O2 hungry myocardium and the blood. (blood is supplied via
the coronary system)
Fibrous Skeleton of the Heart:
o Functions:
Reinforces Myocardium
Anchors muscle fibres + valves + great vessels
Electrically isolates
o 2 Parts:
Septums:
Flat sheets separating atriums, ventricles & left and right sides of the heart.
Electrically isolates the L&R sides of the heart
Rings:
Rings around great vessels & valves stop stretching under pressure
Chambers & Associated Great Vessels:

o 2 Atrias (Superior):
Thin-walled Receiving Chambers
Right Atrium:
Blood enters via 3 veins:
o SVC
o IVC
o Coronary Sinus (collects venous blood draining from the myocardium)
Left Atrium:
Blood enters via:
o 4x Pulmonary Veins (O2 blood)
o 2 Ventricles (Inferior): [Vent = Underside]

Thick, muscular pumping chambers
Right Ventricle:
Anterior Surface of Heart
Thinner – Low Pressure Pulmonary Circulation – Via Pulmonary Arteries
Left Ventricle:
PosteroInferior Surface of Heart
Thicker – High Pressure Systemic Circulation – Via Aorta
Landmarks of the Heart:
Coronary Sulcus (Atrioventricular Groove):
o Encircles the junction between the Atria & Ventricles like a ‘Crown’ (Corona).
o Cradles the Coronary Arteries (R&L), Coronary Sinus, & Great Cardiac Vein
Anterior Interventricular Sulcus:
o Cradles the Anterior Interventricular Artery (Left Anterior Descending)
Posterior Interventricular Sulcus:
o Continuation of the Anterior Interventricular Sulcus
o Cradles the Posterior Descending Artery
Coronary Circulation:
The myocardium’s own blood supply
Arteries lie in epicardium – prevents the contractions inhibiting bloodflow
Arterial Supply:
o Aorta Left & Right coronary arteries
Left Coronary Artery
1. Left Anterior Descending Apex, Anterior LV, Anterior 2/3 of IV-Septum.
2. Circumflex Artery L atrium + Lateral LV
Right Coronary Artery Marginal & Post-Interventricular Artery
R-Atrium
Entire R-Ventricle
Posterior 1/3 of IV-Septum
Heart Valves:
Ensure unidirectional flow of blood through the heart.
2x AtrioVentricular (AV) (Cuspid) Valves:
o Prevent backflow into the Atria during Contraction of Ventricles
Papillary muscles contract before the ventricle to take up the slack in the chordae tendinae
Prevents ballooning of valves under ventricular contraction.
o Tricuspid Valve (Right ):
3 flexible ‘cusps’ (flaps of endocardium + Conn. Tissue)
o Mitral Valve (Left):
2 Leaflets - resembles the 2-sided bishop’s miter [hat]
2x SemiLunar (SL) Valves:

o Open under Ventricular Pressure
o 3x Cusps each
o Pulmonary Valve:
Between Right Ventricle & Pulmonary Trunk
o Aortic Valve:
Between Left Ventricle & Aorta
Valve Sounds:
S1 ( Lubb ):
o AV Valve Closure
o (M1 = Mitral Component)
o (T1 = Tricuspid Component)
S2 ( Dupp ):
o Semilunar Valve Closure
o (A2 = Aortic Component)
o (P2 = Pulmonary Component)
Electrophysiology & ECGs
2 Types of Cardiac Muscle Cells:
- Conductile/Nodal: (Intrinsic)
o Have Spontaneous Electrical Activity Cannot Maintain a Resting Membrane Potential
Spontaneously Depolarises to Threshold (Due to Leaky Na+ Membrane Ion Channels)
NB: Na+ brings to threshold, but Ca+ is responsible for Depolarisation.
Slow ‘Pacemaker’ Action Potentials
o Heirarchy of control depending on Intrinsic Rate.
(SA is fastest :. takes control)
o The SinoAtrial (SA) Node:

= The PaceMaker of the Heart: Unregulated Rate: 90-100bpm......however;
Location: Posterior Wall of the Right Atrium near the opening of the Superior Vena Cava
o The AtrioVentricular (AV) Node:
2nd in Command: Slower than the SA Node: 40-60bpm
Location: Inferior portion of the InterAtrial Septum; Directly above the TriCsupid Valve.
Function: Delays SA Node impulse Approx. 100ms Bundle Branches;
Allows Atrial emptying before Ventricular Contraction
o The Bundle Branches (Bundles of His):
3rd in Command: Slower than AV & SA Nodes: 20-40bpm
Location: Fork of branches – Superior Portion of InterVentricular Septum
Function: Serves as the only connection between the 2 Atria & 2 Ventricles.
o Conduction Path:
SA node
AV node (delays signal – ensures coordinated contraction)
Bundle of His (further delay 0.04secs)
R and L bundle branches
Purkinji fibres
- Contractile:
o Fast Non-Pacemaker Action Potentials
o Have stable membrane potentials.
Depolarisation:
Conductile AP Opens Fast Na+ Channels Massive Na+ influx Depolarisation
Plateau:
Fast Na+ channels close; Voltage-Gated Ca+ channels to open
o Ca Influx + Ca release from Sarcoplasmic Reticulum
[Ca+] causes muscular contraction.
o (Plateau is balanced by Ca+ influx & K+ efflux)
Repolarisation:
Influxing Ca+ channels close; but the effluxing K+ channels remain open;
Excess Ions?:
Excess Na+ & K+ deficit is dealt with by the Na/K-ATPase.
Excess Ca+ from the Plateau Phase is eliminated by a Na/Ca Exchanger.
o The Purkinje Fibres:

= Specialised Myocytes with very few myofibrils (NOT contractile).
Conductile; but...Resembles Ventricular Myocytes
Capable of Spontaneous Depolarisation – 15bpm
Location:
The Inner Ventricular Walls of the Heart – just below the Endocardium
Role in Conduction Network:
Impulse conduction from L & R Bundle Branches to the Ventricles;
o Atrial & Ventricular Myocytes:

Cells with many myofibrils (contractile proteins)
Produce the contraction necessary for heart function.
ElectroCardioGrams (ECG):
- Recording of all Action Potentials by Nodal & Contractile Cells in the heart at a given time.
o NB: It IS NOT a single action potential.
o NB: A “Lead refers to a combination of electrodes that form an imaginary line in the body, along
which the electrical signals are measured.
Ie. A 12 ‘lead’ ECG usually only uses 10 electrodes.
- Graphic Output:
o X-axis = Time
o Y-axis = Amplitude (voltage) – Proportional to number & size of cells.
- Understanding Waveforms:
- ECG Waves:
o P Wave:
Depolarisation of the Atria
Presence of this waves indicates the SA Node is working
o PR-Segment:
Reflects the delay between SA Node & AV Node.
Atrial Contraction is occurring at this time.
o Q Wave:
Interventricular Septum Depolarisation
Wave direction (see blue arrow) is perpendicular to the Main Electrical Axis results in a
‘Biphasic’ trace.
Only the –ve deflection is seen due to signal cancellation by Atrial Repolarisation.
Sometimes this wave isn’t seen at all
o R Wave:
Ventricular Depolarisation
Wave Direction (blue arrow) is the same as the Main Electrical Axis Positive Deflection.
R-Wave Amplitude is large due to sheer numbers of depolarizing myocytes.
o S Wave:
Depolarisation of the Myocytes at the last of the Purkinje Fibres.
Wave Direction (black arrow) opposes the Main Electrical Axis Negative Deflection
This wave is not always seen.
o ST Segment:
Ventricular Contraction is occurring at this time.
Due to the lag between excitation & contraction.
o T Wave:
Ventricular Repolarisation
Positive deflection despite being a Repolarisation wave – because Repol. Waves travel in
the opposite direction to Depol Waves.
The Heart s Electrical A is

o Refers to the general direction of the heart's depolarisation wavefront (or 'mean electrical vector') in the
frontal plane.
o It is usually oriented in a 'Right Shoulder to Left Leg' direction.
o Determining The Electrical Axis From an ECG Trace:
o 3 Methods:
o Quadrant Method (the one you’re concerned with)
o Peak Height Measurement Method
o The Degree Method
o The Quadrant Method:
Effects of the Autonomic Nervous System:
- Parasympathetic NS:
o Innervates SA & AV Nodes
Heart Rate
- Sympathetic NS:
o Innervates the SA & AV Nodes & Ventricular Muscle (& also via Noradrenaline).
Heart Rate
Contractility
Mechanical Events of The Cardiac Cycle
Terms:
- Systole = Myocardial Contraction
- Diastole = Myocardial Relaxation
- Stroke Volume = Output of Blood from the Heart Per Contraction (≈80mL of blood)
- Heart Rate = #Heart Beats/Minute
- Cardiac Output:
o Volume of Blood Ejected from the Heart Per Minute (Typically ≈5L/min)
o Cardiac Output = Heart Rate x Stroke Volume
o Chronotropic Influences:
Affect Heart Rate
o Inotropic Influences:
Affect Contractility (& :. stroke volume)
o Dromotropic Influences:
Affect AV-Node Delay.
- End Diastolic Volume = Ventricular Volume @ end of Diastole (When Ventricle is Fullest)
- End Systolic Volume = Ventricular Volume After Contraction (Normal ≈ 60-65%)
- Preload = The degree of Stretching of the Heart Muscle during Ventricular Diastole.
o ( Preload = cross linking of myofibrils = Contraction (“Frank Starling Mechanism”)
- Afterload = The Ventricular Pressure required to Eject blood into Aorta/Pulm.Art.
o ( Afterload = SV due to ejection time)
- 1. Atrial Systole/Ventricular Filling (Diastole):

- 2. Ventricular Systole:
o a) AV Valves Close:
Ventricular Pressure Exceeds Atrial Pressure AV Valves shut
o b) Semilunar Valves Open:
Ventricular Pressure Exceeds Aortic/Pulm Pressure Blood Ejected
o c) Semilunar Valves Close:
Ventricular Pressure then falls Below Aortic/Pulm Pressure Semilunar Valves Close.
- 3. Ventricular Diastole:
o Ventricles relax Ventricular Pressure falls below Atrial Pressure AV-Valves Open:
Blood from Atria into Ventricles
(NB: Passive filling from venous return is responsible for 70% of ventricular filling.)
CardioDynamics:
- Cardiac Output:
o Determined by 2 Things:
1. Stroke Volume....&
2. Heart Rate
o A erage CO L min (ie. The entire blood supply circulates once per minute)
- Heart Rate:
o Depends on Tissue-Satisfaction with Nutrients & O2.
o Terms:
BradyCardia: HR Slower than normal. (too fast stroke volume & CO suffers)
TachyCardia: HR Faster than normal.
o Regulation of HR:
Autonomic Nervous System:
Parasympathetic: (Vagus Nerve)
o Decrease Heart Rate (-ve Chronotropic Effect)
o Increase AV-Node Delay (-ve Dromotropic Effect)
o NB: ONLY A TINY EFFECT ON CONTRACTILITY
Sympathetic: (Sympathetic Chains)
o Increase Heart Rate (+ve Chronotropic Effect)
o Increase Force of Contraction (+ve Inotropic Effect).
Reflex Control:
Bainbridge Reflex (Atrial Walls):
o Venous Return Heart Rate
o Responsible for 40-60% of HR increases.
BaroReceptor Reflex (Aortic & Carotids):
o BP HR & Contractility (+ Vasodilation)
ChemoReceptor Reflex:
o Low O2 or CO2 in Peripheral-Tissue HR & Resp. Rate
- Stroke Volume:
o Blood output per heart-beat.
o Stroke Volume = End Diastolic Volume End Systolic Volume
o :. SV is by:
Ventricular Filling Time (Duration of Ventricular Diastole)
Venous Return
Arterial BP (Higher harder to eject blood ESV Increases)
o NB: Frank Starling Mechanism :

Preload Contractility Stroke Volume
Control of Circulation (Haemodynamics & BP Regulation)
Resistance:
- 3 Factors Influencing Resistance:
o 1. Blood Viscosity (Fairly Constant)
o 2. Total Vessel Length (Fairly Constant)
o 3. Vessel Diameter (Highly Variable)
Relationship Between Flow, Pressure & Resistance:

- Flow is:
o 1. Directly Proportional to Pressure Gradient
o 2. Inversely Proportional to Resistance
- Therefore:
Effects of Vasomotion on Rate & Velocity of Flow:

- Changes Vessel Diameter:
o The Flow Rate is directly proportional to the 4th Power of the Vessel Diameter.
o Ie. Small changes in diameter Large changes in Flow Rate (by x4).
Factors Influencing Blood Pressure (Long Term):

- Cardiac Output
- Peripheral Resistance
- Blood Volume
:. BP = Cardiac Output X Total Peripheral Resistance
Types of Blood Pressures:

- Systolic: Peak Aortic pressure during ventricular systole.
- Diastolic: Lowest Aortic pressure during ventricular diastole.
- *Pulse Pressure:
o = Systolic Pressure - Diastolic Pressure
o (Eg. 120mmHg – 80mmHg)
o Normal = 40mmHg
- *Mean Arterial Pressure (MAP):
o MAP = Diastolic Pressure + 1/3(Pulse Pressure)
o *The Pressure that Propels Blood to the Tissues – maintains Tissue Perfusion (see below sections).
Control of MAP:
- 3 Main Regulators:
o 1. Autoregulation (@ the Tissue Level):
‘Automatic Vasodilation/constriction @ the tissue relative to metabolic requirements.’
o 2. Neural Mechanisms:
Vasomotor Centres (Medulla):
Baroreceptors & Chemoreceptors
Autonomic Nervous System:
Sympathetic HR & Contractility MAP
Parasympathetic Heart Rate MAP
o 3. Endocrine Mechanisms (Kidney Level):
**Antidiuretic Hormone (ADH) AKA. Vasopressin:
ADH Water Retention Released MAP
Angiotensin II:
AT-II VasoConstriction MAP
Erythropoietin:
EPO Haematopoiesis Blood Volume MAP
Natriuetic Peptides (Released by the heart):
Stretch on Heart NP Release Diuresis Reduces BP & Volume.
Blood Vessels
Introduction to Blood Vessels:
- 3 Classes:
o Arteries Carry blood away from the heart
Elastic Arteries Eg. Aorta & Major Branches (Conducting Vessels)
Muscular Arteries Eg. Coeliac Trunk & Renal Arts. (Distributing Vessels)
Arterioles Eg. Intra-Organ Arteries (Resistance Vessels)
Terminal Arteriole Eg. Afferent Arteriole in kidney
o Capillaries Intimate contact with tissue facilitate cell nutrient/waste transfer
Vascular Shunt
True Capillaries
o Veins Carry blood back to the heart
Post-Capillary Venule (Union of capillaries)
Small Veins (Capacitance Vessels – 65% of body’s blood is venous)
Large Veins (Capacitance Vessels – 65% of body’s blood is venous)
Blood Vessel Structure:

- 3-Layered Wall:
o Tunica Intima:
Ie. The layer in intimate contact with the blood (luminal)
Consists of The Endothelium (Simple Squamous Epthelium)
o Tunica Media:
Middle....& Thickest layer (Smooth Muscle & Elastin)
o Tunica Externa:
Outermost Layer (Loose collagen fibres)
(NB: Also Contains Nerve Fibres, Lymphatics, and Vasa Vasorum (In larger vessels))
Fluid Movements Across a Vessel:

- Determined by the balance of 2 forces:
o 1. Capillary Hydrostatic Pressure:
Capillary blood pressure.
o 2. Colloid Osmotic Pressure:
Balance of Blood Osmolarity vs. Tissue Osmolarity
- (:. Net Filtration Pressure = Net Hydrostatic Pressure – Net Osmotic Pressure)
Foetal Circulation:
B passes Shunts of foetal circulatory system:
o Ductus Venosus
Directs the oxygenated blood from the placental vein into inferior vena cava heart
Partially bypasses the liver sinusoids
o Foramen Ovale
An opening in the interatrial septum loosely closed by a flap of tissue.
Directs some of blood entering the right atrium into the left atrium Aorta.
Partially bypasses the lungs.
o Ductus Arteriosus
Directs most blood from right atrium of the heart directly into aorta
Partially bypasses the lungs
o **All of these “shunts” are occluded at birth due to pressure changes.
NB: The Foramen Ovale can take up to 6 months to close.
Week 2
Electrophysiology & ECGs
The Heartbeat:
- Heart is a Muscle & Requires:
o O2
o Nutrients, &
o Action Potentials; to function.
- However, these neural signals don’t come from the brain;
o Rather, the heart has its own conduction systems.
§ These systems allow it to contract autonomously
o Hence why a transplanted heart still operates (if provided with O2 & nutrients)
- Cardiac Activity is Coordinated:
o To be effective, the Atria & Ventricles must contract in a coordinated manner.
o This activity is coordinated by the Heart’s Conduction Systems......

- The Entire Heart is Electrically Connected...By:
o Gap Junctions:
§ Allows action potentials to move from cell to cell
o Intercalated Discs:
§ Support synchronised contraction of cardiac tissue

The Heart’s Conduction Systems:
- NB: The Amplitude & Steepness of an action potential are important determinants of propagation velocity.

2 Types of Cardiac Muscle Cells:
- Conductile/Nodal: (Intrinsic)
o Slow ‘Pacemaker’ Action Potentials
o Have Spontaneous Electrical Activity – Cannot Maintain a Resting Membrane Potential
§ Spontaneously Depolarises to Threshold
• This gradual depolarisation is called a ‘Prepotential’.
• Due to Leaky Na+ Membrane Ion Channels
• Therefore – Firing Frequency Depends on Na+ Movement
§ Depolarisation:
• Once Threshold is reached, Ca2+ channels open
• Influx of Ca+
• Causes an action potential.
§ Repolarisation:
• Once peak MP is reached, Ca+ channels close, K+ channels open
• K+ Efflux makes MP more –ve.
• Causes repolarisation
§ I.e: Na+ brings to threshold, but Ca+ is responsible for Depolarisation.
o With a Heirarchy of control over the heart.
§ Heirarchy based on natural intrinsic rate. (fastest node (SA node) takes control)


o The SinoAtrial (SA) Node:
§ The region that generates impulses at the highest frequency.
• The “PaceMaker” - Driver of Heart Rate
• Unregulated Rate: 90-100bpm......however;
o Parasympathetic NS lowers heart rate.
§ Keeps Normal Resting Heart Rate at 70bpm
o Sympathetic NS raises heart rate.
• Takes 50ms for Action-Potential to reach the AV Node.
§ Location:
• Embedded in the Posterior Wall of the Right Atrium near the opening of the Superior
Vena Cava
§ Nature of Action Potentials:
• Continually Depolarising 90-100bpm
§ Role in Conduction Network:
• Sets the pace for the heart as a whole.
§ Portion of Myocardium Served:
• Contracts the Right & Left Atrium

o The AtrioVentricular (AV) Node:
§ Location:
• Inferior portion of the InterAtrial Septum; Directly above the TriCsupid Valve.
• Continually Depolarising – but slower than the SA Node.
o 40-60bpm
• To delay the impulse from the SinoAtrial Node à Bundle Branches;
• Delay allows the Atria to empty their contents before Ventricular Contraction
• Delay: Approx. 100ms
• Part of a conducting pathway; serves to pass on the SA Node Impulses to the
Purkinje Fibres (which supply the Ventricular Walls)


o The Bundle Branches/AV Bundle Branches/Bundles of His:
§ Location:
• Fork of branches – Superior Portion of InterVentricular Septum
• Continually Depolarising – Slower than AV & SA Nodes
o 20-40bpm
• Serves as the only connection between the 2 Atria & 2 Ventricles.
• The 2 Atria & 2 Ventricles are isolated by the fibrous skeleton and lack of gap
junctions.
§ Portion of the Myocardium Served:
• Transmits impulses from the AV Node to the R & L Bundle Branches,
o Then along the InterVentricular Septum à Apex of the Heart.
§ NB: Left Bundle is bigger due to larger L-Ventricle.

Nodal Heirarchy:
- Contractile:
o Fast ‘Non-Pacemaker’ Action Potentials
o Have stable membrane potentials.
§ Resting MP:
• Na+ & Ca+ channels are closed.
• Any +ve change to MP causes Fast Na+ channels to open à +ve feedback à
Threshold
§ Depolarisation:
• If MP reaches threshold, all Fast Na+ channels open;
• Massive influx of Na+ into cell
• Membrane depolarises
§ Plateau:
• Fast Na+ channels inactivate.
• The small downward deflection is due to Efflux of K+ ions
• Action potential causes membrane Voltage-Gated Ca+ channels to open
o This triggers further Ca+ release by the Sarcoplasmic Reticulum into the
Sarcoplasm. (“Ca induced Ca Release”)
§ This increased myoplasmic Ca+ causes muscular contraction.
o Plateau is sustained by influx of Ca+, balanced by efflux of K+ ions
§ Repolarisation:
• Influxing Ca+ channels close…..The effluxing K+ channels remain open;
o Result is a net outward flow of +ve charge. à Downward Deflection
o As the MP falls, more K+ channels open, accelerating depolarization.
o Membrane Repolarises & most of the K+ channels close.
§ Excess Ions??
• Excess Na+ in the cell from depolarization is removed by the Na/K-ATPase.
• Deficit of K+ in the cell from repolarisation is replaced by the Na/K-ATPase.
• Excess Ca+ from the Plateau Phase is eliminated by a Na/Ca Exchanger.

o NB: There is a considerable delay between Myocardial Contraction & the Action Potential.

o The Purkinje Fibres:
§ What?:
• Specialised Myocytes with very few myofibrils à don’t contract during impulse
transmission.
§ Location:
• The Inner Ventricular Walls of the Heart – just below the Endocardium
• Begin at the heart apex, then turn superiorly into the Ventricular Walls.
• Conductile; but...
• Resembles those of Ventricular Myocardial Fibers;
o However the Depolarisation is more pronounced & Plateau is longer.
• Long Refractory period
• Capable of Spontaneous Depolarisation – 15bpm
• Carry the contraction impulse from the L & R Bundle Branches to the Myocardium of
the Ventricles;
• Causes Ventricles to Contract.
• R & L Ventricles.

o Atrial & Ventricular Myocytes:
§ Cells with many myofibrils (contractile proteins)
§ Produce the contraction necessary for heart function.

Refractory Periods:
- In Cardiac Muscle, the Absolute Refractory Period continues until muscle relaxation;
o Therefore summation isn’t possible à tetanus cannot occur (critical in heart)
o Ie. The depolarised cell won’t respond to a 2nd stimulus until contraction is finished.
- Absolute Refractory Period:
o Approx 200ms
o Duration: from peak à plateau à halfway-repolarised.
- Relative Refractory Period:
o Na+ channels are closed – but can still respond to a stronger-than-normal stimulus.
o Approx 50ms
o Duration: Last half of repolarisation

Effects of the Autonomic Nervous System:
- Although the heart can operate on its own, It normally communicates with the brain via the A.N.S.
- Parasympathetic NS:
o Innervates SA & AV Nodes
§ Slows Heart Rate
o Direct Stimulation
o Stimulation releases AcetylCholine à Muscarinic receptors in SA/AV Nodes à
§ Causes increased K+ permeability (Efflux) à Hyperpolarises the cell à
• Cell takes longer to reach threshold à Lower Heart Rate
- Sympathetic NS:
o Innervates the SA & AV Nodes & Ventricular Muscle.
§ Raises Heart Rate
§ Increases Force of Contraction
§ Dilates Arteries
o Indirect Stimulation
o Sympathetic Nerve Fibres Release NorAdrenaline (NorEpinephrine) @ their cardiac synapses à
Binds to Beta 1 Receptors on Nodes & Muscles à
§ Initiates a Cyclic AMP Pathway à Increases Na+ + Ca+ Permeability in Nodal Tissue &
Increases Ca+ Permeability(Membrane & SR) in Muscle Tissue.
• Nodal Tissue:
o ++Permeability to Na+ à more influx of Na+ à Membrane ‘drifts’ quicker to
threshold à Increased Heart Rate
o ++Permeability to Ca+ à more influx of Ca+ à Membrane Depolarisation is
quicker à Increased Heart Rate
• Muscle Tissue:
o ++ Membrane Permeability to Ca+ à More influx of Ca+ à
o ++Sarcoplamic Reticulum Permeability to Ca+ àEflux of Ca+ into cytoplasmà
§ Increases available Ca+ for contraction à Contractile Force Increases

ElectroCardioGrams (ECG):
- Recording of all Action Potentials by Nodal & Contractile Cells in the heart at a given time.
o NB: It IS NOT a single action potential.
- Measured by VoltMetres à record electrical potential across cells:
o 3x Bipolar Leads: Measure Voltages between the Arms...OR...Between an Arm & a Leg.
§ I = LA (+) RA (-)
§ II = LL (+) RA (-)
§ III = LL (+) LA (-)
o 9x Unipolar Leads:
§ Look at the heart in a ‘3D’ Image.
o NB: A “Lead” refers to a combination of electrodes that form an imaginary line in the body, along
which the electrical signals are measured.
§ Ie. A 12 ‘lead’ ECG usually only uses 10 electrodes.
o A lead records electrical signals from a particular combination of electrodes placed at specific points
on the body.
- Graphic Output:
o X-axis = Time
o Y-axis = Amplitude (voltage) – Proportional to number & size of cells.
- Understanding Waveforms:
o When a Depol. Wavefront moves toward a positive electrode, a Positive deflection results in the
corresponding lead.
o When a Depol. Wavefront moves away from a positive electrode, a Negative deflection results in the
corresponding lead.
o When a Depol. Wavefront moves perpendicular to a positive electrode, it first creates a positive
deflection, then a negative deflection.

- ECG Waves:
o P – Wave:
§ Depolarisation of the Atria
§ Presence of this waves indicates the SA Node is working

o PR-Segment:
§ Reflects the delay between SA Node & AV Node.
§ Atrial Contraction is occurring at this time.

o Q – Wave:
§ Interventricular Septum Depolarisation
§ Wave direction (see blue arrow) is perpendicular to the Main Electrical Axis à results in a
‘Biphasic’ trace.
• Only the –ve deflection is seen due to signal cancellation by Atrial Repolarisation.
• Sometimes this wave isn’t seen at all

o R – Wave:
§ Ventricular Depolarisation
§ Wave Direction (blue arrow) is the same as the Main Electrical Axis à Positive Deflection.
§ R-Wave Amplitude is large due to sheer numbers of depolarizing myocytes.

o S – Wave:
§ Depolarisation of the Myocytes at the last of the Purkinje Fibres.
§ Wave Direction (black arrow) opposes the Main Electrical Axis à Negative Deflection
§ This wave is not always seen.

o ST – Segment:
§ Ventricular Contraction is occurring at this time.
• Due to the lag between excitation & contraction.

o T – Wave:
§ Ventricular Repolarisation
§ Positive deflection despite being a Repolarisation wave – because Repol. Waves travel in the
opposite direction to Depol Waves.



The Heart’s Electrical Axis:
o Refers to the general direction of the heart's depolarisation wavefront (or 'mean electrical vector') in the
frontal plane.
o It is usually oriented in a 'Right Shoulder to Left Leg' direction.
o Determining The Electrical Axis From an ECG Trace:
o 3 Methods:
o Quadrant Method (the one you’re concerned with)
o Peak Height Measurement Method
o The Degree Method
o The Quadrant Method:
Week 3
Mechanical Events of The Cardiac Cycle

Structure-Function Relationship of the Heart
- The Myocardium is essentially one long muscle orientated in a spiral-like fashion
o This allows the heart to be electrically integrated
o Allows the heart to ‘wring out’ the blood within it
o This setup facilitates a Strong Pumping Action.

Terms:
- Systole:
o When Any Chamber of the Heart Contracts.
o Blood à Out
- Diastole:
o When Any Chamber of the Heart Relaxes.
o Blood à In
- Cardiac Output:
o Output of Blood from the Heart Per Minute
o Cardiac Output = Heart Rate x Stroke Volume
o Chronotropic Influences:
§ Factors affecting Heart Rate
o Inotropic Influences:
§ Factors affecting Force of Contraction (& stroke volume)
o Dromotropic Influences:
§ Factors affecting Conduction Velocity of AV-Node.
- Stroke Volume:
o Output of Blood from the Heart Per Contraction
- Heart Rate:
o #Heart Beats/Minute
- End Diastolic Volume:
o Ventricular Volume during Complete Diastole (end of diastole).
o When Ventricle is at its Peak Fullness
- End Systolic Volume:
o Volume of blood left in Ventricles after Contraction
o NB: not all ventricular blood is ejected during contraction (only 60-65%)
Mechanical Events of the Cardiac Cycle: + Relationships to ECG Trace:
- NB: Contractions of the Heart ALWAYS Lag Behind Impulses Seen on the ECG.
- Fluids move from High Pressure à Low Pressure
- Heart Valves Ensure a UniDirectional flow of blood.
- Coordinated Contraction Timing – Critical for Correct Flow of Blood.

- 1. Atrial Systole/Ventricular Filling (Diastole):
o Contraction of Atria
o IntraAtrial Pressure Increases
o Blood pushed into Ventricles through AV-Valves
o NB: Ventricles are already 70% full from passive Venous Filling.
o At End of Atrial Systole, Ventricles have EDV (End Diastolic Volume) ≈ 130mL

- 2. Ventricular Systole:
o Early Phase:
§ Ventricles Contract
§ Ventricular Pressure Exceeds Atrial Pressure à AV Valves shut
§ IsoVolumetric Contraction Phase:
• The beginning of ventricular systole
• All valves are Closed.
• Where the ventricular pressure rises, but Volume Stays Constant.

o Late Phase:
§ Ventricular Pressure then Exceeds Aortic Pressure à Semilunar Valves Open à Blood
Ejected
• ≈80mL of blood ejected each time (Stroke Volume)
• Ventricular Volume Decreases.
§ Ventricular Pressure then falls Below Aortic Pressure à Semilunar Valves Close.
• Sudden closure of SemiLunar Valves causes the Dicrotic Notch:
o Result of Elasticity of the Aorta & Blood Rebounding off the Closed SL Valve.
o Causes a slight peak in Aortic pressure
§ Ventricles never fully empty:
• ESV (End Systolic Volume) = Amount of blood left in ventricles à 50mLs.
- 3. Ventricular Diastole:
o IsoVolumetric Relaxation Phase:
§ Initially when the Ventricle relaxes, both the Semilunar & AV-Valves are still closed.
• Occurs at a pressure that is still slightly higher than the Atria, but also lower than
Aortic/Pulmonary Arteries.
§ At this time, venous blood is already beginning to fill the atria

o When Ventricular Pressure falls below Atrial Pressure à AV-Valves Open:
§ Blood à from Atria into Ventricles
§ Passive filling of the Atria & Ventricles – responsible for 70% of ventricular filling.

CardioDynamics:
- “The Movement & Forces Generated During Cardiac Contractions”
- Cardiac Output:
o Useful when examining cardiac function over time.
o Determined by 2 Things:
§ 1. Stroke Volume....&
§ 2. Heart Rate

Cardiac Output(mL/min) = Stroke Volume X Heart Rate

o Average CO ≈ 5L/min (ie. The entire blood supply circulates once per minute)
o Is regulated such that peripheral tissues receive adequate blood supply.
o Heart Rate:
§ Depends on Tissue-Satisfaction with Nutrients & O2.
§ Terms:
• BradyCardia: HR Slower than normal. (too fast à stroke volume & CO suffers)
• TachyCardia: HR Faster than normal.
§ Regulation:
• Alterations in SA-Node Firing:
o SA-Node is the Pacemaker.....therefore:
§ Change its rate à change Heart Rate (àchange Cardiac Output)
• Autonomic Nervous System:
o Parasympathetic: (Vagus Nerve)
§ Decrease Heart Rate (-ve Chronotropic Effect)
§ Decrease AV-Node Conduction (-ve Dromotropic Effect)
• Increase delay between Atrial & Ventricular Contraction.
§ NB: ONLY A TINY EFFECT ON CONTRACTILITY
o Sympathetic: (Sympathetic Chains)
§ Increase Heart Rate (+ve Chronotropic Effect)
§ Increase Force of Contraction (+ve Inotropic Effect).

• Reflex Control:
o Bainbridge Reflex (Atrial Walls):
§ Increase in HR in response to increased Venous Return
§ Stretch of Atrial Walls à Stretch Receptors à Symp.NS à ↑HR.
§ Responsible for 40-60% of HR increases.
o BaroReceptor Reflex:
§ 2 Main Baroreceptors:
• Aortic à Vagus Nv. à CV Centre(medulla/pons)
• Carotid à Hering’s Nv. à CV Centre(medulla/pons)
§ Constantly responds to Blood Pressure Changes
• (via stretch in vessel walls)
• More Stretch = More Firing:.leads to:
o Parasympathetic Activation
o Sympathetic De-activation
§ Receptors Never Silent – constantly signalling
§ Quick to respond
§ In Hypertension à receptors recalibrate to the higher BP.
§ Changes HR accordingly

o ChemoReceptor Reflex:
§ Responds mostly to O2 & CO2 levels in Peripheral-Tissue.
§ If O2 low à Respiratory Rate Increases (Small Increase in HR also)
• Venous Return:
o Venous Return Fills Atria With Blood.
§ When Venous Return ↑, Atrial Walls Stretch à Stretches SA-Node.
o Stretching of SA-Node Cells à More Rapid Depol. à ↑HR
o Responsible for 15% of HR increases.
o Influenced by:
§ Arterial Pressure
§ Peripheral Compliance
§ Local Blood Flow
§ Capillary Exchange

• Chemical Regulation:
o Hormones:
§ Adrenaline
§ Thyroxine
§ Insulin
o Ions:
§ Na+
§ K +
§ Ca2+
o Other Factors:
§ Age (Old à Lower Resting-HR)
§ Gender (Females à Higher Resting-HR)
§ Physical Fitness (Fit à Lower Resting-HR)
§ Temperature (Hot à Higher Resting-HR)

o Stroke Volume:
§ Blood output per heart-beat.
§ Useful when examining a single cardiac cycle.

Stroke Volume = End Diastolic Volume – End Systolic Volume

§ ↑End Diastolic Volume = ↑Stroke Volume
§ EDV Influenced by:
• 1. Filling Time (Duration of Ventricular Diastole)
• 2. Venous Return (Rate of Venous Flow during Filling Time)
§ ESV Influenced by:
• 1. Arterial BP (Higher à harder to eject blood à ESV Increases)
• 2. Force of V.Contraction (Higher à more blood ejected à ESV Decreases)

§ Regulation of SV:
• PreLoad: Degree of Stretch of Heart Muscle:
o The degree of Stretching of the Heart Muscle during Ventricular Diastole.
§ Caused by amounts of blood from venous return.
o Preload ↑ as EDV↑. (Directly Proportional)
§ ↑End Diastolic Volume = ↑Stroke Volume (Frank-Starling Law)
o Affects % of actin/myosin contact in myocytesà Affects cross-bridge cycling:
§ à Affects muscle’s ability to produce tension.
o Preload Varies with demands placed on heart.
o Contractility:
§ Inotropy
§ Force produced during contraction at a given Preload.
§ Influences End Systolic Volume (↑Contractility = ↓ESV)

• Afterload: Back Pressure Exerted by Arterial Blood:
o The tension needed by Ventricular Contraction to Open Semilunar Valve.
§ Ie. The pressure the heart must reach to eject blood.
o ↑Afterload = ↑ESV = ↓SV
o Afterload is increased by anything that Restricts Arterial Blood Flow.

• Venous Return:
o What determines the preload of the heart
o Influenced by:
§ Arterial Pressure
§ Peripheral Compliance
§ Local Blood Flow (depending on the demands of those tissues)
§ Capillary Exchange.

Week 4
Blood Vessels

Objectives:
- Functional differences between arteries/veins/capillaries
- Anatomical & functional difference of each of the vessel layers
- How Capillary Beds Work
- Explain Net Filtration Pressure of a Capillary Bed
- How Oedema occurs.

Introduction to Blood Vessels:
- 3 Classes:
o Arteries – Carry blood away from the heart
§ Elastic Arteries (Conducting Vessels)
§ Muscular Arteries (Distributing Vessels)
§ Arterioles (Resistance Vessels)
§ Terminal Arteriole
o Capillaries – Intimate contact with tissue à facilitate cell nutrient/waste transfer
• Precapillary Sphincters
§ Vascular Shunt
• MetarteriolàThoroughfare Channel
§ True Capillaries
• Continuous Capillaries
• Fenestrated Capillaries
• Sinusoids (Leaky Capillaries)
o Veins – Carry blood back to the heart
§ Post-Capillary Venule
§ Small Veins (Capacitance Vessels)
§ Large Veins (Capacitance Vessels)

- NB: Arterial blood isn’t always oxygenated; In Foetal & Pulmonary Circulation, placental & pulmonary
arteries both carry deoxygenated blood.

Blood Vessel Structure:
- 3-Layered Wall:
o Tunica Intima:
§ Ie. The layer in intimate contact with the blood (luminal)
§ Minimises friction (flow resistance)
§ Consists of The Endothelium:
• Simple Squamous Epthelium
• Lines the lumen
• Continuation of the Endocardium (inside lining of the heart)
§ Larger vessels have a Sub-Endothelial Layer:
• Basement membrane...&
• Loose Connective Tissue.
o Tunica Media:
§ Middle....& Thickest layer
• Circulating Smooth Muscle
• Sheets of Elastin
§ Regulated by Sympathetic Nervous System + Chemicals
§ Contraction/Dilation Maintains Blood Pressure.
o Tunica Externa:
§ Outermost Layer
§ Mostly loose collagen fibres
• Protection
• Reinforcement
• Anchorage to tissues
§ Contains:
• Nerve Fibres
• Lymphatics
• Vasa Vasorum (In larger vessels)
o A system of tiny vessels
o Nourish the tissues of the vessel wall


More Detail:
The Arterial System:
- Elastic (Conducting) Arteries:
o Eg. The Aorta + its major branches
o Close to the Heart.
o Thick-Walled
o Large Lumen = Low resistance
o Highest Proportion of Elastin:
§ Withstands Pressure Fluxes
§ Smoothes out Pressure Fluxes
§ ‘Stretch’ = potential energy à helps propel blood during diastole.
o Also Contain a lot of smooth muscle, but are relatively inactive in vasoconstriction.
§ Ie. Function of Elastic Arteries = simple elastic tubes.
- Muscular (Distributing) Arteries:
o Distal to Elastic Arteries
o Deliver blood to specific body organs
o Diameter: 0.3mmà1cm
o Thickest Tunica Media:
§ Due to smooth muscle
o Highest Proportion of Smooth Muscle:
§ Are active in vasoconstriction
§ Are therefore less distensible (less elastin)
- Arterioles:
o Smallest Arteries
o Larger Arterioles have all 3 Tunics (Intima/media/externa).....
§ Most of the T.Media is Smooth Muscle
o Smaller Arterioles – lead to capillary beds
§ Little more than 1 layer of smooth muscle around the endothelial lining.
o Diameter:
§ Controlled by:
• Neural (electrical) signals
• Hormonal signals (NorAdrenaline/Epinephrine/Vasopressin/Endothelin-1/etc)
• Local chemicals
§ Controls blood flow to Capillary Beds
• When constricted – tissues served are bypassed
• When dilated – Tissues served receive blood.
o Biggest controller of Blood Pressure

The Capillary System:
- Smallest blood vessels - microscopic
- Thin, thin walls – Tunica Intima Only – Ie. Only 1 layer thick.
- Average length = 1mm
- Diameter: The width of a single RBC.
o RBC’s flow through capillaries in single file
o RBC’s shape allows them to stack up efficiently against each other.
- Invades most tissues.
o (except tendons/ligaments/cartilage/epithelia. – but receive nutrients from vessels nearby)
- Main Role:
o Exchange of Gases/Nutrients/Hormones/Wastes
o Exchange occurs between Blood & Interstitial Fluid.
- 3 Types:
o Continuous Capillaries:
§ Most common
§ Abundant in Skin & Muscles.
§ ‘Continuous’ = uninterrupted endothelial lining.
• Adjacent cells form Intercellular Clefts:
o Joined by incomplete-tight-junctions
o (ie. Allow limited passage of fluids & solutes)
• NB: in the brain, the tight-junctions are complete à blood brain barrier.

o Fenestrated Capillaries:
§ Abundant wherever active absorption/filtration occurs.
• Ie. Intestines
• Kidneys
• Endocrine organs (allow hormones rapid entry to blood)
§ Similar to Continuous Capillaries but….
• Endothelial cells are riddled with oval pores (Fenestrations = windows)
• Much more permeable to fluids & solutes than continuous capillaries.

o Sinusoids (Sinusoidal Capillaries):
§ AKA “Leaky Capillaries”
§ Found ONLY in:
• Liver
• Bone Marrow
• Lymphoid Tissues
• Some Endocrine Organs
§ Large Irregularly-shaped lumens
§ Usually fenestrated
§ ‘Discontinuous’ = interrupted by Kupffer Cells:
• Remove & destroy bacteria
§ Intercellular clefts à larger + have fewer tight junctions
• Allow large molecules & leukocytes passage through to Interstitial Space.

- Capillary Beds:
o Capillaries are only effective in numbers:
§ Form networks called ‘capillary beds’
o Facilitates ‘Microcirculation’: Blood-Flow from an Arteriole à Venule
§ Consist of 2 Types of Vessels:
• Vascular Shunt:
o From Metarteriole à Thoroughfare Channel
o Short vessel – directly connects Arteriole with Venule.
• True Capillaries:
o The ones that actually take part in exchange with tissues.
o Usually branch off the Metarteriole (proximal end of vascular shunt)
o Return to the Thoroughfare Channel (distal end of vascular shunt)
o Precapillary Sphincters:
§ Smooth muscle Cuffs
§ Surround the roots of each true capillary (arterial ends)
§ Regulates blood flow into each capillary
§ Ie. Blood can either go through capillary or through the shunt.
o A Cap. Bed may be flooded with blood or bypassed, depending on conditions in the body or that
specific organ.
Vascular Anastomosis:
- Anastomosis = “Coming Together”
- Hence...where vascular channels unite
- Arteries supplying the same territory often merge (anastomose)
o Form alternate pathways
o Aka. Collaterals
- Venous Anastomoses are also very common.
- Often occur around Joints/Abdominal Organs/Brain/Heart
- Also occur between Arterioles & Venules – “Arteriovenous Anastomoses”
o Aka. = Metarteriole-Thoroughfare Channels See below sections...

The Venous System:
- Vessels carry blood back towards the Heart. (From Capillary Beds)
- Vessels gradually increase in Diameter & Thickness towards the heart.
- 2 Types:
o Venules:
§ Formed by union of capillaries (post-capillary venules)
§ Consist entirely of Endothelium
§ Extremely porous; Allows passage of:
• Fluid &
• White Blood Cells (migrate through wall into inflamed tissue)
§ The larger venules:
• Have 1or2 layers of smooth muscle (ie. Tunica Media)
• Have a thin Tunica Externa as well
o Veins:
§ Formed by union of Venules
§ 3 distinct Tunics (but walls thinner than corresponding arteries)
• Thinner walls due to lower Blood Pressure
§ Tunica Media:
• Poorly developed
• Some smooth muscle
• Some elsastin
• Tend to be thin even in large veins.
§ Tunica Externa:
• Heaviest layer (thicker than Media)
• Thick longitudinal collagen bundles
• Thick elastic networks
§ Lumens larger than corresponding arteries
• The reason 65% of body’s blood is in the veins.
• Therefore Veins: aka “Capacitance Vessels”
§ Lower Blood Pressure than arteries:
• Require structural adaptations to get blood à heart:
o Large lumen (low resistance)
o Valves
§ Venous Valves:
• Folds of Tunica Intima (resemble Semilunar Valves)
• Prevent blood flowing backward
• Ensures unidirectional flow
• Often have to work against gravity.
• If Faulty:
o Causes thrombosis (eg. Varicose veins)


Body fluid – distributed between:
- Extracellular:
o Blood Plasma
o Interstitial Fluid
- Intracellular:
o Cytoplasm

Interstitial Fluid:
- Contains Thousands of Substances:
o Amino Acids
o Sugars
o Fatty Acids
o Vitamins
o Chem. Messengers
o Salts
o Wastes...etc.

Oedema:
- Abnormal accumulation of fluid in the Interstitial Space = ie. Tissue Swelling
- Caused by: increase in Flow of Fluid à Out of Vessel OR Lack of Re-Absorption à Into Blood Vessel
- Usually reflects an imbalance in Colloid Osmotic Pressure on the 2 sides of the Capillary Membrane.
o Eg. Low levels of plasma protein (reduces amount of water drawn into capillaries.
- Contributing Factors:
o High BP (Hydrostatic Pressure):
§ Can be due to incompetent valves...OR
§ Localised Blood Vessel Blockage...OR
§ Congestive Heart Failure (Pulmonary Oedema – due to blockage in pulmonary circuit)...OR
§ High Blood Volume
o Capillary Permeability:
§ Usually due to a Inflammatory Response

Fluid Movements:
- Fluid flows across capillary walls due to 2 forces:
o Capillary Hydrostatic Pressure:
§ The force the blood exerts against the capillary wall.
§ Hydrostatic pressure = capillary blood pressure ≈35mmHgArterial End /15mmHgVenous End
§ Tends to force fluids through the capillary’s Intercellular Clefts (between endothelial cells)
• Capillary hydrostatic pressure drops as blood flows from arteriole à venule.
§ Net Hydrostatc Pressure = Capillary Hydrostatic Pressure – Interstitial Hydrostatic Pressure.
• NB: Interstitial Hydrostatic Pressure ≈ 0mmHg

o Colloid Osmotic Pressure:
§ Opposes hydrostatic pressure
§ Due to large, non-diffusible molecules (Plasma Proteins) drawing fluid into capillaries.
§ Typically ≈25mmHg
• Relatively constant at both Arterial & Venous ends
§ Net Osmotic Pressure = Capillary Osmotic Pressure – Interstitial Osmotic Pressure.
• NB: Interstitial Osmotic Pressure ≈ 1mmHg

- Hence Fluid is Forced Out @ Arterial End & Reabsorbed @ Venous End
- The amount of fluid forced out – determined by the balance of net Hydrostatic & Osmotic forces.
o Ie. Net Filtration Pressure = Net Hydrostatic Pressure – Net Osmotic Pressure

Injury to blood vessels
1. Early Athersclerotic lesions - lipid streaks.
i. Ie the formation of fatty plaques
ii. Fatty plaques begin to ulcerate
iii. NB: Arterosclerosis is different = hardening of the vessel wall

2. Coronary Blockages due to fatty plaque buildup
i. Due to processed foods, saturated fats, bad diet.
ii. Tends to be seen in many people these days

o Elastic Arteries:
• Elastic due to concentric sheets of elastin
• Can, however, lose their elasticity
• Due to having thinner walls, they're more prone to aneurysm (bulging & potentially rupturing)
§ Results in pooling of blood --> eventual rupture.

o Muscular Arteries:
• Those supplying specific organs
• Less elastin, more muscle
• Only a single sheet of elastin
§ More likely to have a tear in vessel wall.
• Dissecting aneurysms (blood builds up between the layers of the wall & eventually press the vessel
closed)
Smooth Muscle & Movement of Blood:
o Elastic Vessels:
• Limited effect due to small muscle layer
• Mainly elasticity mobilises blood
o Muscular Vessels:
• Muscle will prevent rapid movement (vasoconstriction)
• Control vessel diameter & influences BP (More next week)

Nervous System input in smooth muscle in arteries & its role in vasoconstriction:
o Alpha adrenergic receptors in smooth muscle of vasculature
o Sympathetic releases NA = vasoconstriction
o Beta Adrenergic receptors in coronary arteries --> Vasodilation --> increases blood flow to the heart
o Skeletal muscle blood vessels have Beta 2 recepors & some muscarinic receptors....why:?

Key Concepts of This Week:
o Arterial System
• Vessel structure:
§ Layers
§ Wall structure
• Movement of blood
§ In each of the 3 artery types:
§ Ie. Elastic arteries use their stretch...but in Muscular arteries & arterioles...blood moves due to
pressure gradients
• Smooth Muscle
§ Constriction
§ Dilation
§ Highly innervated by the sympathetic NS
• Alpha Receptors (systemic vasculature)
• Beta (coronary vasculature)
o Venous System:
• Vessel Structure:
§ Larger lumen
§ Collapsible
• Venous Return:
§ Valves
§ Muscular Pump
§ Respiratory Pump (by breathing in, the vessels in abdomen are compressed, milking blood back to
the heart....while in the chest, the vessels are opened up...)
o Capillary System:
• Vessel Structure:
§ 3 types
• Capillary Bed:
§ Vascular shunt (metarteriole thoroughfare channel)
§ Precapillary sphincters
• Movement of fluid:
§ Pressure gradients (arteriole end & venule end) IE. Capillary Hydrostatic Pressure
§ Coloid Osmotic Pressure - due to plasma proteins in blood drawing fluid from interstitial space.
o Location of Major blood vessels:
• Coronary Vessels - all major ones
§ + what part of the heart these vessels are supplying
• Others: use the page numbers below in marieb.
§ Know:
• The blood vessels to this level of detail:
• Marieb P.746-747 Table 19.4
• Marieb P.758-9 Table 19.9



Week 5
Control of Circulation (Haemodynamics & BP Regulation)

Blood Flow:
- The Amount of blood flowing through a vessel/organ/system per unit time. (mLs/min)
- Determined by pressure gradient & resistance.
- NB: NOT SPEED
o Systemic Blood Flow = Cardiac Output (relatively constant)
o Specific Organ Blood Flow – may vary widely due to its immediate needs.

Velocity of Flow:
- Velocity of Flow ≠ Blood Flow:
o Blood Flow = AMOUNT of flowing blood. (mL/min)
o Velocity of Flow = SPEED of flowing blood. (mm/sec)
o NB: A constricted vessel will have a lower flow rate, but a higher velocity of flow. (ie. Garden hose)
o NB: Velocity tends to change by a greater magnitude than the change in Flow Rate.

Blood Pressure: (**continued on page 4)
- The Pressure exerted on the vessel wall by contained blood. (mmHg)
- Decreases with distance from heart. (arterial system)
- Decreases with 10%+ decrease blood volume.
- Increases with vessel constriction (provided same blood volume)

Resistance:
- The amount of Friction blood encounters as it passes through the vessels.
- 3 Factors Influencing Resistance:
o Blood Viscosity (↑Viscosity = ↑Resistance... Fairly Constant)
o Total Vessel Length (longer vessel = ↑ resistance... Fairly Constant)
o Vessel Diameter (thinner vessel = ↑↑resistance...Frequently Changes)
§ Most Responsible for changes in BP
- Systemic Vascular Resistance = Combination of the Above Factors

Relationship Between Flow, Pressure & Resistance:
- 1. Flow is Directly Proportional to Pressure Gradient between 2 points (Change in Pressure)
- 2. Flow is Inversely Proportional to Resistance
- Therefore:
'()**+() ,(-./)01 (∆')
!"#$ ! =
5)*/*1-06)

NB: Resistance is far more important in determining local blood flow than the Pressure Gradient.

Effects of Vasomotion on Rate & Velocity of Flow:
- Constriction/Dilation:
- Changes Vessel Diameter:
o Influence on Flow Rate:
§ The Flow Rate is directly proportional to the 4th Power of the Vessel Diameter.
§ Ie. Small changes in vessel diameter à Changes Flow Rate by an exponent of 4.
(Poiseuille’s Law)

o Influence on Flow Velocity:
§ Flow Rate is inversely proportional to the vessel’s cross-sectional area.
§ Ie. An ‘α’ x Increase in cross-sectional area à Decreases Flow Velocity by a factor of ‘α’.

Properties of the Systemic Circuit:
- a) Individual Vessel Diameter:
- b) Total Combined Cross-Sectional Area of Vessels:
- c) Average Local Blood Pressure:
- d) Local Velocity of Blood Flow:

Blood Pressure Continued:

Factors Influencing Blood Pressure (Long Term):
- Cardiac Output:
o ↑Cardiac Output = ↑ BP
- Peripheral Resistance:
o Causes backpressure in blood (arterial system)
- Blood Volume:
o (assuming constant vessel diameters) ↑Blood Volume = ↑BP
o Its affect depends on vessel compliance

BP = Cardiac Output X Total Peripheral Resistance
Types of Blood Pressures:
- Systolic:
o Peak Aortic pressure reached during ventricular systole.
o Function of:
§ Peak rate of ejection
§ Vessel wall compliance
§ Diastolic BP
o Normal = 120mmHg
- Diastolic:
o Lowest Aortic pressure reached during ventricular diastole, due to blood left after peripheral runoff.
o Function of:
§ Blood Volume
§ Heart Rate
§ Peripheral Resistance
o Normal = 80mmHg
- *Pulse Pressure:
o Difference in Systolic & Aortic Pressure (120mmHg – 80mmHg)
o Normal = 40mmHg
o If Lower – may be an indication of Aortic Stenosis or Atherosclerosis (slowed peripheral runoff)
- *Mean Arterial Pressure (MAP):
o MAP = Diastolic Pressure + 1/3(Pulse Pressure)
o *The Pressure that Propels Blood to the Tissues – maintains Tissue Perfusion (see below sections).
§ Maintains flow through capillary beds
o Must be high enough to overcome peripheral resistance – (if not blood doesn’t move)
o Finely Controlled: See Below:

Tissue Perfusion:
- Blood flow to the tissues.
- Adequate Tissue Perfusion for:
o Demands (O2/nutrients) of organs/tissues.
o Gas exchange in lungs
o Nutrient Absorption in GIT
o Urine formation in Kidneys.

Control of MAP:
- 3 Main Regulators:
o 1. Autoregulation (Local):
§ ‘The automatic immediate adjustment of blood flow to each tissue relative to the tissue’s
requirements at any instant.’
§ Local (tissue bed) Level
• Ie. Control of flow within a single capillary bed.
• Ensures perfusion of the ‘Needy’ Tissues.
§ Short Term – Immediate Adjustments – Due to:
• Metabolic Controls: à Vasodilation:
o Low Oxygen levels
o Low Nutrient levels
o Nitric Oxide
o Endothelin
o Inflammatory Chems: (histamine/kinins/prostaglandins)
o NB: Was thought that Symp-ANS dilates à wrong! It only Constricts!
• Myogenic Control: à Vasoconstriction:
o Sheer Stress: Vascular smooth muscle responds to passive stretch
(↑vascular pressure) with increased tone.
§ Prevents excessively high tissue perfusion that could rupture smaller
blood vessels.
o Reduced stretch promotes vasodilation à flow increases.
o 2. Neural Mechanisms:
§ Short-term Immediate adjustments:
§ Aims to:
• Adjust Cardiac Output
• Maintain adequate MAP by altering vessel diameter.
• Alter blood distribution due to specific demands of various organs.
§ Mediated by the Nervous System.
• Respond to changes in Arterial Pressure & Blood Gas Levels.
o Vasomotor Centres:
§ Neuron Cluster in Medulla:
• Take info from receptors:
o Baroreceptors (primarily)
o Chemoreceptors (lesser degree)
• Transmit impulses via SNS:
o ↑ sympathetic activity = vasoconstriction = ↑ BP
o ↓ sympathetic activity = vasodilation = ↓ BP
o CardioVascular Centres of ANS:
§ CardioAcceleratory (Sympathetic):
• Active in times of Stress
• ↑HR & Contractility
§ CardioInhibitory (Parasympathetic)
• Active at Rest
• ↓Heart Rate

Effects of CV Centres on Cardiac Output


Baroreceptor Reflex

Chemoreceptor Reflex
o 3. Endocrine Mechanisms:
§ More Long Term BP & Bl-Volume regulation:
§ AT THE KIDNEY LEVEL:
• **Antidiuretic Hormone (ADH) – AKA. Vasopressin:
o Released due to Low blood volume
• Angiotensin II:
o Released due to Low blood pressure
o Potent VasoConstrictor
o Increases CO & Blood volume
o (NB: ‘ACE’ (Angiotensin I Converting Enzyme) activates it to Angiotensin II.
Hence ‘ACE-Inhibitors’ are often used as AntiHypertension medicine)
• Erythropoietin:
o Released due to Low Pressure & Low O2 Levels.
o Increases RBC production to increase Blood Volume.
• Natriuetic Peptides:
o Released by the heart due to High Blood Pressure & Volume.
o Inhibits ADH & Angiotensin II à Reduces BP & Volume.



Week 6
Hypertension & Shock

Hypertension:
- What is it?:
o Consistent Diastolic of +90mmHg AND/OR
o Consistent Systolic of +140mmHg.

- General Info:
o Is a Risk Factor For:
§ Coronary Artery Disease
§ Stroke
§ Heart Failure
§ Renal Failure
§ Peripheral Vascular Disease
o Big problem in Aus – 2.2Mil People à $1Bilion/Year
o Usually Asymptomatic – many don’t know they have it.
o Often Misdiagnosed Due To:

- Classifications (In Adults):
o Different Classes Based on BP Ranges:
- 2 Types of Hypertension:
o (Based on Aetiology.)
o 1. Primary (Essential) Hypertension:
§ 90-95% of cases
§ No specific cause.
§ But Related to:
• Obesity
• ↑Cholesterol
• Atherosclerosis
• ↑Salt Diet
• Diabetes
• Stress
• Family History
• Smoking
§ Diastolic Hypertension:
• Elevated Diastolic Pressure
• Relatively Normal Systolic (or slightly elevated)
• Mostly Middle-Aged Men
§ Isolated Systolic Hypertension:
• Elevated Systolic Pressure
• Normal Diastolic Pressure
o Ie. High Pulse Pressure
• In Older Adults (60yrs+):
o May be due to reduced compliance of the aorta with increasing age.
• In Younger Adults (17-25):
o May be due to Overactive Sympathetic NS à ↑Cardiac Output
o Or Congenitally Stiff/Narrow Aorta

o 2. Secondary (Inessential) Hypertension:
§ 5-10% of cases
§ Secondary to Another Diseases – Eg:
• Renal Disease.
• Endocrine Disorders
• Pregnancy (Pre-Eclampsia) – in 10% of pregnancies. (@ 20wks of gestation)
• Other –, Cancers, Drugs, Alcohol

- Organ Damage Caused By Hypertension:
o Relationship between Degree of hypertension & Degree of Complications.
o Heart:
§ Increased Afterload:
• ↑ Workload of Heart à ↑Afterload à Pumps Harder à Hypertrophy à Failure
§ L-Vent. Hypertrophy:
• To compensate for higher workload
• à Compromised L-Ventricular Volume à ↓Stroke Volume à↓Cardiac Output

o Lungs:
§ Pulmonary Congestion:
§ Backing up of blood in Pulmonary Circuit.
§ Why: ↑BP = ↑Aortic-BP = ↑Afterload = ↓SV = ↑ESV = ↓Pulmonary Blood Flow

o CerebroVascular:
§ Stroke – Typically Intracerebral Haemorrhage
§ Rupture of Artery/Arterioles in brain

o Aortia/Peripheral Vascular:
§ Arterial Mechanical Damage (eg. Aneurysms/Dissecting Aneurysms)
§ Accelerated Atherosclerosis

o Kidneys:
§ Nephrosclerosis – (hardening of kidney blood vessels)
§ Renal Failure
- Short-Term Control of BP:
o The Baroreceptor Reflex:
- Risk Factors Of Hypertension:
o Age:
§ BP normally increases with age.
• Baby: 50/40
• Child: 100/60
• Adult: 120/80
• Aged: 150/85 (quite normal)
§ Due to Loss of Elasticity of Blood Vessels with age - Compliance↓.
§ & Atherosclerosis

o Race:

o Obesity:
§ Fatty Diet à Atherosclerosis
§ Body Fat à kms more vessels à ↑Peripheral Resistance à Hypertension
§ Physical Weight of fat – may impede venous return
§ Kidney Dysfunction à Loss of long-term BP (Blood Volume) Control.

o Excess Na+ Intake:
§ If Normal Kidney Function:
• Na+ intake à Slight BP increase (due to fluid retention)
• But Excess Na+ & H2O excreted by kidneys à BP returns to normal.
§ If Impaired Kidney Function:
• Na+ intake à Larger BP increase...
• Because Excess Na+ & H2O Not excreted by kidneys (less efficiently)

- Basic Hypertension Treatment Plan:
- AntiHypertensive Drugs:
o Diuretics:
§ Increases urination à ↓Blood Volume
§ Aim = To reduce workload on heart by reducing preload
o Sympatholytics:
§ Reduces Sympathetic Activity (Prevents ↑HR/↑Contractility = Decrease in CO)
§ ‘Beta-Blockers’.
o Vasodilators:
§ Reduce Peripheral Resistance
§ à Reduce Afterload
§ à Reduce Workload on Heart.
o Renin-Angiotensin Antagonists (ACE Inhibitors):
§ Decreases affects of Renin-Angiotensin System:
• Decreases Sympathetic Drive
• Decreases Vasoconstriction
• Decreases Fluid Retention
• Decreases Preload
• Decreases Afterload

↑....For your own Interest....↑

Shock:
- What is it?:
o Profound Haemodynamic/Metabolic Disorder due to Inadequate Blood Flow & O2 Delivery.

- Common Causes:
o Hypovolemic Change:
§ Severe Dehydration
§ Haemorrhage
o Cardiogenic Change:
§ Heart Failure (heart isn’t getting enough blood out)
§ ↓Venous Return
o Distributive Alteration:
§ Excessive metabolism – ie. Even a normal CO is inadequate.
§ Abnormal Perfusion Patterns – ie. Most of CO perfuses tissues other than those in need.
§ Neurogenic Shock – Ie. Sudden loss of Vasomotor Tone à Massive VenoDilation.
§ Anaphylactic Shock – Drastic Decrease in CO & BP due to Allergic Reaction
§ Septic Shock – Disseminated bacterial infection in Body à Extensive Tissue Damage.

- 3 Stages of Shock:
o 1. Non-Progressive:
§ Stable, not self-perpetuating.
§ Symptoms:
• Hypotension (Low BP)
• Tachycardia (High HR – body’s attempt to compensate for poor perfusion)
• Tachypnoea (High Breathing-Rate – Phrenic Nerve Stimulation – Diaphragm)
• Oliguria (Low Urine Production by Kidney)
• Clammy Skin
• Chills
• Restlessness
• Altered Consciousness
• Allergy symptoms (if anaphylaxis)
§ The Body’s Compensatory Mechanisms (below) will prevail without intervention.
• Aim to increase BP:
o 2. Progressive Stage:
§ Unstable, viscous cycle of Cardiovascular Deterioration – Self-Perpetuating.
§ Compensatory Mechanisms are insufficient to raise BP.
§ Perfusion continues to fall à Organs become more Ischemic (incl. Heart à Failure)
• Cardiac Depression (due to O2 Deficit to Heart)
• Vasomotor Failure (due to O2 Deficit to Brain)
• “Sludged Blood” (Viscosity ↑. – Harder to move)
• Increased Capillary Permeability
§ Symptoms:
• Beginning of organ failure
• Severely Altered Consciousness
• Marked Bradycardia (initially tachycardic – but now the body is giving up)
• Tachypnea (Fast Breathing) with Dyspnea (No breathing)
• Cold, lifeless skin
• Acidosis - (CO2 equation affected)
§ Treatment:
• Identify & Remove Causative Agents
• Volume Replacement for Hypovolemia
• If Septic Shock: Antibiotics
• Sympathomimetric Drugs: If Neurogenic Shock (loss of vasomotor tone -vasodilation)
§ Fatal if untreated.

o 3. Irreversible Stage:
§ Advanced stage where the body is irrecoverable.
§ Usually any form of therapy is ineffective.
• Eg. Transfusion is ineffective because the tissue/organ damage is too advanced.
§ Symptoms:
• Organ Dysfunction (Renal/Cardiac/Pulmonary/CNS)
• Renal Failure
• Heart Failure
• Severely compromised CO & BP
• Worsening Acidosis
• Ischaemic Cell Death
• Coma.

Shock-Induced Cell Death
- Self Perpetuating Cascade
Week 8
Myocardial Ischaemia

‘Ischaemia’:
• = Restraint of Blood (Ie. Insufficient Blood)
• Leads to Imbalance Between Oxygen Supply & Demand.
• Oxygen Supply – Increased By:
o ↑Coronary Blood Flow:
§ ↑Aortic, Diastolic Perfusion Pressure:
• Aortic Pressure During L-Ventricular Diastole
• If High à ↑Coronary Perfusion
• Influenced by:
o Hypotension
o Aortic Regurgitation
§ ↓Coronary Vascular Resistance:
• Resistance to Coronary Blood Flow
• Depends on Vascular Diameter...
• Influenced by:
o External Compression (eg. Oedema)
o Intrinsic Regulation (Dilation/Constriction).
§ Metabolites
§ Neural
o ↑O2-Carrying Capacity of Blood:
§ Influenced By:
• Hb Saturation
• Hb Levels (Anaemia)
• Blood pH
• CO Poisoning
• Lung Disease
• Oxygen Demand – Increased By:
o ↑Wall-Tension Force:
§ ↑Preload – (Degree of Stretch of Myocardium):
• The degree of Stretching of the Heart Muscle during Ventricular Diastole.
§ ↑Afterload – (Back Pressure Exerted by Arterial Blood):
• The tension needed by Ventricular Contraction to Open Semilunar Valve.
o ↑Heart Rate (Chronotropic State)
o ↑Force of Contraction (Inotropic State)

*Ischaemia Vs. Hypoxia Vs. Infarction:
• Ischaemia: A ‘FLOW’ Limitation, Typically due to Coronary Artery Stenosis (Narrowing)
• Hypoxia: An ‘O2’ Limitation,Typically due to High-Altitude/Respiratory Insufficiency/etc.
• Infarction: Irreversible Cell-DEATH, Typically due to sustained Ischaemia.
• NB: Ischaemia can lead to Hypoxia & Infarction.

Myocardial Ischaemia:
- Largest Cause of Deaths (50% of all deaths) in Western Society
- Mostly Attributed to ↓Coronary Blood Flow – Due to Plaque/Thrombosis.
- Regional Ischaemia:
o Ischaemia Confined to Specific Region of Heart.
o Due to Plaque/Thrombosis
- Global Ischaemia (Rare):
o Ischaemia of Entire Heart
o Due to Severe Hypotension/Aortic Aneurysm/Open-Heart-Surgery

What Happens During Myocardial Ischaemia:
- Myocardial Damage:
o Inner-Myocardium will become Ischaemic first, then progress Outwards.
o (Same with necrosis/infarction)

- Metabolic Changes – (Aerobic à Anaerobic):
o ↑Lactate (Anaerobic Metabolism), ↓pH
o ↓ATP, ↑ADP, ↑Pi
o ↓Glycogen
- Pain:
o Nociceptor (pain receptor) Activation à Angina Pain
- Acute Ischaemic Attack:
o SNS & PNS Stimulation à Tachycardia, Sweating, Nausea......
- Reversible Cell Injury:
o ↓Blood-Flow à ↓Myocardial Relaxation (diastolic) à Stiffening of L-Ventricle à ↑LVDP
- Reperfusion Injury:
o Cell Damage that occurs When Blood Supply is Restored (after being stopped)
o Due to inflammation and oxidative damage through the induction of oxidative stress.
- Pulmonary Congestion:
o Stiffening of L-Ventricle & ↑LVDP à ↑Pulmonary Vascular Pressure
§ à Pulmonary Congestion
§ à Shortness of Breath
- Ventricular Arrhythmias:
o Due to Myocyte Ion-Disturbances:
§ ↑ Extracellular K+
§ ↑ Intracellular Na+
§ ↑ Intracellular Ca+ (“Calcium-Loading”) – If Ischaemia is Prolonged à Irreversible Damage
o à Alters Conduction Patterns of the Heart à Arrhythmias


Clinical Presentations of Myocardial Ischaemia:
- Ischaemic Heart Failure:
o Weakness of Heart Muscle à Difficulty Breathing + Peripheral Oedema
- Angina Pectoris:
o Substernal/Precordial Chest Pain – Due to Myocardial Ischaemia à No Cell Necrosis
o Pain Usually lasts up to 15min.
o 3 Subtypes:
§ Stable Angina (Typical):
• Angina-Pain During Exertion/Stress
• No Permanent Injury
• ST-Depression (Indicates Subendocardial Ischaemia)
• Treated with Vasodilators
§ Variant Angina (Prinzmetal):
• Angina-Pain Unrelated to Activity
• Due to Coronary Vascular Spasm
• ST-Elevation (Indicates Transmural Ischaemia)
§ Unstable Angina (Dangerous):
• Occurs @ Rest – Prolonged Pain
• Increasing Frequency & Duration of Angina-Pain
• Due to unstable Atherosclerotic Plaque
• Can Lead to Myocardial Infarction (if untreated)
- Silent Ischaemia:
o No Pain
o Abnormal ECG (ST-Elevation)

Prolonged Ischaemic à Irreversible Damage à Leads to:
- Ca+ Loading Within Cell:
o Ca+ Recycling Cycle (between Sarcoplasmic Reticulum, Sarcoplasm & Actin) Changes.
o Marks the transition between Reversible & Irreversible Damage.
- Heart Failure – Due to:
o Lethal Arrhythmias
o ↑LVDP à Pulmonary Congestion à R-Heart Failure.
- Infarction (Necrosis):
o Irreversible Cell Death – Due to Ischaemia/Acute Thrombus
o Myocyte Membrane damage à Cell Enzymes/Proteins into Blood à Used as blood Markers:
§ Troponin I (Preferred)
§ Creatinine Kinase
ECG Changes Due to Ischaemia:
- Normally:
o QRS = Ventricular Depolarisiation
o T-Wave = Ventricular Repolarisation
§ NB: Ven.Repol – Very sensitive to myocardial perfusion. (ie. Lack of blood supply alters
Ven.Relaxation)

- Subendocardial Ischaemia:
o Poor Perfusion à Altered Ven.Repolarisation à
§ ST-Depression
§ T-Wave Inversion
- Transmural Ischaemia:
o Full-thickness of the heart wall is damaged à Altered Ven.Repolarisation à
§ ST-Elevation

Myocardial Infarction (Heart Attack):
- *90% Infarcts due to Thrombosis from Ruptured Atherosclerotic Plaque.
- Diagnosis Requires 2 of the Following:
o History of Ischaemic-Related Chest Pain:
§ Eg. Angina
o Changes on Sequential ECGs:
§ ST-Segment Elevation à Indicates Transmural Ischaemia:
• Where the full-thickness of the heart wall is damaged.
• NB: ST-Elevation isn’t always due to MI.
o Rise/Fall in Serum Cardiac Markers:
§ Spilt contents of dead cells à Blood
§ Eg. Cardiac Troponin & Creatinine Kinase
- Ensuing Inflammatory Response:
o When Cells Die à Neutrophils Infiltrate Area à Attack/Decompose/Phagocytose Dead Cells
o After Inflammatory Response à Fibrosed Scar Tissue (Such Tissue in Heart is Non-Contractile*)


Week 12
The Ageing Heart

What Happens in an Normal Ageing Heart?:
- Physical Changes:
o Heart Dilation – (Lumen Size of L-Atrium & L-Ventricle Increases with Age.)
o Increased Capillary Density
o Valves become calcified – (Mitral Valve closes more slowly with age à ↑L-Vent. Filling Time)
o Fibrosis increases
o Arteries become less compliant
- Histological Changes:
o The number of myocytes decreases
o The remaining myocytes enlarge
o Heart Wall thickens to compensate for extra stress from stiffer blood vessels.
- Functional Changes:
o Decreased Heart Rate During Exercise
o Decreased Contractility
- Physiologic Changes:
o Myocardial metabolism decreases (Reduced mitochondrial metabolism)
o Altered Sarcoplasmic Reticulum function (Lower Ca+ in SR & Fewer Ca+ pumps/cell) à decreased
contractility
- Sensitivity Changes:
o β-Adrenergic Sensitivity Decreases
§ (less Ca+ enters the cell à Max HR & Contractility decreases)
o Baroreceptor Sensitivity Decreases
o Chemoreceptor Sensitivity Decreases
- Conductivity Changes:
o Conduction pathways become calcified
o Reduced Number of SinoAtrial Node Pacemaker-Cells à DECREASED HEART RATE
o Impaired Sinoatrial (Pacemaker) Function à Atrial Fibrillation, Arrhythmias

- NB: These Changes = Normal = “Normal Ageing Myopathy”

These Above Changes Make Old Age a Risk Factor For Heart Failure:
- Incidence of Chronic Heart Failure Increases with Age...WHY?
o 1. The above changes may interact with each other à Heart Failure
§ Eg. Decreased Myocytes (contractility) + Valve Calcification à ↓SV à Heart Failure

o 2. The above changes may interact with an existing cardiovascular disease:
§ Eg. Valvular Stenosis + Fibrosis + Less Compliant Arteries à ↓SV à Heart Failure
§ Eg. Atherosclerosis + ↓Contractility à ↓Coronary Perfusion à Ischaemia à Heart Failure
§ Eg. Hypertension + Calcified Valves + Less Compliant Arteries à ↓SV à Heart Failure

- Ie. The normal physiological effects of ageing, even if healthy, increases the presence of many Heart-
Failure Risk Factors.

Healthy 20yr-old Vs. Healthy 80yr-old (At Rest)
- Heart Rate (Resting) is 10% Lower in Old Heart:
o Older hearts have a 10% lower Resting Heart Rate than Young.

- Stroke Volume (At Rest) is 10% Higher in Old Heart:
o Ie. An Old Heart pumps 10% more blood/beat than a Young Heart (At Rest), despite being a weaker
pump.
o ...How?:
§ Older Heart Compensates for its ↓Contractility by Dilating more during Diastole to Increase
Ventricular Filling (Preload/End-Diastolic Volume) à ↑Stroke Volume.

- Same Resting Cardiac Output:
o Ie. An Old Heart pumps out the same amount of blood/min (at rest) as a Young Heart.
o ...How?:
§ Older hearts have a 10% Higher Stroke Volume + but 10% Lower Heart Rate à Same Cardiac
Output (At Rest) compensates for its ↓Contractility by Dilating more during Diastole to
Increase Ventricular Filling (Preload/End-Diastolic Volume) à ↑Stroke Volume.
o However, the older heart has a narrower ‘Scope’ for Activity – Meaning it can only match a young
heart’s increase in Stroke Volume (during exercise) up until a point, after which the younger heart is
superior.

- Same Resting Ejection Fraction:
o Ie. An Old Heart has the same ‘Ejection Fraction’ (≈67%) as a Young Heart.
§ NB: Ejection Fraction = The Percentage of The End Diastolic Volume Ejected Each Beat.
o However, the older heart has a narrower ‘Scope’ for Activity – Meaning it can only match a young
heart’s Increase in Ejection Fraction (during exercise) up until a point, after which the younger heart
is superior.

Healthy 20yr-old Vs. Healthy 80yr-old (During Exercise):
- Higher Preload/End-Diastolic Volume (During Exercise) in Older Heart:
o The older heart compensates for its ↓Contractility by Dilating more & Decreasing Heart Rate to
Increase Filling Volume & Filling Time à ↑Preload
§ Increased Preload (End-Diastolic Volume) à ↑Stroke Volume.

- Lower Max. Heart Rate (During Exercise) in Older Heart:

- Same Stroke Volume (During Exercise):
o Due to Increased Preload/EDV via Dilation & ↓HR.

- 25% Lower Cardiac Output (During Exercise) in Older Heart:
o Primarily Due to decreased heart rate. NB: SV stays same.
§ (The young heart can increase CO from 5L/min @ rest to about 35L/min)
§ (The old heart can only increase CO from 5L/min @ rest to about 15L/min)

- Lower VO2max (Max O2 Consumption) in Older Person:
o Old Person’s VO2max is half that of a Young Person.
o Due to:
§ Lower Muscle Mass (Ie. Less muscle uses less energy à ↓O2 Consumption)
§ Changes in Muscle Metabolism (↓enzyme efficiency/manufacture etc.)
§ Decreased Number of Mitochondria/Cell.

- Lower Max. Ejection Fraction (During Exercise) in Older Heart:
o Young heart can increase its ejection fraction from 67% à 89%.
§ - by ↑Contraction & ↑Heart Rate.
o However, the Old heart can only increase its EF from 67% à 71%.
§ - by Dilating.

Summary:
- Young Heart: In Exercise – its contractility is higher, so when the body requires a higher cardiac output, the
heart contracts more than normal by balling up tighter in each contraction à decreasing End-Systolic
Volume à Increasing Stroke Volume à Increasing Cardiac Output.

- Older Heart: In Exercise – Its contractility is lower (Approx 60% lower than 20yr old heart – mostly due to
sedentary lifestyle), so when the body requires a higher cardiac output, the heart compensates by dilating
more to increase filling (End-Diastolic Volume) à Increasing Preload àIncreasing Stroke Volume à
Increasing Cardiac Output.

- NB: This compensatory mechanism of Dilating to increase L-Heart Pressures can lead to Symptoms of Heart
Failure (Ie. Shortness of Breath, Loss of Pump Function & Pulmonary Oedema). However, this is not strictly
Heart Failure, because Cardiac Output is not Severely Compromised.

Benefits of Aerobic Exercise on CardioVascular Ageing:
- Huge Benefits:
o ↑Max O2 Consuption
o ↑Ejection Fraction
o ↑Contractility
o (↑Contractility à Less need to Dilate for Increased Stroke Volume)
o Less Dilation à ↓EDV & ↓LAP.
o Less Arterial Stiffness.
- Ie. It seems that a large part of CV-Ageing is Related to a Sedentary Lifestyle.

Combating CV-Ageing with Pharmaco-Therapies:
- Drugs that ↑Vascular Compliance
- Drugs that reduce Cardiac Fibrosis
- Drugs that reduce Ventricular Hypertrophy
- Antioxidants – Prevents damage due to free radicals
- Anti-Inflammatory Drugs – CV-Ageing has a small underlying inflammatory component.
- Exercise

CARDIOVASCULAR Pathology:
ACUTE CARDIOGENIC PULMONARY OEDEMA
ACUTE CARDIOGENIC PULMONARY OEDEMA

- Aetiology:
o Severe Decompensated LV-Failure (CCF)
- Pathophysiology:
o Severe Decompensated LV-Failure (CCF) Fluid Accumulation in Alveoli & Interstitium Dyspnoea
Impaired Gas Exchange & Respiratory Failure
- Clinical Features:
o Symptoms:
Tachycardia
Tachypnoea
Diaphoresis
Wet Cough w. Frothy Sputum
o Signs:
Respiratory Distress ( SpO2)
Bi-Basilar Crackles
Splitting of S2
Dullness to Percussion
(+/- Signs of RV-Failure [↑JVP, Peripheral Oedema, Ascites])
- Investigations:
o CXR – (Pulmonary Congestion/Oedema, Cardiomegaly, Effusions)
o ECG – (Dx Previous/Current IHD, Rule out Arrythmias)
o Echo (TTE) – (Assess Ventricular Function [Ejection Fraction])
o +(FBC [ Hb/Infection], UEC, eLFT [Alcohol], TSH [↑Thyroid], Lipids [IHD], BSL/HbA1c [Diabetes])
- Management:
o Pt will most likely already be on CCF Regime. Ie:
ACEi (Perindopril) / ARB (Candesartan)
B-Blocker (Carvedilol)
Diuretics (Frusemide / Spirinolactone)
Fluid Balance (Daily weights/Fluid restriction/ Na diet)
o “LMNOP” Protocol:
L – Lasix (↑Diuresis & Fluid Restriction) – [Frusemide / Spirinolactone]
M – Morphine (Anxiolytic & Vasodilation)
N – Nitrates (GTN)
O – Oxygen
P – Positive Pressure Ventilation (CPAP / BiPAP)
HEART FAILURE . . . CONT.
❏ other agents
• ß blockers - recommended for functional class (FC) II-III patients
• should be used cautiously, titrate slowly because may initially worsen CHF
• postulated that these agents interfere with neurohormonal activation
• carvedilol confers survival benefit in FC II-III CHF
• metoprolol has been shown to delay time to transplant, decreased hospitalizations in dilated
cardiomyopathy and to decrease mortality (MERIT study)
• CCB (have equivocal effect on survival)
• antiarrhythmic drugs
• if required, amiodarone is drug of choice
• class I anti-arrhythmics associated with increased mortality in CHF
ACUTE CARDIOGENIC PULMONARY EDEMA
Definition
❏ left-sided backward heart failure leading to severe pulmonary congestion with extravasation of capillary fluid
into the pulmonary interstitium and alveolar space
Clinical Manifestations
❏ tachycardia, tachypnea, diaphoresis
❏ severe left-sided venous congestion
Management, use mnemonic "LMNOP"
❏ make sure to treat any acute precipitating factors (e.g. ischemia, arrhythmias)
❏ sit patient up with legs hanging down if blood pressure is adequate
❏ L - Lasix - furosemide 40 mg IV, double dose q1h as necessary
❏ M - Morphine 2-4 mg IV q5-10 minutes
• decreased anxiety
• vasodilation
❏ N - Nitroglycerine topical 2 inches q2h (or IV)
❏ O - Oxygen
❏ P - Positive airway pressure
• (CPAP or BiPAP) decreased need for ventilation and decreased preload
❏ other vasodilators as necessary in ICU setting
• nitroprusside (IV)
• hydralazine (PO)
• sympathomimetics
• potent agents used in ICU/CCU settings
• dopamine
• agonist at dopamine D1 (high potency), ß1-adrenergic (medium potency),
and α1-adrenergic receptors (low potency)
• "low-dose" causes selective renal vasodilation (D1 agonism)
• "medium-dose" provides inotropic support (ß1 agonism)
• "high-dose" increase systemic vascular resistance (SVR),
which in most cases is undesirable (α1 agonism)
• dobutamine
• acts at ß1 and α1 adrenoceptors
• selective inotropic agent (ß1 agonism)
• also produces arterial vasodilation (α1 antagonism)
• phosphodiesterase inhibitors (amrinone, Inocor)
• effects similar to dobutamine (inhibits PDE ––> cAMP ––>
inotropic effect and vascular smooth muscle relaxation (decrease SVR)
• adverse effect on survival when used as long-term oral agent
❏ inotropic support (dopamine, dobutamine) if necessary
❏ consider PA line to monitor capillary wedge pressure
❏ consider mechanical ventilation if needed
❏ rarely used but potentially life-saving measures
• rotating tourniquets
• phlebotomy
CARDIAC TRANSPLANTATION
❏ indications - end stage cardiac disease (CAD, DCM, etc.)
• failure of maximal medical/surgical therapy
• poor 6 month prognosis
• absence of contraindications
• ability to comprehend and comply with therapy
❏ 1 year survival 85%, 5 year survival 70%
❏ complications: rejection, infection, graft vascular disease, malignancy
MCCQE 2002 Review Notes Cardiology – C31
CVS Pathology:
Aneurysms & Dissections
Aneurysms (General Info):

- Definition:
o Dr. Martin A Increase in the Si e of an Artery Above its Normal Si e
Eg. Normal Infra-Renal Aorta = 2cm :. An Aneurysm would be >3cm.
(90% of AAAs are Infra-Renal)
o Robbins a Localised abnormal dilation of a BLOOD VESSEL OR THE HEART
- True Vs. Pseudo- Aneurysms:
o True Aneurysms – (Full Thickness Aneurysms)
o False/Pseudo Aneurysms – (Partial Thickness Aneurysms)
- Classification (Size/Shape):
o “Saccular Aneurysms”: Hemispherical Outpouchings involving ONLY PART of the vessel wall
o “Fusiform Aneurysms”: CIRCUMFERENTIAL Dilation of a vascular segment
o “Dissecting Aneurysms”:Blood within the Arterial wall itself.
- Aetiologies:
o Atherosclerosis - (Typically AAAs)
o Hypertension - (Typically Thoracic Aortic Aneurysms)
o Myocardial Infarction - (Typically Ventricular Aneurysms)
o (Others: Congenital – Eg. Downs/Marfan’s/Ehlers-Danlos Syndrome/Conn.Tissue Disorders/Etc)
- Risk Factors:
o Age >65
o Male
o Atherosclerosis
o ↑Cholesterol
o HTN
o Smoking
o FamHx
- ABDOMINAL AORTIC ANEURYSM:
o Aetiology:
Atherosclerosis
o Pathogenesis:
Atherosclerotic Plaque Weakening of Vessel Wall Aneurysm
o Morphology:
90% of AAAs are INFRA-RENAL
Saccular OR Fusiform
o Clinical Features:
Presentation:
Typically Asymptomatic (Hence Sudden Death”)
But Symptoms Include:
1. Pulsatile Abdo Mass.
2. Pain - Back/Flank/Abdo/Groin
3. DVT (From Venous Compression)
4. “Trash Foot” – from Thrombo-Emboli
o Investigations:
Clinical Suspicion + Examination
**Abdo USS – (100% Sensitive)
CT/MRI
o Complications:
#AAA – (NB: SIZE = #1 Predictor of Rupture):
Classic Triad of Rupture:
1. Sudden Pain – (Abdo/Back)
2. Shock – (Hypotension/ALOC)
3. Pulsatile Mass
+ Acute Abdomen
+ Grey Turners Sign
Occlusion of a Branch-Vessel:
Eg. Pre-Renal Failure
Eg. Mesenteric Ischaemia
Thromboemboli:
Renal Infarction
Mesenteric Infarction
“Trash Foot” – Focal Gangrene.
o Management:
AAAs <5cm Diameter Watchful Waiting (6mthly)
+ Risk Factor Modification
AAAs >5cm Diameter Surgical Repair (Due to ↑ Rupture Risk)
(Open Vs. Endovascular Repair)
#AAA EMERGENCY SURGERY:
+ 2x Large Bore Cannulas
+ Fluid Resuscitation (Bolus + Maintenance; Target BP 80 Systolic)
+ Group & Hold + X-Match for Transfusion
o Prognosis:
Pre-Rupture: Good Prognosis
Post Rupture: 95% Mortality – (Only 30% Make it to Hospital; 20% of those Survive).
- THORACIC AORTIC ANEURYSMS:
o Aetiology:
Hypertension
Complications:
Mediastinal Compression (Heart & Lungs)
Dysphagia
Cardiac Disease (Eg. Aortic Regurgitation, Myocardial Ischaemia/Infarction)
Rupture
- AORTIC DISSECTION:
o Aetiology:
Hypertension
M:F = 4:1
o Pathogenesis:
Hypertension Intimal Tear Blood Enters False Lumen Dissection Continues
o Morphology:
#1. Ascending Type (Ascending Aorta):
Bad because can Occlude Brachiocephalic Trunk/Internal Carotid/Subclavian.
Descending Type (Descending Aorta):
Bad because can Dissect all the way to legs GI/Renal/Limb Ischaemia
Sudden Excruciating Chest Pain Radiating to the Back between Scapulae
Radio-Radial Delay
+/- Signs of Complications:
Rupture Cardiac Tamponade & Shock
Valvular Aortic Regurgitation Diastolic Murmur (Due to Dilation)
Vessel Occlusion MI, Stroke, Limb Ischaemia, Mesenteric Ischaemia, Renal Fail
o Investigations:
CXR – Wide Mediastinum, L-Pleural Effusion
CT – 100% Sensitive
TOE (Echo) – 100% Sensitive, but slow.
o Management:
1. Aggressive BP-Reduction (Nitrates + B-Blocker) Slows Progression
If Ascending: EMERGENCY SURGERY
If Descending: Initial Medical Mx
CEREBRAL ANEURYSM (Congenital Berry Anerysms – See Sub-Arachnoid Haemorrhage Notes):

o Symptoms for an aneurysm that has not yet ruptured –
Fatigue
Loss of perception
Loss of balance
Speech problems
o Symptoms for a ruptured aneurysm –
Severe headaches
Loss of vision
Double vision
Neck and and/or stiffness
Pain above and/or behind the eyes.
VASCULAR - ARTERIAL DISEASES . . . CONT.
CRITICAL ISCHEMIA
❏ arterial compromise eventually leading to necrosis
❏ signs and symptoms (see Colour Atlas PL5)
• rest pain, night pain
• ulcerations, gangrene of toes
• pallor on elevation, dependent rubor, slow capillary refill
• decreased or absent pulses
• significant bruits may be heard (at 50% occlusion) – if stenosis severe, no bruit will be heard
• ABI < 0.5
❏ investigations
• as above
❏ management
• needs immediate surgery due to risk of limb loss
• initial procedures: transluminal angioplasty, laser, atherectomy and stents
❏ operations include
• inflow procedures for aortoiliac disease
• endarterectomy
• reconstructive procedures for superficial femoral artery occlusion
• profundoplasty
• femoropopliteal bypass
• aortoiliac or aortofemoral bypass
• axillofemoral bypass (uncommon)
ABDOMINAL AORTIC ANEURYSM (AAA)
❏ aneurysm: localized dilatation of an artery that is 2x normal diameter
• true aneurysm: wall is made up of all 3 layers of the artery
• false aneurysm: defect in arterial with aneurysmal sac composed of fibrous tissue or graft
❏ classification
• etiology: congenital
• Marfan syndrome, berry aneurysms acquired
• metabolic / endocrine
• degenerative
• inflammation / infection - syphilis
• neoplastic
• dissection
• shape:Fusiform (true aneurysms)
Saccular (false aneurysms)
• location: aortic
peripheral arteries
splanchnic
renal
❏ structure true or false
❏ inflammatory
❏ infected
❏ 95% of AAA’s are infrarenal
❏ incidence 4.7 to 31.9 per 100,000 person from 1951-1980
❏ the average expansion rate (80% of aneurysms) is 0.2cm/yr for smaller aneurysms (< 4 cm)
and 0.3-0.5 cm/yr for larger aneurysms (> 4-5 cm)
❏ may be associated with other peripheral aneurysms
❏ etiology
• cystic medial necrosis – likely due to enzymatic abnormalities in the aortic wall
• atherosclerosis
❏ high risk groups
• 65 years and older
• male:female = 3.8:1
• peripheral vascular disease, CAD, CVD
• family history AAA
❏ clinical presentation
• common
• 75% asymptomatic (often discovered incidentally)
❏ symptoms due to acute expansion or disruption of wall
• syncope, pain (abdominal, flank, back)
• uncommon
• partial bowel obstruction
• suodenal mucosal hemorrhage ––> GI bleed
• erosion of aortic and duodenal walls ––> aortoduodenal fistula
• erosion into IVC ––> aortocaval fistula
• distal embolization
❏ signs
• hypotension
• palpable mass felt at/above umbilicus
• pulsatile mass, in 2 directions
• bounding femoral pulses
• distal pulses may be intact
CVS24 – Cardiac and Vascular Surgery MCCQE 2002 Review Notes
❏ investigations
• U/S (100% sensitive, able to measure up to +/– 0.6 cm accuracy); however, operator dependent, and
may not be possible with obese patients, excessive bowel gas or periaortic disease
• Aortogram (not useful because lumen may not change in size due to thrombus formation)
• CT (accurate visualization, determines size)
• MRI (very good imaging, but limited access)
• Doppler/Duplex (to rule out aneurysmal disease elsewhere in the vascular tree)
❏ treatment and prognosis
• decision to treat is based on weighing the risk of OR to disease complications (such as rupture)
• risk of rupture depends on
• size %/yr
• 4-5 cm – 2-3%
• 5-6 cm – 5-8%
• > 7 cm – 25-40%
• > 10 cm – 100%
• rate of growth (> 0.4 cm/yr)
• presence of symptoms, hypertension, COPD
• consider operate at > 5 cm since risk of rupture greater than or equal to risk of surgery
• mortality of elective repair = 2-3% (mostly due to MI)
• consider revascularization for patients with CAD before elective repair of CAD
• conservative
• reduce risk factors
• smoking
• HTN
• DM
• hyperlipidemia
• exercise
• watchful waiting if <4-5cm re-U/S q6mo
❏ surgery
•procedure
• laporotomy performed firm xyphoid process to symphis pubis
• aorta is dissected out
• distal clamp is placed onto aorta
• proximal clamp is placed onto aorta or common iliacs
• aneurysm opened
• removal of thrombis
• graft put into place: tube/bifurcation
• graft sewn into proximal site
• graft suture site tested
• graft sewn into distal site - last stitch not closed until integrity of anastomosis tested
• aorta wall sewn over graft
• indications for surgery
• ruptured
• symptomatic or rapidly expanding aneurysms
• asymptomatic aneurysms >5cm
• contraindications
• less than 1 year to live
• terminal underlying condition (cancer)
• overwhelming medical conditions
• recent MI, unstable angina, decreased mental acruity, advanced age
• early post-op complications
• myocardial ischemia
• arrhythmias
• CHF
• pulmonary insufficiency
• renal damage
• bleeding
• infection
• cord injury
• impotence
• late complications
• graft infection/thrombosis
• aortoenteric fistula
• anastomotic aneurysm
• infection
MCCQE 2002 Review Notes Cardiac and Vascular Surgery – CVS25
• post-op orders
• bedrest (24-48 hr)
• NPO
• NG ––> straight drainage, record drainage q12h +/– NG losses 1:1 q shift Ns with 10 mEq KCl/L
• Foley ––> straight drainage
• +/– PA line
• +/– arterial line
• routine post-op vitals q15min until stable then q1h
• routine CU ICU admission blood work
(includes CBC, lytes, BUN, Cr, PLT, PT, PTT, glucose)
• CXR on CUICU admission and daily until extubated
• ECG on admission q8h x 24 hrs and PRN after
• ABI’s/pedal pulses q1h x 4 h then q shift
• chest physiotherapy assessment and treatment
• weaning protocol as per CUICU portocol
• titrate FiO2 to keep PO2 > 90 mmHg or O2 sat > 95% c/c
• ventilation (if required) Vt 700 mL, FiO2 > 50% c/c, rate 12/min, PEEP 5 cm/H2)
to keep PaCo2 35-45 mmHg
• incentive spirometry when extubated
• epidural proticol if required
• IV’s: N/S or RL at 150 cc/hr x 24 hr; reassess at 24 hrs
• morphine 2-10 mg IV q1h PRN
• midazolam 2-4 mg IV q1h PRN max 20 mg/24hr
• dimenhydrinate 12.5-25 mg IV q4h PRN
• heparin 5,000U SC q12h for DVT prophylaxis start post-op
• sulcrote 1 gm NG q4h
• may require inotropic agents
• may require antiphypertensive agents
ABDOMINAL AORTIC DISSECTION
❏ Stanford Surgical Classification
• Type A: involves the ascending and aortic arch; requires emergency surgery
• Type B: involves the aorta distal to subclavian artery; emergency surgery only if
complications of dissection (require long-term follow-up to assess aneurysm size)
❏ male:female = 3-4:1
❏ predominantly older patients
❏ etiologic factors
• hypertension
• cystic medial necrosis (not atherosclerosis)
❏ associated factors
• Marfan's Syndrome
• coarctation of aorta
• congenital bicuspid aortic valve
❏ pathogenesis (usually in thoracic aorta)
• intimal tear ––> entry of blood separates media ––> false lumen
created ––> dissection often continues to aortic bifurcation
❏ symptoms and signs
• sudden searing chest pain that radiates to back
• asymmetric BPs and pulses between arms
• branch vessel "sheared off" – ischemic syndromes
• MI with proximal extension to coronary arteries
• "unseating" of aortic valve cusps
• new diastolic murmur in 20-30%
• neurologic injury - stroke (10%), paraplegia (3-5%)
• renal insufficiency
• lower limb ischemia
• cardiac tamponade - false lumen ruptures into pericardium
• hypertension (75-85% of patients)
❏ diagnosis and investigations
• CXR
• Pleural cap
• Widened mediastinum
• Left pleural effusion with extravasation of blood
• ECG - most common abnormality is LVH (90%)
• TEE, CT, aortography
❏ management
• sodium nitroprusside and B-blocker to lower BP and decrease cardiac contractility
• ascending aortic dissections operated on emergently
• descending aortic dissections initially managed medically
• 10-20% require urgent operation for complications
RUPTURED ABDOMINAL AORTIC ANEURYSM (RAAA)

❏ narrow window of opportunity
❏ usually present with classical diagnostic triad (50% cases)
• sudden abdominal or back pain
• SHOCKY (Hypotensive, faintness, cool, mottled extremities)
• pulsatile mass
❏ may be confused with renal colic
❏ ECG confusing - may show cardiac ischemia
❏ diagnosis by history and physical
❏ do not waste time in radiology if RAAA strongly suspected
❏ if patient stable without classic triad ––> consider CT
❏ management
• initial resuscitation including vascular access, notify OR,
• ensure availability of blood products, invasive monitoring
• emergency laparotomy as soon as IV and cross-match sent
• upon opening - gain centre of aorta proximal to rupture with cross clamp
❏ prognosis
• 50% survival for patients who make it to OR
• 100% mortality if untreated
• overall mortality 90%
CAROTID SURGERY (see Neurosurgery Chapter)
VASCULAR – VENOUS DISEASE

ANATOMY
❏ the venous system is divided into 4 general areas
• superficial venous system (subcutaneous veins and the greater and lesser saphenous veins)
• communicating venous system (perforating veins)
• deep venous system (tibial, popliteal, femoral and iliac veins)
• venous valves (in all infra-inguinal veins)
DEEP VENOUS THROMBOSIS (DVT) (ACUTE)
❏ occlusion of the deep venous system, typically of the lower extremity that can extend up to the right atrium.
❏ pathogenesis (Virchow's Triad)
❏ flow stasis
❏ postulated that stasis protects activated pro-coagulants from circulating inhibitors,
fibrinolysis and inactivation in the liver
❏ surgery
❏ trauma and subsequent immobilization
❏ immobilization due to: acute MI, stroke, CHF
❏ compression of veins by tumours
❏ shock (decreased arterial blood flow)
❏ hypercoagulability
❏ states that increase coagulability of the blood (ex. Increased fibrinogen or prothrombin) in which there is a
deficiency of anti-coagulants (anti-thrombin III, Protein C+S), e.g.
• pregnancy
• estrogen use
• neoplasms: diagnosed, occult, undergoing chemotherapy
• tissue trauma: activation of coagulation
• nephrotic syndrome
• deficiency of anti-thrombin III, protein C or S
• endothelial damage
❏ exposure of the underlying collagen in a breach of the intimal layer of the vessel wall leads to
platelet aggregation, degranulation and thrombus formation. There also appears to be a
decrease endothelial production of plasminogen and plasminogen activators, e.g.
• endothelial damage: venulitis, trauma
• varicose veins
• previous thrombophlebitis
Week 13
Arrhythmias

Characteristics of a Normal ECG:
- Sinus Rhythm/Rate:
o Between 60-100 bpm.
o Initiated by SA-Node
o NB: it’s intrinsic rate is higher, but is suppressed by constant Parasympathetic-NS Influence
- P-Wave:
o Rounded
o Between 0.5-2.5 mm Tall
o Less than 0.1 Seconds Duration
- PR-Interval:
o Fixed
o Between 0.12-0.20 Seconds
- QRS-Complex:
o Clean & Sharp
o Normally Less Than 25mm Tall
o QRS Interval: Between 0.06-0.12 Seconds Duration
- Q-T Interval:
o Between 0.35-0.45 Seconds Duration
- S-T Segment:
o Normally ≈0.08 Seconds Duration
- T-Wave:
o Prominent
o Rounded
o Less Than 5mm Tall (Limb) or Less Than 10mm Tall (Precordial)
- U-Wave

Week 13
Arrhythmias

Characteristics of a Normal ECG:
- Sinus Rhythm/Rate:
o Between 60-100 bpm.
o Initiated by SA-Node
o NB: it’s intrinsic rate is higher, but is suppressed by constant Parasympathetic-NS Influence
- P-Wave:
o Rounded
o Between 0.5-2.5 mm Tall
o Less than 0.1 Seconds Duration
- PR-Interval:
o Fixed
o Between 0.12-0.20 Seconds
- QRS-Complex:
o Clean & Sharp
o Normally Less Than 25mm Tall
o QRS Interval: Between 0.06-0.12 Seconds Duration
- Q-T Interval:
- S-T Segment:
o Normally ≈0.08 Seconds Duration
- T-Wave:
o Prominent
o Rounded
o Less Than 5mm Tall (Limb) or Less Than 10mm Tall (Precordial)
- U-Wave

CVS Pathology:
Arrhythmias
BACKGROUND INFO:
- Working knowledge of ECG and Cardiac Cycle is Essential:
o P Wave = Atrial Depolarisation
o QRS Complex = Ventricular Depolarisation
o T Wave= Ventricular Repolarisation
o Normal Rate 70bpm
o Tachycardia = >100bpm
o Bradycardia = <60bpm
- Revision of the Cardiac Cycle:

o P-Wave = Atrial Systole
o QRS-Complex = Start of Ventricular Systole
o T-Wave = Ventricular Filling
o First & Second Heart Sounds:
1. Lubb (AV Valve Closure)
2. Dupp (Semilunar Valve Closure)
Mechanisms of TachyArrhythmias

Mechanism of Re-Entry:
- Accounts for ≈75% of Tachycardias
- Causes of Re-Entry:
o Ischaemic Heart Disease
o Ion-Channel Mutations
o Electrolyte Disturbances
- Results in an “Ectopic Focus”:
o = An area in the heart that initiates abnormal beats. (Aka: An Ectopic Pacemaker)
o Ectopic foci may occur in both healthy and diseased hearts
o Usually associated with irritation of a small area of myocardial tissue.
o Creates a Single Additional Beat, OR a Full Rhythm.
- How It Occurs:
o Normally, an Impulse from Conductile Tissue transmits into Myocytes (Contractile Cells), then
spreads amongst the myocytes. All Myocytes receive the Impulse and Contract.
o NB: Once a cell receives a signal, it won’t receive another.

àààààààààààààààààààààààààààààààààààààààààààààààà

o However, for Re-Entry to occur, an initial momentary/transient Block is required. See Below:



Early After-Depolarisations:
- Occur During Repolarisation Phase
o (Where K+ is Flowing OUT)
o (Where Ca+ has STOPPED Flowing IN)
- More Likely to occur when Action-Potential Duration is Increased...WHY?
o The Absolute Refractory Period for the Na+ Channels (those responsible for depol) only lasts for a
small period of time. Usually this period is enough for repolarisation to occur.
o However, if the AP-Duration is increased, the membrane will still be in Plateau when the Na+
Channels enter the Relative Refractory Period, meaning a further stimulus will cause another action
potential.
- Early After-Depolarisations can result in:
o Torsades de pointes (Twisting of the Points)
o Tachycardia
o Other Arrhythmias

Delayed After-Depolarisations:
- Depolarisation during phase 4 (after repolarization is completed, but before another action potential would
normally occur)
- Due to High Intracellular Ca2+ Concentrations Caused by TOO MUCH DIGOXIN.
o NB: Digoxin is a drug used to treat Atrial Flutter & Atrial Fibrillation by Decreasing Conduction
Through the AV-Node. Ie. DIGOXIN à DECREASED HEART RATE

- Digoxin – Mechanism of Action:
o 1. Blocks the Na+/K+-ATPase on the cell.
§ à Accumulation of Na+ inside the cell
§ à Deficit of K+ inside the cell
o 2. The Secondary Active Na/Ca-Exchanger (That normally relies on the High Extracellular Na+
Gradient to remove Ca+ from the cell) ceases to work.
§ à Accumulation of Ca+ inside the cell à ↓Rate of Depol & Repol of Pacemaker Action
Potentials à Stops Atrial Flutter/Fibrillation/other atrial tachycardia.

- NB: This accumulation of Na+ & Ca+ in the cell makes the Resting Membrane More Positive.
o à Action Potentials are easier to stimulate
o Can Lead to A Series of Rapid Depolarisations.

LOOKING AT ECGs:
- Check Pt ID
- Check Voltage & timing
o 25mm/sec
o 1large square = 0.2s (1/5sec)
o 1small square = 0.04s
- What is the rate?
o 300/number of large squares between QRS Complexes
Tachycardia
>100bpm
Bradycardia
<60bpm
- What is the Rhythm?
o Sinus? (are there P-Waves before each QRS complex)
o If Not Sinus?
Is it regular
Irregular?
Irregularly Irregular (AF)
Brady/Tachy
- Atrial Fibrillation:
o Irregularly Irregular
o P-Waves @ 300/min
- QRS:
o Is there one QRS for each Pwave?
o Long PR Interval? (1st degree heart block)
o Missed Beats? (Second degree block)
o No relationship? Complete heart block
- Look for QRS Complexes:
o How wide should be < 3 squares
o If wide It is most likely Ventricular
o (Sometimes atrial with aberrant conduction (LBBB/RBBB)
o IF Tachycardia, & Wide Complex VT is most likely. (If hypotensive Shock; if Normotensive
IV Drugs)
- Look for TWaves:
o Upright or Inverted
- Look at ST-Segment
o Raised, depressed or inverted
o ST Distribution Tells you which of the coronaries are blocked/damaged
Inferior ischaemia (II, III, AVF)
Lateral ischaemia (I, II, AVL, V5, V6)
Anterior ischaemia (V, leads 2-6)
o NB Normal ECG Doesn e cl de infarc
o ST Depression Ischaemia
o ST Elevation Infarction
o If LBBB or Paced, you CANNOT comment on ST-Segment
COMMON TACHYCARDIAS:
DDX #1 SUPRAVENTRICULAR TACHYCARDIAS:

- SINUS TACHYCARDIA:
o = Sinus Rhythm of 100+Beats/min
Shortened T-P Interval (But All Waves Visible)
o Management:
Carotid Massage
(B-Blocker if Symptomatic)
- ATRIAL PREMATURE BEATS (APBs):

o = Single Ectopic P-Wave QRS
o Management:
Nil
(If Symptomatic B-Blocker or Ca-Ch-Blocker)
- ATRIAL FLUTTER:
o = Atrial Rate of 300bpm; But NOT Sinus Rhythm!
Sa oo h P-Waves
Ventricular Conduction Variable (Eg. 2:1 / 3:1 / 4:1 Block etc)
o Mechanism: Re-Entry (See End)
o Treatment:
Rate Control (B-Blocker, Ca-Ch-Blocker [Verapamil], Digoxin)
Electrical Cardioversion (NB: Different to Defibrillation)
- ATRIAL FIBRILLATION (AF):

o = Sinus Rate of -600Beats/min; Irregular QRSs.
NB: Poor Atrial Contraction Thromboemboli Common. (Requires Warfarin)
o Causes PIRATE SHIV
PE, IHD, Rh-Heart Disease, Anaemia, Thyroid, ETOH, Sepsis, HTN, Iatrogenic, Valvular
o Treatment:
Vent-Rate Control (B-Blocker / Ca-Ch-Blocker [Verapamil] / Digozin)
Anticoagulation (Warfarin)
Cardioversion (Medical [Sotalol/Amiodarone] or Electrical)
- PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT):

o = Sudden Onset Regular Tachycardias (Typically Atrial Re-Entry)
+
Ra e bpm (Regular)
o Diagnosis:
ECG
Adenosine Trial (Dromotropic Slows SA-Node) :. If Rate slows = SVT.
(If not, consider ventricular cause)
o Management:
Rate Control (B-Blocker / Ca-Ch-Blocker [Verapamil] / Dogoxin)
(Definitive Catheter Ablation.)
DDX #2 VENTRICULAR TACHYCARDIAS:
- PREMATURE VENTRICULAR COMPLEXES (PVCs):
o = Additional QRS s with No Preceding P-Wave.
Wide QRS & Bizarre Shape
o Complication Consecutive PVCs = VENTRICULAR TACHYCARDIA.
o Management:
Nil Necessary
B-Blocker (if Symptomatic)
- VENTRICULAR TACHYCARDIAS:
o = 3 or more Consecutive PVCs.
>30sec = Sustained VT
<30sec = Non-Sustained VT
o Mechanism: Re-Entry (Typically due to IHD)
o Treatment If Sustained (>30s):
Cardioversion
+/- Anti-Arrhythmic Drugs (Type 1a Antiarrhythmics [Eg. Procainamide])
- VENTRICULAR FIBRILLATION:
o = Disordered, Rapid Ventricular Depolarisation with NO Coordinated Contraction.
No Coordinated Contraction No Cardiac Output
A Ca se of S dden Death
o Mechanism: Often Preceded by PVCs or Ventricular Tachycardia.
o Treatment:
Defibrillation (Much Stronger than Cardioversion & isn imed
+/- CPR
+/- Anti-Arrhythmic Drugs.
- TORSADES DE POINTES ( TWISTING OF THE POINTS ):

o = Polymorphic VT with QRS-Complexes of Changing Amplitude
o Ra e -250bpm
o Causes:
Long-QT-Syndrome (An inherited ion channel mutation)
(Drugs) eg. K+ Channel Blockers
Electrolyte Disturbances (Hypokalaemia / Hypomagnasaemia)
o Management:
IV Magnesium
Temporary Pacing
DC Cardioversion - (If Haemodynamic Compromise)
COMMON BRADYCARDIAS:
SINUS BRADYCARDIA:
- = Sinus Rhythm of <60 Beats/min (SA-Node is still the pacemaker)
o Prolonged TP-Interval; All Waves Visible
- Normal (At rest/Sleeping/In Elite Athletes)
- Pathological ( SA-Node Firing (Eg. IHD/Old Age), Cardiomyopathy).
- Management:
o Atropine (If symptomatic) (+/- Pacing)
ESCAPE RHYTHMS (SINUS ARREST/EXIT BLOCK):

- = SA-Node Failure (No P-Wave) AV-Nodal E ca e Rh hm .
o AV-Node Rate -60bpm (Compared to the SA-Node s -100bpm)
- Management:
o Cease Dromotropic Drugs (B-Blockers / Ca-Ch-Blockers / Digoxin)
Conduction Blocks:
- = Impaired AV-Conduction
o Often due to IHD
o Often Escape Rhythm.
- Types of Conduction Blocks:
o Vertical - Between Atria & Ventricles
o Lateral - Between L-Heart & R-Heart
- AV-Conduction Blocks 1 of 3 Degrees:
o 1. FIRST-DEGREE HEART BLOCK:
= Prolonged AV-Delay (Greater than 0.2sec)
Ie. Prolonged PR-Interval (But P:QRS ratio = 1:1)
Management:
Nil.
o 2. SECOND-DEGREE HEART BLOCK:

MOBITZ TYPE-I (WENCKEBACH):
= Gradual Lengthening of PR-Interval until a QRS is lost.
Management:
o Nil; (Atropine if Symptomatic)
MOBITZ TYPE-II:
= Intermittent Loss of AV-Conduction with FIXED PR-Interval
o Block may last for 2/more beats.
Management:
o Pacemaker
o 3. THIRD-DEGREE HEART BLOCK (AKA: COMPLETE HEART BLOCK):

= Complete AV-Conduction Failure.
No P:QRS Relationship
Cardiac Output (Disordered Contraction of Atria & Ventricles)
Management:
Pacemaker.
- Bundle Branch (Lateral) Blocks (Ie. @ L/R Bundle-Branches):
o LEFT BUNDLE-BRANCH BLOCK:
= When Left Bundle-Branch is unable to conduct impulses to L-Ventricle.
Therefore, R-Bundle-Branch depolarizes R-Ventricle First, then the impulse travels
to L-Ventricle causing it to depolarize.
Ie. Ventricles depolarize Consecutively rather than Simultaneously.
Widened & Split QRS-Complex
o RIGHT BUNDLE-BRANCH BLOCK:
= When Right Bundle-Branch is unable to conduct impulses to R-Ventricle.
Therefore, L-Bundle-Branch depolarizes L-Ventricle First, then the impulse travels
to R-Ventricle causing it to depolarize.
Ie. Ventricles depolarize Consecutively rather than Simultaneously.
Widened & Split QRS-Complex
DRUGS FOR ARRHYTHMIAS:
Therapeutic Management of Dysrhythmias (Arrhythmias) (Anti-Arrhythmics):
- Class-I Antiarrhythmics (VG-Na+ Channel Blockers):
o General Info:
Indication:
Ie. Typically Re-Entrant Tachycardias (But Not 1st line)
Mechanism of Action:
Selective VG-Na+ Channel Blockade (in Contractile Cells):
o Slows down Re-Entrant Foci Restores SA-Nodal Control of HR.
Typical Agents:
1a Quinidine, Procainamide (Intermediate Association/Dissociation)
1b Lidocaine, Tocainide (Fast Association/Dissociation)
1c Flecainide, Encainide (Slow Association/Dissociation)
- Class-II Antiarrh thmics 1-Blockers):

o Classical Agents:
**Propanolol
Atenolol
o Mechanism of Action:
-Adrenergic Receptor Blockade Inhibit Sympathetic NS
Conductile System HR
Contractile Cells Contractilit
o Indications:
Atrial Fibrillation (Or other Sinus Tachycardia)
SVT
(Hypertension.)
Ischaemic Heart Disease Cardiac Workload (Ie. Metabolic Demands)
o Contraindications:
Asthma Can cause Bronchoconstriction.
Ca+ Channel Blockers (Verapamil/Nifedipine) Can cause Fatal Bradycardia.
o Side Effects:
Sinus Bradycardia.
Bronchoconstriction in Asthmatic Patients.
(Rebound Tachycardia if stopped abruptly; Must be weaned off)
- Class-III Antiarrhythmics (VG-K+ Channel Blockers):
o Classical Agents:
**Amiodarone
VG-K+ Channel Blockers Prolongs Plateau Phase of AP HR
o Indications:
*1st Line in Re-Entrant Tachycardias. V-Tac, V-Fib, A-Fib & A-Flutter.
o KEY Side Effect/s:
Bradycardia
Early-After-Depolarisation (PVCs/Ectopic Beats)
- Class-IV Antiarrhythmics (VG-Ca+ Channel Blockers):

o Classical Agents:
**Verapamil (Selective for the Heart)
Nifedipine (Selective for Vessels) (Used in Angina & Heart Failure)
**Heart:
VG-Ca+ Channel Blockade
o @ SA/AV Nodes HR
o @ Myocytes Ca Infl Contractility)
(Vessels Used in Angina):
VG-Ca+ Channel Blockade
o @ Vascular Smooth Muscle Vasodilation BP & Afterload
o Indications:
SVT (Supraventricular Tachycardias)
Variant Angina
-Blockers (Since Ca+ Channel Blockers also Inhibit Ca+ Influx) Fatal Bradycardia.
o KEY Side Effect/s:
Heart Block
Bradycardia.
Also H po ension Di iness d e o Con rac ili
- Other Agents:
o Digoxin:
2x Clinical Uses:
1. Heart Failure (Especially Pts with coincident Atrial Fib. Kill birds
2. Long Term SVT (Eg. AF) Management
2x Mechanisms of Action:
1. Inotropic: Myocytes: Na/K-ATPase Inhibitor Contractility.
o Use: Heart Failure
o Side Effect: Earl Af er Depolarisa ions (Ectopic Beats/SVT)
2. Dromotropic: AV Node: K+ Channel Agonist Slows AV Conduction.
o Use: SVT (Supraventricular Tachycardia)
o Side Effect: Heart Block (if HR <60bpm)
Summary of Actions & Potential Side Effects:
NB: Not to be given if HR less than 60bpm Brady/Heart Block.
NB: Also, Dosage is very important for reducing side effects.
*(NB: Also require K+ Monitoring - & Supplements if on K+ Wasting Diuretic)
o Adenosine:
Clinical Use:
Diagnostically to distinguish V-Tac from SVT.
NB: Extremely short T1/2 - Only Effective in Emergency Situations to stop SVT.
o (Digoxin is used for long-term SVT Management)
Adenosine Receptor Agonist @ SA & AV Nodes Delays AV-Node Conduction.
(HR will slow if it is an SVT) / (If HR is unchanged, then it is V-Tac)
Side Effect/s:
IMPENDING DOOM!!! P s li erall feel like he re d ing
o Atropine:
Clinical Use:
Acute Bradycardias/Asystole HR. (However can cause V-Tac).
Chronotropic: Anti-Muscaranic (Blocks Parasympathetic NS) HR
KEY Side Effect/s:
Overdose Ventricular Tachycardia
CVS Pathology:
Atherosclerosis
TERMINOLOGY:
Arteriosclerosis Hardening of Any Artery:
o **Macroangiopathy = A he o cle o i - Hardening of Large & Medium Arteries
o Microangiopathy = A e iolo cle o i Hardening of Small Arteries
Hyperplastic
Hyaline
Arteritis Inflammation of Any Artery. (Next Week)
**ATHEROSCLEROSIS:
- = A Progressive Chronic Inflammation of Arteries characterised by:
o 1. Inflammation, (Macrophages engulf LDLs Foam Cell
o 2. Fibrosis, (Conn. Tissue Matrix/Collagen/Elastin)
o 3. & Lipid Deposition (Cholesterol Esters & Cholesterol in Cells)
o A he o Fa Scle o i Ha dening
- Aetiology:
o BEGINS with Endothelial Injury
o BIG Inflammatory Component
o Risk Factors:
Non Modifiable: Age (40-60), Male, FamHx, Indigenous
Modifiable: Cholesterol, HTN, Smoking, Diabetes, Obesity, Metabolic Syndrome
- Pathogenesis
o 1. Endothelial Injury & Activation (HTN/Smoking/DM/Turbulence/Toxins/Infection/Immune).
o 2. Endothelial Inflammation (Macrophage & Smooth Muscle Migration)
o 3. Accumulation of Lipoproteins Fatty Streak Formation.
o 4. Proliferation & Fibrosis (Conversion of Fatty Streak into a Mature Atheroma)
o 5. Complicated plaque formation (Thin Fibrous Cap Rupture Thrombus ACS)
- Clinical Features/Complications:
o Multi-Organ Disease:
Heart IHD (Angina, MI).
Brain Cerebral Infarction (Stroke)
Kidneys Renal Infarction
GIT GI-Ischaemia/Infarction
Lower Extremities PVD (Eg. Claudication, Gangrene of Legs, Arterial Leg Ulcers)
- Investigations:
o Coronary Angiogram
- Management:
o Risk Factor Modification:
Statins - ( Cholesterol)
ACE-I/B-Blocker - (HTN)
Control DM
Die Physical Exercise (For Obesity)
Smoking, Alcohol
o Prevent Thrombosis:
Aspirin/Clopidogrel
o Surgical Intervention:
Balloon Angioplasty/Stent AngioplastyBypass Surgery:
Week 7
Atherosclerosis

Atherosclerosis: A General Overview:
- “Athero” = Gruel/Porridge (ie. The fat in the blood)
- “Sclerosis” = Hardening

- A Progressive Chronic Inflammatory Disease of the Blood Vessel Wall
o Due to Vessel Injury à Fatty Plaque Formation à Occlusion of Blood Vessel
§ Reduced blood flow to local area à Imbalance of Supply & Demand.

- Occurs Silently Over Many Decades

- Advanced Plaque & Thrombus:
o If ‘Apical Cap’ becomes unstable à Ruptures à Massive Thrombus (Clot) à
o Thrombus Completely Occludes Vessel

- Characterised By Accumulation of:
o 1. Lipids (Cholesterol Esters & Cholesterol in Cells)
o 2. Fibrous Elements (Conn. Tissue Matrix/Collagen/Elastin) &
o 3. Local Inflammatory Response (Macrophages engulf LDLs à “Foam Cells”)

- Principle cause of Heart Disease & Stroke
o Cause of 90% Myocardial Ischaemia
§ Due to Occlusion of Coronary Circulation
o Cause ≈50% of deaths in Western Society.

Lipids: The Main Culprits! (A Review)
- 3 Types of Lipids in Plasma:
o 1. Cholesterol + Ch. Esters
o 2. Phospholipids
o 3. Triglycerides (Fatty Acids + Glycerol)
- Lipid Transport:
o Insoluble In Water à Must be Packaged to be suspended in plasma.
o Fats Absorbed in GI à Packaged into Chylomicrons (in S.I.) à Lymphatics à
§ Lymphatics à Circulation (Left Sub-Clavian Vein) àLiver.
o Liver Repackages Chylomicron Remnants à Lipoproteins à Circulation

NB: LDLs Attribute to Atherosclerosis
NB: HDLs Help Prevent Atherosclerosis

What Is The Process?:
1. Vessel Injury – Endothelial Damage:
a. Risk Factors:
i. High Cholesterol
ii. Hypertension – High Pressure can split arteries (Particularly where they branch)
iii. Smoking – Toxins from cigarettes.
iv. Toxins/Poisons
v. Virus
vi. Bacteria
vii. Immune Reactions
viii. Diabetes
b. Endothelium Becomes Activated:
i. Increased Vessel Permeability – Become ‘Leaky’
ii. Platelets Adhere
iii. Monocytes Adhere à Transform to Macrophages
iv. Blood LDLs Enters à Bind to their Apolipoprotein ‘Receptors’ à Activated & Oxidised à
v. Oxidised LDL Presence à Causes Inflammation:
c. Local Inflammation:
i. Oxidised LDLs – Attract Immune Cells/Cytokines/Platelets/Smooth Muscle/Conn. Tissue
ii. Macrophages Engulf Oxidised LDL à Transform to Lipid-Laiden Foam Cells.
iii. Plaque Building Slowly Begins.

2. Fatty Streak Formation:
a. Fat Deposition Under the Tunica-Intima Vessel-layer.
b. The Typical Early Atherosclerotic Lesion.
i. Majority Are Clinically Silent
ii. Are Reversible – eg. If Diet Changes
c. Yellow Colour Reflects:
i. Oxidized Lipids
ii. Presence of ‘Foam Cells’

3. Lipid Plaque:
a. Fatty Streak gets more profound
b. ‘Foam Cells’ Unable to Digest Lipid Contents à Die
i. à Extracellular Lipids
ii. à Cell Debris
c. Oxidised LDLs – Attract Immune Cells/Cytokines/Platelets/Smooth Muscle/Conn. Tissue
i. Positive Feedback.
d. Plaque Builds.

4. Complicated Plaques:
a. ‘Cap’ forms on plaque à Becomes more ‘Unstable’ à May rupture à Thrombus à Occlusion
b. Clinical Manifestations (Different Types of ‘Complicated Plaques’):
i. **Plaque Rupture à Thrombosis (Responsible for 90+% of MI’s)
ii. Narrowing/Calcification à Vessel Rigidity & Fragility
iii. Haemorrhage Into Plaque à Narrowing of Lumen
iv. Fragmentation of Plaque à Distal Emboli
v. Weakening of Vessel Wall à Aneurysms

Simplified Summary Of Process Of Atherosclerosis:
Whole Process

Diagnosis Of Atherosclerosis:
- (Old) Invasive Method:
o Catheter via Femoral Artery à Coronary Artery à X-Ray Angiogram.
- (Current) Non-Invasive Method:
o Contrast-Enhanced CT-Scan
o Takes 15sec.

Preventing Atherosclerosis:
- Drugs:
Reparative Surgery:
- Balloon Angioplasty:
o Balloon-tipped tube inserted in coronary artery
o Balloon Expanded multiple times – Stretches lumen.

- Balloon Stent Angioplasty:
o Stent-Tipped Balloon-Tipped Tube inserted in coronary artery
o Balloon (+ Stent) expanded
o Balloon deflated & withdrawn
o Stent stays in & open.

- Bypass Surgery:
o The use of a distal vessel as a substitute for Blocked Artery.
o Eg. Radial Artery Bypass
o Eg. Saphenous Vein Bypass
SS Questions:
1. What is the difference between Arteriosclerosis & Atherosclerosis?
a. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large
arteries, whereas...
b. Atherosclerosis is the hardening of an artery specifically due to an atheromatous (atherosclerotic)
plaque.

2. What are the 3 Types of Arteriosclerosis?
1. Atherosclerosis - 2. Arteriosclerosis Obliterans - 3. Medial Calcific Sclerosis - mostly in elderly -
Atheroma Plaque Fibrosis of intima _ Calcification Calcification of Internal Elastic Lamina, but without
of Media. thickening of intima or narrowing of vessel.

3. What is the effect of Diabetes on the Vascular System?
a. Chronic elevation of blood glucose level leads to damage of blood vessels (angiopathy). The
endothelial cells lining the blood vessels take in more glucose than normal, since they don't depend
on insulin. They then form more surface glycoproteins than normal, and cause the basement
membrane to grow thicker and weaker.
CVS Pathology:
Carcinoid Heart Disease
CARCINOID HEART DISEASE:

- Aeitology:
o Cardiac Manifestation of the Systemic Syndrome caused by Carcinoid Tumours.
- Pathogenesis:
o Carcinoid Tumour Releases Vasoactive Hormones into Venous Circulation
Serotonin / Bradykinin / Histamine / Prostaglandins
o Venous Drainage of these Hormones R-Heart R-Heart Endocardial & Valvular Fibrosis.
(Generally Fibrosis of R-Heart Valves (Tricuspid/Pulmonary))
- Clinical Signs:
o “Carcinoid Syndrome”:
Episodic flushing of skin
Cramps
Nausea/Vom/Diarr.
o Heart Manifestations (RV-Failure due to..):
*Tricuspid Regurgitation (Most Common)
Hepatomegaly/Pain
Pulsatile Liver
↑JVP with Prominent V-Waves
Systolic Murmur @ 4th ICS, L-Sternal Border, Louder on Inspiration
*Pulmonary Regurgitation
Dyspnoea
Diastolic Murmur @ 2nd ICS, L-Sternal Border, Louder on Inspiration
(+ Features of RV-F):
Peripheral Oedema
Organomegaly
Portal HTN (Caput Medusa, Spider Naevi)
↑JVP
- Investigations:
o 24hr Urinary 5-HIAA (A Serotonin Metabolite)
o Abdo CT + Somatostatin Receptor Scintigraphy (SRS) – (Tumour Localisation)
o Abdo MRI + Contrast
o Cardiac Ix (ECG, CXR, ECHO)
- Management:
o Medical Somatostatin Analogues (Octreotide)
+/- Interferon-A in Palliative Pts.
o Surgery Tumour Resection + Valuloplasty
- Prognosis:
o Can Metastasize :. Early Removal is Essential
(A, Characteristic endocardial fibrotic lesion involving the right ventricle and tricuspid valve. B, Microscopic
appearance of carcinoid heart disease with intimal thickening.)
CVS Pathology:
CARDIOMYOPATHIES
CARDIOMYOPATHIES (“Heart Muscle Diseases”):

- 1. DILATED CARDIOMYOPATHY (Most Common):
o Aetiology:
***Idiopathic
**Chronic Alcoholism
*Post-Viral (Myocarditis)
Genetic
Chemotherapy
Chronic Anaemia
o Pathogenesis:
Progressive Dilation & Hypertrophy Systolic Dysfunction.
Enlarged, Flabby Heart
Mural Thrombi (Can embolise)
AV-Valve Regurgitation (Due to Chamber Dilation)
Any Age (Incl. Childhood).
Presentation: Congestive Heart Failure:
Dyspnoea/Orthopnoea/PND
Exercise Tolerance
Fatigue
Wet Cough
o Complications:
Mitral Regurgitation
Arrhythmias
Possible Thrombotic Embolism
o Investigations:
ECG
CXR (Globular Heart)
Echo (Assess Vent Function)
o Management:
ETOH
CCF Triple Therapy:
ACEi (Perindopril) / ARB (Candesartan)
Diuretic (Frusemide)
Warfarin (Prevent Thromboembolism)
FluVax & PneumoVax
** Heart Transplant
o Prognosis:
50% 5yr Mortality Unless Heart Transplant.
- 2. HYPERTROPHIC CARDIOMYOPATHY (AKA: HOCM – Hypertrophic Obstructive Cardiomyopathy)
o Aetiology:
**Genetic
o Pathogenesis:
Genetic Mutation Hypertrophy Diastolic Dysfunction ( Filling Chamber Size
NB: End Stage can Focal Ischaemia (Even in absence of Coronary Artery Disease)
o Clinical Features & Complications:
CCF (Dyspnoea, Orthopnoea, PND, Cough)
Ventricular Outflow Obstruction Syncope + Harsh Systolic Murmur
Angina
Arrhythmias
Mural Thrombus Embolisation (eg. Stroke)
Sudden Death
o Investigations:
ECG (LVH, Path Q Waves)
Echo (LVH, Diastolic Dysfunction, Poor EF)
o Management:
Medical β-Blockers Heart Rate Contractility
Surgical Septal Myomectomy (Relieves the outflow tract obstruction)
+/- ICD (If Arrhythmias)
A, The septal muscle bulges into the left ventricule, left atrium is enlarged.
B, Extreme hypertrophy, branching of Myocytes, and the characteristic interstitial fibrosis (collagen is blue).
- 3. RESTRICTIVE CARDIOMYOPATHY
o Aetiology:
**Amyloidosis/Sarcoidosis/Scleroderma/Haemochromatosis
o Pathogenesis:
Stiffening of Myocardium Diastolic Dysfunction ( Filling) Heart Failure
Ventricles Normal Size Volume
Myocardium is Firm & Non-Compliant
o Clinical Features & Complications:
Heat Failure Symptoms:
Cough, Dyspnoea, PND, Orthopnea
Fatigue
Chest Pain, Palpitations
Signs:
Elevated JVP
Lung Crepitations
Peripheral Oedema
Arrhythmias
o Investigations:
ECG (Low Voltage)
CXR – (CCF Signs)
Echo – (Diastolic Failure, Poor EF)
Myocardial Biopsy (To Determine Aetiology)
o Management:
Medical:
CCF Triple Therapy (ACEi/ARB + B-Blocker + Diuretics)
Warfarin
+/- Anti-Arrhythmics
Definitive: Requires Heart Transplant.
- (4. “COR PULMONALE”):
o RV Hypertrophy AND Dilation. (Secondary to COPD/Chronic Pulmonary Hypertension)
- (5. “STRESS CARDIOMYOPATHY”):

o AKA:
Broken Heart Syndrome
Takotsubo Cardiomyopathy
Apical Ballooning Cardiomyopathy
o Aetiology:
(NON-ischaemic)
Stress-Related (High Catecholamines)
o Pathogenesis:
Stress High Catecholamines Coronary Vasospasm Myocardial Stunning
Bulging of the LV-Apex with Hypercontractile LV-Base. Octopus Trap Shape
o Clinical Presentation & Complications:
Acute, Reversible LV Systolic Dysfunction
Sudden Onset CCF
Chest Pain
Dyspnoea
Lethal Ventricular Arrhythmias + Other ECG Changes (Similar to MI)
Ventricular Rupture
o Investigations:
ECG – (ST-Elevation)
Troponins – (Elevated)
CXR
Echo – (Characteristic Regional Wall Motion Abnormalities)
Serum Catecholamines
o Management:
Supportive Therapy
CCF Triple Therapy:
ACEi (Perindopril)
Diuresis
Inotropes (If Hypotensive) (Dopamine)
Aspirin
+/- Warfarin
Week 8 & 9
Preventative Medicine & Addiction Studies Notes
CARDIOVASCULAR DISEASE & OBESITY; NUTRITION & PHYSICAL EXERCISE

CARDIOVASCULAR DISEASE:

What is CVD?
- Heart Disease
- Stroke
- Blood-Vessel Disease
- NB: The Leading Cause of Death.
- NB: Signs & Symptoms are often Silent until Acute Event.

Epidemiology:
- CVD Mortality Has Declined Significantly:
o Better Drugs
o Better Surgery
o Falling Smoking Rates
- However, CVD Rates are Increasing due to:
o Ageing Population
o ↑Overweight/Obesity (Doubled since ‘80s)
o ↑Diabetes (Doubled since ‘90s)
o ↑Sedentary Behaviour
o NB: Hypercholesterolaemia Hasn’t Changed.
- ATSI Populations Suffer Most:
o 3x Rate of Major Coronary Events (incl. Heart Attack)
o 3x as likely to Die from CVD
o 15-25% More Likely to die from Acute Rheumatic Fever & Chronic Rheumatic Heart Disease.
o Why? – Tend to have multiple CV Risk Factors & more of them.

THE 3 MAJOR RISK FACTORS FOR CVD:
- Smoking
- Hypertension
- Hypercholesterolaemia

Other Risk Factors for CVD:
- Unavoidable Factors:
o Sex
o Age
o Family history
o Personality type
- Avoidable/Changeable Factors:
o Nutrition & Inactivity /Sedentary Lifestyle
§ Obesity
§ Hypertriglyceridaemia
§ Hypertension
o Diabetes
o Psychosocial factors (depression, social isolation, poor social support)
o NB: All of the above can be improved by 2 things: - NUTRITION & PHYSICAL EXERCISE.

Lifestyle Measures to Reduce Risk Factors for Chronic Disease:
- *Control Blood Pressure:
o Lose Weight
o Regular Physical Activity
o Nutrition
- *Maintain a healthy Weight:
o Nutrition
- *Physical Activity:
o ↑Activity; ↓Sedentary Behaviour
- *Nutrition:
o Adequate Fruit/Veg
o 2x Fish/Week – (Omegas - Essential Fats)
o Limit Alcohol
o Limit Saturated Fats
o Calcium (At least 800mg/day) à Helps reduced BP in Hypertension.

Role of the National Heart Foundation in CVD:
- Aim: To reduce Suffering & Death from Heart/Stroke/Vessel Disease in Australia.
- How?:
o Fund Scientific Research
o Public Education Resources
§ Public Awareness Programs
§ Assist in Making Healthier Choices
§ Educate Community about Recognising Warning Signs of Heart Attack:
• Jaw Pain
• Neck Pain
• Back Pain
• Shoulder Pain
§ Especially Women – Leading cause of death in Women (4x Breast Cancer)
o Guidelines for Health Professionals:
§ Lipid Management
§ Acute Coronary Syndrome Management
§ Heart Failure Management
§ Hypertension Management
§ Guidelines for Physical Activity (For healthy people & with CVD)
§ Guidelines on Diagnosis/Management of Acute Rheumatic Fever & Rheumatic Heart Disease.
§ Guidelines for Reducing risk of Coronary Heart Disease.
§ ‘Cardiovascular Risk Calculator’
o National Programs:
§ “Tick Program” – (The Heart-Foundation Approved “Tick” on foods.)
§ “Time for Action”
o Advocates of Anti-Tobacco Legislation.
o Advocates of Physical Activity for CVD & Obesity Prevention:
§ Walking Groups – Encourage more people to walk.
o Advocate & Actively Contribute to Improving ATSI Health:
§ Projects to Improve Smoking Cessation.
§ Promoting Physical Activity
§ Promoting Good Nutrition
§ Guidelines on Diagnosis/Management of Acute Rheumatic Fever & Rheumatic Heart Disease.

- Cardiac Rehabilitation
o Assist CVD Patients by promoting Treatment & Rehabilitation:
§ “Heartmoves” – Safe exercise program for Stable CVD Pts/High-Risk Pts/Chronic Disease.
§ Walking Groups – Encourage more people to walk.
§ “My Heart My Life” – Cardiac Rehabilitation:
• (An education booklet resource)
• Phase 1 – Counselling & Education of Cardiac Patients:
o Basic Understanding of Heart Disease
o Angina Recognition & Home-Management.
o Medication Education à ↑Compliance
o Recognition & Modification of Risk Factors
• Phase 2 – Improving Condition & Education of Patient:
o Regain Pre-Hospital Activities.
o Action Plans to Modify Risk Factors.
o Psychological Recovery
o Regular Physical Exercise.
• Physical Activity Guidelines:
o Walk 5-10mins Twice Daily (Post- Surgery/Cardiac-Event)
o Avoid Upper Body Activity (Sternotomy)
o Sleep on back (not side) for 4-6weeks post-op.
o Post-Discharge walking program:

o NB: Shouldn’t do Too Much Physical Activity:
§ Walk & Talk test – (Tests breathlessness)
§ If Previous Day’s Exercise has left you Tired or Sore, have a day off.
o Stairs?:
§ Increase Gradually Within Your Own Limits.
§ (If you can walk normally, you should be fine with 2 Flights of Stairs)
o Sport?:
§ Most sports are fine After 6 Weeks.
§ However, must check with Cardiologist.
o Sex?:
§ Same as 2 flights of stairs.
§ (If you can walk normally, you should be fine with sex)

OVERWEIGHT & OBESITY:

Obesity is due to:
- ↑Processed (High GI) Foods & Drinks
- ↑Fatty foods
- ↑Sedentary Behaviour
- ↑Effort-saving inventions
- Possibly genetically determined (and Epigenetics)
- Epigenetics – events during childhood can change the expression of certain genes which predispose patient
to Obesity (Changes are Permanent & Heritable)
- Leptin Deficiency & Obesity:
o Leptin Deficiency causes Hyperphagia à Obesity
o However, there have only ever been 12 cases worldwide

The General Effect of Fat on the Body:
- ↑Fat Mass à ↑Blood Vessels à↑Peripheral Vascular Resistance à ↑Strain on the Heart à↑CVD
- ↑Fat Mass à ↑Body Weight à ↑Wear & Tear on Joints (Particular weight-bearing)à Arthritis
- ↑Fat Mass à Endocrine Imbalances à Glucose Tolerance .... à Diabetes.
- Many More – Ie. The Whole Body has to work harder to compensate.

What is a Healthy Weight?
- BMI:
o Normal = 18.5-24.99
o Overweight = >25.00
o Obese = 30.00à
- Waist Circumference:
o Better than BMI
o Abdominal Adiposity, Regardless of BMI, Increases Risk of Certain Obesity-Related Conditions.
o NB: Fat deposited elsewhere (hips/buttocks) seems to be less of a risk.
o Healthy Measurements:
§ Women: Waist Circumference of 88cm or Less.
§ Men: Waist Circumference 94cm or Less.

Regulation of Appetite:
- Central Signals:
o Appetite Stimulating
§ Neuropeptide Y
§ Agouti Related Peptide
o Appetite Inhibiting
§ Α-MSH
§ 5HT
§ NE
- Peripheral Signals:
o Positive Feedback:
§ Ghrelin
§ Cortisol
o Negative feedback:
§ Leptin
§ Insulin

- NB. The CNS Appetite-Centre has evolved around the idea that “there is not enough”.
o Ie. There are several Safeguards Against Weight Loss.
o Ie. There is NO Safeguard Against Weight Gain.

↑Mortality increases exponentially with ↑BMI:
- Almost all body organs are affected

Managing Obese Patients:
- Weight loss improves all of:
o Cholesterol
o Glucose tolerance
o HBA1C
o Blood lipids
- Obesity Treatment Pyramid:
o Lifestyle Mods at the foundation (Nutrition/Dieting & Physical Exercise)
o Pharmacotherapy
o Surgery (at the top)

- Nutritional Advice & Food Diaries:
o Useful for recording what/how much/where/ate too much?/calories etc.
o Also useful for monitoring alcohol intake
o NB: There is NO particular Diet that is proven to cause weight loss:
§ Instead, it is an Energy Balance.
§ If by eating low-energy density foods, you create an energy deficit in your body, which is
supplemented by burning fats.
§ Summary:
• Low energy density, calorie controlled style of eating
o Increased fruit & veg
o Reduce sat fat
o Reduce portion size
o Regular meals especially breakfast
o Eat slowly
o Self-Monitoring (food diary)
§ NB: Plateaus in weight loss charts are normal & predictable:
• Patients plateau after losing an amount of weight because their energy intake (which
was previously creating an energy deficit) is now neutral since his body uses less
energy to move the increased body mass. (which is now not there)

- Physical Activity:
o ↑Incidental Movement (Movt is an opportunity rather than inconvenience)
o Increase aerobic capacity
o Resistance training
o NB: Aerobic fitness almost halves risk of cardiovascular disease mortality.
o NB: Increased body fat increases CVD
o However, even a fit, obese person has a lower risk of CVD than an unfit, thin person.
o Benefits of regular physical activity:
§ ↓loss of fat-free mass associated with weight loss
§ Improves maintenance of weight loss
§ Improves cardiovascular risk regardless of weight loss.
- Psychological Component of weight Loss:
o Self monitoring
o Systematic approach to solving problems
o Contingency plans for times of overeating
o Stimulus control (identify triggers for overeating)
o Stress management
o Social Support (important for both exercise & maintaining dietary change) – eg. Wife
o Cognitive Restructuring
§ Changing style of thinking
§ Changing Dichotomous thinking (all or nothing; passed or failed; good or bad)
§ Reassessing Unrealistic Goal Setting
§ Body image issues.

- Bariatric Surgery:
o Indications:
§ BMI over 40
§ Or life-threatening CVD/diabetes/lifestyle impairment
§ Failure to achieve adequate weight loss with non0surgical treatment
§ High Risk Heart Disease
§ Uncontrolled Depression/Psychotic Illness
§ Active Substance Abuse

BRUCE:
- 55yrs
- 84kg à 110kg due to sedentary job, too much food & alcohol. (BMI 35)
- Waist 110cm
- Tried many times to diet/exercise etc, but largely ineffective.
- Motivation – excercise intolerance, uncomfortable, avoid medication, avoid premature death, poor body
image.
- Goal – to be under 90kg.
- Med Hx:
o Impaired glucose tolerance (Elevated fasting BSL)
o Unfavourable lipid profile
o Recently hypertensive 155/90
o Mild osteoarthritis of knees.
- Fam Hx:
o Bowel Cancer
o Myocardial Infarction
o Ischaemic Heart Disease
- Social Hx:
o Poor sleep
o Late to bed, & tired in morning
- Treatment (Physical Exercise):
o Bike riding
o Walked to and from work
o Pedometer
o Supervised resistance training with Exercise Physiologist
o Decreased screen time (Sedentary time)

LIFESTYLE FACTORS & CHRONIC DISEASE

NB: Lifestyle Measures in Treatment of Chronic Disease is INDIVIDUAL:
- Ie. Not one size fits all – (Ie. The same ‘lifestyle prescription’ doesn’t suit everyone.)
- Dietary Advice should be Adapted Depending on the Patient’s Situation:
o Eg. Obese with CVD
o Eg. Normal weight with CVD
o Eg. Diabetes and obese
o Eg. Diabetes and normal weight

Lifestyle Measures to Reduce Risk Factors for Chronic Disease:
- *Control Blood Pressure:
o Lose Weight
o Nutrition
- *Maintain a healthy Weight:
o Nutrition
- *Physical Activity:
o ↑Activity; ↓Sedentary Behaviour
- *Nutrition:
o 2x Fruits/Day
o 5x Vegs/Day
o 2x Fish/Week – (Omegas - Essential Fats)
o Legumes
o Limit Alcohol
o Limit Alcohol
o Limit Saturated Fats
o Calcium (At least 800mg/day) à Helps reduced BP in Hypertension.

- NB: Notice how all of the above tie in with each other?
- Therefore, the 2 MOST IMPORTANT Lifestyle Measures that cover all the bases in reducing Chronic Disease
are Nutrition & Physical Activity.

NUTRITION:

- The Role of Nutrition in Promoting Health & Preventing Chronic Disease:
o Helps Control Blood Pressure
o Helps Control Hypercholesterolaemia
o Helps Maintain/Achieve a Healthy Body Weight
o Good Diet Promotes Good Health – by supplying the body with all essential vitamins/minerals.

- The Role of Nutrition in Management of Chronic Disease:
o Nutrition & Obesity – An Energy Balance:
§ Losing/Maintaining Weight is a simple Energy Balance:
• Ie. Energy Input (Caloric Intake) </= Energy Expenditure (Physical Activity).
• NB: There are certain Energy-Dense foods to avoid (Sweets/Cheese/Butter/Etc),
However, you can still get fat if you eat LOTS of “Healthy” foods.

o Nutrition & Cholesterol – A Problem of SAT-FATs:
§ Apparently Saturated Fats à ↑LDL Levels:
• Don’t know how, Just Know that it Does. (Possible Controversy)
• (NB: LDLs – Low density lipoproteins – are “Bad Cholesterol”)
§ SOURCES OF SATURATED FAT
• ANIMAL PRODUCTS
o Fat on meat
o Skin on chicken
o Dairy fats
o Some “deli meats”
• • VEGETABLE PRODUCTS
o Coconut (milk/cream/oil)
o Palm oil
o Tropical oil
o Vegetable oil (unspecified) eg fish shops
o Many roasted nuts
§ REPLACING SATURATED FAT:
• If Pt. Is Fat: Carbohydrates
• If Pt. Is Thin: Poly- or mono-unsaturated fats
• (Decision depends on BMI)

- Role of Dieticians in Managing Patients with Chronic Disease - Giving Nutritional Advice:
o *Tell them what to eat, rather than what not to eat:
§ 2x Fruits/Day
§ 5x Vegs/Day
§ 2x Fish/Week – (Omegas - Essential Fats)
§ Legumes
§ Limit Alcohol
§ Limit Alcohol
§ Limit Saturated Fats
§ Calcium (At least 800mg/day) à Helps reduced BP in Hypertension
o IF you tell them what to avoid:
§ Many will starve themselves
§ Others will find it too hard & give up

o Nutrition knowledge quiz - Hawkes and Nowak 1998
§ 1. To reduce your cholesterol level do you think you should eat less:
• Cakes/biscuits - yes
• Ice cream - yes - (No if made with Skim Milk)
• Fat on meat - yes
• Peanuts - yes – (Salted Peanuts require oil for the salt to stick)
• Coconut - yes
• Skim milk - (Has NO fat – so makes no difference)
• Sugar – (Sugar will make you fat, but doesn’t affect cholesterol)
• Bread – (It’s what you put on the bread)
• Avocados – (Contains Good Cholesterol)
§ 2. Cholesterol is only found in animal products?
• True – Plants don’t have sat-fats)
• (NB: Saturated Fats apparently increases Bad (LDL) Cholesterol Levels)
§ 3. To reduce your blood cholesterol level is it more important to eat less saturated fat or
less cholesterol?
• Saturated fat
• (NB: Dietary Cholesterol has little/no effect)
§ 4. Which has LESS fat (pick one)
• Butter
• Margarine
• They are equal – (Fat content goes by Weight, therefore 1g of Marg = 1g of Butter)
o (The Only difference is Margarine contains Poly-Unsaturated Fats)
§ 5. Which has LESS fat (pick one)
• Olive oil
• Vegetable oil
• They are equal
§ 6. The correct way to lose weight is to eat LESS:
• Cheese - yes
• Butter - yes
• Cakes - yes
• Margarine - yes
• Bread – (It’s what you put on the bread)
• Bananas – (Depends how much you eat)
• Potatoes - (Depends how much you eat)
• Grapes - (Depends how much you eat)
• Rice yes - (Depends how much you eat)
• NB: While there are some things to avoid to lose weight Faster, it still comes down
to HOW MUCH you eat – (Energy Balance)

§ 7. Are these foods HIGH in fat?
• Toasted muesli - yes – (Muesli is Toasted in Oil. NB: NON-Toasted is fine)
• Nuts - yes – (50% Oil, 50% Protein; Where do you think they get peanut oil from?)
• Margarine - yes – (Even though it contains poly-unsaturated fats, it still has fat)
• Olive oil - yes – (Oil IS Fat in Liquid Form)
• Carob bar - yes – (Requires oil to form it into Bars & Resemble the Texture of Choc)
• Spaghetti – (No – Just carbs)
• Rice – (No – Just carbs)
• Bread – (No – Just carbs)
§ 8. The Main Ingredient in a food is listed FIRST on a food label:
• True
§ 9. Does one teaspoon of fat weigh:
• 0.1 gram
• 1 gram
• 4 grams
• 10 grams
• not sure
§ 10. Which of these foods contain fibre?
• Oranges - yes
• Bread - yes – (NB: White Bread has very little; unless fortified with fibre)
• Baked beans – yes
• Steak – (NO – Just Protein)
• apple juice – (NO – unless freshly squeezed with pulp)
• fish - (NO – Just Protein)

PHYSICAL ACTIVITY:
- The Role of Physical Activity in Promoting Health & Preventing Chronic Disease:
o NB: DECREASING Sedentary Behaviour is MORE EFFECTIVE than INCREASING Exercise.
§ Both are good, but doing exercise is pointless if you lead a Sedentary Lifestyle.
§ What you WANT to do is ↑PHYSICAL ACTIVITY.
§ Ie. Exercise ≠ Physical Activity:
• Exercise = Dedicated Physical Exertion
• Physical Activity = Miscellaneous Day-to-Day Activity.

- The Perils of Sedentary Behaviour:
o Sedentary Behaviour is DIRECTLY LINKED to:
§ ** CVD (NB: All of the below further contribute to CVD)
§ *Obesity
§ *Depression
§ *Diabetes (Typically type 2)
§ Osteoporosis
§ Stroke
§ Hypertension
§ High Cholesterol
o Exercise is known to a) Reduce the Risk of these conditions, but b) Also Decrease their Severity.
§ Ie. Any Increase in Physical Activity (be it small/large) is immensely beneficial, Even in
patients who already have these diseases.

- The Rewards of ↑Physical Activity:
o ↑Lean body mass
o ↑Bone density
o ↑Cardiac output
o ↑Oxygen carrying capacity & exchange
o ↑Metabolism
o Improved neurotransmitter regulation
o Improved mood, self-efficacy
o Improved QOL

- Physical Activity Guidelines:
§ (NB: Moderate Activities = Brisk walk, a Bike ride or Active Play)
§ (NB: Vigorous Activities = Anything that makes the kid “huff and puff” (Ie. Sports))
o 5-12 year olds:
§ Combination of Moderate and Vigorous Activities for At Least 60mins/day.
§ NB: Children & Adolescents require almost Double.
o 12-18 year olds:
§ At least 60mins of Moderate to Vigorous Physical Activity Every Day.
§ NB: Children & Adolescents require almost Double.
o Adults:
§ Step 1 – Think of movement as an opportunity, not an inconvenience
§ Step 2 – Be active every day in as many ways as you can
§ Step 3 – At least 30mins of Moderate Physical Activity per day. (At least 5 days a week)
§ Step 4 – Some Regular, Vigorous Activity for extra health and fitness.
§ NB: If Exercise is being used as a disease Intervention, the recommendations are Doubled.
o Elderly/Completely Sedentary:
§ ANY Physical Activity is Beneficial.

- Rate of Perceived Exertion – RPE – “Borg’s RPE Scale”:
o Measures Perceived Exertion on a scale of 0-20:
§ 0 = Falling Asleep; 6 = Very Very Light Exertion; 20 = Maximal Exertion
o Why? – Because HR alone is an unreliable measure of exertion in patients on Cardio-Drugs.

- How do we Ensure the Exercise is Safe for the Patient?:
o NB: Low-Risk Patients can start exercise Immediately.
§ However, Moderate-High-Risk Patients should undergo medical testing before undertaking
any exercise.
o Risk Stratification Flow-Chart:

NB: I Doubt you’ll have to memorise this. For your interest & understanding only.

- The Role of Physical Activity in Management of Chronic Disease:
o PA & Management of Cardiovascular Disease (Post Myocardial Infarction):
§ Post-MI Exercise is Immediate:
• Ie. Within days after the MI.
• NB: However, It is only LOW INTENSITY.
• NB: Cardiac Rehab is usually done as an INPATIENT under close supervision.
§ Recommendations (MI)
• Begin ASAP
• 3days/wk
• 20-60 min (cardiac rehab) PLUS home-based
• Start @ 40-60% Heart-Rate Reserve; progress to 85%
• (HR Reserve = 220 – Age – Resting HR.)
§ Benefits (MI):
• Improved cardio-respiratory function
• Protection against exertional MI trigger
• Reduced HR, BP, LDL, TC
§ Contraindications (CVD):
• Change in Resting ECG Indicating Ischemia/MI/Unstable Angina/Uncontrolled
Dysrhythmias.
• Symptomatic Aortic Stenosis
• Uncontrolled Heart Failure
• Pulmonary Embolus/infarction
• Myo-/Pericarditis
o PA & Management of Diabetes:
§ Diabetics are advised to Cycle/Swim instead of Running:
• Because Peripheral Vasculopathy & Neuropathy in Diabetes à Repetitive Trauma to
feet + Little Sensation à Formation of Ulcers.
§ Benefits:
• Improved Action of Insulin (Insulin Sensitivity)
o NB: Exercise + Normal dose of Insulin = Additive Effect; can cause
hypoglycaemic shock. Therefore Necessary to ↓Insulin dose with Exercise.
o NB: Can even Reverse Type-2 Diabetes.
• Improved Glucose tolerance
• Improved weight management
• Improved BP à Decreased CVD Risk
• Improved Lipid profiles àDecreased CVD risk
§ Recommendations:
• Aerobic Exercise: (20-60min @ Heavy Exertion (High RPE) At least 4 Times/wk)
• Strength: (Low Resistance @ Moderate Exertion (RPE 11-16) 2-3 Times/wk.)
• Flexibility, balance & coordination: (2-3xwk)
§ Precautions:
• Effects of insulin & exercise are ADDITIVE - (Adjust insulin dose accordingly)
• If BG <4 or >17 mmol/L, delay exercise until stable
• Always have glucose handy (honey, jelly beans) in case of Insulin Overdose.
• Illness, infection, retinal haemorrhage, peripheral neuropathy.

o PA & Management of Depression:
§ Benefits:
• Improved Self-esteem
• Improved Mood
• Opportunity for participation in community/family events/tasks
§ Recommendations:
• HIGH Intensity, FUN Exercise is recommended à Mental Distraction.
o NB: The opposite (Anxiety), requires long, slow, exercise à Calming.
• The longer the duration, the greater the benefit
• Exercise is As Effective as psychotherapy
§ Precautions:
• CVD risk factors
• Stage of change & motivation
• Must vary exercises, repetition leads to boredom.

o PA & Management of Cancers:
§ Benefits:
• Preservation/Improvement in Muscle Mass & Strength
• Preservation/Improvement of CV fitness
• Preservation/Improvement of Immune Function
• Preservation/Improvement Self-Esteem
• Decrease in side-effects & symptoms
• Decreased hospitalisation length, depression & anxiety
§ Recommendations:
• Large muscle groups (Moderate Daily Aerobic Exercise ≈ 20-30 min total)
§ Precautions:
• Swimming (Infection/catheters/wounds)
• Limited Balance/Coordination (eg. Treadmill, Yoga) when sensory neuropathy, dizzy.
§ Contraindications:
• On days of IV Chemotherapy.
• Platelets<50,000; WBC<3,000
• Unusual weakness/malaise, dehydration, nausea
- Allied Health Professionals & Physical Activity:
o Exercise Scientists (3Yr Degree):
§ Mainly Involved in Disease PREVENTION in Healthy Patients:
• Kids/teenagers:
o • active after school program
o • sporting groups
• • Adults:
o • community projects (healthy hearts, 10,000 steps)
o • workplace health promotion (corporate challenges)
• • Elderly:
o • group exercise (aqua)
o Accredited Exercise Physiologists (4Yr Degree):
§ Mainly Involved in Management & Rehabilitation of Chronic Disease Patients:
• Musculoskeletal conditions
o Athletic/Workplace injury
o Osteoarthritis/Osteoporosis/Back pain
• Neurological conditions:
o Multiple Sclerosis, stroke, ABI, SCI, Epilepsy, Cerebral Palsy, Parkinsons
Disease
• Cardio-respiratory conditions:
o CVD, asthma, COPD, emphysema, cystic fibrosis
• Metabolic conditions:
o Obesity, diabetes
• Cancers
§ NB: AEPs Have Medicare Provider Numbers – Pts are covered.
CVS Pathology:
Congenital Heart Defects
Review of Foetal Circulation:

B passes Sh n s of foe al circ la or s s em
o Ductus Venosus
Shunts O2-Blood from Placental Vein IVC R-Atrium
Bypasses the Liver
o Foramen Ovale
Shunts O2-Blood from R-Atrium L-Atrium.
Bypasses the Lungs.
o Ductus Arteriosus
Shunts O2-Blood from Pul-Artery Aorta
Bypasses the Lungs
o ( All of these “shunts” are should close after birth due to pressure changes)
NB: The Foramen Ovale can take up to 6 months to close.
CONGENITAL HEART DEFECTS:

NB: 50- of Children ha e Innocen Hear M rm rs Red Flag = Murmur + Cyanosis/ Perfusion.
L R (Non-Cyanotic) Shunts (ASD, VSD, PDA)
o VSD = Commonest
R L (Cyanotic) Shunts (TETRALOGY & TRANSPOSITION)
Obstructive Defects (COARCTATION, Valvular Stenoses)
Genetic Associations:
- MARFAN S SYNDROME
o Autosomal Dominant Disorder
o CV-Defects: - (Mitral Prolapse / Tricuspid Prolapse / ASD / Others)
- DOWN S SYNDROME
o Trisomy 21
o CV-Defects: - (Valvular Malformations / ASD / VSD)
Left Right (NON-Cyanotic) Shunts.
- PATENT DUCTUS ARTERIOSUS (PDA):
o = Malocclusion of Ductus Arteriosus after birth.
L R Shunt from Aorta Pulmonary Artery
Pulmonary Hypertension
Murmur (Continuous, Harsh “Machinery-like” Murmur).
o Complications:
Soon After Irreversible Obstructive Pulmonary Vascular Disease (Pulmonary Vessel
Hypertrophy & Vasoconstriction Resistance SHUNT REVERSAL Cyanosis
o Investigations:
CXR (Pulmonary Congestion, Cardiomegaly)
ECG (LVH, RVH)
ECHO (Definitive)
o Management:
(*PDAs should be closed as early in life as possible)
Medical: Indomethacin (Prostaglandin Inhibitor)
(NB: In Cyanotic Heart Defects, Prostaglandin is actually Given to maintain a PDA)
Surgical: Surgical Ligation
- ATRIAL SEPTAL DEFECT (ASD):

o = Hole in the Interatrial Septum. (NB: NOT a patent Foramen Ovale)
Shunt from L-Atria R-Atria:
RV-Hypertrophy & Pulmonary HTN.
Asymptomatic in Childhood (Symptom onset yrs).
Murmurs:
Diastolic ASD Murmur (During Atrial Contraction)
(Systolic Pulmonary Flow-Murmur (Hyperdynamic))
(Splitting of S2 (Delayed P2))
RV-Hypertrophy Parasternal Heave
o Complications are Rare, but Include:
CCF Pulmonary Oedema (Dyspnoea) + Peripheral Oedema, Ascites, etc.
Parado ical Embolisa ion (DVT Stroke)
o Investigations:
ECG (RV-Hypertrophy, RAxDev)
CXR (Pulmonary Congestion & Oedema)
ECHO (Definitive)
o Management:
Surgical Endovascular Closure of Defect
- VENTRICULAR SEPTAL DEFECT (VSD):
o (*The Most Common Congenital Heart Disease)
o = Hole in the Interventricular Septum.
Shunt from L-Vent. R-Vent.
LV-Failure (CCF, Pulm.HTN, RV-Hypertrophy).
Asymptomatic if Small (& Close Spontaneously)
Failure to Thrive if Large (& Requires Surgical Closure)
Murmurs:
Pansystolic VSD Murmur (+/- L-Sternal Thrill)
Pulmonary Valve Flow Murmur
CCF (Dyspnoea, Cough, Peripheral Oedema)
o Complications:
Initially a L-R-Shunt Pulmonary HTN RV-Hypertrophy
Later Irreversible Obstructive Pulmonary Vascular Disease SHUNT REVERSAL:
R-L Shunt ( O2 Blood Systemic Circulation Cyanosis/Death)
o Investigations:
CXR (Pulmonary Congestion, Cardiomegaly)
ECG (LVH & RVH)
ECHO (Definitive)
o Management:
Early surgical intervention is Critical for normal lifespan
Right Left (CYANOTIC SpO2 <75%) Shunts
- TETRALOGY OF FALLOT C ano ic Hear Bl e Bab S ndrome
o 4 Features:
1. VSD
2. Overriding Aorta:
Aortic Valve sits above the VSD :. Connected to both the R & L-Ventricle.
3. Subvalvular Pulmonic Stenosis:
RV-Outflow Obstruction R-L-Shunt Hyopxemia/Cyanosis
4. R-Ventricular Hypertrophy:
Due to R-Vent. Worlkload
(5. Sometimes Patent Ductus Arteriosus)
If Mild Pulm. Stenosis Resembles an isolated VSD. (L-R-Shunt) [Non Cyanotic]
If Severe Pulm. Stenosis R-L-Shunt
Chronic Cyanosis SpO2 <75%
Fingernail Clubbing
Polycythaemia RBC
Symptoms:
Blue Baby
Paroxysmal Tachypnoea
Irritability/Crying
o Complications:
“Paradoxical Embolism – (DVT Stroke)
Seizures
o Investigations:
ECG (RV-Hypertrophy)
CXR (Boot-Shaped Heart)
ECHO (Definitive)
o Management:
Medical:
Supp O2
B-Blocker
Surgical:
Definitive Repair
- TRANSPOSITION OF GREAT VESSELS:
o = Aorta & Pulmonary Artery are switched.
(NB: Atrioventricular Connections are correct)
(NB: Venous Return is correct – IVC/SVC & Pulmonary Veins)
Hence, the Pulmonary & Systemic Circuits run in Parallel, rather than Series.
o NB: Incompatible with Post-Natal Life Unless a Shunt exists for Mixing of Blood:
Eg. TGV + VSD = Stable Shunt. (Adequate mixing)
Eg. TGV + Patent Foramen Ovale = Unstable Shunt (Tends to close).
Severe Hypoxemia & Cyanosis
Blueness of skin & mucous membranes
Fingernail Clubbing
Polycythaemia RBC
o Complications
Prominent R-Ventricular Hypertrophy (R-V Pressure overload)
Atrophy/Thinning of L-Ventricle
o Investigations:
ECG (RAxDev, RVH)
CXR (Egg-Shaped Heart w. Narrow Mediastinum – “Egg on a string heart”)
ECHO (Definitive Dx)
o Management:
Prostaglandin Infusion (To maintain PDA & allow mixing of blood)
Surgical repositioning of Great Vessels
o Prognosis:
90% 1yr Mortality without Surgery.
Obstructive Defects:
- COARCTATION OF AORTA
o = Narrowing/Constriction of the Aorta.
2M:1F
50% have Bicuspid Aortic Valve
o Pathophysiology 2 Types:
Preductal:
Proximal to Ductus Arteriosus
• R-L-Shunt (Pulm.Artery Aorta).
• Cyanosis of Lower Half of body.
Postductal:
Distal to Ductus Arteriosus.
• L-R-Shunt from Aorta Pulm.Artery
• Pulmonary HTN & CCF
Symptoms:
Leg Claudication
NB: Presentation may take up to 10 years – As the Coarctation doesn’t grow with
the rest of the body Only symptomatic when peripheral demand > Aortic Flow.
Signs:
Upper limb BP > Lower limb BP.
RF-Delay
Cold Legs & CRT
Systolic Murmur
LV-Hypertrophy
o Investigations:
ABI - (Asymmetrical)
ECG (LV-Hypertrophy)
o Management:
Surgery – (Balloon Angioplasty & Stenting).
- AORTIC STENOSIS:
o = Narrowing/Obstruction of the Aortic Valve.
LV-Afterload Cardiac Output LV-Failure (Pul.HTN, Dyspnoea)
- PULMONIC STENOSIS:
o = Narrowing/Obstruction of the Pulmonary Valve OR Artery.
RV-Afterload Pulmonary Output RV-Failure (Peripheral Oedema)
Week 11
Congenital Heart Defects

Basics of Foetal Development of the Heart:
- Begins at Wk 3 of Gestation
- Why? Because by this stage, the foetus is too large for nutrient/gas exchange to be via simple diffusion.
o Therefore, an active nutrient/gas distribution system is needed for continual growth of Foetus.
- Beating occurs @ week 4/5

- The “Cardiac Tube”:
o The primordial tubular heart in the embryo, before its division into chambers.

o This cardiac tube begins to fold & twist on itself until it is laid out in the basic heart-like structure.

- Septation:
o Between 4-6 weeks
Foetal Circulation:
• Foetal circulation is different from neonatal circulation.
o Has to integrate circulation of placenta.
o Blood flow to non-functional lungs & liver are partially bypassed.
• “Bypasses” / “Shunts” of foetal circulatory system:
o Ductus Venosus
§ Directs the oxygenated blood from the placental vein into inferior vena cavaàheart
§ Partially bypasses the liver sinusoids
o Foramen Ovale
§ An opening in the interatrial septum loosely closed by a flap of tissue.
§ Directs some of blood entering the right atrium into the left atrium à Aorta.
§ Partially bypasses the lungs.
o Ductus Arteriosus
§ Directs most blood from right atrium of the heart directly into aorta
§ Partially bypasses the lungs
o **All of these “shunts” are occluded at birth due to pressure changes.
§ NB: The Foramen Ovale can take up to 6 months to close.
• NB: At Birth, the Pulmonary Vascular Resistance Falls Due to:
o 1. Mechanical Inflation à Increased Radial Traction of Vessels
o 2. Vasodilation – due to ↑Oxygen-Tension in the Lungs

Types of Congenital Heart Defects:

Septal Defects:
- A hole in the septum (Either Atrial/Ventricular) Leading to the Mixing of Blood from one side to the other.
o This ‘mixing’ (shunt) typically occurs from Left to Right (Due to Higher L-Heart Pressure)
o However, the shunt may reverse to RightàLeft (If Pulmonary Blood Volume Reaches a Critical Level)
- Treatment: Direct suture closure with a pericardial/synthetic patch.

• Atrial Septal Defects:
o Opening in the Inter-Atrial Septum – Usually at the level of the Foramen Ovale.
o NB: This is different from a ‘patent foramen ovale’ (Normal for up to 6-12 months old) in that an
‘Atrial Septal Defect’ is just a hole, not a flap.
o Leads to: Oxygenated Blood is shunted from the L-Atrium to the R-Atrium.

• Ventricular Septal Defects:
o Opening in the Inter-Ventricular Septum – Vary greatly in size.
§ Most smaller shunts close spontaneously by 2 yrs.
§ Larger shunts tend to remain open
o Leads to: Blood shunted from L-Ventricle to R-Ventricle àIncreased output to Pulmonary Circulation
§ Can result in Pulmonary Hypertension à R-Heart failure & Hypertrophy
à The Shunt may Reverse à Causing Deox. Blood to
flow into L-Ventricle (Therefore Systemic Circulation) à Systemic Cyanosis.
(Eisenmenger Syndrome)

Patent Ductus Arteriosus:
- Where the Foetal Shunt that connects the Pulmonary Artery to the Aorta Doesn’t Close off.
o Normally, Rising O2 Tension & Decreasing Prostaglandins cause it to Close.
- Leads to: Shunting of Oxygenated (Aortic) Blood back into the Pulmonary Artery (Deox) à Lungs.
o NB: In Utero, Blood flows the other way (From the Pulmonary Artery to the Aorta)

Valvular Stenosis:
- Aortic Stenosis:
o Narrowing/Obstruction of the Aortic Valve.
o Typically presents as a Bi-Leaflet, instead of the normal Tri-Leaflet Formation.
o Most common in males.
o Leads to: Increased Afterload à ↑L-Ven. End Systolic Volume à ↓Cardiac Output à Hypotension
(↓Cardiac Output à Backup of Blood in Lungs à Pul.Congestion)
à L-Ventricular Hypertrophy à Possibly Left Heart Failure

- Pulmonic Stenosis:
o Narrowing/Obstruction of the Pulmonary Valve OR Artery.
§ 90% = Valvular
§ 10% = Elsewhere in the Pulmonary Artery
o Leads to: Increased Afterload à ↑R-Ven. End Systolic Volume à ↓Pulmonary Output
(↓Pulmonary Output à Backup of Blood in Body à Syst.Oedema)
à R-Ventricular Hypertrophy à Possibly Right Heart Failure

Coarctation of the Aorta:
- Narrowing of the Aortic Lumen Either Before or After the Ductus Arteriosus.
o “Preductal” Coarctation of the Aorta
o “Postductal” Coarctation of the Aorta
- Leads to: Increased Afterload à ↑L-Ven. End Systolic Volume à ↓Cardiac Output à Hypotension
(↓Cardiac Output à Backup of Blood in Lungs à Pul.Congestion)
à L-Ventricular Hypertrophy à Possibly Left Heart Failure
àDecreased Perfusion to Abdominal Organs & Lower Limbs.
- NB: Clinical Presentation may take up to 10 years – Due to the fact that the Coarctic bit doesn’t grow, while
the rest of the heart grows around it. Hence, it only presents itself when the body’s demand for increased
cardiac output exceeds the flow rate of the Aorta.
- Treated By: Surgery or Balloon Angioplasty & Stenting.

Preductal Coarctation Postductal Coarctation

Tetrology of Fallot:.
- Consists of 4 Abnormalities:
o 1. Ventricular Septal Defect
o 2. Subvalvular Pulmonic Stenosis
o 3. R-Ventricle Hypertrophy (Due to Pulmonic Stenosis)
o 4. Overriding Aorta (Valve sits over the Vent.Septal Defect – ie. Receives Blood from Both Ventricles)
- Most Common Cause of CYANOSIS after Infancy.
- Symptoms:
o Cyanosis
o Irritability
o Hyperventilation (Due to Cyanosis–low [O2] stimulates peripheral chemoreceptors à ↑Respirations)
o Occasional Syncope (Fainting)
o Occasional Convulsion
- Symptoms Alleviated by Increasing Systemic Vascular Resistance:
o Eg. By squatting (kinking femoral artery)
o à Means more blood being ejected via the Pulmonary Artery à Better Oxygenation.

Transposition of the Great Vessels:
- Where the Aorta comes off the R-Ventricle & the Pulmonary Artery comes off the L-Ventricle.
- Hence, the 2 Circuits (Pulmonary & Systemic) are running in Parallel, rather than Series.
o Pulmonary Circuit:
§ L-Vent. Blood à Pulmonary Artery à Lungs à Pulmonary Vein à L-Atrium à L-Vent.
o Systemic Circuit:
§ R-Vent. Blood à Aorta à Systemic Circulation à Vena Cavae à R-Atrium à R-Vent.

- The Most Common Cause of Cyanosis (“Blue Babies”) during Infancy
- Leads to:
o Severe Hypoxia & Cyanosis
- Typically Incompatible with Life:
o 30% die within a week
o 90% die within a year
- The Baby May Survive If:
o 1. The Foramen Ovale Remains Patent...and
o 2. The Ductus Arteriosus Remains Patent
o – These shunts maintain some communication between the parallel circuits à may prolong life.
o – Therefore the doctor may give Prostaglandins to Maintain Patency of the Ductus Arteriosus as a
short-term treatment until surgery is available.
- Treatment (Surgery):
o Atrial Switch (Mustard/Senning Procedure):
§ Where the Systemic Venous Blood is diverted to the Left Atrium à L-Ventricle à Lungs.
§ And the Pulm-Venous (Oxy) Blood is diverted to the R-Atrium à R-Ventricle à Aorta
§ - The Disadvantage = The R-Heart becomes responsible for Systemic Circulation (which it is
not designed to do)
o Arterial Switch:
§ Where the Pulmonary Artery & Aorta are switched.

Atrial Swich Operation Arterial Switch Operation
Marfan’s Syndrome:

- Autosomal Dominant Disorder
- Common CV Abnormalities
o Mitral Valve Prolapse - (L-AV Valve) this can lead to a mitral valve regurgitation. (blood will flow back
from the ventricle to the atrium)
o Tricuspid prolapse
o ASD
o Many More.....

Down’s Syndrome:

- 40% of Down’s Syndrome Patients have congenital Heart Defects
- Common CV Abnormalities:
o Atrio-Ventricular Canal - (Incomplete formation of AV Valves)
o Atrial Septal Defects
o Ventricular Septal Defects

CVS Pathology:
DVT & PE
DEEP VEIN THROMBOSIS “PHLEBOTHROMBOSIS” “THROMBOPHLEBITIS” :

- Aetiology:
o **Deep Venous Valve Incompetence of Lower Limbs:
Blood Stasis Thrombosis
o + **Prolonged Immobilisation:
Blood Stasis Thrombosis
o +Risk Factors:
“Virchow’s Triad”
1. Vessel Damage:
o Surgery/Smoking/Hypertension
2. **Stasis
o Flight/Long Travel/Prolonged Bedrest/Surgery
o Obesity/Pregnancy/Congestive Heart Failure
o Post Operative
3. Hypercoagulabiltiy
o Cancer (Eg. Adenocarcinoma Paraneoplastic Syndrome)
o Congenital: Eg. Antithrombin III Def./Factor 5 leiden
o Drugs: Eg. Oral Contraceptive/HRT
o Hyperviscosity: Eg. Pregnancy/Polycythaemia
- Pathogenesis:
o Failure/Inactivity of the Venous Calf Pump (Immobility/Valve Insufficiency)
Blood Stasis & Pooling in Leg Veins Coagulation Thrombosis
o Symptoms:
Localized Symptoms (Typically in Calf):
Tenderness (Elicited by Pressure/Passive Dorsiflexion)
Heat, Redness, Swelling
Distal Oedema
Distal Cyanosis
Superficial Venous Dilation
**Pulmonary Embolism – May be the 1st Manifestation:
Thromboembolism into Pulmonary Artery Biventricular Heart Failure
o Sudden Chest pain, Dyspnoea, Haemoptysis, Collapse, Death.
- Investigations:
o Duplex Doppler USS (93% Sensitive; 98% Specific)
- Management:
o **Heparinization (LMW-Heparin) 1wk
Then Convert to Warfarin 6mths
o +/- Thrombectomy
o +/- IVC Filter (To Prevent Pulmonary Embolus)
PULMONARY EMBOLISM
- Aetiology:
o 95% = DVT Thrombo-Emboli
- Pathogenesis:
o DVT Thrombo-Emboli Lodges in Pulmonary Arteries
1. VQ-Mismatch Respiratory Compromise (Respiratory Failure)
2. ↑Pulm.Vas.Resistance Haemodynamic Compromise (Heart Failure).
o Severity Depends on Size/Number of Emboli (Extent of Obstruction)
o If Severe Instant Death!! (Due to sudden Cardiac Failure)
o Symptoms
Pleuritic Chest Pain (+ Pleural Rub)
Dyspnoea/Tachypnoea
Cough/Haemoptysis
(+ DVT Symptoms)
o Signs:
RV-Failure (↑JVP, Tricuspid Regurg)
Shock/Syncope
Fever
- Diagnosis:
o **CTPA (CT-Pulmonary Angiogram): Shows Large Emboli lodged in Major Pulmonary Artery
o ECG: Classical S1Q3T3 Pattern
o VQ Scan: Shows VQ Mismatch
o CXR (Later >1day): Shows Wedge-Shaped Pulmonary Infarct
- Treatment:
o Give Oxygen
o **Heparinization (LMW-Heparin) 1wk
Then Convert to Warfarin 6mths
o TPA-Thrombolysis (If Haemodynamic Compromise)
o (+/- Trombectomy & IVC Filter)
- Prevention (in High Risk Individuals):
o Elastic/Compression Stockings
o Anticoagulation
o If Severe Risk, Insertion of a IVC-Filter

• pulsatile mass
❏ management
❏ prognosis

ANATOMY
❏ flow stasis
❏ surgery
• pregnancy
• estrogen use
• varicose veins
VASCULAR - VENOUS DISEASE . . . CONT.
❏ signs and symptoms

• most frequent site of thrombus formation is calf
• isolated calf thrombi often asymptomatic
• 30-50% are asymptomatic or minimal symptoms
• 20-30% extend proximally and account for most clinically significant emboli
• classic presentation < 1/3
• calf/thigh discomfort, edema, venous distension
• investigations (refer to PIOPED study for details)
• history and physical
• calf tenderness (if elicited on ankle dorsiflexion = Homan’s sign)
• wider circumference of affected leg
• fever POD #7-10
• clinical assessment incorrect 50% time, therefore must confirm by objective method
• non-invasive tests
• duplex doppler U/S
• 93% sensitive and 98% specific for symptomatic patients, decreased for asymptomatic patients
• detects proximal thrombi
• initial negative exam should be repeated 6-7 days later to detect proximal extension
• invasive testing
• ascending phlebography (venogram)
• the gold standard but costly
• detects distal and proximal thrombi
• complicated by contrast-induced thrombosis of peripheral veins (2-3%)
❏ management
• goals of treatment
• prevent formation of additional thrombi
• inhibit propagation of existing thrombi
• minimize damage to venous valves
• prevent pulmonary emboli (PE)
• 25% develop PE if untreated; 5% if treated
• aggressive medical management
❏ treated as outpatient
❏ fragment / low molecular weight heparin (LMWH)
❏ coumadin
❏ advantage: avoid hospitalization
• conservative medical management
• IV heparin, 5,000 U bolus + 1,000 U/hr to keep aPTT 2-2.5x control
• convert to warfarin 3-7 days after full heparinization; warfarin for 3-6 months
• risks of therapy - bleeding, heparin-induced thrombocytopenia, warfarin is teratogenic
• surgical
• venous thrombectomy - if arterial insufficiency with extensive iliofemoral thrombosis,
+/– venous gangrene
• inferior vena cava (IVC) (Greenfield) filter- inserted percutaneously, indications:
• recurrent PE despite anticoagulation
• contraindication to anticoagulation e.g. intra-cranial trauma
• certain operations for cancer, pulmonary embolectomy
• septic emboli refractory to combination antibiotic and anticoagulation
• "free-floating" thrombus loosely adherent to wall of IVC or pelvic veins
• IVC ligation, surgical clips - increases risk of venous insufficiency; rarely used
❏ DVT prophylaxis
• conservative
• minimize risk factors
• early ambulation, passive range of motion
• anti-embolism stockings
• pneumatic sequential compression devices
• elevation of limb
• medical prophylaxis
• optimize hydration to prevent hemoconcentration
• ECASA, warfarin, minidose heparin(5,000 U SC q8-12h) in high risk situations
❏ complications
• pulmonary embolus (PE)
• varicose veins
• chronic venous insufficiency
• venous gangrene
• phlegmasia cerulea dolens (PCD) - massive DVT with clot extension to iliofemoral
system and massive venous obstruction resulting in a cyanotic, immensely swollen,
painful and critically ischemic leg
• risk venous gangrene
• phlegmasia alba dolens (PAD) - as above with additional reflex arterial spasm
resulting in less swelling than PCD
• cool leg and decreased pulses
CVS Pathology:
Dyslipidaemia
DYSLIPIDAEMIA:
- Dyslipidaemia = a blanket term for Elevated Blood levels of Fats (cholesterol and/or triglycerides).
- Review of physiology of cholesterol and other lipids:
o Five Lipid Transporters:
1. Chylomicrons Made by Small Intestine:
Transport Dietary Fats from SI Liver (Via Lymph).
Ver Lo Densit Lipoproteins VLDL s Made by Liver:
Transports Fats from Liver Tissues.
Intermediate Densit Lipoproteins IDL s Made by Liver:
Essentially a VLDL with some lipid and protein removed.
4. Low Density Lipoproteins (LDL s) BAD
Delivers Cholesterol to Liver and Tissues.
NB: Fat Consumption [LDL] ATHEROSCLEROSIS.
5. High Density Lipoproteins GOOD
Cholesterol Re-Uptake from Tissues Liver
- Aetiologies:
o Primary Hyperlipidaemias (Genetic):
Eg. Familial Hyperlipidaemia
Eg. Lipoprotein lipase deficiency
o Secondary Hyperlipidaemia (Acquired):
Eg. Obesity
Eg. Hypothyroidism
Eg. Diabetes mellitus
Eg. Nephrotic syndrome
Eg. Liver Failure
Eg. Drugs: (eg. Oral contraceptives/Retinoids/thiazide diuretics)
- Diagnosis & Screening (for high risk Pts):
o FamHx of CVD/IHD/MI/ Cholesterol
o Physical Signs (Xanthomata, Xanthelasma)
o Comorbidities (Eg. Obesity, Diabetes, HTN, Hypothyroid).
- Investigations:
o Serum TGLs - (Normal = <2mmol/L):
*>6mmol/L Requires Intervention - (<6mths Lifestyle Modification Statin Therapy).
o Cholesterol - (Normal = <4mmol/L):
*>6.5mmol/L Requires Intervention - (<6mths Lifestyle Modification Statin Therapy).
(Target = <4mmol/L total cholesterol or LDL-CK less than 1.8mmol/L)
- Management:
o **1. Lifestyle Modification:
Diet ( Sat.Fat/Cholesterol Intake, Fibre intake, Alcohol, Smoking, Weight Loss)
Exercise
o **2. Pharmacological:
**Statins (HMG-CoA Reductase Inhibitors):
Classical Agents: (Simvastatin, Atorvastatin)
MOA: HMG-CoA Reductase Inhibitor Cholesterol Synthesis
Side Effects:
o Statin-Induced Myopathy/Myositis/Rhabdomyelosis Muscle
Pain/Weakness + CK-Levels
o (Other Lipid-Lowering Agents (Only Recommended If CHD or Intolerant to Statins)):
*Fibrates: (Fenofibrate)
Bile Acid-Binding Resins (Ion Exchange Resins): (Cholestyramine)
Ezetimibe: (Ezetimibe)
Fish Oil (Omega-3) Prophylactic?
CVS Pathology:
HEART FAILURE
HEART FAILURE:
- Insufficient Cardiac Output to meet the demands of the body Organ Perfusion
- NB: 30% die within 1yr of Dx.
Where is the Failure?:
- Myocardial Failure (Ie. Systolic/Diastolic Dysfunction (Heart Muscle Itself) Pumping Function):
o (Eg. Ischaemic Heart Disease, Myocarditis, Cardiomyopathies, etc.)
- Valvular Heart Failure (Ie. A problem with the Heart-Valves Pumping Function):
o (Eg. Stenosis/Regurgitation)
- Circulatory Failure - (Ie. Defect in the Peripheral Circulation Vascular System Dysfunction):
o (Eg. Haemorrhage/Shock)
What side is the Failure?

- Left Heart Failure (LSHF):
o = L-Ventricle CO into Systemic Circulation
o Common Causes:
Systolic Failure: Weak LV (IHD, Dilated Cardiomyopathy, Alcoholism, Myocarditis)
Diastolic Failure: Stiff LV (Eg. Amyloidosis, Sarcoidosis, Hypertrophic Cardiomyopathy).
Valve Dysfunction: (Aortic Stenosis/Regurg, Mitral Stenosis/Regurg)
Excessive Afterload: (Eg. HTN, Coactation of Aorta, Dissecting AAA)
o Consequences & Clinical Features:
Pulmonary Congestion CCF Cough/Dyspnoea/Or hopneoa P can lie fla /PND.
CO (Kidneys Pre-Renal Failure), (Brain Irritability, ALOC)
LV-Hypertrophy Initially Adaptive, then Weakens Worse LV-Failure
- Right Heart Failure (RSHF):
o = R-Ventricle CO into Pulmonary Circulation
o Common Causes:
Isolated RHF is Rare (Typically caused by LSHF, Aka. “Cor Pulmonale )
“Cor Pulmonale : LSHF Pulmonary Hypertension RSHF.
o Consequences & Clinical Symptoms:
Pulmonary Congestion CCF Cough/Dyspnoea/Orthopneoa P can lie fla /PND.
PLUS Systemic Congestion Peripheral Oedema/Organomegaly/Pleural Effusion/Ascites
Signs of Cardiac Output:
- Thready Pulse (Due to Low Arterial Pressure)
- Tachycardia (A Compensatory Mechanism)
- Exercise Intolerance (Due to Ti e Perf ion & Pulmonary Congestion)
- Dyspnoea (Due to In Pulmonary Congestion)
- Peripheral Oedema (Venous Overload)
The Body’s Responses to Heart Failure:
- Short Term (Adaptive):
o Peripheral Shutdown (To maintain BP of Vital Organs. Af erload
o Salt & H2O Retention To Blood Vol me Preload
o Preload To S roke Vol me
o Sympathetic Tone To Hear Ra e Ejec ion
o Hypertrophy To M cle Ma o Con rac ile S reng h
- Long Term (Maladaptive):
o Peripheral Shutdown Afterload L-Heart Failure
o Salt & H2O Retention Fluid Overload Pulmonary & Peripheral Oedema
o Hypertrophy Myocardial Ischaemia + Diastolic Failure
Investigations:
- B-Natriuretic Peptide (BNP) (If >500 = Heart Failure)
- CXR (Pulmonary Congestion/Oedema, Cardiomegaly, Effusions)
- ECG (Dx Previous/Current IHD, Rule out Arrythmias)
- Echocardiogram (TOE/TTE) (Assess Ventricular Function [Ejection Fraction])
- +(FBC [Anaemia/Infection], UEC, eLFT [Alcohol], TSH [Hyperthyroid], Lipids [IHD], BSL/HbA1c [Diabetes])
Week 9
Heart Failure

Heart Failure:
- Where an abnormality in cardiac function à poor cardiac output à isn’t enough to supply the demands of
the body à low perfusion of organs à hypoxia etc.
- Ie. The heart can’t maintain circulation to tissues for normal metabolism.

Revision of Cardiac Output
- Cardiac Output = Heart Rate x Stroke Volume
§ = End Diastolic Volume – End Systolic Volume
§ ≈ 70mL/min
o Heart Rate Determined by:
§ Chronotropic Factors
§ Autonomic Nervous System
o Stroke Volume Determined by:
§ Contractility (NB: a direct effect of Ca+ at the cellular level.)
§ Preload (Degree of Ventricular Filling During Diastole. High à ↑SV)
§ Afterload (ie. Resistance to Ventricular Ejection (ie. Due to ↑Aortic Blood Pressure)
- ‘Ejection Fraction’: % of the End Diastolic Volume that is Ejected in Systole.
o Stroke Volume/End Diastolic Volume
o ≈60%

Types of Failure:
- Heart Failure:
o Failure of the Heart as an organ to pump enough blood to satisfy the Periphery.
o Myocyte Function May Be Normal.
§ Eg. Heart Valve Failure:
• Ie. A problem with the Heart-Valves
• Eg. Valve Incompetence/Regurgitation
• Eg. Valve Stenosis (Narrowing)
• Result = Changes in Preload/Afterload à Altered Cardiac Output
- Myocardial Failure:
o Ie. Defect in Myocardial Contration (Heart Muscle Itself)à Leads to deficit in Pump Function
o Eg. Myocyte Death Due to Infarction à↓Myocyte Mass
o Result = Decreased/Altered Pump Function
- Circulatory Failure:
o Ie. Defect in the Peripheral Circulation
o Eg. Haemorrhage/Shock/Cardiogenic Shock/Hypoxia
o Result = Reduced Peripheral Perfusion
- Congestion:
o Peripheral or Pulmonary Oedema - Due to:
§ Inadequate Pumping of the Heart
§ High Heart-‘Filling’
§ High Venous Pressures à Backlog
§ Ie. When one side of the heart isn’t ‘pulling its weight’àBackglog
Forward/Backward Heart Failure:
- Forward Heart Failure:
o Reduced Output due to Inadequate Discharge of Blood into Arterial System.
- Backward Heart Failure:
o Where One/Both Ventricle
§ 1. Fails to Discharge its Contents OR
§ 2. Fails to Fill Normally
o Results in ↑Atrial Pressure + ↑Pressure in Venous System Behind the Failing Ventricle.
- NB: Most Patients Have Both (Because Blood Flows in a Circle)
o Eg. Forward Heart Failure à Low Cardiac Output à Less Venous Return à Backward Heart Failure.

Left/Right Heart Failure:
- Left Heart Failure:
o Inability of L-Heart to Pump into Systemic Circulation
o What Happens:
§ Heart Tries to Compensate by Pumping Harder
§ àL- Heart Becomes Weaker
§ à ↑L-Ventricular End Systolic Volumes
§ à ↑L-Ventricular End Diastolic Volumes
§ à ↑L-Atrial Pressure
§ à ↑Pulmonary-Vein Pressure
§ à Shortness of Breath (Dyspnoea) & Pulmonary Oedema
§ à Fatigue

- Right Heart Failure:
o Inability of R-Heart to Pump into Pulmonary Circulation
o What Happens:
§ Blood Backs-Up in Peripheral Circulation
§ à ↑Venous Pressure
§ à Peripheral Oedema (Especially Legs & Abdominal Organs (Mainly Liver))
• & Renal Insufficiency (Due to ↓Perfusion of Kidneys) – Hence Renal & Heart Failure
go hand in hand.
§ Ie. A Congestive Heart Failure

- NB: L-Failure can lead to R-Failure:
o Eg. L-Failure à Pulmonary Hypertension à ↑Afterload on R-Ventricle à R-Ventricular Failure.

Signs of ↓Cardiac Output:
- Low Arterial Pressure (Due to weaker heart muscle)
- Tachycardia (A Compensatory Mechanism)
(Due to [Carotid/Aortic] BaroReceptor-Reflex In Response to ↓BP)
(Also due to the ↑Venous Pressure of Systemic Backlog (↑Systemic Blood Volume)
àAtrial Stretchà Bainbridge Reflex à Vagal (Parasympathetic) Withdrawal à↑HR)
- Exercise Intolerance (From ↓Tissue Perfusion)
- Difficulty Breathing (eg. In Pulmonary Congestion)
- Peripheral Oedema (eg. Due to R-Sided Heart Failure)

New York Heart Association – Grading of Heart-Failure Symptoms:
- 5 Classes
The Body’s Responses to Heart Failure:
- Short Term (ie. Acute Heart Failure):
o Mainly Adaptive:
§ Vasoconstriction (To maintain BP of Vital Organs. à ↑Afterload)
§ Salt & H2O Retention (To ↑Blood Volume à ↑Preload)
§ Increased Preload (To ↑ Stroke Volume)
§ ↓Parasympathetic (To ↑ Heart Rate & Ejection)
+ ↑ Sympathetic
§ Increased HR (To ↑ Cardiac Output)
§ Hypertrophy (To ↑ Muscle Mass to ↑ Contractile Strength)

- Long Term (ie. Chronic Heart Failure/Congestive Heart Failure):
o Mainly Maladaptive:
Over a long period, the Heart simply Can’t maintain the compensatory mechanisms of increasing CO.
§ Vasoconstriction à L-Heart Failure + ↑Myocardial Oxygen Consumption (MVO2)
§ Salt & H2O Retention à Pulmonary / Peripheral Oedema
§ Increased HR à ↑Energy Demand
§ Hypertrophy à Myocyte Energy Starvation + Impaired Relaxation

3 Compensatory Mechanisms:
- 1. Frank-Starling Law/Mechanism:
o “↑Preload à ↑Stroke Volume”
o Incomplete Chamber Emptying à↑PRELOAD à ↑Cardiac Output BY ↑STROKE-VOLUME.
o BENEFICIAL in Short-Term
o DETRIMENTAL in Long-Term
§ Ie. In Severe Heart Failure, Starling Curve is Flatter than normal.
§ àEven large Increase in End-Diastolic Volume has Little Effect on Stroke Volume & CO.
§ Also, ↑Vent-EDV à ↑Atrial Pressure à ↑Pulmonary Pressure

- 2. Myocardial Hypertrophy:
o Pressure Overloaded Hypertrophy:
§ In response to ↓Cardiac Output: When↓CO is due to ↑↑Afterload (↑Arterial Pressure)
§ “Concentric Hypertrophy”: Muscle Thickens – Due to Synthesis of Sarcomeres in PARALLEL.
o Volume Overloaded Hypertrophy:
§ In response to ↑Volumes:
§ Ie. ↑EDV à Ventricle Stretches (Dilates) à Cannot Generate Enough Force to Pump Blood.
§ “Eccentric Hypertrophy”: Heart Balloons Out – Due to Synthesis of Sarcomeres in SERIES.

o Increased Ventricular Mass = Cell Hypertrophy (↑Size) & Hyperplasia (↑Numbers).
§ Helps Maintain CO
§ Helps Reduce Wall Stress (By Increasing Thickness & Radius of Ventricle)
§ To Increase Contractility BUT Doesn’t Work!
• Heart becomes Rounder & Larger
• Muscles Thicken, Lose Elasticity & Stiffen à Hard to relax.
o àDecreased Compliance à ↑ESV à ↑Atrial Pressure à ↑Pul.Pressure.
• Ventricle Stretches (Dilates) à Cannot Generate Enough Force to Pump Blood.
• Cells Actually Become WEAKER!

- 3. Neurohormonal Systems:
o Nor-Adrenaline/Epinephrine:
§ Baroreceptors sense ↓CO as ↓Perfusion-Pressure àStimulates Sympathetic:
• à↑ Heart Rate
• à↑ Contractility
• à↑ Vessel Tone à To Increase Venous Return
• à↑Preload (àSV àCO)

o Renin-Angiotensin-Aldosterone System (RAAS)/Anti-Diuretic-Hormone Release:
§ Due to ↓Renal Perfusion-Pressure à Stimulates Renin Secretion from Juxtaglomerular Cells.
• àVasoconstriction (Angiotensin-II = Potent Vasoconstrictor)
• à↑Fluid Retention (Increases Intravascular Volume)
• à↑Blood Pressure
• à↑Preload (àSV àCO)

o Atrial Natriuretic Peptide:
§ Produced by Heart – But has NEGATIVE effects.
§ Released due to High Filling Pressures (within heart) – Via L-Atrial & Arterial Baroreceptors.
§ Important INDICATOR of Heart Failure
§ Function: à Reduce Fluid Retention (ie. Diuretic)
• àVasorelaxation
• à↓BP Therefore Inhibits RAAS.
• à↑Renal Excretion (Na+ & H2O)

o NB: The Neurohormonal Compensatory Mech = Viscious Cycle:
§ Strain on heart à Activation of Neurohormonal Mechanisms à↑Preload & BP à Extra
Strain on the heart.
§ Heart Responds by Remodelling à Larger & Rounder à Weaker.

Management of Chronic CCF:
- 1. Correct Systemic Factors & Comorbidities (Eg. Thyroid, Infection, Diabetes, COPD)
- 2. Lifestyle Mods ( Smoking/Alcohol, Weight Loss)
- 3. Fluid Restriction - Sal In ake Fl id Restriction, Daily Weights)
- 4. Antihypertensives ( Preload & :. CO :
o ACE Inhibitors (Perindopril)/ARBs (Candesartan):
MOA: AT-II Va odila ion Fl id Re en ion SNS Preload Afterload
Dose: Start Low &Go Slow.
(Side Effects: Persistent Dry Cough, Postural Hypotension, K+, Renal Impairment)
o β-Blockers (Carvedilol, Metoprolol, Bisoprolol):
MOA: Workload of Heart (+ Preload Cardiac Output) & Triggers Remodelling.
(Side Effects: Postural Hypotension, Dizziness)
- 5. Diuretics ( Fluid Overload):
o Loop Diuretics (Fr emide La i )
o [IF SEVERE] Aldosterone Antagonists (Spirinolactone) (Also K+ Sparing)
- (+/- Digoxin to Contractility ; or Rate Control in AF) (Symptomatic Improvement, but no Mortality)
- (+/- Oxygen if SpO2 <88%)
- (+/- Vasodilators Eg. Hydralazine / Nitrates)
- (+/- Internal Cardiac Defibrillator as 50% of mortality is due to sudden lethal arrhythmias)
Management of Acute, Decompensated CCF:

- As Above (ACEi + B-Blocker)
- + Diuretics (Frusemide)
- + Digoxin (For Inotropic Support)
- +/- Nitrates
Complications:
- Sudden Lethal Arrhythmias (VT/VF) Death
- Acute (Cardiogenic) Pulmonary Oedema (See CVS PATH Acute Cardiogenic Pulmonary Oedema)
Other Info:
-
- NYHA Functional Classification:
o Class I: No Limitation in ANY Activities; (Asymptomatic)
o Class II: Slight Limitation of Activity; (Asymptomatic with Mild Exertion).
o Class III: Marked Limitation of Activity; (Comfortable ONLY @ Rest).
o Class IV: Symptoms Occur at Rest or with ANY Physical Activity.
CVS Pathology:
Hypertension
HYPERTENSION:
- What is it?:
o Consistent Systolic of +140mmHg. AND/OR
o Consistent Diastolic of +90mmHg
- Aetiologies & Types:

o Primary “Essential” Idiopathic Hypertension:
Idiopathic Likely multifactorial (not curable)
Risk factors for HT:
GENETICS/FamHx
High Cholesterol/Salt Diet
Diabetes/Obesity
Smoking/Alcohol
Stress
Age
Subtypes:
Isolated Diastolic HTN (Typically Older Men)
Isolated Systolic HTN (Eg. >160/<90)
o In Young Adults (Due to Overactive Sympathetic NS CO)
o In Older Adults - (Due to Arterial Compliance (Calcification/Fibrosis))
o 5% = Secondary Hypertension:
Cardio - Coarctation, Hypervolaemia, Rigid Aorta
Renal - Acute Glomerulonephritis, CKD , Polycystic Kidneys, Renal Artery Stenosis
Endocrine Hyper-Adrenalism, Acromegaly, Hypo/hyperthyroidism, Phaeo C hing .
Neurologic - Psychogenic, Raised ICP, Sleep Apnea, Acute Stress
Pre-Eclampsia: (10% of pregnancies) - Placental Ischaemia Placental vasoactive
mediators Ma e nal BP in effo o Placen al Pe f ion
o Accelerated “Malignant” Hypertension :
= Rapid in BP (>200/120mmHg) Sufficient to cause Vascular Damage
Retinopathy (Papilloedema, Haemorrhages, Bulging Discs)
Brain (Mental Status Changes)
Renal (Creatinine Rise)
Rapid Organ Failure
NB: Malignan HTN i a e, but can arise in HT of any Aetiology.
Pathophysiology Not well Understood:
Common Causes:
o Cessation of Antihypertensives (Rebound HT)
o Sympathetic Hyperactivity
o Stimulants (Cocaine/Amphetamines)
o Glomerulonephritis (Nephritic Syndrome)
o Head Trauma ICP
o Tumours (Eg. Thyroid, Phaeo, Adrenal)
o Pre-Eclampsia
Symptoms Include:
Vision Disturbance (Papilloedema/Retinal Bleed)
Headache, Drowsiness, Confusion
Nausea, Vomiting
Management:
Smoothly Reduce BP over 24 to 36 hours to <150 / 90
(NB: Excessive reduction may Coronary/Cerebra/Renal Ischaemia)
o Symptoms:
Typically Asymptomatic (Unless Malignant Headache, Dizziness, N/V, Visual Changes)
o Signs:
Signs of 1o causes Eg. Thyroid, C hing Acromegaly, Polycythaemia, CKD, Pregnancy.
Abdomen: Renal or Adrenal Masses (for possible causes), or for AAA
Renal Bruit: (Renal Artery Stenosis)
o Diagnosis Essential Vs. Secondary?:
If Essential HT: Diastolic Pressure will RISE on standing.
If Secondary HT: Diastolic Pressure will FALL on standing.
o Classification (Adults):
- Diagnostic Evaluation:
o >3 Consecutive Readings of >140/>90 over 6mths = HTN
o BUT: Needs to be >Stage 2 (>160/>100) to Prescribe Antihypertensives.
o +FBC (Eliminate Polycythaemia)
o +Lipids Sc een Ri k F fo IHD
o +UEC (Screen Renal Failure, Electrolyte Disturbances)
o +Urinalysis (Screen Renal Failure & Urine Electrolytes)
o +BSL (Screen Diabetes)
o +ECG (Screen IHD)
Category Systolic (mmHg) Diastolic (mmHG) % Population

Normal 120-140 80-90 83
Stage 1 Hypertension (Mild) 140-160 90-100 13.5
Stage 2 Hypertension (Moderate) 160-180 100-110 2
Stage 3 Hypertension (Severe) 180-210 110-120
Stage 4 Hypertension (Severe) 1
- MANAGEMENT:
o (Identify & treat underlying causes)
o (NB: Reduction should be SLOW, otherwise can be fatal)
o 1. Lifestyle changes:
Reduce Risk Factors (Eg. Quit Smoking, -Fat Diet, Alcohol Salt, Exercise)
o 2. Treatment drugs (If >Stage 2 [>160/>100]):
Monotherapy First, Then Add ONE Other (In Order of Recommendation):
ACEi (Perindopril [ Coversyl ]) / ARB (Candesartan A acand
o NB Be a e K+)
o (Beware Dry Cough)
Ca-Ch-Blocker (Amlodipine No a c / Nifedipine Adalat
Thiazide Diuretic (Hydrochlorothiazide Ami ide
o NB Be a e K+)
{B-Blocker (Carvedilol Dila end Atenolol No en } Now Controversial!
o Only used if Pt also has IHD / CCF.
(Therapeutic Target <140/90mmHg or <130/80mmHg in diabetics)
o + (3. Home BP Monitoring):
If: Non-Complian Diabe ic Whi e-Coa HTN
- Complications of Hypertension:
o Is a Major Precursor For:
CAD/IHD
Hypertensive Heart Disease (Heart Failure, Hypertrophic Cardiomyopathy)
Stroke
Aortic Dissection
PVD
Renal Failure
Microangiopathy/ Ar eriolosclerosis (Small Vessel Diseases)
o Relationship between Degree of hypertension & Degree of Complications.
o Heart:
Afterload LV-Hypertrophy Eventually Diastolic Failure
Workload O2 Demand Exacerbated Coronary Ischaemia
o Lungs:
Pulmonary Congestion Pulmonary Oedema & RV-Hypertrophy
o CerebroVascular:
Intracerebral Haemorrhage (Rupture of Artery/Arterioles in brain)
o Aortia/Peripheral Vascular:
Mechanical Arterial Damage (eg. Aneurysms/Dissecting Aneurysms/Atherosclerosis)
o Kidneys:
Nephrosclerosis (hardening of kidney blood vessels) Renal Failure
CVS Pathology:
Infective Endocarditis
INFECTIVE ENDOCARDITIS
- = Infection of the Endothelial Lining of the Heart (including the heart valves)
- Risk Factors:
o Valve Abnormality (Valve Murmurs, Calcification, Congenital, Artificial)
o Open-Heart Surgery
o Poor Dental Hygiene (Source of Bacteria)
o Bacteraemia
o IV Access (Haemodialysis, IVDU, Surgery)
o Immunosuppression
- Aeitologies:
o Subacute Bacterial Endocarditis (Most Common - 50-60% of Cases):
(Oral) Strep Viridans/(Surgical) Strep Epidermidis (Low Virulence)
Epi: Recent Oral Surgery, or Post-Prosthetic Valve Insertion.
o Acute Bacterial Endocarditis (Rare 10-20% of Cases):
Staph. Aureus (High Virulence - 50% Mortality)
Epi: IV Drug Users
- Pathogenesis:
o Bacterial Infection of Valves/Endocardium Vegetations on Valve Cusps
Typically Strep. Viridans (Subacute-BE) or Staph Aureus/MRSA (Acute-BE)
Affects Aortic & Mitral Valves.
(RH-Valves may be affected in IV Drug Users)
- Clinical Signs:
o Symptoms:
**Fever + New Murmur** = Endocarditis until proven otherwise
+Fatigue, Malaise, Weight Loss
o Physical Signs:
Septic Emboli Infarcts:
Splinter Haemorrhages (In the nail bed)
Osler s Nodes (painful erythematous nodules in pulp of digits)
Janeway Lesions (Red, nontender lesions on palms/soles)
Roth Spots (Retinal Haemorrhages - red ring lesions with a yellow centre)
Splenomegaly
Arrhythmia
o Complications Begin ks af er onse
Renal Failure (Renal Emboli/Immune Complex Deposit Glomerulonephritis, Haematuria)
TIA (Cerebral Septic Embolism Ischaemia TIA/Stroke)
Septicaemia
CCF
- Investigations:
o Clinical (Fever + New Systolic Murmur +/- Septic Emboli)
o 3x Blood Cultures (@ Different Times & From Different Sites Eliminate Contamination)
o ECG (Rule out Ischaemia/MI/Arrhythmias)
o Echo (Valvular Vegetations & Mitral Regurgitation)
- Management:
o 2-6wks of High Dose IV Vancomycin - (Initially Empirical; Then Culture-Directed Therapy).
o Refer to Cardiac Surgeon (For ?Valve Replacement Surgery?):
If IV-ABs are Unsuccessful.
Or If Valve is Destroyed (Ie. In Acute-BE) Heart Failure
- Prognosis:
o 30% Mortality with Rx.
NON-INFECTIVE ENDOCARDITIS (NBTE - Non Bacterial Thrombotic Endocarditis):
- Aetiology:
o Hypercoaguable States Eg. DIC, Malignancy, Sepsis, SLE, Pregnancy.
- Pathogenesis:
o Deposition of small Sterile Th bi leafle f Ca diac Val e Ie The ffi i i i NOT c ec
o Preference for Valves: Mitral>Aortic>Tricuspid>Pulomonary
- Clinical Signs:
o Signs:
Of Hypercoaguable States:
DIC: Acutely Ill, Shocked, Widespread Haemorrhage (Mouth, Nose, Bruising, Renal)
Sepsis: Fever, Acutely Ill, Shocked, Infective Focus
SLE: Fever, Fatigue, Malaise, Butterfly/Malar Rash, Lymphadenopathy, Arthritis
Pregnancy: Baby Bump, DVT
Of NBTE:
Heart Murmurs
Stroke
MI
If 2o Infective-BE:
Fever + New Murmur
Septic Infarcts (Splinters, Oslers, Janeways, Roths, Abscesses, Haematuria)
o Symptoms are those of Systemic Arterial Embolism (Complications):
Thrombo-Embolic Infarcts (eg. Brain Stroke; Heart MI)
Secondary Bacterial Colonisation on Vegetations.
- Investigations:
o Clinical (Fever + New Systolic Murmur +/- Septic Emboli)
o 3x Blood Cultures (@ Different Times & From Different Sites Eliminate Contamination)
o + Coags Screen!!
o ECG (Rule out Ischaemia/MI/Arrhythmias)
o Echo (Valvular Vegetations)
- Management:
o Treatment of Underlying Aetiology
o Anticoagulant Therapy (Heparin Then Warfarin)
o +(If 2o Bacterial Endocarditis 2-6wks of High Dose IV Vancomycin)

o Refer to Cardiac Surgeon (For ?Valve Replacement Surgery?):
If IV-ABs are Unsuccessful.
Or If Valve is Destroyed (Ie. In Acute-BE) Heart Failure
VALVULAR HEART DISEASE
❏ see Cardiac Surgery Chapter
INFECTIVE ENDOCARDITIS (IE)

Etiology
❏ Strep viridans (commonest, spontaneous bacterial endocarditis (SBE) on abnormal valve – prosthetic, MVP, etc.)
❏ Enterococcus (Group D strep, SBE)
❏ Staph aureus (enter through break in skin: IV drug abusers, usually rightsided, catheter-associated sepsis)
❏ Staphylococcus epidermidis (prosthetic valve)
❏ Strep bovis (underlying GI malignancy)
❏ others: gram-negative bacteria, Candida, HACEK organisms (Haemophilus species, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella, and Kingella), Pseudomonas (IV drug)
❏ frequency of valve involvement: MV >> AV > TV > PV
❏ risk of IE in various cardiac lesions (JAMA 1997;227:1794)
• high risk: prosthetic heart valves, previous IE, complex cyanotic congenital heart disease,
surgically constructed systemic to pulmonary shunts or conduits
• moderate risk: most other congenital cardiac malformations, acquired valvular dysfunction,
HCM, MVP with MR and/or thickened leaflets
Pathogenesis and Symptomatology
❏ usually requires source of infection, underlying valve lesion, +/– systemic disease/immunocompromised state
❏ portal of entry: oropharynx, skin, GU, drug abuse, nosocomial infection ––> bacteremia ––>
diseased valve/high flow across valve ––> turbulence of blood across valve ––>
deposition of bacteria on endocardial surface of valve
(vegetation = clump of fibrin, platelets, WBCs and bacteria) ––> endocarditis ––> septic embolization
❏ symptoms
• fever, chills, rigors
• night sweats
• 'flu-like' illness, malaise, headaches, myalgia, arthralgia
• dyspnea, chest pain
Signs
❏ fever, regurgitant murmur (new onset or increased intensity), constitutional symptoms, anemia
❏ signs of CHF (secondary to acute MR, AR)
❏ peripheral manifestations: petechiae, Osler's nodes ("ouch!" raised, painful, 3-15 mm, soles/palms),
Janeway lesions ("pain away!" flat, painless, approx. 1-2 cm, on soles/plantar surfaces of toes/palms/fingers),
splinter hemorrhages (especially on proximal nail bed, distally more commonly due to local trauma)
❏ CNS: focal neurological signs (CNS emboli), retinal Roth spots
❏ clubbing (subacute)
❏ splenomegaly (subacute)
❏ microscopic hematuria (renal emboli or glomerulonephritis) ± active sediment
❏ weight loss
Investigations
❏ blood work: anemia, uncreased ESR, positive rheumatoid factor
❏ serial blood cultures (definitive diagnosis)
❏ echocardiography (transesophageal > sensitivity than transthoracic)
• vegetations, degree of regurgitation valve leaflet perforation, abscess
• serial ECHO may help in assessing cardiac function
Natural History
❏ adverse prognostic factors
• CHF, Gram (–) or fungal infection, prosthetic valve infection, abscess
in valve ring or myocardium, elderly, renal failure, culture negative IE
❏ mortality up to 30%
❏ relapses may occur - follow-up is mandatory
❏ permanent risk of re-infection after cure due to residual valve scarring
Complications
❏ CHF (usually due to valvular insufficiency)
❏ systemic emboli
❏ mycotic aneurysm formation
❏ intracardiac abscess formation leading to heart block
❏ renal failure: glomerulonephritis due to immune complex deposition; toxicity of antibiotics
C36 – Cardiology MCCQE 2002 Review Notes
VALVULAR HEART DISEASE . . . CONT.
Management
❏ medical
• antibiotic therapy tailored to cultures (penicillin, gentamicin, vancomycin, cloxacillin) minimum
of 4 weeks treatment
• serial ECGs - increased PR interval
• prophylaxis (JAMA 1997;227:1794)
• dental/oral/respiratory/esophageal procedures
• amoxicillin 2 g 1 hour prior
• GU/GI (excluding esophageal) procedures
• high risk: ampicillin + gentamicin
• moderate risk: amoxicillin, ampicillin, or vancomycin
❏ surgical
• indications: refractory CHF, valve ring abscess, valve perforation, unstable prosthesis, multiple major
emboli, antimicrobial failure, mycotic aneurysm
RHEUMATIC FEVER
Epidemiology
❏ school-aged children (5-15 yr), young adults (20-30 yr), outbreaks of Group A ß-hemolytic Streptococcus,
upper respiratory tract infection (URTI), social factors (low socioeconomic status (SES), crowding)
Etiology
❏ 3% of untreated Group A ß-hemolytic Streptococcus (especially mucoid, highly encapsulated stains,
serotypes 5, 6, 18) pharyngitis develop acute rheumatic fever
Diagnosis
❏ 1. Modified Jones criteria (1992): 2 major, or 1 major + 2 minor
• major criteria
• pancarditis
• polyarthritis
• Sydenham's chorea
• erythema marginatum
• subcutaneous nodules
• minor criteria
• previous history of rheumatic fever or rheumatic heart disease
• polyarthralgia
• increased ESR or C-reactive protein (CRP)
• increased PR interval (first degree heart block)
• fever
plus
❏ 2. Supported evidence confirming Group A Streptococcus infection: history of scarlet fever, group A
streptococcal pharyngitis culture, rapid Ag detection test (useful if positive), anti-streptolysin O Titers (ASOT)
Clinical Features
❏ Acute Rheumatic Fever: myocarditis (DCM/CHF), conduction system(sinus tachycardia, A fib), valvulitis
(acute MR), pericarditis (does not usually lead to constrictive pericarditis)
❏ Chronic: Rheumatic Valvular heart disease: fibrous thickening, adhesion, calcification of valve leaflets resulting
in stenosis/regurgitation, increased risk of IE +/– thromboembolic phenomenon. Onset of symptoms
usually after 10-20 year latency from acute carditis of rheumatic fever. Mitral valve most commonly affected.
Management
❏ acute treatment of Streptococcal infection (benzathine penicillin G 1.2 MU IM x 1 dose)
❏ prophylaxis to prevent colonization of URT (age < 40): benzathine penicillin G 1.2 MU IM q3-4 weeks,
within 10 yr of attack
❏ management of carditis in rheumatic fever: salicylates (2g qid x4-6 wk for arthritis), corticosteroids
(prednisone 30 mg qid x4-6wk for severe carditis with CHF)
AORTIC STENOSIS
Etiology
❏ congenital (bicuspid > > unicuspid) ––> calcified degeneration or congenital AS
❏ acquired
• degenerative calcified AS (most common) - "wear and tear"
• rheumatic disease
Definition
❏ AS = narrowed valve orifice (aortic valve area: normal = 3-4 cm2
severe AS = < 1.0 cm2
critical AS = < 0.75 cm2 )
❏ Note: low gradient AS with severely reduced valve area (< 1.0 cm2) and normal gradient in setting of
LV dysfunction
Pathophysiology
❏ pressure overloaded LV: increased LV end-diastolic pressure (EDP), concentric LVH, subendocardial ischemia
––> forward failure
❏ outflow obstruction: fixed cardiac output (CO)
❏ LV failure, pulmonary edema, CHF
Symptomatology
❏ ASD (triad of Angina, Syncope, and Dyspnea; prognosis associated with onset)
❏ angina (exertional): due to concentric LVH and subendocardial ischemia (decreased subendocardial flow and
increased myocardial O2 demand), may have limitation of normal activity or resting angina in tight AS
(associated with < 5 year survival)
❏ syncope: due to fixed CO or arrhythmia (< 3 year survival)
❏ dyspnea (LV failure): systolic +/– diastolic dysfunction, pulmonary edema, may have orthopnea, if secondary
RHF may have ascites, peripheral edema, congestive hepatomegaly (< 2 years)
Signs of AS
❏ pulses
• apical-carotid delay
• pulsus parvus et tardus (decreased amplitude and delayed upstroke) narrow pulse pressure,
brachial-radial delay
• thrill over carotid
❏ precordial palpation
• PMI: sustained (LVH) +/– diffuse (displaced, late, with LV dilation)
• +/– palpable S4
• systolic thrill in 2nd right intercostal space (RICS) +/– along left lower sternal bender (LLSB)
❏ precordial auscultation
• most sensitive physical finding is SEM radiating to right articular head
• SEM – diamond shaped (crescendo-decrescendo), harsh, high-pitched, peaks progressively later
in systole with worsening AS, intensity not related to severity, radiates to neck, musical quality of
murmur at apex (Gallavardin phenomenon)
• +/– diastolic murmur of associated mild AR
• S2 – soft S2, absent A2 component, paradoxical splitting (severe AS)
• ejection click
• S4 – early in disease (increased LV compliance)
• S3 – only in late disease (if LV dilatation present)
Investigations
❏ 12 lead ECG
• LVH and strain +/– LBBB, LAE/A fib
❏ chest x-ray
• post-stenotic aortic root dilatation, calcified valve, LVH + LAE, CHF (develops later)
❏ ECHO
• test of choice for diagnosis and monitoring
• valvular area and pressure gradient (assess severity of AS)
• LVH and LV function
• shows leaflet abnormalities and "jet" flow across valve
❏ cardiac catheterization
• r/o CAD (i.e. especially before surgery in those with angina)
• valvular area and pressure gradient (for inconclusive ECHO)
• LVEDP and CO (normal unless associated LV dysfunction)
Natural History
❏ asymptomatic patients have excellent survival (near normal)
❏ once symptomatic, untreated patients have a high mean mortality
• 5 years after onset of angina, < 3 years after onset of syncope; and < 2 years after onset of CHF/dyspnea
❏ the most common fatal valvular lesion (early mortality/sudden death)
• ventricular dysrhythmias (likeliest cause of sudden death)
• sudden onset LV failure
❏ other complications: IE, complete heart block
Management
❏ asymptomatic patients - follow for development of symptoms
• serial echocardiograms
• supportive/medical
• avoid heavy exertion
• IE prophylaxis
• avoid nitrates/arterial vasodilators and ACEI in severe AS
❏ indications for surgery
• onset of symptoms: angina, syncope, or CHF
• progression of LV dysfunction
• moderate AS if other cardiac surgery (i.e. CABG) required
❏ surgical options (see Cardiac and Vascular Surgery Chapter)
• AV replacement
• excellent long-term results, procedure of choice
• open or balloon valvuloplasty
• children, repair possible if minimal disease
• adults (rarely done): pregnancy, palliative in patients with comorbidity, or to stabilize patient
awaiting AV replacement - 50% recurrence of AS in 6 months after valvuloplasty
• complications: low CO, bleeding, conduction block, stroke
CVS Pathology:
Ischaemic Heart Disease
Review of Coronary Anatomy:
LAD Apex, Anterior LV, Anterior 2/3 of IV-Septum

LCX Lateral LV
RCA Entire RV, Postero-Superior LV, Posterior 1/3 of IV-Septum
Degrees of Coronary Blockage:

– <70% Occlusion: Asymptomatic
– 70-75% Occlusion: Angina
– 90% Occlusion: Chronic IHD
– Unstable Plaque: Unstable angina +/- Rupture Acute MI
– > 90% Occlusion: MI
*Ischaemia Vs. Hypoxia Vs. Infarction:

Ischaemia: A FLOW Limitation, Typically due to Coronary Artery Stenosis (Narrowing)
Hypoxia: An O2 Limitation,Typically due to High-Altitude/Respiratory Insufficiency/etc.
Infarction: Irreversible Cell-DEATH, Typically due to sustained Ischaemia.
Regional Vs. Global Myocardial Ischaemia:

- Regional Ischaemia:
o Local Atherosclerosis/Thrombosis Ischaemia Confined to Specific Region of Heart.
- Global Ischaemia (Rare):
o Severe Hypotension/Aortic Aneurysm Ischaemia of Entire Heart
What Happens During Myocardial Ischaemia:

- Myocardial Damage: Initially Subendocardial -Ischaemia/Infarction (ST-Depression & T-Wave Inversion)
Progresses to Transmural -Ischaemia/Infarction (ST-Elevation & Pathological Q-Waves).
- Metabolic Changes (Aerobic Anaerobic): Lactate Anaerobic Metabolism pH

- Pain: Nociceptor (pain receptor) Activation Angina Pain
- Global Autonomic Symptoms: Tachycardia, Sweating, Nausea.
- Pulmonary Congestion: Eg. LV-Failure Pulmonary Congestion Shortness of Breath
- Ventricular Arrhythmias: Eg. SVT or VT or VF (due to Re-Entrant Focus & Altered Conduction Patterns)
ANGINA PECTORIS:
- Aetiology:
o Myocardial Perfusion (relative to demand) due to Coronary Insufficiency.
o Causes: **Atherosclerosis / Vasospasm / Embolism / Ascending Aortic Dissection
o Exacerbated by (Vent-Hypertrophy, Tachycardia, Hypoxia, Coronary Arteritis (e.g. in SLE))
- Pathogenesis:
o (= A Late Sign of Coronary Atheroma Symptoms Imply >70% Occlusion!!)
o Insufficient Coronary Perfusion Relative to Myocardial Demand
o Stable Angina:
Due to: Stable Atherosclerotic Coronary Obstruction (No Plaque Disruption)
Presentation: Chest Pain on Physical Exertion, which fades quickly with Rest (minutes)
o Variant/Prinzmetal Angina:
Due to: Coronary Vasospasm (May not be Atheroma).
Presentation: Angina Unrelated to Activity (Ie. At Rest)
o Unstable Angina “Pre-Infarction Angina” :
Due to: Unstable Atherosclerotic Plaque (+/- Plaque Disruption & Thrombus).
Presentation: Prolonged Angina @ Rest (Either New-Onset/ Severity/ Frequency).
**NB: = Red Flag that MI may be Imminent
o Silent Ischaemia:
Due to: Ischaemia masked by neuropathy (eg. Diabetes/ B12/etc)
Presentation: Painless, but may have Nausea, Vomiting, Diaphoresis + Abnormal ECG
- Clinical Features of Angina:
o Common Presentation:
**<15mins of Crushing, Central, Retrosternal Chest Pain Radiating to Arms, Neck or jaw:
(Stable: On exertion)(Prinzmetal: Rest)(Unstable: Worsening/Prolonged/@Rest)
+Dyspnoea (Pulm.Congestion)
+ Fear of Impending Doom
o Signs:
Sympathetic Drive Diaphoresis
Hypotension Cold/Clammy/Peripheral Shut-Down/Thready Pulse
Pulmonary Congestion Dyspnoea, JVP
- Investigations:
o (1st Line) Resting ECG:
During Attack: ST-Depression, T-wave Inversion (Normal between Attacks)
(Path-Q-Waves if Previous MI).
nd
o (2 Line) Cardiac Stress Test + ECG: Suggests Severity of CAD (Any ST Depression is a +Ve Result)
o (3rd Line) Stress Echocardiography: Assess Ventricular Function
o (4th Line) Coronary Angiography (Cath-Lab): Pre-Angioplasty to Map the Coronary Anatomy
o (5th Line) Myocardial Perfusion Scans (Nuclear Medicine):
- Management/Treatment:
o (Prevention/Management of CV Risk Factors):
Smoking/Hypertension/Hyperlipidaemia/Diabetes/Obesity/Etc.
o Medical Therapy (Maintenance):
1. Anti-Anginal Therapy:
Nitrates (GTN) Coronary Vasodilation Cardiac Perfusion
B-Blockers (Metoprolol) To Workload of the Heart
Ca-Channel Blockers (Diltiazem/Verapamil) To Afterload
2. Antiplatelet Therapy:
Aspirin / Clopidogrel
3. Lipid-Lowering Therapy:
Atorvastatin/Simvastatin
o Revascularisation (Definitive) - OPTIONAL:
PCI (Per-Cutaneous Intervention)/Coronary Angioplasty:
Balloon Dilation/Stenting of Coronary Arteries via Femoral Artery
OR... CABG - (Coronary Artery Bypass Grafting):
Harvested Vein (Saphenous/Wrist) Bypasses the blockage
Acute Coronary Syndromes - (Unstable Angina/STEMI/NSTEMI):
- Aetiology:
o Unstable Atheroma
- Pathogenesis:
o Unstable Atheroma Rupture Prolonged Ischaemia Necrosis/Death of Myocardium.
( Sudden Death, Acute Systolic Dysfunction & Heart Failure, Vent.Rupture)
o Progression of Ischaemic Necrosis “ST-ELEVATION?”:
1. Initially “Subendocardial Necrosis” NON-ST-ELEVATION MI:
ST-Depression + T-Wave Inversion (As with Angina)
2. Then “Transmural Necrosis” ST-ELEVATION MI:
ST-Elevation + T-Wave Inversion + Path.Q-Waves
NB: The Endocardium is spared due to O2/Nutrients of Ventricular Blood.
o Most Common Coronary Obstruction & Locations of Ischaemia:

50% - LAD Obstruction:
Anterior-LV + Apex + Ant.2/3 of IV-Septum
30% - RCA Obstruction:
Posterior-LV + Posterior Septum + Free wall of RV.
20% - LCX (Left Circumflex) Obstruction:
Lateral LV (except for the apex.)
(NB: Nearly ALL Infarcts involve a portion of the LV)
- Clinical Features of NSTEMI/STEMI:

o Common Presentation:
**>20mins Crushing, Central, Retrosternal Chest Pain Radiating to Arms, Neck or Jaw.
NB: Some are Silent Eg. Diabetes, Post Cardiac Surgery, Elderly)
+Dyspnoea (Pulm.Congestion)
+ Fear of Impending Doom
o Signs:
Sympathetic Drive Diaphoresis
Hypotension Cold/Clammy/Peripheral Shut-Down/Thready Pulse
Pulmonary Congestion Dyspnoea/Tachypnoea/ JVP
Signs of PVD
- Investigations:
o (1st Line):
Serial Resting 12Lead ECGs (Every 15 Mins):
ST-Changes and Diagnosing MI:
o V1, V2, V3, V4 = Anterior MI
o II, III, AVF = Inferior Wall MI
o I, AVL, V5, V6 = Lateral
3-Lead Cardiac Telemetry (Screening for Arrhythmias)
Serial Troponin Levels (Cardiac Troponin-I/T, or CK-MB):
1st. On Presentation
2nd. @ 6hrs ( Troponin = MI)
3rd. Within 24hrs
+ Bloods (FBC, Serum Electrolytes, Glucose, Lipids)
o (2nd Line):
TTE/TOE Transthoracic/Transoesophageal Echo:
Assess LV-Function
(+ Excludes DDXs - Aortic Dissection / Pericarditis / Pulmonary Embolism)
Myocardial Perfusion Scans (Nuclear Medicine):
? Location of Infarct
- Management (As with Angina PLUS MORPHINE, O2 & ANTICOAGULATION + DEFINITIVE Mx):
o (Simplified: MONA = Morphine, Oxygen, Nitrates, Aspirin)
o 1. Medical Therapy (Maintenance):
1. Anti-Anginal Therapy:
Nitrates (GTN/Isosorbide Mononitrate) Coronary Vasodilation Cardiac Perfusion
B-Blockers (Propanolol/Metoprolol) To HR & Contractility Cardiac Workload
Ca-Channel Blockers (Nifedipine/Verapamil) To Afterload Cardiac Workload
2. Antiplatelet Therapy:
(Aspirin / Clopidogrel)
3. Lipid-Lowering Therapy:
(Atorvastatin/Simvastatin)
+4. Morphine: (Analgesia + Vasodilation)
+5. Oxygen: (To Maximize O2 @ Myocardium)
+6. Anticoagulation: (Heparin/LMWH or Warfarin) (Prevent Further Thrombogenesis).
o 2. STAT Revascularisation (Definitive) WITHIN 4 HRS:
**PCI (Per-Cutaneous Intervention)/Coronary Angioplasty:
Balloon Dilation/Stenting of Coronary Arteries via Femoral Artery
OR... Thrombolysis/Fibrinolysis (With TPA “Tissue Plasminogen Activator “Alteplase ):
Contraindicated in: Hx of CVA, Stroke <3mths, Aortic Dissection, Active Bleeding.
+/- CABG:
- Complications:
o Acute Complications:
LV-Failure: Acute Pulmonary Oedema, Shock (70% Mortality)
Lethal Arrhythmias: VT, VF
Weakening of Necrotic Myocardium Myocardial Rupture: Tamponade / Acute VSD
Stasis Mural Thrombosis Embolization Stroke
o Chronic Complications:
Ventricular Aneurysm, Papillary Muscle Rupture Mitral regurgitation, CCF.
ISCHEMIC HEART DISEASE (IHD)
BACKGROUND
Epidemiology
❏ commonest cause of cardiovascular morbidity and mortality
❏ male: female ratio
• = 2:1 with all age groups included (Framingham study)
• = 8:1 < age 40
• = 1:1 > age 70
• disparity due to protective effect of estrogen
❏ peak incidence of symptomatic IHD is from ages 50 to 60 in men and ages 60 to 70 in women
❏ spectrum of IHD/CAD ranges anywhere from asymptomatic to sudden death
Atherosclerosis and IHD
❏ atherosclerosis and thrombosis are by far the most important pathogenetic mechanisms in IHD
Major Risk Factors For Atherosclerotic Heart Disease
❏ smoking
• risk can be halved by cessation of smoking
❏ diabetes mellitus (DM)
• micro and macrovascular complications
❏ hypertension (HTN)
• depends on degree and duration
❏ family history (FHx)
• first degree male relative < 55 or first degree female relative < 60
❏ hyperlipidemia
Other Minor Risk Factors
❏ obesity
• > 30% above ideal weight
❏ sedentary lifestyle
❏ hyperhomocysteinemia
Preventative Measures
❏ smoking cessation
❏ tight glycemic control in diabetics
❏ BP control
• major reason for the recent decrease in IHD
❏ lipid-modifying therapy
❏ dietary measures e.g. mild alcohol consumption
❏ weight loss
❏ exercise improves weight, HTN, cholesterol and glycemic control
❏ family screening (high risk groups)
ANGINA PECTORIS
Definition
❏ symptom complex resulting from an imbalance between oxygen supply and demand in the myocardium
Pathophysiology of Myocardial Ischemia
O2 O2
Demand Supply
Heart Rate Length of Diastole
Contractility Coronary Diameter
Wall Tension Hemoglobin
SaO2
Figure 9. Physiological Principles
Etiology
❏ decreased myocardial oxygen supply
• atherosclerotic heart disease (vast majority)
• coronary vasospasm (variant angina= Prinzmetal’s Angina)
• severe aortic stenosis or insufficiency
• thromboembolism
• severe anemia
• arteritis (e.g. Takayasu’s syndrome, syphilis, etc.)
• aortic dissection
• congenital anomalies
ISCHEMIC HEART DISEASE (IHD) . . . CONT.
❏ increased myocardial oxygen demand

• myocardial hypertrophy
• severe tachycardia
• severe hyperthyroidism
• severe anemia
DDx
❏ musculoskeletal (MSK) disease
• rib fracture
• intercostal muscle tenderness
• costochondritis (Tietze’s syndrome)
• nerve root disease (cervical radiculitis)
❏ gastrointestinal (GI) disease
• peptic ulcer disease (PUD)
• reflux esophagitis
• esophageal spasm and motility disorder (may be improved by NTG)
❏ pulmonary disease
• pulmonary embolism (PE)
• pneumothorax
• pneumonia
❏ cardiovascular (CV) disease
• aortic dissection (asymmetrical BP and pulses, new AR murmur)
• pericarditis
❏ Other
• intercostal neuritis (shingles)
• anxiety
❏ note
• careful history and physical required
• consider risk factors for each entity
• beware cardiac and non-cardiac disease may coexist
Diagnosis of Angina Pectoris
❏ history
• classically precordial chest pain, tightness or discomfort radiating to left shoulder/arm/jaw
• dyspnea or fatigue may present as "chest pain equivalents," especially in females
• associated with diaphoresis or nausea
• predictably precipitated by the "3 E's" Exertion, Emotion and Eating
• brief duration, lasting < 10-15 minutes and typically relieved by rest
• note: always list the presence or absence of the cardiac risk factors in a separate subsection
in the history (e.g., + FHx, + HTN, +DM, + smoking, - hypercholesterolemia)
❏ stress testing (see Cardiac Diagnostic Tests section)
Variant Angina (Prinzmetal’s Angina)
❏ vasospasm of coronary arteries results in myocardial ischemia
• may occur in normal or atherosclerotic vessels
❏ typically occurs between midnight and 8 am
❏ unrelated to exercise; relieved by Nitrates
❏ typically ST elevation on ECG (may be confused with acute MI)
❏ diagnose by provocative testing with ergot vasoconstrictors (rarely done)
Syndrome X
❏ patient has typical symptoms of Angina yet has normal angiogram
❏ may show definite signs of ischemia during exercise testing
❏ pathogenesis thought to be due to inadequate vasodilator reserve of coronary resistance vessels
❏ has better prognosis than patient with overt atherosclerotic disease
Medical Treatment
❏ ß blockers (first line therapy)
• decrease overall mortality
• decrease heart rate, contractility, and to a lesser degree, blood pressure (afterload)
• increase coronary perfusion
• avoid agents with intrinsic sympathomimetic activity (ISA) (e.g. Acebutolol) (these increase demand)
❏ nitrates
• used for symptomatic control
• no clear impact on survival
• decrease myocardial work and, therefore, oxygen requirements
through venous dilatation (decrease preload) and arteriolar dilatation (decrease afterload)
• dilate coronary arteries
• maintain daily nitrate-free intervals to try to prevent nitrate tolerance
❏ calcium channel blockers (CCB)
• variably decrease afterload, decrease heart rate and decrease contractility, produce coronary dilatation
❏ ECASA
• all patients
• decrease platelet aggregation
❏ lipid lowering
Coronary Artery Disease (CAD) Lipid Therapy
Trial Drug Dose CHD Event Reduction
primary WOSCOPS pravastatin 40 31%

prevention AFCAPS lovastatin 20-40 24%
secondary LIPID pravastatin 40 23%
prevention 4S simvastatin 20-40 34%
CARE pravastatin 40 24%
2000 Canadian Guidelines for Treatment of Dyslipidemia

Target Values
Level of Risk LDL TC:HDL Ratio Tryglycerides
(Definition)
Very High
(History of cardiovascular < 2.5 <4 <2
disease or 10 yr risk of CAD > 30%)
High
(10 yr risk of CAD 20-30%) <3 <5 <2
Moderate
(10 yr risk 10-20%) <4 <6 <2
Low
(10 yr risk < 10%) <5 <7 <3
Risk calculated based on Framingham data: dertermined by gender, age group, total cholesterol level, HDL level, SBP, history of smoking
❏ treatment strategy
• short acting nitrates on PRN basis to relieve acute attacks
and PRN prior to exertion
• be careful when combining ß blockers and verapamil/diltiazem
• both decrease conduction and contractility and may result in sinus bradycardia or AV block
• use nitrates and CCB for variant angina
low likelihood intermediate likelihood high likelihood
non-nuclear otherwise healthy poor surgical candidate

with multiple co-morbidities
+
– nuclear stress testing nuclear stress testing
–
– + +
medical follow-up cath medical follow-up
low risk high risk
medical management PTCA, CABG
Figure 10. Diagnostic Strategies in the Management of IHD
Indications for Angiography

❏ strongly positive exercise test
❏ significant, reversible defects on thallium scan
❏ refractory to medical therapy or patient unable to tolerate medical therapy
❏ unstable angina
Percutaneous Transluminal Coronary Angioplasty (PTCA)

❏ uses a balloon inflated under high pressure to rupture atheromatous plaques
❏ may be used as primary therapy in angina, acute MI, post-MI angina or in patients presenting
with bypass graft stenosis
❏ optimally used for proximal lesions free of thrombus and distanced from the origins of large vessel branches –
not in Left Main
❏ primary success rate is > 80%
❏ use of intracoronary stent is associated with a lower restenosis rate (compared with PTCA alone)
❏ complications (overall 3-5%)
• mortality < 1%
• MI 3-5%
• intimal dissection + vessel occlusion requiring urgent CABG
Surgical Treatment- Coronary Artery Bypass Grafting (CABG)
❏ indications - for survival benefit, or symptomatic relief of angina
• stable angina (survival benefit for CABG shown)
• left main coronary disease
• three-vessel disease with depressed LV function
• multi-vessel disease with significant proximal LAD stenosis
• unstable angina (see below)
• above indications or
• continuing angina despite aggressive medical therapy
• complications/failed PTCA
❏ comparison of CABG with PTCA
• studies: RITA, GABI, BARI, EAST, ERACI, CABRI
• highly select patient population - no left main disease and minimal LV dysfunction
• overall no difference in survival, but PTCA group had more recurrent
ischemia and required more interventions
• BARI, subset analysis - CABG superior in patients with DM and multi-vessel IHD
❏ predictors of poor outcome
• poor LV function (EF < 40%), history of CHF, NYHA III or IV
• previous cardiac surgery
• urgent/emergent case, preoperative IABP
• gender (relative risk for F:M = 1.6:1)
• advanced age (> 70), DM, co-morbid disease
❏ CABG operative mortality
• elective case < 1%
• elective case, poor LV function 1-3%
• urgent case 1-5%
• overall (1980-1990) 2.2%
❏ efficacy: > 90% symptomatic improvement in angina
❏ conduits and patency
• internal mammary (thoracic) artery 90% patency at 10 years
• saphenous vein graft 50% patency at 10 years
• radial/gastroepiploic/inferior 85% patency at 5 years
epigastric arteries (improving with experience)
ACUTE CORONARY SYNDROMES (ACS)

Spectrum of ACS
A. Unstable Angina
B. Acute Myocardial Infarcion
C. Sudden Death
A. UNSTABLE ANGINA/NON ST ELEVATION MI (NSTEMI)
Definition
❏ accelerating pattern of pain
• increased frequency
• longer duration
• occurring with less exertion
• less responsive to treatment (eg. require higher doses or more frequent doses)
❏ angina at rest
❏ new onset angina
❏ angina post-MI
❏ post-angiography
❏ post-CABG
❏ note that unstable angina is a heterogeneous group and can be divided into a higher and lower risk groups
Significance
❏ thought to represent plaque rupture and acute thrombosis with incomplete vessel occlusion
Diagnosis
❏ history
❏ ECG changes
• ST depression or elevation
• T wave inversion
❏ no elevation of cardiac enzymes
Management
❏ oxygen
❏ hospitalization/monitoring
❏ bed rest
❏ anti-anginal medications
• sublingual or IV nitroglycerine
• ß blockers are first line therapy
• aim for resting heart rate of 50-60
• CCB are second line therapy (use if ß blockers contraindicated, or if patient has refractory symptoms
despite aggressive treatment with ECASA, nitrates, and ß blockers)
• evidence suggests that they do not prevent MI or decrease mortality
• be cautious using verapamil/diltiazem with ß blockers
• use non-dihydropyridines if cannot use ß blockers otherwise may use amlodipine
or long-acting nifedipine if concomitant ß blockade
❏ ECASA
• 160-325 mg/day
❏ IV heparin or Plavix (GPIIB/IIIA inhibitor)
❏ angiography with view to potential PTCA or CABG – used to map areas of ischemia
❏ if aggressive medical management is unsuccessful
• may use intra-aortic balloon pump (IABP) to stabilize before proceeding
with revascularization – used to increase coronary perfusion during diasole
• proceed to emergency angiography and PTCA or CABG
B. ACUTE ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

Definition
❏ syndrome of acute coronary insufficiency resulting in death of myocardium
Infarct Diagnosis Based on 2 of 3 - History, ECG, Cardiac Enzymes
❏ history
• sudden onset of characteristic chest pain for > 30 minutes duration
• may be accompanied by symptoms of heart failure (e.g. SOB, leg edema, etc.)
❏ ECG changes
• criteria: ST elevation of at least 1 mm in limb leads and 2 mm in precordial leads
• evolution of ECG changes in Q-wave MI
• 1st – abnormal T waves
• 2nd – ST-T elevations (hours post-infarct)
• 3rd – significant Q waves (hours to days post-infarct)
• 4th – inverted T waves, or may become flat or biphasic (days to weeks)
❏ cardiac enzymes
• follow CK-MB q8h x 3, Troponin q8h x 3
❏ cardiac Troponin I and/or T levels provide useful diagnostic, prognostic information and permit early
identification of an increased risk of mortality in patients with acute coronary syndromes
• Troponin I and T remain elevated for 5 to 7 days
❏ beware
• up to 30% are unrecognized or "silent" due to atypical symptoms
• DM
• elderly
• patients with HTN
• post heart-transplant (because of denervation)
❏ draw serum lipids within 24-48 hours because the serum values are unreliable after 48 hours,
but become reliable again 8 weeks post-MI
Patient Evaluation “unstable angina”
history • physical exam • ECG • enzymes
ST elevation non ST elevation
presumed acute MI sample enzymes
assess for positive enzymes negative enzymes

thrombolysis acute MI
unstable angina non cardiac chest pain
Figure 11. Diagnostic algorithm in acute IHD
Etiology
❏ coronary atherosclerosis + superimposed thrombus on ruptured plaque (vast majority)
• vulnerable "soft" plaques more thrombogenic
❏ coronary thromboembolism
• infective endocarditis
• rheumatic heart disease
• intracavity thrombus
• cholesterol emboli
❏ severe coronary vasospasm
❏ arteritis
❏ coronary dissection
❏ consider possible exacerbating factors
• see Angina Pectoris section
Plasma
Enzyme CK-MB
Level x
Normal
ISCHEMIC
HEART DISEASE
. . . CONT.
DAYS POST-MI
Figure 12. Cardiac Enzyme Profile in Acute MI
Further Classification of MIs

❏ Q wave
• associated with transmural infarctions, involving full thickness of myocardium
❏ non-Q wave
• usually associated with non-transmural (subendocardial) infarctions,
involving 1/3 to 1/2 of myocardial thickness
• in-hospital mortality from non-Q wave infarction is low (< 5%)
but 1 year mortality approaches that of Q wave infarction
Management
❏ goal is to minimize the amount of infarcted myocardium and prevent complications
❏ emergency room measures
• ECASA 325 mg chewed stat
• oxygen
• sublingual nitroglycerine
• morphine for pain relief, sedation, and venodilation
• ß blockers to reduce heart rate if not contraindicated
❏ thrombolytic therapy (see Table 7)

• benefits of thrombolysis shown to be irrespective of age, sex, BP, heart rate, or history of MI or DM
• indications for thrombolytic therapy
A. at least 0.5 hours of ischemic cardiac pain and
B. any of the following ECG changes thought to be of acute onset
• at least 1 mm of ST elevation in at least two limb leads
• at least 1 mm of ST elevation in at least two adjacent precordial leads or
• new onset complete BBB
C. presentation within 12 hours of symptom onset
• choice of thrombolytic agents include streptokinase and rt-PA
• patients having previously received streptokinase must
receive alternate agent due to development of immunity
❏ heparin
❏ PTCA, CABG
Long-Term Measures
❏ antiplatelet/anticoagulation therapy
❏ ECASA 325 mg daily
❏ nitrates
• alleviate ischemia but may not improve outcome
• start immediately and continue indefinitely if no contraindications
• decrease mortality
❏ CCB
• NOT recommended as first line treatment - Short Acting Nifedipine is contraindicated!
• Diltiazam and Verapamil are contraindicated in MI with associated LV dysfunction
❏ ACEI
• stabilize endothelium and prevent adverse ventricular remodeling
• strongly recommended for
• symptomatic CHF
• reduced LVEF (< 40%) starting day 3 to 16 post-MI (SAVE trial)
• anterior MI
❏ lipid lowering agent (HMG-C0A reductase inhibitors or niacin)
• if total cholesterol > 5.5 or LDL > 2.6
❏ coumadin (for 3 months)
• for large anterior MI, especially if LV thrombus seen on 2D-ECHO
❏ see Figure 13 for post critical care unit (CCU) strategy
Table 7. Contraindications to Thrombolytic Therapy in AMI
Absolute Relative
• active bleeding • GI, GU hemorrhage or stroke within past 6 months
• aortic dissection • major surgery or trauma within past 2-4 weeks
• acute pericarditis • severe uncontrolled hypertension
• cerebral hemorrhage • bleeding diathesis or intracranial neoplasm
(previous or current) • puncture of a noncompressible vessel
• significant chest trauma from CPR
❏ Indications for Post-thrombolysis Heparin
• tPA used for thrombolysis
• Anterior MI
• Ventricular aneurysm
• Post-thrombolysis angina
• A fib
• Previous deep vein thrombosis (DVT), PE, or ischemic stroke
Prognosis
❏ 20% of patients with acute MI die before reaching hospital
❏ 5-15% of hospitalized patients will die
• risk factors
• infarct size/severity
• age
• co-morbid conditions
• development of heart failure or hypotension
❏ post-discharge mortality rates
• 6-8% within first year, half of these within first 3 months
• 4% per year following first year
• risk factors
• LV dysfunction
• residual myocardial ischemia
• ventricular arrhythmias
• history of prior MI
• resting LVEF is most useful prognostic factor
Table 8. Complications of Myocardial Infarction

Complication Etiology Presentation Therapy
Arrhythmia
(a) tachycardia sinus, AF, VT, VF early/late see Arrhythmia section
(b) bradycardia sinus, AV block early
Myocardial
Rupture
(a) LV free wall transmural infarction 1-7 days pericardiocentesis or surgery
(b) papillary muscle inferior infarction 1-7 days surgery
(MR) anterior infarction
(c) ventricular septum septal infarction 1-7 days surgery
(VSD)
Shock/CHF LV/RV infarction within 48 hours fluids, inotropes, IABP
aneurysm
Post Infarct Angina persistent coronary stenosis anytime aggressive medical therapy
multivessel disease PTCA or CABG
Recurrent MI reocclusion anytime see above
Thromboembolism mural thrombus in Q wave 7~10 days, heparin, warfarin
infarction up to 6 months
Pericarditis post-MI 1-7 days NSAIDs
(Dressler's) autoimmune (Dressler’s) 2-8 weeks NSAIDs, steroids
Acute MI Risk Stratification
Cardiogenic Shock ST Elevation or LBBB No ST Elevation

Acute Phase
(5% - 10%) and Presentation ≤ 12 hours and Presentation > 12 hours

(25% - 45%) (50% - 70%)
Thrombolysis
CCU Phase
? Rescue PTCA, CABS

No Reperfusion Reperfusion
(19% - 45%) (55% - 81%)
Non-Acute Risk Stratification

In-Hospital Phase
High-Risk (30% - 35%) Intermediate/Low-Risk

• prior MI (65% - 70%)
• CHF
• Recurrent Ischemia
• High-Risk Arrhythmia Non-invasive Stress Testing
Cardiac Catheterization
Ischemia or Normal Results
Poor Functional Status
Cardiac Catheterization No further testing at this time

••Please note that Echocardiography is done routinely post-MI.
It is controversial whether an EF < 40% is by itself an indication for coronary angiography.
Figure 13. Acute MI and Predischarge Risk Stratification
C. SUDDEN DEATH
Definition
❏ unanticipated, non-traumatic death in a clinically stable patient, within 1 hour of symptom onset
❏ immediate cause of death is
• V fib (most common)
• ventricular asystole
Significance
❏ accounts for ~ 50% of CAD mortalities
❏ initial clinical presentation in up to 20% of patients with CAD
Etiology
❏ primary cardiac pathology
• ischemia/MI
• LV dysfunction
• severe ventricular hypertrophy
• hypertrophic cardiomyopathy (HCM)
• AS
• QT prolongation syndrome
• congenital heart disease
❏ high risk patients
• multi-vessel disease
• LV dysfunction
Management
Acute
❏ resuscitate with prompt CPR and defibrillation
Long Term Survivors
❏ identify and treat underlying predisposing factors
❏ IHD
• cardiac catheterization to evaluate cardiac anatomy, LV function and need for revascularization
❏ Holter monitoring
❏ electrophysiologic studies
Treatment
❏ antiarrhythmic drug therapy
• amiodarone, ß blockers
❏ surgery
• revascularization to treat ischemia
• map-guided subendocardial resection
• cryoablation, radiofrequency ablation
❏ implantable cardioverter-defibrillator
Prognosis
❏ 1 year mortality post-resuscitation 20-30%
❏ predictors of recurrent cardiac arrest in the "survivor" of sudden cardiac death
• remote MI
• CHF
• LV dysfunction
• extensive CAD
• complex ventricular ectopy
• abnormal signal-averaged ECG
HEART FAILURE
❏ overall, CHF is associated with a 50% mortality rate at five years
❏ see Colour Atlas R3 and R4
Definitions and Terminology
❏ inability of heart to maintain adequate cardiac output to meet the demands of whole-body metabolism
and/or to be able to do so only from an elevated filling pressure(forward heart failure)
❏ inability of heart to clear venous return resulting in vascular congestion (backward heart failure)
❏ either the left side of the heart (left heart failure) or the right side of the heart (right heart failure) or both
(biventricular failure) may be involved
❏ there may be components of ineffective ventricular filling (diastolic dysfunction) and/or emptying
(systolic dysfunction)
❏ most cases associated with poor cardiac function (low-output heart failure) but some are not due to intrinsic
cardiac disease (high-output heart failure; this is discussed separately below)
❏ CHF is not a disease itself - it is a syndrome involving variable degrees of both forward and backward
heart failure
CVS Pathology:
Lymphangitis
LYMPHANGITIS:
- Aetiology:
o Commonly β-Haemolytic-Strep or Staphylococcus Aureus
- Pathogenesis:
o Bacterial Infection Spread to Lymphatics Acute Inflammation
If Severe Cellulitis/Abscesses
If Very Severe Bacteraemia/Sepsis
o Fever/Chills/Malaise
o Painful Red Subcutaneous Streaks
o Painful Lymphadenitis (Swollen draining lymph nodes)
- Complications:
o Abscesses
o Cellulitis
o Sepsis
- Investigations:
o Blood Culture + Swab any open wounds.
o FBC +/- CRP
- Management:
o Immobilisation of Limb
o Antibiotics
o Analgesia
CVS Pathology:
Myocarditis - Viral & Toxic
MYOCARDITIS VIRAL & TOXIC:

- Inflamma ion of he Hear M scle
o + Characterized by Myocyte Necrosis – (Positive Troponin I results seen in 35% of Myocarditis)
- 2 Main Aetiologies:
o Viral Myocarditis. (Eg. Coxsackievirus, Rhinovirus, Influenza, Parvovirus B19, etc)
Either Direct Myocardial Injury OR 2o AutoImmune Response
Heart Thickens & Weakens Systolic Heart Failure
o Toxic Myocarditis (Eg. Chemo Drugs, Cocaine, Alcohol, Diuretics, Antibiotics, Venom, CO, etc)
Myocardial Damage & Inflammation due to Either:
Hypersensitivity to Drugs
Direct Toxic Damage
o (May be Asymptomatic)
o Symptoms:
Flu-Like Syx - (Fever, Fatigue, Malaise)
LV-Failure – (Dyspnoea/Orthopnoea/PND/Cough)
Chest Pain – (Due to Myocarditis +/- Pericarditis)
Palpitations (Arrhythmias)
- Complications:
o Cardiomyopathy Heart Failure
o Arrhythmias Sudden Death
o Pericarditis Pericardial Effusion
- Investigations:
o ECG & Continuous Telemetry
o Serial Troponins I/T - (Immediately, then @6hrs, then @24hrs)
o FBC (↑WCC), CRP (↑), ESR (↑)
o CXR (Cardiomegaly)
o Echo (Dilated, Poor Vent-Function)
- Management:
o **Bed Rest
o **CCF Triple Therapy (ACEi/ARB + B-Blocker + Diuretics)
o **Warfarin (Prevent Thromboembolism)
o Supportive Rx. (Fluids, Analgesia)
o Treat Underlying Cause if Possible
CARDIOMYOPATHIES . . . CONT.
MYOCARDITIS
❏ inflammatory process involving the myocardium (an important cause of dilated cardiomyopathy)
Etiology
❏ idiopathic
❏ infectious
• viral: Coxsackie virus B, Echovirus, Poliovirus, HIV, mumps
• bacterial: S. aureus, C. perfringens, C. diphtheriae, Mycoplasma, Rickettsia
• fungi
• spirochetal (Lyme disease – Borrelia burgdorferi)
• Chagas disease (Trypanosoma cruzi), toxoplasmosis
❏ acute rheumatic fever (Group A ß-hemolytic Streptococcus)
❏ drug-induced: emetine, doxorubicin
❏ collagen vascular disease: systemic lupus erythematosus (SLE), polyarteritis nodosa (PAN),
rheumatoid arthritis (RA), dermatomyositis (DMY)
❏ sarcoidosis
❏ giant cell myocarditis
❏ constitutional illness
❏ acute CHF
❏ chest pain - associated pericarditis or cardiac ischemia
❏ arrhythmias (may have associated inflammation of conduction system)
❏ systemic or pulmonary emboli
❏ sudden death
Investigations
❏ 12 lead ECG
• non-specific ST-T changes +/– conduction defects
❏ blood work
• increased CK, Troponin, LDH, and AST with acute myocardial necrosis
+/– increased WBC, ESR, ANA, rheumatoid factor, complement levels
❏ perform blood culture, viral titers and cold agglutinins for Mycoplasma
❏ chest x-ray
• enlarged cardiac silhouette
❏ echocardiography
• dilated, hypokinetic chambers
• segmental wall motion abnormalities
Natural History
❏ usually self-limited and often unrecognized
❏ most recover
❏ may be fulminant with death in 24-48 hours
❏ sudden death in young adults
❏ may progress to dilated cardiomyopathy
❏ few may have recurrent or chronic myocarditis
Management
❏ supportive care
❏ restrict physical activity
❏ treat CHF
❏ treat arrhythmias
❏ anticoagulation
❏ treat underlying cause if possible
CVS Pathology:
Pericarditis
PERICARDITIS:
- Aetiology:
o Usually Secondary to:
Infection (**Viruses**, Bacteria, Fungi, Parasites)
Immuno (Rheumatic Fever, SLE, Post-MI, Drug Hypersensitivity)
Other (MI, Post-Cardiac Surgery, Neoplasia, Trauma, Radiation)
- Classification:
o According to Composition of Pericardial Exudate:
Serous (Non-Infectious Inflammatory Diseases – SLE, Uraemia, Tumours)
Purulent (Infective - by Microbes)
Fibrinous/Serofibrinous (Due to Acute MI, Ch. Radiation, SLE, Trauma)
Caseous (Tuberculosis)
Haemorrhagic (Due to Metastasis, Cardiac Surgery).
- Pathogenesis:
o Various Aetiologies Inflammation of the Pericardium
Thickening of Pericardium Pericardial Exudate (Serous Fluid + Pus/Fibrin/Blood)
Rubbing of Parietal & Visceral Pericardium Further Inflammation & Exudate.
- Clinical Features & Complications:
o Symptoms:
Pleuritic Chest Pain (Better on Sitting Forward; Worse on Inspiration & Lying Down)
Fever, Fatigue
Dry Cough
Syx of CCF (Dyspnoea, Fatigue)
o Signs:
Fever, Tachycardia
Muffled Heart Sounds.
Friction Rub
↑JVP
Heart Failure Signs if Tamponade
o Complications:
Cardiac Tamponade/Pericardial Effusion
If >3mths Chronic Constrictive Pericarditis (Requires Surgery)
- Diagnosis:
o ECG – (Classical PR-Depression + ST-Elevation + Tachycardia)
o CXR – (Pulmonary Congestion)
o ECHO – (?Pericardial Effusion)
- Management:
o Rx Underlying Cause
o Anti-Inflammatories (NSAIDs / Steroids)
o Analgesia
CVS Pathology:
Peripheral Vascular Disease, Varicose Veins & Chronic Leg Ulcers
Revision of Lower Limb Vascular Anatomy:

- Arterial & Venous Circulation of the Legs:
o
- T eM ceP
o
- Superficial & Deep Leg Veins:
ACUTE ARTERIAL OCCLUSION CRITICAL LIMB ISCHAEMIA :
- NB: Emboli Can also Deposit in Other Arteries Too:

o Eg. Mesenteric Ischaemia Ischaemic Gut (++ Painful + Bloody Diarrhoea)
o Eg. Renal Art.Thrombosis Abdo/Back/Flank Pain, ARF, Oliguria, Hypertension
PERIPHERAL VASCULAR DISEASE (AKA: Peripheral ARTERIAL Disease):
- Definition:
o Obstruction of any of the PERIPHERAL ARTERIES (Not including Coronaries/Aortic Arch/Brain)
- Aetiologies:
o **Atherosclerosis (Most Common)
o (Major Risk Factors):
Smoking (10x) - the single greatest modifiable cause of PVD.
Diabetes
Dyslipidaemia
Hypertension
- Pathogenesis:
o Atherosclerosis Obstruction of Peripheral Arteries Chronic Ischaemia
Eg. Arterial Ulcers, Leg Claudication, Ra na d s Phenomenon
o Symptoms:
(Acute Critical Limb Ischaemia See Prev. Page):
Pain, Pallor, Paraesthesia, Paralysis, Pulseless
Chronic:
Mild-Severe Claudication (Leg Pain/Cramping/Weakness on Exercise)
o 1. On Exertion (Typically in Calves)
o 2. Relived by Rest (2-3mins)
o Reprod cible Same Cla dication Distance
o (+ Rest Pain if SEVERE)
Distal Pulses Weak/Absent
Skin Changes (Hair-Loss, Atrophic Skin, Ulcerations, Gangrene)
Other Atherosclerotic Lesions (Impotence, CVD, CAD)
- Investigations:
o Non-Invasive:
ABI (Ankle-Brachial Index):
Ankle BP <90% of Brachial BP = Abnormal
ABI <0.3 Rest Pain & Night Pain *( Risk of Critical Limb Ischaemia)
Doppler Ultrasound
Contrast CT-Angiogram
o Invasive:
**Femoral Angiography (DSA Lab) = Gold Standard
o (NB: Check for Carotid-Artery Stenosis!!)
- Treatment:
o 1. Conservative Mx Can 70% Improvement:
Stop Smoking, ETOH, Control Diabetes/ Dietary Cholesterol/HTN.
Exercise
o 2. Medical Management:
Cholesterol-Lowering (Statins/Fibrates/Bile-Resins(Cholestyramine)/Ezetimibe)
Antihypertensives (B-Blockers, ACE-Is/ARBs, Ca-Ch-Blockers)
Diabetes Mx
Champix
o 3. Surgery:
Angioplasty (Balloon + Stent)
Bypass Grafting (Eg. Femoral-Popliteal Bypass)
Plaque Excision (Endarterectomy)
Amputation
VARICOSE VEINS:
- Aetiology:
o Mechanical: Prolonged Leg Dependence
o (Risk Factors = Obesity, Pregnancy, Familial)
- Pathogenesis:
o Superficial Valve Incompetence (Due to Incompetent Valves & Venous Dilation)
Further Venous Stasis, Congestion, Oedema, Pain & Thrombosis.
o (NB: Can Also Occur in Oesophagus, Rectum, & Scrotum)
o Symptoms:
Diffuse Aching, Tightness & Night-Cramping
Persistent Leg Oedema
Wound Healing
o Signs:
Distended, Tortuous Superficial Veins
Ischaemic Skin Changes (Eg. Stasis Dermatitis)
Venous Leg Ulcers
o NB: Embolism is RARE since only Superficial Veins are affected!!!!
o Complications:
Recurrent Superficial Thrombophlebitis (See Below)
Lipodermatosclerois
Haemorrhage
Ulceration
- Investigation:
o Trendelenberg Test (Pt Supine; Raise leg & occlude Saphenous Vein @ Thigh. Then convert to
standing and let go. If Veins Fill From The Top = Positive Test)
- Management:
o Conservative: Elevation + Compression Stockings
o Surgical: Stripping of Varicose Veins
CHRONIC SKIN ULCERS (Lower Limbs Most Common):
- Locations:
o Venous Gaiter Region
o Arterial Foot Region, Anterior Shin & Pressure Points
o Neuropathic Pressure Points
- PRESSURE ULCERS:
o Aetiology:
Long-Term Pressure (Elderly, frail, bedridden, paraplegia, coma)
o Pathogenesis:
Long-term skin pressure Skin Ischaemia Necrosis Ulcer
Location & Appearance:
Bony Prominences (sacrum, coccyx, heels, occiput, knee, elbow)
Initially Non-blanching Erythema Wet, oozing ulcer.
Pain:
Often Painful unless Neuropathic/Paraplegia/etc.
o Treatment:
Pressure Redistribution (Regular Turning, Air Mattress)
Debridement & Dressings
Antibiotics
- ARTERIAL ULCERS:
o Aetiology:
Arterial Insufficiency (PVD) (Typically due to Atherosclerosis)
**Common in Diabetes
o Pathogenesis:
Arterial Insufficiency Tissue Hypoxia/Ischaemia Skin Necrosis + Wound Healing
(NB: Often occurs following Trivial Trauma or Localised Pressure)
Locations:
Anterior Shin
Pressure Points of Ankle & Foot (Bony Prominences)
Appearance:
Superficial
Well Defined Edges
Pale, Non-Granulating Base (Often Necrotic)
Does not bleed to touch
*No surrounding dermatitis (As opposed to Venous Ulcers)
(Cold, Pale feet + Absent Pulses)
Symptoms:
**Severely Painful - Relieved by Depression
(+ Claudication)
o Management;
(DO NOT use Compression Bandage!!)
Control Risk Factors Smoking Diabetes H pertension Lipids
Clean Wound +/- Debride
Reperfusion (Surgery/Angioplasty)
- VENOUS ULCERS:
o Aetiology:
Venous Valve Insufficiency of the legs Sustained Venous Hypertension
(May be Associated with Varicose Veins)
o Pathogenesis:
Venous Insufficiency of legs Venous Hypertension & Stasis Ulceration
Gaiter Region Above Malleoli
Wet, Oozing**
Moist, Granulating Base Bleeds on touch.
S rro nding Stasis Dermatitis Ec emato s
Oedematous
Presence of Varicose veins
Symptoms:
**Only Mild Pain - Relieved by Elevation
Dependent Oedema
Treatment:
Compression Bandage
Elevation @ Rest
Exercise
Clean Wound
- NEUROPATHIC ULCERS:
o Aetiology:
**Diabetic Neuropathy + **Arterial Insufficiency
o Pathogenesis:
Diabetic Neuropathy Damage/Injury goes Unnoticed Further Tissue Damage/Necrosis
(+ Arterial Insufficiency Tissue Hypoxia/Ischaemia Tissue Damage/Necrosis)
Occurs over Pressure Points
Deep P nched-O t lcers
***Often with surrounding Calluses (Hyperkeratosis)
Don t Bleed to To ch
Symptoms:
**Painless
Treatment:
(DO NOT apply Compression Bandage!!)
Debride (+/- Amputation)
Antibiotics
Fastidious Foot Care (Clean Wound, Podiatrist)
Control Other Risk Factors Esp Diabetes Smoking H pertension Lipids
CVS Pathology:
Rheumatic Fever & Rheumatic Heart Disease
RHEUMATIC FEVER & RHEUMATIC HEART DISEASE

- Background:
o Rheumatic Fever (RF) = Delayed Autoimmune Complication of a GA H S ep Tonsillo/Pharyngitis.
o Acute Rheumatic Fever / Carditis (Acute Phase of Rheumatic Fever)
o Chronic Rheumatic Heart Disease (RHD) (Typically Mitral Stenosis)
o (NB: Rheumatic Fever (RF) & Rheumatoid Arthritis (RA) are 2 different diseases)
RF - Licks joints but bites heart! (Temporary Arthritis, but Permanent Valvular Damage)
RA – Licks heart but bites joints! (Mild Myocarditis, but permanent Severe Arthritis)
- Aetiology 3 Factors:
o 1. Environmental factor Group-A-Beta-Haemolitic Strep (Pyogenes) Pharyngitis
o 2. Genetic Susceptibility (3% of Population) HLA DR-2 & DR-3 Positive
o 3. Autoimmunity Autoantibodies (Antigenic Mimickery)
GABH-Strep Production of Anti-M-Protein Ab Cross React with Cardiac Conn. Tissue.
- Pathogenesis Mitral Stenosis:
o 1. GABH Strep Pharyngitis (In HLA-DR2/3-Positive Person)
o 2. 2wks Later, Immune Response to GABH-Strep Rheumatic Fever Carditis
(NB: 2wk Delay due to Lymphocyte Activation)
o 3. Subsequent GABH-Strep Infections Secondary (STRONGER) Immune Responses:
Recurrent Rh-Fever Cumulative Valve Damage (Fibrosis) Rheumatic Heart Disease
- Clinical Features & Diagnosis:

o Acute Rheumatic Fever:
o Jones Criteria Rules - Must Have:
1) Evidence of Previous GABH-Strep (Strep. Pyogenes) Infection
2) (2x Major Criteria) OR (1 Major + 2 Minor)
o 1. (Evidence of Previous Strep Infection):
Anti-Streptolysin-O Titre
Anti-DNaseB Antibodies
Positive Throat Swab Culture
o 2a. (Major Criteria)
J Joints (Migratory Polyarthritis Not necessarily arthralgia)
Carditis (Incl. Pericarditis Friction Rub, Quiet Heart Sounds, Tachy)
N Nodules (Subcutaneous, painless, on extensor surfaces)
E Erythema Marginatum (Non-Pruritic, Tinea-like Rings on Trunk & Limbs)
S S denham Chorea (Rapid, Involuntary Movements)
2b. (Minor Criteria)
(Fever)
(Arthralgia)
(Elevated ESR)
(Prolonged PR-Segment)
o Chronic Rheumatic Heart Disease:
Cardiac Murmurs (Typically L-Heart):
Mitral Stenosis (+/- Regurg)
Aortic Stenosis (+/- Regurg)
Mitral Stenosis:
Mi ral Facie (Malar/Butterfly Rash over Cheeks & Nose)
Mid-Diastolic Rumbling Murmur (Loudest @ Apex on Expiration & Axilla).
Pulm.Congestion & CCF (RV-Hypertrophy, Exertional Dyspnoea)
Atrial Fibrillation (From Atrial Stretch due to Mitral Stenosis)
Risk of Infective Endocarditis
- Management:
o (Primary Prevention Rx of Strep Pharyngitis):
10days PO Penicillin-V (Or Amoxicillin or Cephalexin)
o Secondary Prevention:
Admit on Suspicion:
Based on Jones Criteria
Treating Acute Rheumatic Fever:
GABH Strep Eradication (Single dose IM Benz-Pen-G)
Joint pain (Arthralgia) (NSAIDs or Codeine).
Chorea (Carbamazepine or Valproate if Necessary)
Carditis/Heart Failure (ACEi + B-Blocker + Diuretics)
Treating to Prevent Recurrent Attacks:
Continuous AB-Prophylaxis for Minimum 10 years after last ARF Episode.
o ***First-line: Monthly IM Ben-Pen-G
o **Second-line: BD Oral Pen-V
o *(If Penicillin Allergy: BD Oral Erythromycin).
o (Tertiary Prevention):
Cardiac Surgery - Mitral Valve Replacement
- GLS Question - What is the difference between Rheumatic Fever (RF) & Rheumatic Heart Disease (RHD)?
o (NB: Neither RF or RHD is an Infection, and Both can affect the Heart.)
(The Distinction is whether it is Reversible (RF) or Irreversible (RHD).)
o Rheumatic Fever:
An acute, Post-GAS-Infection Inflammatory Disease.
Occurs a few weeks After a GAS Infection.
If not treated aggressively Acute Rheumatic Carditis Valvular Deformities.
o Rheumatic Heart Disease:
The Chronic Stage which causes Irreversible Myocardial Damage & Heart Valve Damage.
Management
❏ medical
❏ surgical
RHEUMATIC FEVER
Epidemiology
Etiology
Diagnosis
• major criteria
• pancarditis
• polyarthritis
• minor criteria
• polyarthralgia
• fever
plus
Clinical Features
Management
AORTIC STENOSIS
Etiology
❏ acquired
Definition
LV dysfunction
Pathophysiology
Symptomatology
Signs of AS
❏ pulses
• ejection click
Investigations
❏ 12 lead ECG
❏ chest x-ray
❏ ECHO
Natural History
Management
• IE prophylaxis
• AV replacement
CVS Pathology:
Shock
SHOCK:
- EXAM Definition = Indequate Perfusion of Vital Organs (Heart/Brain/Kidneys)
- Aetiologies:
o Hypovolemic Shock:
Severe Dehydration - (Eg. Sweating, Vom/Dia, DKA & Diuresis, Seeping Burns)
Severe Blood Loss/Haemorrhage
o Cardiogenic Shock:
Heart Failure - (Eg. Acute MI, Valvular, Cardimyopathy, Myocarditis)
o Distributive Shock:
Septic Shock (Extracellular Fluid Shift Hypotension Shock)
Anaphylactic Shock (Extracellular Fluid Shift Systemic Oedema & Hypotension).
Neurogenic Shock (Sudden loss of Vasomotor Tone Massive VenoDilation)
o Obstructive Shock:
Massive PE
Cardiac Tamponade (Massive Pericardial Effusion Ventricular Filling SV CO)
Tension Pneumothorax
- Compensatory Mechanisms:
o CARDIAC RESERVE = Maximal % that CO can Increase Above Normal. (Typically 300-400%)
o (IMMEDIATE) Sympathetic Tone:
Baroreceptors SNS HR & Contractility CO
o (DELAYED) Renal:
Angiotensin-II General Vasoconstriction BP
Vasopressin (ADH) Urine Output Blood Volume BP
EPO Haematopoiesis Blood Volume BP
- 3 Stages of Shock:
o 1. Non-Progressive Stage (<15% (<750mL)Blood Loss):
Stable & Reversible.
Signs of Compensated Hypovolaemia:
Tachycardia
Oliguria (Low Urine Production)
o 2. Progressive Stage (15-40% (750-2000mL)Blood Loss):
Unstable, Decompensating, Reversbile.
Signs of Decompensation:
Hypotension
Delayed CRT ( Peripheral Perfusion)
Tachycardia
Organ Failure (Anuria, Confusion/ALOC, Heart Failure, Tachypnoea, Acidosis)
But Still Reversible with Treatment:
Reverse Causative Agents + Volume Replacement (Bolus 2L IV) +/- Inotropes
(Otherwise Fatal if Untreated)
o 3. Irreversible Stage (>40% (>2000mL) Blood Loss):
Unstable, Irrecoverable Organ Failure.
Pt WILL Die Treatment will delay death, but NO treatment will save Pt s life.
Symptoms:
Multi-Organ Failure (Renal/Cardiac/Pulmonary/CNS)
Acidosis
Anuria.
Coma.
- Recognising And Assessing Shock ?
o Obvious Causes? (Eg. Bleeding, seeping burns)
o Compensation? (Eg. Tachycardia)
o Hypotension? (Despite Compensation)
o Poor Tissue Perfusion?
Peripheral Shutdown? (Eg. Cold, sweaty)
Renal Failure? ( Urine Output)
Brain Hypoxia? (Confusion, ALOC, Coma)
Myocardial Ischaemia (Chest Pain, Heart Failure)
BASIC SHOCK MANAGEMENT:

- Hypovolaemic Shock: Recognise Severity, Replace Loss (Normal Saline), Stop Ongoing Losses
- Septic Shock: Blood Culture, IV ABs, IV Fluids, Inotropes, Vasopressors, Remove Infective Focus
- Anaphylactic Shock: ABC 1o Assessment, IM/IV/SC Adrenaline, +/- Steroids
- Cardiogenic Shock: Inotropes, Nitrates/Angioplasty/Reperfusion, Valvuloplasty, Transplant
- Mechanical:
o Tamponade: Pericardiocentesis, Correct Cause (Trauma/Infection)
o Pneumothorax: Thoracocentesis (Pleural Tap), Correct Cause (Trauma/Infection/Fluid Overload)
o PE: Thrombolysis (TPA/Alteplase), Thrombectomy
FLUID RESUSCITATION PRINCIPLES See Fluid Management Surgical Context for more Info :
- How Much???
o 1. Bolus (Vol. Of Estimated Acute Losses)
o 2. Maintenance ***(4,2,1 Rule)***:
4ml/kg/hr for 1st 10kg
2ml/kg/hr for 2nd 10kg (Ie. 60ml/hr for 1st 20kg)
1ml/kg/hr for every kg thereafter. (Ie. 100ml/hr for 1st 60kg Plus 1ml/kg/hr onwards)
- What happens to the Different IV Fluids?:
o Crystalloids (IV Saline Hartmann’s) Na Redistributed into ECF & Blood due to Na/K-ATPase.
(25% remains in Blood)
:. Somewhat useful in Pressure Fluid Resuscitation.
o Colloid (Albumin, Gelatine) Colloid Is Not Redistributed (Stays in blood).
(ALL fluid given remains in Circulation) - (500mL of Colloid = 2L of Crystalloid)
:. Most effective fluid in Pressure Fluid Resuscitation.
o IV Dextrose Actively taken into cells :. None Remains in Blood.
:. NOT Suitable for Pressure Fluid Resuscitation. (Good for Hypoglycaemia & Post-Surgery)
- Blood:
o = The best fluid to replace blood loss
o But Saline/Hartmanns or Colloid are still ok.
o BUT Blood has risks (immunogenic/infections/etc)
GLS SHOCK CASES:
Case 1 - Bart:
- He is pale and sweaty, has a distended abdomen and obvious bilateral femoral fractures. His pulse is 140 and
his blood pressure is 75/40.
What signs of shock are evident?
o Pale and Sweaty
o Tachycardic
o Hypotensive
What Type of Shock is This?
o Hypovolaemic (Haemorrhagic) Shock:
Seems to be bleeding into abdomen Hypovolaemia CO Hypotension +
Compensatory Tachycardia
Could Bart be shocked without a change in BP?
o Yes. Young, healthy people are able to compensate for up to 1500mL of blood loss by Tachycardia &
Vasopression, but then deteriorate rapidly afterwards.
Is this consistent with our definition of shock ?
o No - Our definition stipulates a loss of blood pressure.
o (Clinically important - Need to remember that relying on blood pressure changes alone to diagnose
shock means that we will not recognise shock until a patient has lost 30 - 40 % of their blood volume
(class 3))
Initial Treatment:
o Fluid Replacement (For Hypovolaemia)
Case 2 Homer:
- Suddenly collapsed and clutched his chest. He is pale and sweaty. His pulse is 40 and his blood pressure is
85/60. He is feeling short of breath. You note that his JVP is raised. Moe thinks that Homer has had a heart
attack.
o Pale & Sweaty
o Hypotensive
o Bradycardic Suggests Cardiogenic Shock
o Cardiogenic Shock:
Myocardial Infarction Heart Failure ( CO Bradycardia BP.
H e ECG a a a e ca d a fa c . Why might this have caused him to be shocked
?
o Myocardial Infarction Disrupted heart Contraction & Conduction HR (in this case), and CO
If Homer has a heart that is not pumping properly (decreased contractility) which direction will his Starling
curve move?
o His starling curve will shift Downwards (Ie. Stroke Volume & CO will be Less @ any given End-
Diastolic Volume)
Initial Treatment:
o Inotropes (For the Bradycardia)
Case 3 - Marge:
- Marge has bought a special new brand of extra strong hairspray. Begins to feel very itchy and notices small
bumps coming up on her head. She collapses. She is conscious but confused. Skin is bright red & covered in
raised lumps. Her pulse is 120 and her blood pressure is 90/60.
o Tachycardic
o Hypotensive
o Distributive (Anaphylactic) Shock:
Itchy, red, bumps on skin + History of new Hairspray Allergy (Systemic release of
Histamine & Other Vasoactive Mediators Loss of Vasomotor Tone BP &
Compensatory Tachycardia.
What has happened to her:
o Venous Tone? Decreased
o Venous Capacitance? Increased
o Venous Return? Decreased
o Preload? Decreased
o Stroke Volume? Decreased
o Cardiac Output? Decreased
Why has she collapsed?
o Due to Postural Hypotension Hypo-Perfusion of Brain Momentary loss of consciousness.
(Regained once supine)
Initial Treatment:
o Adrenaline (For the Anaphylaxis)
Case 4 Lisa:
- Lisa has been playing her saxophone. She collapsed gasping for breath. Her pulse is 120 and her Blood
Pressure is 65/45. Neck veins are distended. No breath sounds on the left side. Tension pneumothorax.
o Tachycardic
o Hypotensive
o Obstructive Shock:
Spontaneous Tension Pneumothorax from Playing Saxophone Intra-Thoracic Pressure
Inhibits Cardiac Filling (Seen as raised JVP) CO Hypotension & Compensatory
Tachycardia
How might Lisa’s tension pneumothorax cause her to be shocked?
o If pressure in the tension pneumothorax is high enough it may:
Compress (Decrease) Venous Return to the chest & heart CO Shock
Shift the Mediastinum such that one more of the Great vessels gets kinked CO
Shock
Initial Treatment:
o Chest Drain For the Pneumothorax.
Case 5 - Maggie:
- Her dummy fell in dog poo. Now very sleepy. Her skin is a mottled grey colour. Pulse of 180 and blood
pressure is 60/40. Angry inflamed area on her face which has pus in the middle of it.
o Tachycardic
o Hypotensive
o Grey, colourless skin
o Distributive (Septic) Shock:
Bacterial infection from dog faeces Endo/Exo Toxin Systemic Cytokine Release Loss
of Vasomotor Tone BP Compensatory Tachycardia
How have the following been affected ?
o Venous tone? Decreased
o Vessel Permeability? Increased
o Myocardial function? Inotropic
Initial Treatment:
o Antibiotics
o (Also check Lactic Acid Level):
High levels can indicate severe infection
& Can indicate lack of Tissue Perfusion & Production of Lactica Acid by Anaerobic Metabolic
Pathways.
CVS Pathology:
Tumours of Vessels
Tumours of Vessels (Blood & Lymphatics): p520

- HAEMANGIOMA:
o = Closely Packed Aggregates of Sub-Cutaneous Capillaries filled with Blood.
o Congenital & Benign
- PYOGENIC GRANULOMA:
o = A Granulating Haemangioma
o Rapidly Growing Cutaneous/Mucosal Red Nodule (Bleeds Easily & Often Ulcerated.)
o Consist of Capillaries, Granulation Tissue & Bacteria
o Often follow Trauma (Inflammatory tissue due to injury)
- TELANGIECTASIA:
o = A Tiny AV-Malformation
o Blanching, Spider-Like, Red Lesions.
o Composed of Capillaries, Venules & Arterioles.
o (Usually in Skin/Mucous Membranes)
- LYMPHANGIOMA:
o = Benign Lymphatic Version of a Haemangioma – (= Aggregations of Lymphatic Vessels)
o May be Simple Capilla L mphangioma; or Ca e no L mphangioma C ic H g oma .
- KAPOSI SARCOMA “ANGIOSARCOMA” :

o = Highly Malignant Endothelial Tumour Caused by HHV-8 Infection.
o Typically in Terminal AIDs Pts (Or other Immunodeficiency)
o Early Stages = Asymptomatic Surgical Excision effective.
o Late Stages = Metastatic Chemotherapy Required.
CVS Pathology:
Valvular Heart Disease & Murmurs
VALVULAR HEART DISEASE:

- 4 Most Common Murmurs & Their Causes:
Valve Lesion Aetiology/Pathological Cause
Mitral Stenosis **Rheumatic Fever (Post Inflamm. Scarring)
Mitral Regurgitation Mitral Prolapse M omato s Degeneration
Rheumatic Fever (Post Inflamm. Scarring)
MI (Papillary Muscle Fibrosis/Dysfunction)
Rupture of Papillary Muscles/Chordae Tendineae
Dilated Cardiomyopathy (Dilation of Valve Annulus)
Congenital (Degeneration of Cusps)
Aortic Stenosis Age-Related Calcification
Aortic Regurgitation Age-Related Dilation of the Ascending Aorta
HT-Related Dilation of the Ascending Aorta
Marfan s S ndrome
Syphilitic Aortitis
Rheumatoid Arthritis
Ankylosing Spondylitis
- (Red = Most Common)
- Other Less Common Murmurs:

Cause Diastolic/Systolic?
Pulmonary Stenosis Congenital Heart Defect Systolic
Rheumatic Heart Disease
Pulmonary Regurgitation Pulmonary Hypertension Diastolic
Tricuspid Stenosis Rheumatic Fever Diastolic
Tricuspid Regurgitation R-Ventricular Dilation (Eg. R-V Systolic
Infarction)
MITRAL STENOSIS:
- Aeitiology:
o 99% Rheumatic Heart Disease
- Pathogenesis:
o Recurrent Acute Rheumatic Fever Autoimmune Mitral Valve Fibrosis Stenosis
- Clinical Features
o Symptoms:
CCF (Exertional Dyspnoea/Orthopnoea/PND/Wet cough (Pulmonary Oedema))
o Signs:
Low-Volume Pulse
Mid-Diastolic Rumbling Murmur (Loudest @ Apex on Expiration & Axilla).
Mi al Facie (Malar/Butterfly Rash over Cheeks & Nose)
Pulm.Congestion & CCF (RV-Hypertrophy, Exertional Dyspnoea)
If Cor-Pulmonale (RV-Failure) JVP, Pulsatile Liver, Ascites, Peripheral Oedema)
- Investigations:
o ECHO (Diagnostic)
o ECG (May have A.Fib, LA-Hypertrophy, RVH)
o CXR (LA-Hypertrophy, Pulmonary Congestion)
- Management:
o Medical Treat A.Fib, Warfarin, CCF Triples (ACEi + B-Blocker + Diuretics)
o Surgical Mitral Valvuloplasty (Repair) or Replacement
MITRAL INCOMPETENCE/REGURGITATION:
- Aeitiology:
o Myxomatous Degeneration, Rheumatic Fever, Infective Endocarditis or Ischaemia
- Pathogenesis:
o Myxomatous Degeneration (Pathological weakening of valve connective tissue)
o Rheumatic Fever Autoimmune Mitral Valve Fibrosis Stenosis & Regurg
o Infective Endocarditis Vegetations on Valve Edges Improper Closure Regurg
o Ischaemia (Post MI Papillary Rupture Ballooning of Mitral Valve during Systole)
o Symptoms:
Exertional Dyspnoea
Wet Cough (Pulmonary Oedema)
o Signs:
High-Pitched Pansystolic Murmur (Loudest @ Apex on Expiration Axilla)
L-Parasternal Heave (L-Atrial Hypertrophy)
- Investigations:
o ECHO (Diagnostic)
o ECG (LAH, LVH)
o CXR (LAH, LVH, Pulmonary Congestion)
- Management:
o Medical CCF Triples (ACEi + B-Blocker + Diuretic)
o Surgical Mitral Valvuloplasty (Repair) or Replacement
AORTIC STENOSIS:
- Aeitiology:
o Age-Related Calcification (Wear & Tear)
o (Also Rheumatic Heart Disease in 10% of cases)
- Pathogenesis:
o Wear & Tear Degeneration + Calcification.
o Symptoms:
Ao ic S eno i T iad
1. Angina - (Due to LV-Hypertrophy & Demand)
2. Exertional Dyspnoea - (Due to Congestive Heart Failure)
3. Syncope/Dizziness - (Due to Cerebral Perfusion)
o Signs:
LV-Hypertrophy Displaced Apex Beat.
Loud Ejection Systolic Murmur +/- Thrill (Loudest @ 2ndICS R-Sternal Border)
Worse on Expiration
Radiates to Carotids
Congestive Heart Failure Dyspnoea + Pulmonary Oedema
- Investigations:
o ECHO (Diagnostic)
o ECG (LV-Strain & LVH)
o CXR (Calcified Valve, LVH, CCF/Pulmonary Oedema)
- Management:
o If Symptomatic Requires Cardiac Surgery:
Aortic Valve Replacement.
Or Balloon Valvuloplasty
AORTIC INCOMPETENCE/REGURGITATION:
- Aeitiology:
o Age/H e en ion S hili ic Ao i i Aortic Root Dilation
- Pathogenesis:
o Dilation of Aortic Root Valve Leaflets Misalignment Aortic Regurg
o Symptoms:
Aortic Triad:
1. Angina - (Due to LV-Hypertrophy & Demand)
2. Exertional Dyspnoea - (Due to Congestive Heart Failure)
3. Syncope/Dizziness - (Due to Cerebral Perfusion)
o Signs:
Waterhammer Pulse (Bounding and Rapidly Collapsing)
Displaced Apex Beat (Due to LV-Hypertrophy)
Diastolic Decrescendo Murmur (Loudest @ R.2ndICS on Expiration)
Tachycardia (Compensation for CO)
- Investigations:
o ECHO (Diagnostic)
o ECG (LAH + LVH)
o CXR (LAH + LVH, CCF/Pulmonary Oedema)
- Management:
o Medicine: Vasodilators + CCF Triple Therapy (ACEi + B-Blocker + Diuretic)
o Surgery: Aortic Valve Replacement
CVS Pathology:
Vasculitides
NB Raynaud s Phenomenon A common feature of Blood Vessel Disorders):

- Aetiology: Exaggerated Vasoconstriction of Digital Arteries (Cold/Emotional Trigger)
- Clinical Features: Paroxysmal Pallor/Cyanosis of Digits (hands/feet)
o Usually benign
Vasculitis (General Vessel Inflammation):

- NB The e a e diffe en fo m of Va c li i Only focus on those Highlighted)
- 2 Aetiologes:
o Immune...OR...Infective
o (NB: MUST distinguish between aetiologies since treatments Contradict each other)
- Signs/Symptoms:
o Generals Fever, Malaise, Myalgias & Arthralgias.
o Specifics - Depend on Vessels Affected.
VASCULITIS IN LARGE ARTERIES:
** GIANT CELL (TEMPORAL) ARTERITIS:

- Aetiology:
o Chronic, Autoimmune Disease of TEMPORAL and OPHTHALMIC Arteries
- Pathogenesis:
o Autoimmune Inflammation of Temporal & Ophthalmic Arteries
o (Typically in o
o Temporal Arteritis Triad:
1. Headaches
2. Jaw Claudication
3. Tender Temples
o + Fever, Fatigue, Weight Loss
o +/- Sudden Painless Blindness (Transient or Permanent)
o Sometimes Polymyalgia Rheumatica (Neck, Shoulder & Hip Pain/Stiffness)
- Complications:
o **RED FLAG If Untreated, can BLINDNESS
o Aortic Arch Syndrome Aortic Aneurysm +/- Rupture.
- Investigation:
o ESR + CRP **Temporal Artery Biopsy
(NB: Biopsy = Definitive Diagnosis)
o +/- Cranial Angiography
- Treatment:
o High-Dose Prednisone
o (+/- Azathioprine or Methotrexate if severe)
VASCULITIS IN MEDIUM ARTERIES (MUSCULAR ART):
POLYARTERITIS NODOSA:
- Aetiology:
o SYSTEMIC Autoimmune Inflammation of Medium Arteries.
- Pathogenesis:
o Immune Complex Deposition in Arteries (Particularly Renal Arteries)
Necrosis of Vessels Rupture/Thrombosis/Aneurysms Infarct/Ischaemia.
o General Symptoms:
**Fever
Rash
Malaise
Weight Loss
o Organs-Specific Symptoms:
Skin Palpable Purpura, Ulcers
End-Arteries Gangrene, Digital Infarcts
Muscles Myalgia
Joints - Arthralgia
Kidneys - Hypertension
Heart Angina, MI, CCF
GIT Abdo Pain, Haematemesis, Malena, Ischaemic Gut
Liver Jaundice
Neuro Peripheral Neuropathy, Paraesthesia, Weakness
- Complications:
o Rupture/Thrombosis/Aneurysms Localised Infarct/Ischaemia
- Investigation:
o ESR + CRP
o Vascular Biopsy
o Or Angiogram
- Treatment:
o Prednisone
o + Cyclophosphamide (Chemotherapy)
KAWASAKIS DISEASE Mucocutaneous Lymph Node Syndrome :

- See Paediatrics
VASCULITIS IN SMALL ARTERIES (CAPS & ARTERIOLES):
WEGENER S GRANULOMATOSIS:
- Aetiology:
o Autoimmune (Probably Hypersensitivity to Inhaled Agents)
- Pathogenesis:
o Autoimmune Hypersensitivity Reaction to Inhaled Agent Necrotizing Lung Granulomas (~TB)
(Also Renal Glomerulonephritis).
- Morphology:
o Granulomatous Inflammation in Lungs & URT
URT Mucosal Granulomatous Lesions
Granulomas (which may cavitate) in the Lungs
o Necrotizing Vasculitis around Small Vessels (Particularly Renal/Glomerular).
Focal (early) or Diffuse (late) Glomerular Necrosis Glomerulonephritis
o Systemic:
Fever, Malaise, Weakness, Myalgia, Rash.
o Respiratory:
Initially (Flu-like Illness):
Fever
Cough
Rhinorrhoea
Otitis Media
Later (Similar Features to TB):
Haemoptysis
Chronic Pneumonitis
Bilateral Cavitary Granulomas in Lungs
Chronic Sinusitis
o Renal:
Glomerulonephritis (Nephrotic +/- Nephritic Syndrome)
- Investigations:
o American College of Rheumatology Criteria (>2 of):
URTI Inflammation (Nasal/Oral)
CXR (Nodules/Cavitations)
Urinalysis (Protein/Casts)
Biopsy (Granulomatous Inflammation)
o + ANCA
o ESR & CRP
- Treatment:
o Prednisone (+/- Cyclophosphamide)
o + High-Dose Methotrexate
o (NB: 80% 1yr Mortality if Not Treated)
CHURG-STRAUSS SYNDROME:
- Aetiology:
o Unknown
- Pathogenesis:
o Granulomatous Inflammation of Small/Medium-Sized Vessels.
o Churg-Strauss Triad:
Systemic Vasculitis
Asthma
Allergic Rhinitis
o Others (Angina, Myocarditis, Neuropathy)
- Investigation:
o +ANCA
o ESR
o FBC (Eosinophilia)
- Management:
o Prednisone +/- Cyclophosphamide
o Then Methotrexate
BUERGER S DISEASE THROMBOANGIITIS OBLITERANS

- Aetiology:
o **Cigarette Smoking Direct Endothelial Toxicity
- Pathogenesis:
o **Cigarette Smoking Direct Endothelial Toxicity Vasculitis Ischaemia Gangrene
o ***Occurs in Chronic HEAVY Smokers
o Digital Infarcts - Gangrene
o Distal Limb Ischaemia (Claudication, Arterial Ulcers, Gangrene)
- Treatment:
o Smoking Cessation (In early stages) Dramatic Relief.
(Lumen is occluded by thrombus containing abscesses (arrow), and the vessel wall is infiltrated with leukocytes.)
CARDIAC AND
VASCULAR SURGERY
Dr. D.S. Kucey and Dr. C.M. Peniston
Alex Kulik and Ted Rapanos, chapter editors
Neety Panu, associate editor
PREOPERATIVE ASSESSMENT . . . . . . . . . . . . 2 CARDIAC TRANSPLANTATION . . . . . . . . . . . . . 17

History and Physical Exam
Consent CONGENITAL HEART SURGERY . . . . . . . . . . . . 18
Preadmission Tests and Orders Palliative Procedures
Preoperative Medications Pure Obstructive Lesions
Simple Left-to-Right Shunts
ASSESSING RISK AND BENEFIT OF . . . . . . . 3 Right-to-Left Shunts
SURGERY Complex Cyanotic Defects
COMMON POSTOPERATIVE . . . . . . . . . . . . . . . 4 VASCULAR - ARTERIAL DISEASES . . . . . . . . . 22
COMPLICATIONS Acute Arterial Occlusion/Insufficiency
Arrhythmias Chronic Aterial Occlusion/Insufficiency
Bleeding Critical Ischemia
Renal Failure Abdominal Aortic Aneurysm (AAA)
Respiratory Failure Abdominal Aortic Dissection
Low Cardiac Output (CO) and Ruptured Abdominal Aortic Aneurysm
Intra-aortic Balloon Pump (IABP) Cartoid Surgery
Cardiac Tamponade
Perioperative Myocardial Infarction VASCULAR - VENOUS DISEASES . . . . . . . . . . . 27
Hypertension Anatomy
Postoperative Fever Deep Venous Thrombosis (DVT) (Acute)
CNS Complications Superficial Thrombophlebitis
Varicose Veins
CARDIAC ANESTHESIA . . . . . . . . . . . . . . . . . . . 7 Chronic Deep Venous Insufficiency (post phlebitic
Preoperative Syndrome, Ambulatory Venous Hypertension)
Intraoperative Anesthesia Lymphatic Obstruction/Lymphangitis
Intraoperative Monitoring
Postoperative VASCULAR - TRAUMA . . . . . . . . . . . . . . . . . . . . . 31
Penetrating (Laceration)
PRINCIPLES OF CARDIOPULMONARY . . . . . 8 Blunt (Contusion, Spasm, Compression)
BYPASS (CPB)
REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32
MYOCARDIAL PROTECTION AND . . . . . . . . . 10
CARDIOPLEGIA
CORONARY ARTERY BYPASS GRAFT . . . . . . 11
SURGERY
VALVE REPLACEMENT AND REPAIR . . . . . . 13
Aortic Stenosis (AS)
Aortic Regurgitation (AR)
Choice of Aortic Valve Prosthesis
Mitral Stenosis (MS)
Mitral Regurgitation (MR)
Choice of Mitral Valve Prosthesis
AORTA REPLACEMENT AND REPAIR . . . . . . 16
Thoracic Aortic Dissection
Thoracic Aorta Aneurysm
Traumatic Aortic Disruption

PREOPERATIVE ASSESSMENT
HISTORY AND PHYSICAL EXAM
❏ history of present illness
• inquire about symptoms of cardiac disease i.e. chest pain, dyspnea, fatigue, hemoptysis, syncope,
palpitations, peripheral edema, cyanosis
• determine the degree of physical disability caused by cardiac symptoms
(angina, shortness of breath (SOB), undue fatigue, palpitations) using the
New York Heart Association (NYHA) functional classification (see Table 2 Cardiology Chapter)
• determine severity of angina pectoris using the Canadian Cardiovascular
Society classification (see Table 1 Cardiology Chapter)
❏ past medical history
• cardiac risk factors: smoking, family history, elevated cholesterol,
diabetes mellitus (DM), hypertension (HTN), +/– elevated homocysteine levels
• previous operations: thoracotomy, saphenous vein stripping/ligation, peripheral vascular surgery,
carotid endarterectomy
• allergies, medications i.e. anticoagulants, antiarrhythmics,
antiplatelet agents, ACE inhibitors, diuretics, etc.
❏ family and social history
• family history of coronary artery disease (CAD), congenital heart disease, Marfan syndrome,
malignant hyperthermia and other hereditary disorders should be noted
• consider marital status and living conditions in discharge planning
❏ review of symptoms
• cardiovascular: past cardiac procedures, and investigations
• CNS: previous transient ischemic attack (TIA) or stroke (requires full neurologic work-up)
• respiratory: if chronic obstructive pulmonary disease (COPD) is suspected, obtain spirometry,
pulse oximetry and ABG pre-op
• endocrine: DM and its complications should be noted
• hematologic: bleeding disorders, sickle cell screening if African heritage
• renal: impaired renal function and renal dialysis increase the risk of perioperative complications;
renal transplant patients should be followed by renal transplant service
perioperatively to manage medications
• gastrointestinal (GI): active peptic ulcer disease, active hepatitis, cirrhosis,
and other GI problems can seriously affect the outcome of cardiac surgery
• peripheral vascular: venous and arterial disease should be noted; intra-aortic balloon pump insertion
through a femoral artery may be difficult with aorta-iliac occlusive disease
• genitourinary (GU): prostate problems may impair Foley catheter insertion
• musculoskeletal (MSK): major skeletal deformities or active arthritic conditions may interfere
with airway management, ambulating, and recovery
❏ physical examination
• height, weight, and vital signs
• examine mouth, airway, neck, chest and abdomen
• assess all peripheral pulses and auscultate the carotid and subclavian arteries for bruits
• examine saphenous veins
• perform Allen's test on both hands in case a radial artery is used as a bypass conduit
for coronary artery bypass
• infection following cardiac surgery can be disastrous, therefore rule
out skin infections and dental caries (especially prior to valve surgery)
CONSENT
❏ risks and benefits of surgery should be clearly outlined to the patient and his/her family
(with patient's permission)
❏ serious complications should be explained, such as death, stroke, myocardial infarction (MI), infection, etc.
PREADMISSION TESTS AND ORDERS

❏ CBC, PTT, INR, electrolytes, glucose, BUN, creatinine, and other special blood tests as needed
❏ urinalysis
❏ PA and lateral CXR (+/– CT chest, especially in re-operations to determine relation
of sternum to heart and ascending aorta)
❏ ECG to diagnose heart rhythm abnormalities and myocardial ischemia
❏ cross and type for 2 units PRBCs
❏ NPO after midnight
❏ Dulcolax suppository preop
❏ ancef 1 g IV to be given in OR (vancomycin 1 g IV or clindamycin 600 mg IV if penicillin allergic)

PREOPERATIVE ASSESSMENT . . . CONT.
PREOPERATIVE MEDICATIONS
❏ All regular cardiac medications should be continued to the morning of surgery (including nitro patch), except:
• amiodarone - should be stopped 4 weeks preop to avoid potential intraoperative problems
(resistant bradycardia, hypotension, etc.)
• ACE inhibitors - small risk of hypotension perioperatively with these drugs,
therefore stop 24 hours preop (controversial)
❏ anticoagulants
• warfarin - stop 4-5 days prior to surgery; admit and start on IV heparin if high risk of thrombosis
large left atrium, atrial fibrillation (A fib), mitral valve prosthesis
• heparin - IV heparin should be stopped 2-3 hours preop
(unless on intra-aortic balloon pump (IABP) support)
• ASA/Ticlodipine/NSAIDs - stop 7-10 days preop if possible
❏ psychotropic drugs
• MAO inhibitors - discontinue 3 weeks preop if long acting, 1 week if short acting
❏ others
• steroids and anti-rejection drugs (transplant patients) must be continued
ASSESSING RISK AND BENEFIT OF SURGERY

❏ ventricular function
• the most important determinant of outcome of all heart diseases
• patients with severe left ventricular (LV) dysfunction usually have a poor prognosis,
but surgery can sometimes dramatically improve LV function
• patients with severe LV dysfunction but good arteries to bypass usually do very well from the
operative risk viewpoint, but those with bad ventricles and marginally graftable coronary arteries
are usually poor surgical candidates
• to assess viability of non-functioning myocardial segments, use thallium and
sestamibi myocardial imaging, PET scanning or MRI (see Cardiology chapter)
• surgically correcting volume overloading conditions such as aortic or mitral regurgitation (AR/MR)
may not change the prognosis (due to irreversibly damaged myocardium)
but symptomatology can be improved
• depressed ventricular function caused by aortic stenosis almost always improves
following relief of obstruction
❏ coronary artery disease (CAD)
• isolated proximal disease in large coronary arteries (>1.0 - 1.5 mm) is ideal for bypass surgery
• small, diffusely diseased coronary arteries are not suitable for bypass surgery
• see Cardiology Chapter for discussion of PTCA vs. surgery
❏ heart valve disease
• repair of heart valves is preferable to replacement because the ideal artificial valve
has not yet been developed
• repair is not feasible in all patients with heart valve disease, therefore valve replacement is necessary
❏ numerous risk factors for CABG mortality have been identified in several major studies
(in decreasing order of significance)
• urgency of surgery (emergent or urgent)
• reoperation
• older age
• poor ventricular function
• female gender
• left main disease
• others include catastrophic conditions (cardiogenic shock, ventricular septal rupture, ongoing CPR),
dialysis-dependent renal failure, end-stage COPD, diabetes, cerebrovascular disease,
and peripheral vascular disease
❏ commonly identified factors found to increase CABG post-operative morbidity or length of stay
(in decreasing order of significance):
• reoperation
• emergent procedure
• preoperative usage of intra-aortic balloon pump (IABP)
• congestive heart failure (CHF)
• CABG-valve surgery
• older age
• renal dysfunction
• COPD
• DM
• Cerebrovascular disease (CVD)
❏ see Table 1 - Cleveland Clinic Clinical Severity Scoring System

ASSESSING RISK AND BENEFIT OF SURGERY . . . CONT.
Table 1. Cleveland Clinic Clinical Severity Scoring System

Preoperative Factor Score Added Score Morbidity* Mortality
Emergency Case 6 0-2 4-7% 0-2%
Creatinine 141-167 umol/L 1 3-5 10% 2-4%
Creatinine >168 umol/L 4 6 18% 5%
Severe LV dysfunction 3 7-9 23% 7%
Reoperation 3 10+ > 50% > 25%
Mitral Regurgitation 3
Age 65-74 1
Age 75+ 2
Prior vascular surgery 2
COPD 2
Hematocrit <34% 2
Aortic stenosis 1
Weight <65 kg 1
Diabetes 1
Cerebrovascular disease 1
*Morbidity defined as myocardial infarction requiring use of IABP, mechanical ventilation for 3+ days, neurological deficit, oliguric or anuric renal
failure, or serious infection.
Adapted from Higgins et al. Stratification of morbidity and mortality outcome by preoperative risk factors in coronary artery bypass patients. JAMA. 1992:267:234-8.
COMMON POSTOPERATIVE COMPLICATIONS

ARRHYTHMIAS
❏ ventricular ectopy most common
• premature ventricular contractions (PVC's) are usually benign, but may reflect marginal coronary
perfusion and ongoing myocardial ischemia
• if frequent (> 6-10/min) or multifocal PVCs, check serum electrolytes,
repeat 12 lead ECG and assess hemodynamics
• treatment
• Lidocaine 100 mg IV bolus (may repeat 50 mg IV bolus), followed by drip at 1-4 mg/min
• Magnesium sulfate 2-4 g IV, may repeat
• Amiodarone 150 mg IV slowly over 15-30 minutes,
then 900-1,200 mg (in 250 cc D5W) over 24-48 h
• cardioversion needed if progresses to symptomatic ventricular tachycardia (VT)
or if patient develops ventricular fibrillation (V fib)
• atrial or atrioventricular pacing at a slightly higher rate may suppress ectopy
❏ nodal or junctional rhythm
• treatment may not be necessary (assure no hypotension)
• rule out digoxin toxicity, make certain serum K+ > 4.5, rule out hypomagnesemia
• may require A-V sequential pacing if loss of atrial kick has significant hemodynamic sequelae
❏ supraventricular tachycardia (SVT) - includes atrial fibrillation (A fib) and flutter
• onset may be heralded by multiple premature atrial contractions (PAC's)
• atrial ECG using atrial pacing leads often helpful in distinguishing fibrillation from
flutter during rapid rates
• treatment of A fib
• digoxin used to control rate - 0.5 mg IV once, then 0.25 mg q6h x 2,
then 0.125-0.375 mg PO daily depending on body weight and renal function
• if no asthma/COPD: metoprolol 5 mg IV q15min x 3, then 25-50 mg PO bid
• if asthma/COPD: diltiazem 0.25 mg/kg IV bolus (further 0.35 mg/kg bolus if
inadequate response), then switch to amiodarone 400 mg PO tid x 3-5 days,
then 200 mg PO od after loading dose
• if unstable or Grade IV LV: consider amiodarone 150 mg IV bolus (can repeat),
then 900 mg IV over 24 h, then switch to PO amiodarone as above
• treatment of atrial flutter
• rapid atrial pacing > 400 bpm
• digitalization followed by IV beta blocker
• IV verapamil followed by digitalization (calcium channel blockers must be used judiciously
as wide complex SVT can mimic VT)
• in both instances, the arrhythmia should be treated with synchronous direct current (DC) cardioversion
at 25-50 joules should there be a significant drop in blood pressure (BP) or cardiac output (CO)
• never give IV CCB and B blocker together
• adenosine can be used as a diagnostic and therapeutic intervention
(transient bradycardia/asystole to allow interpretation of rhythm, may be therapeutic)

COMMON POSTOPERATIVE COMPLICATIONS . . . CONT.
BLEEDING
❏ causes include medications, clotting deficits, prolonged operation, emergency surgery,
technical factors, deep hypothermia, renal impairment, and transfusion reactions
❏ patients at high risk for bleeding complications: endocarditis, aortic dissection, redo cases
❏ treatment
• assure normothermia
• measure clotting factors stat: INR, PTT, fibrinogen, platelet count, activated clotting time
• tranexamic acid bolus (50 mg/kg) occasionally given if > 150 cc/h chest tube output
• correct with fresh frozen plasma, cryoprecipitate, platelets, DDAVP,
protamine for continued heparinization
• transfusion reaction protocol if suspected
❏ indications for surgical exploration of post-operative hemorrhage
• mediastinal tube output > 300 cc/h despite correction of clotting factors
• 1.5% rate for CABG, 4% rate for valve surgery
• technical factors found as cause > 50% of time
RENAL FAILURE
❏ incidence is 0.3-1%
❏ diagnosis - prerenal vs. renal vs. postrenal
❏ management
• optimize volume status and cardiac output
• discontinue nephrotoxic drugs (indomethacin, aminoglycosides, ACE inhibitors)
• maintain urine output > 40 cc/h using low-dose dopamine (1-3 ug/kg/h),
furosemide 10-300 mg IV bolus +/– 10-20 mg/h drip, or ethacrynic acid (50-100 mg IV bolus) as indicated
• furosemide/mannitol drips if persistent oliguria
• dialysis
• continuous arterial-venous hemodialysis (CAVHD) or continuous venous-venous (CVVHD)
approach are most suitable for hemodynamically unstable patients
• for hemodynamically stable patients, consider intermittent hemodialysis or peritoneal dialysis
(peritoneal cavity may communicate with mediastinum and be ineffective)
❏ outcome
• mortality rates 0.3-23% depending on the degree of azotemia
• if dialysis is required, mortality ranges from 27-53%
RESPIRATORY FAILURE
❏ mechanical - mucous plugging, malpositioned endotracheal tube, pneumothorax,
pre-existing COPD, bronchospasm
❏ intrinsic - volume overload, pulmonary edema, atelectasis, pnemonia, pulmonary embolus
(uncommon), acute respiratory distress symptom (ARDS)
❏ management
• examine patient and evaluate CXR for correctable causes
• if intubated: add positive end-expiratory pressure (PEEP) (7.5-10 cm H2O),
increase % oxygen inspired (FiO2), diuresis, consider bronchoscopy with lavage for sputum,
bronchodilators
• if extubated: pain control, chest physio, diuresis, increase FiO2,
facial continuous positive air pressure (CPAP), bronchodilators
• if pneumonia: sputum culture and gram stain, bronchoscopy,
consider antibiotics early if prosthetic materials in heart
LOW CARDIAC OUTPUT (CO)
❏ cardiac index < 2.0 L/min/m2
❏ signs - decreased urine output, acidosis, hypothermia, altered sensorium, cool clammy skin
❏ assessment - heart rate and rhythm (ECG: possible acute MI), preload and afterload states
(Swan-Ganz catheter readings), measurement of CO
❏ treatment
• stabilize rate and rhythm
• optimize volume status, systemic vascular resistance (SVR)
• consider ECHO to rule out tamponade
• give calcium chloride 1 g IV until more definitive diagnosis reached
• correct acidosis, hypoxemia if present (CXR for pneumothorax)
• inotropic agents if necessary - see Table 4
• Dopamine: increases SVR, protects renal function (increases renal blood flow,
GFR and sodium excretion), produces tachycardia only in high doses
• Dobutamine: increases CO, decreases LV pressure, decreases SVR
• Epinephrine: increases heart rate, contractility and stroke volume (SV), decreases urine flow
• Norepinephrine: increases mean arterial pressure (MAP) with less increase in HR
compared to epinephrine
• Milrinone: improves cardiac output and myocardial contractility, decreases systemic
and pulmonary vascular resistance without increasing HR, used for right ventricle (RV)
failure or high pulmonary artery (PA) pressure
• Amrinone: similar to milrinone but more prone to cause arrhythmias in high doses
• persistent low cardiac output despite inotropic support requires placement of IABP
❏ intra-aortic balloon pump (IABP)

• augments cardiac function without increasing oxygen demand
• inflation during diastole augments coronary perfusion and oxygen delivery
• deflation during systole reduces afterload, therefore decreasing oxygen demand
• indications: unable to wean from cardiopulmonary bypass, cardiogenic shock unresponsive
to medical therapy, low output syndrome, unstable angina, ventricular tachyarrhythmias
caused by ischemia, bridge to transplantation
• contraindications: aortic regurgitation, aortic dissection, aortic aneurysm (thoracic or abdominal),
severe peripheral vascular disease (consider transthoracic route instead), severe blood dyscrasias
Table 2. Adrenergic Catecholamine Receptor Activity

Agent α1 α2 ß1 ß2 Dopamine
Dopamine ++ + + + +++
Dobutamine s s +++ ++ s
Epinephrine +++ +++ ++ ++ s
Norepinephrine +++ +++ + s s
Adapted from Cheng DCH, David TE eds. Perioperative care in cardiac anesthesia and surgery. Austin: Landes Bioscience, 1999.
CARDIAC TAMPONADE
❏ onset - suggested by increased filling pressures (> 20 mmHg) with decreased CO,
decreased urine output (U/O), hypotension, poor peripheral perfusion, pulsus paradoxus, quiet and distant
heart sounds, absence of chest tube drainage, eventual equalization of right and left-sided atrial pressures
❏ high degree of suspicion when coincides with excessive post-operative bleeding
❏ echocardiogram if high index of suspicion; CXR may demonstrate wide mediastinum
❏ treatment
• emergent re-exploration is treatment of choice and may be needed at bedside
for sudden hemodynamic decompensation
• transfuse to optimize volume status and inotropic support
• avoid increased PEEP
PERIOPERATIVE MYOCARDIAL INFARCTION (MI)
❏ incidence: 2.4% CABG, 1.3% valve surgery
❏ diagnosis: new onset Q waves (or loss of R waves) post-operatively, new ST segment elevation,
serial isoenzymes (CK-MB, troponin), segmental wall motion abnormalities by ECHO
❏ treatment
• vasodilation (IV nitroglycerine is preferred to nitroprusside)
• intra-aortic balloon pump if continued hemodynamic deterioration
(unloads the ventricle, and may preserve non-ischemic adjacent myocardium)
❏ outcome - associated with increased morbidity and mortality as well as poorer long-term results
HYPERTENSION (HTN)
❏ incidence 30-50% following cardiopulmonary bypass
❏ predisposes to bleeding, suture line disruption, aortic dissection, increased myocardial oxygen requirements,
depressed myocardial performance
❏ treat if systolic pressure > 130 mmHg
❏ treatment
• resume preoperative medications when tolerated
• nitroglycerin 100 mg in 250 cc D5W at 5-50 cc/h (good for ischemia or high filling pressures)
• sodium nitroprusside 50 mg in 250 cc D5W at 5-50 cc/h (good to reduce afterload)
• beta-blockers (esmolol 10-20 mg IV bolus, metoprolol 1-5 mg IV bolus, etc.)
• CCB (nifedipine 10 mg sublingual for arterial spasm, diltiazem 5-10 mg IV q1h)
• ACE inihibitor if poor LV function and good renal function
POSTOPERATIVE FEVER
❏ definition: core body temperature > 38.0ºC
❏ common in first 24 h post-operatively
❏ etiology unknown but likely due to atelectasis or may be associated
with pyrogens introduced during cardiopulmonary bypass
❏ treat with acetaminophen, add cooling blankets (associated hypermetabolism and
vasodilation may be detrimental to hemodynamic status and increase myocardial work)
❏ post-operative patients receive cefazolin 1 g IV q8h (total 3-6 doses), or if pen-allergic then
vancomycin 1 g IV q12h (1 dose CABG, 2 doses valve) or clindamycin 600 mg IV q8h (6 doses)
❏ if patient febrile beyond 24 hours, culture urine, blood, sputum, and check WBC count

❏ consider early antibiotic treatment if patient has prosthetic material

❏ arterial and central lines should be changed prophylactically every 7-10 days unless obviously infected
❏ inspect sternal wound daily for drainage and stability (sternal wound infections are disastrous
and require operative debridement, 0.8% incidence)
❏ post-pericardiotomy syndrome
• characterized by low grade fever, chest pain, malaise and pericardial rub on auscultation
• usually 2-3 weeks post-op
• treatment - NSAIDs, rarely steroids are necessary
CNS COMPLICATIONS
❏ causes - pre-existing CVD, prolonged cardiopulmonary bypass, intra-operative hypotension,
emboli (air or particulate matter)
❏ transient neurologic defecit - occurs in up to 12% of patients, with improvement usually within several days
❏ permanent deficit - suspect in patients with delayed awakening post-op or with pathologic reflexes present
❏ stroke incidence: 1.4% CABG, 2.5% valve surgery, 6.6% aorta surgery
❏ CT scan early for suspected localized lesion, EEG in patients with extensive dysfunction
❏ treatment - optimize cerebral blood flow, avoid hypercarbia
❏ post-cardiotomy psychosis syndrome
• incidence 10-24%
• begins post operative day (POD) #2 with anxiety and confusion,
progressing to disorientation and hallucinations
• rule out organic causes of delirium: substance withdrawal,
hypoxemia, hypoglycemia, electrolyte abnormalities, etc.
• treatment - rest and quiet environment, Haloperidol 2-10 mg IV q1h PRN
❏ post-op seizures
• check serum electrolytes (calcium, magnesium, sodium) and glucose
• treatment: diazepam 2-5 mg IV or lorazepam 1-2 mg IV, then
phenytoin 10-15 mg/kg IV load with 3-5 mg/kg/day maintenance
CARDIAC ANESTHESIA
PREOPERATIVE
❏ preoperative patient education of the perioperative course is important to reduce anxiety
and establish patient's expectations
❏ preadmission clinic and same day admission reduce hospital length of stay and reduce delay
from last minute abnormal blood tests or suboptimal clinical condition of patients
INTRAOPERATIVE ANESTHESIA
❏ premedication: lorazepam 1-3 mg sublingually, 1 h preoperation
❏ prophylactic antifibrinolytic treatment with tranexamic acid 50-100 mg/kg IV intraoperatively
(reduces perioperative blood loss)
❏ induction: propofol (0.5 mg/kg) or thiopental (1 mg/kg), low dose narcotic (fentanyl total 10-15 ug/kg),
pancuronium (0.15 mg/kg), midazolam (1-3mg)
❏ precardiopulmonary bypass: isoflurane (0.5-2%), midazolam (total 0.07-0.1 mg/kg)
❏ a baseline activated clotting time (ACT) is drawn after operation has commenced, and then
heparin 3-4 mg/kg (300 units/kg) is administered prior to cannulation of cardiopulmonary bypass
to maintain ACT over 480 seconds
(minimizes activation of coagulation system and formation of fibrin monomers)
❏ to reduce risk of myocardial necrosis and ventricular arrhythmias during prebypass period,
control myocardial oxygen demand by keeping heart rate less than 90 and systolic pressure
less than 130 mmHg (pulse-pressure product < 12,000)
❏ maintain stable hemodynamics and aggressively control arrhythmias
• use fluids and alpha-agents to counteract vasodilation, beta-blockers or additional
anesthetic agents for hypertension or tachycardia, and nitroglycerin for ischemia
❏ during cardiopulmonary bypass: propofol infusion 2-6 mg/kg/h
❏ postcardiopulmonary bypass: postoperative analgesia is essential (indomethacin or diclofenac 50-100 mg PR
unless contraindicated) and sedation (propofol) are titrated to allow for early tracheal extubation
(within 1-6 hours)

PRINCIPLES OF CARDIOPULMONARY BYPASS
INTRAOPERATIVE MONITORING
❏ standard monitors include:
• five-lead ECG monitoring with ST segment analyses (leads II, V5)
• noninvasive blood pressure measurement
• direct arterial pressure
• pulse oximetry
• end tidal gas analysis (capnography)
• temperature (nasopharyngeal in all patients, also rectal in infants)
• urine Foley catheter
• central venous pressure (CVP) (assess filling of right ventricle)
❏ commonly used monitors
• Swan-Ganz catheter
• monitors central venous pressure (CVP), pulmonary artery pressure,pulmonary capillary wedge
pressure (PCWP), CO (as needed), and mixed venous gas measurements (as needed)
• indications for use: LV dysfunction (EF<40%), poor distal vessels (high risk of poor
revascularization), preoperative hemodynamic instability, anticipated long cardiopulmonary
bypass time, significant coexistent medical disease (pulmonary, cerebral, renal)
• transesophageal echocradiography (TEE)
• indications: significant atheromatous disease of aorta, mitral valve repair, aortic valve
repair/replacement, adult/pediatric congenital heart disease, ventricular myomectomy,
ventricular remodeling procedures, endocarditis, cardiac tumour resection, heart transplant,
perioperative cardiovascular instability or difficult cardiopulmonary bypass separation
• contraindications: esophageal pathology (stricture, cancer, diverticulae), c-spine instability,
lack of informed consent
❏ monitors added at conclusion of operation:
• pacing wires (by convention atrial on right side and ventricular on left)
• mediastinal and pleural chest tubes
POSTOPERATIVE
❏ accelerated weaning and tracheal extubation of patients allows for earlier chest tube removal, mobilization,
and oral intake of food on POD #1, facilitating ICU and early hospital discharge
❏ mediastinal tubes are discontinued when drainage is less than 200 cc/8 h and
no air leak is present (usually POD #1-2)
❏ if no arrhythmias, pacing wires are removed at 4 days or the day prior to discharge
PRINCIPLES OF CARDIOPULMONARY BYPASS

❏ cardiopulmonary bypass (CPB) and cardioplegia provides a still bloodless heart by
diverting blood into a heart-lung machine (extracorpeal circuit) that performs the functions
of respiration, circulation and temperature regulation while the heart and lungs are not functioning
❏ CPB is required when manipulation of the heart significantly compromises
systemic blood pressure and when intracardiac surgery is performed
❏ the cardiopulmonary circuit (see Figure 1)
• venous blood drains by gravity from the right atrium (RA) or vena cavae into a reservoir,
passes through an oxygenator/heat exchanger attached to a heating/cooling machine,
and is returned to the arterial system through a filter using either a roller or centrifugal pump
• the membrane oxygenator is ventilated with 100% O2, run through a blender to control the
pO2 between 100-200 mmHg and pCO2 between 35-40 mmHg
• a priming solution (mostly crystalloid) is circulated through the lines to remove air
• the arterial cannula is usually placed in the ascending aorta or arch
• occasionally, the arterial cannula is placed in the femoral or axillary artery
(e.g. aortic dissection surgery)
• additional suction lines can be used for intracardiac venting and scavenging of blood from
the operative field, and this blood passes through a microporous filter
(to remove particulate matter) before returning to the cardiotomy reservoir

PRINCIPLES OF CARDIOPULMONARY BYPASS . . . CONT.
Blood drains by gravity through the

(A) venous lines into a
(B) cardiotomy reservoir, is
(C) pumped through the
(D) oxygenator/heat exchanger and
arterial line filter back into the
A (F) arterial circuit. Additional suction
lines
G (G) can be used for intracardiac venting
F B and scavenging of blood from the
operative field.
water out
C
water in
Figure 1. The Cardiopulmonary Circuit

Illustration by Ken Vanderstoep
❏ initiating bypass
• 3-4 mg/kg heparin is administered systemically, and the activated clotting time (ACT)
is monitored (a value over 400 is required before bypass is started)
• blood pressure is usually maintained between 55-65 mmHg using vasodilators or vasopressors
(cerebral blood flow is usually maintained by autoregulation until the pressure falls below 40 mmHg)
• the lungs are not ventilated during bypass
• pump flows are usually around 2.24 L/min/m2 and is non-pulsatile
(pulsatile flow used if significant renal disease)
• the patient may be warmed or cooled depending on the procedure and the surgeon's preference
❏ terminating bypass
• the patient is warmed to normothermia
• air is removed from the LV and aorta with a needle or venting cannula
• the lungs are ventilated and cardiac pacing is initiated as necessary
• the heart is filled by restricting venous return as bypass flow is reduced and turned off
• alpha agents (e.g. dopamine 1-5 ug/kg/min) and calcium chloride (1 g) are often used to improve
contractility and systemic blood pressure and facilitate weaning from CPB
• inotropic support is considered for poor cardiac performance
• when the patient is stable, protamine is administered to reverse the heparin effect
(1.0 to 1.5 times the original heparin dose), and the cannulas are removed
• blood remaining in the oxygenator and lines at the end of bypass (as well as shed mediastinal blood)
can be transfused back to the patient at the conclusion of the operation
• see Table 3 - Postoperative Orders
❏ adverse effects of CPB
• CPB activates numerous cascades (coagulation, complement, fibrinolytic, and kallikrein systems)
• proinflammatory cytokines are released that can cause a systemic inflammatory response and
contribute to myocardial reperfusion damage, lung injury, and generalized capillary leak
• CPB can also cause a coagulopathy (dilution of clotting factors and platelets, platelet dysfunction)
and renal and splanchnic hypoperfusion
❏ circulatory arrest
• necessary for some operations on the ascending aorta and all aortic arch operations to allow the
surgeon to operate without the constraints of vascular clamps and a blood obscured field
• the patient is cooled systemically to 18-20ºC at which the EEG is flat, and the head is packed with ice
• the arterial line is clamped, the CPB machine is turned off, and blood is drained from the circulation
(the venous line is intermittently clamped to prevent excessive drainage from the patient)
• after completing the distal anastomosis of the prosthetic graft to the distal ascending/
transverse aorta, the arterial inflow cannula is positioned through the graft, the open
end of the prosthetic graft is clamped, and full bypass is resumed before the proximal
anastomosis is performed
• the "safe" upper limit for circulatory arrest is 45-60 minutes at 18ºC
• administering blood retrograde into the brain through a cannula in the superior vena cava (SVC)
may extend this safe upper limit by providing additional cooling and possibly some oxygen and
nutrition to the brain
• retrograde perfusion also maintains cerebral hypothermia and flushes air and debris out
of the cerebral vessels
PRINCIPLES OF CARDIOPULMONARY BYPASS . . . CONT.
Table 3. Intensive Care Unit (ICU) Post-operative Orders for Cardiac Surgery
1. Vital signs q15min, then q1h when stable
2. Urine output q1h until extubation, then q2h
3. Chest tubes at -20 cm H2O suction. Record chest tube loss q15min x 1h, then q1h if hemodynamically stable
4. Auto-transfuse chest drainage
5. Cardiac output calculations now and q6h
6. Check peripheral pulses q1h x 4 then q4h
7. Central line IV D5W TKVO
8. K+ replacement - to be decided depending on urine output and last K+ value
9. Peripheral IV NS TKVO
10. 12 lead ECG now then daily x 3 days
11. Ventilation e.g. VT 700 mL, FiO2 50%, Rate 12/min, Peep 5 cm/H2O to keep PaCO2 between 35-45 mmHg
12. Titrate FiO2 to keep PO2 > 90 mmHg or O2 sat > 95%
13. Suction ETT prn and chest care as per assessment
14. Physiotherapy: assessment and treatment
15. Pacemaker connected and checked by MD
16. Morphine sulphate 1-6 mg IV q1h PRN
17. Indomethacin supp 50-100 mg pr q1h x 2 PRN (avoid if diabetic, renal failure, peptic ulcer disease, or age > 75)
18. Gravol 25-50 mg IV/IM q4h PRN x 2 days
19. Cefazolin 1 g IV q8h in 50 cc D5W x 3 doses (Vancomycin 300 mg to 1 g IV q12h if pen-allergic)
20. Propofol 200 mg IV in 100 cc D5W PRN
21. Sodium nitroprusside 50 mg IV in 250 cc D5W to keep SBP < 140 mmHg
22. Nitroglycerin 100 mg IV in 250 cc D5W PRN
23. Dopamine 200 mg IV in 250 cc D5W PRN to keep SBP > 90 mmHg
MYOCARDIAL PROTECTION AND CARDIOPLEGIA

❏ nearly all intracardiac procedures and most coronary bypass operations
require a quiet, bloodless field that allows for precise surgical techniques
❏ cardioplegia is used to arrest the heart (reducing the oxygen demand of the heart nearly 90%),
and hypothermia is used to further reduce myocardial metabolism
❏ without this reduction in myocardial metabolism by hypothermia or chemical cardiac arrest,
crossclamping the aorta for more than 20 minutes would result in myocardial anaerobic metabolism and
severe myocardial dysfunction and necrosis
❏ blood cardioplegia is used (rather than crystalloid solutions) because it improves postoperative ventricular
function by increasing oxygen delivery and preserving myocardial high-energy phosphate stores
❏ a wide variety of cardioplegia solutions exist
• one example is a blood-crystalloid solution mixed at a ratio of 8:1, with a crystalloid composition
of 6 meq/L magnesium sulfate, 50 mmol/L dextrose and potassium (30 meq/L KCl for cardiac arrest,
8 meq/L for maintenance) in sterile water
❏ cardioplegia can be administered at various temperatures
• cold cardioplegia (4ºC)
• advantages: decreases myocardial metabolism, allows for prolonged cardioplegic interruptions
to facilitate exposure for complex surgical procedures
• disadvantages: delays recovery of cardiomyocyte metabolism and function
• warm cardioplegia (37ºC)
• advantages: rapid recovery of myocardial metabolism, metabolic enhancement for patients
with active ischemia
• disadvantages: requires near continuous delivery because of the tendency for the heart to
resume electrical activity at normothermia, continuos delivery may obscure operative field,
questionable increased risk of neurologic injury
• tepid cardioplegia (29ºC)
• may optimize myocardial protection

MYOCARDIAL PROTECTION AND CARDIOPLEGIA . . . CONT.
❏ cardioplegia can be administered antegrade via the aortic root or coronary ostia, retrograde via the
coronary sinus, or combined (antegrade via completed saphenous vein grafts plus retrograde)
• antegrade
• advantages: simple to use
• disadvantages: suboptimal perfusion distal to coronary occlusions, risk of coronary
embolization in redo CABG, frequent interruptions (administered intermittently to
maintain cardiac arrest), aortic root cardioplegia contraindicated in severe aortic insufficiency
(but can administer via coronary ostia)
• retrograde
• advantages: allows for near continuous delivery
• disadvantages: decreased perfusion of right ventricle and posterior interventricular septum,
large amount of nonnutritive flow through Thebesian channels, damage to coronary
sinus at pressures > 40 mm Hg
• combined
• advantages: maximizes myocardial perfusion
• disadvantages: relatively complex delivery system
❏ with near continuous cardioplegic delivery, the large volumes of cardioplegia administered may result in
hyperkalemia (consider treating with furosemide 40 mg IV and/or insulin 10 units IV)
CORONARY ARTERY BYPASS GRAFT (CABG) SURGERY

❏ the objective of CABG is complete revascularization of the myocardium
❏ arteries with severe stenoses (> 50% diameter reduction) are bypassed, except those of small caliber
(< 1mm in diameter)
❏ indications
• class 3 or 4 chronic stable angina, either to improve prognosis and/or relieve symptoms
• unstable angina refractory to medical management
• acute ischemia or hemodynamic instability post-PTCA (rate of emergency surgery post-PTCA is 3-4%,
with 5-6% operative mortality)
• post-MI angina
• acute evolving infarction within 4-6 hours of onset
• ventricular arrhythmias with coronary disease
• markedly positive stress test before major intra-abdominal or vascular surgery
• ischemic pulmonary edema
• usually left main or triple vessel disease, impaired LV function
(70% 2 year mortality managed medically)
• to improve survival in patients (even if asymptomatic)
• left main stenosis > 50% (annual mortality 10-15%)
• left main equivalent: > 70% stenosis of proximal left anterior descending (LAD)
and proximal circumflex artery (PCA)
• three vessel disease with ejection fraction (EF)< 50%
• three vessel disease with EF> 50% but significant inducible ischemia
• one and two vessel disease with extensive myocardium at risk but lesions
not amendable to PTCA
• other
• significant coronary lesions accompanying other cardiac lesions requiring surgical correction
• congenital coronary anomalies
❏ approach to reading coronary angiograms
• see selected angiograms in Colour Atlas (see Colour Atlas CS1-CS3)
• angiographic atherosclerotic stenoses are expressed as a percent reduction of the lumen
diameter compared to an area of adjacent normal vessel
• the catheter usually is a size 6 French catheter (1.8 mm in diameter) - comparing the size of vessels
to the size of the catheter can help distinguish graftable from non-graftable (< 1 mm) vessels
• right coronary artery divides to posterior interventricular (PIV) artery (also known as posterior
descending artery) and posterolateral branches (PIV can be identified by the presence of septal
perforating branches)
• left main coronary artery divides to the LAD and circumflex (LAD can be identified by the
presence of septal perforating branches and its approach towards the apex)
• left ventriculogram assesses the global and regional contractile performance of the heart,
and presence and degree of MR
❏ surgical approach (see Figure 2)
• right coronary artery - common site of distal anastomosis is just before the bifurcation at the crux, or
directly to the posterior descending artery if the bifurcartion is diseased
• left main coronary artery - not directly grafted because it is inaccessible without dividing the aorta and
pulmonary artery (therefore graft LAD and obtuse marginals of circumflex for left main stenosis)
• left anterior descending (LAD) - distal anastomosis is usually placed from midpoint on; diagonal
branches > 1-1.5 mm in diameter are also bypassed especially if they are diseased
• circumflex coronary artery - difficult to approach since located below great cardiac vein, therefore
bypass circumflex artery system by grafting to obtuse marginal branches
CORONARY ARTERY BYPASS GRAFT SURGERY . . . CONT.
LIMA to LAD
SVG to circumflex
marginal artery
SVG to right
The internal mammary artery has been placed to the LAD.
corornary artery Aortocoronary saphenous vein grafts have been sewn to the
RCA and circumflex obtuse marginal artery.
Figure 2. Coronary Artery Bypass Grafting

Illustration by Mi Ji Kim
❏ conduits for coronary bypass surgery

• saphenous vein grafts
• at 10 years, 50% occluded, 25% stenotic, 25% angiographically normal
• internal thoracic (mammary) artery - anastamosed to LAD
• at 10 years, 90-95% patency
• increased 10-year patient survival
• improved event-free survival (angina, MI)
• no increase in operative risk
• contraindications: inadequate mammary blood flow, occluded abdominal aorta,
chest wall irradiation, avoid bilateral internal thoracic arteries in diabetics or obese patrients
• right gastroepiploic artery
• good long term patency
• usually long enough to bypass any of the 3 vessels
• concerns: can not use as free graft, laparatomy incision (increased morbidity),
arterial graft (therefore vasoreactive postoperatively)
• radial artery
• time consuming to harvest
• approximately 90% patency at 5 years
• prone to severe vasospasm postoperatively ("no touch" technique during harvest
of the radial artery pedicle) - avoid with CCB (Adalat XL 20 mg PO OD) for 6 months
❏ redo bypass grafting
• operative mortality 2-3 times higher than first operation
• 10% perioperative MI rate
• reoperation undertaken only in symtomatic patients who have failed medical therapy and in whom
angiography has documented progression of the disease
• increased risk with redo-sternotomy
• adhesions may result in laceration to aorta, RV, LITA and other bypass grafts
(consider preop CT chest)
• myocardial protection is very important
• cardioplegia should be given through the aortic root through the new bypass grafts as
constructed and retrograde via the coronary sinus to protect ischemic areas
• distal and proximal incision of old atherosclerotic grafts should be undertaken as early
as possible on CPB to prevent atherosclerotic emboli down these grafts
• consider using right or left IMA's, lesser or greater saphenous veins if available,
or right gastroepiploic artery
• only arteries that are > 1.5 mm in diameter should be grafted at the second operation

VALVE REPLACEMENT AND REPAIR
❏ see Cardiology Chapter for etiology, symptoms, imaging and medical management of valvular disease
AORTIC STENOSIS (AS)
• symptomatic patients with valve gradient of > 50 mm Hg or valve area < 0.8 cm2 (normal 3-4 cm2)
• asymptomatic patients with significant stenosis and LVH should also be considered
• moderate AS if other cardiac surgery is required (i.e. CABG)
❏ surgical options
• balloon valvuloplasty
• for critically ill patients with end-stage AS as a "bridge" to aortic valve replacement
• also considered in pregnancy or if significant comorbidity and high surgical risk
• 50% recurrence of AS in 6 months
• decalcification/debridement
• in patients with mild to moderate AS in whom the primaryindication for surgery
is coronary artery disease
• commissurotomy
• useful in a small percentage of patients with aortic rheumatic valve disease
with a trileaflet valve and minimal to no calcification
• valve replacement
• practically all patients with severe AS require aortic valve replacement (see Figure 3)
Aorta
(A) An aortotomy incision has

Left coronary been made, the valve is
artery removed with scissors, and
the annulus is debrided.
(B) Horizontal mattress
sutures (often with pledgets)
are placed through the annu-
right coronary lus and the sewing ring of the
artery valve. The valve is seated,
the sutures tied, and the aor-
totomy incision is closed.
Figure 3. Aortic Valve Replacement:

Illustration by Teresa McLaren
AORTIC REGURGITATION (AR)

•
acute AR with CHF
•
class III-IV symptoms
•
endocarditis with hemodynamic compromise or recurrent emboli
•
evidence of LV decompensation in the asymptomatic patient
• EF <55%
• end-diastolic dimension > 70 mm
• end-systolic dimension > 55 mm
• valve repair
• involves resection of portions of the valve leaflets and reapproximation to improve
leaflet coaptation (especially for bicuspid valves), often with a suture annuloplasty
• valuable in younger patients
• practically all patients with AR require aortic valve replacement
• Bentall procedure
• a valved conduit is used if an ascending aortic aneurysm (annuloaortic ectasia) is also present

VALVE REPLACEMENT AND REPAIR . . . CONT.
CHOICE OF AORTIC VALVE PROSTHESIS

❏ the aortic valve can be replaced with either a valve (mechanical or porcine bioprosthetic tissue valve)
or graft (autograft or homograft)
❏ mechanical valve
• durable valves but require continuous anticoagulation with coumadin (contraindicated if
previous bleeding history), requiring patient to take daily medication and have periodic blood tests
(to maintain INR 2-3)
• in carefully anticoagualated patients, the risk of hemorrhage is 1-2% per year,
and the risk of thromboembolic events is 1-3% per year
• preferred valve replacement if long life expectancy or if risk of reoperation is considered high
• preferred valve replacement if small aortic root (bioprosthetic aortic valve placement in a
small aortic orifice may result in obstruction and unacceptably high gradients)
❏ bioprosthetic valve
• low embolic rate in the absence of anticoagulation (1-2% risk of thromboembolic events)
• less durable than mechanical valves and require reoperation due to degeneration and structural failure
• however, structural degeneration of bioprosthetic valves is rare in elderly patients
• preferred valve replacement if life expectancy of patient is shorter than the known durability
of the bioprostheses
• also considered if potential for pregnancy (coumadin is teratogenic)
❏ pulmonary autograft
• Ross procedure: replace the diseased aortic valve with the patient's own pulmonary valve and
implant a semilunar valve homograft (e.g. pulmonary valve homograft) in the pulmonary position
• pulmonary autograft failure is rare in carefully selected patients, but 20% will require reoperation
at 10 years because of stenosis of the pulmonary homograft
• technically demanding operation
• ideal for children and young adults to avoid anticoagulation
• contraindicated in patients with dilated aortic root (Bentall procedure recommended instead)
❏ aortic homograft
• particularly suitable for children, women of child-bearing age, and patients with active endocarditis
(e.g. aortic root abscess)
• durability is limited with 20% 10 year reoperation rate (higher in younger patients)
• procurement a problem: valves from donors older than 40 years of age are often not good
MITRAL STENOSIS (MS)
• MV area < 1.5 cm2 (normal is 4-6 cm2)
• NYHA classes III-IV
• NYHA class II when MV area < 1 cm2 (critical mitral stenosis)
• history of atrial fibrillation and/or systemic emboli (from left atrial thrombus)
• worsening pulmonary hypertension
• percutaneous balloon mitral valvuloplasty
• for young rheumatic patients with pure MS and good leaflet pliability,
minimal chordal thickening and good subvalvular mechanism
• also considered in pregnant patients with critical MS in whom CPB should be avoided
• contraindicated if left atrial thrombus
• open mitral commisurotomy
• for patients with mild calcification and mild leaflet/chordal thickening +/– other
coexistent diseased valves (e.g. aortic and/or tricuspid)
• technique involves incision of both commissures, incision/resection of fused chordae,
and occasionally incision into papillary muscle to increase mobility
(if evidence of chordae shortening from scarring and fibrosis)
• 50% of patients will require reoperation 8 years following initial commisurotomy
due to restenosis
• for moderate to severe calcification with severely scarred valve leaflets or subvalvular apparatus

VALVE REPLACEMENT AND REPAIR . . . CONT.
MITRAL REGURGITATION (MR)

• acute MR associated with CHF or cardiogenic shock
• acute endocarditis with hemodynamic compromise or recurrent emboli
• NYHA class III-IV
• Class I-II symptoms with onset of atrial fibrillation or evidence of deteriorating LV function
• EF < 55%
• end-diastolic dimension > 75 mm
• end-systolic dimension > 45 mm
• valve repair
• applicable to more than 75% of patients with MR
• the ideal pathology for mitral valve repair is myxomatous degeneration of the MV
• several techniques include annuloplasty rings, leaflet repairs, patch repair
(for endocarditis), and chordal transfers, shortening or replacement
• prolapse of the posterior leaflet is usually corrected by rectangular resection
of the prolapsing segment and plication of the annulus
• prolaspe of the anterior leaflet is corrected by transposition of chordae
from the posterior leaflet (neo-cordae)
• chordal enlongation is corrected by invaginating the excess length of chordae
into a trench in the papillary muscle
• a ring annuloplasty or Gortex is often used in MV repair to reshape the annulus
to its normal elliptical configuration and to maintain stability
• indicated only when satisfactory repair cannot be accomplished
• most patients with MR due to ischemic heart disease, rheumatic heart disease
or advanced myxomatous disease need MV replacement
• replacement usually required if heavily calcified annulus or if papillary muscle rupture
• chordal preservation of the posterior leaflet should be strongly considered for all
MV replacements (to improve ventricular function and minimize risk of posterior LV wall rupture)
❏ the advantages of repair vs. replacement are the low rate of endocarditis
and lack of need for long-term anticoagulation
CHOICE OF MITRAL VALVE PROSTHESIS
❏ the current choice for mitral valve replacements include mechanical prostheses
(e.g. ball valve, tilting disc, bileaflet, etc.) and bioprosthetic valves
❏ the main factors affecting choice of prosthesis are anticoagulation, and the
attitude of the patient and surgeon regarding reoperation
❏ bioprosthetic valves
• require anticoagulation only for first 3 months
• lower durability and require reoperation due to degeneration and structural failure
(20-40% fail by 10 years)
• however, structural degeneration of bioprosthetic valves is rare in elderly patients
• bioprosthetic valves in the mitral position are not as durable as in the aortic position
• preferred valve replacement if life expectancy of patient is shorter than the
known durability of the bioprostheses
• also considered if potential for pregnancy (coumadin is teratogenic)
❏ mechanical valves
• require continuous anticoagulation (contraindicated if previous bleeding history)
• in the setting of chronic A fib, patient is already anticoagulated, and therefore mechanical valve used
• preferred valve replacement if long life expectancy or if risk of reoperation is considered high

AORTA REPLACEMENT AND REPAIR
THORACIC AORTIC DISSECTION
❏ see Abdominal Aortic Dissection for more details
❏ DeBakey classification
• Type I - intimal disruption of ascending aorta, which dissects to involve the descending aorta
and abdominal aorta
• Type II - involving the ascending aorta only (stops at the innominate artery)
• Type III - descending aorta only (distal to left subclavian artery)
❏ Stanford classification
• Type A - any dissection that involves ascending aorta
• Type B - dissection involves only the descending aorta
❏ multiple causes - atherosclerosis, cystic medial necrosis (i.e. Marfan's syndrome), infectious, trauma,
coarctation, bicuspid aortic valve, pregnancy
❏ diagnosis is usually made by chest CT or echocardiography
❏ preoperative control of hypertension with beta blockers (+/– nitroprusside if necessary)
is an essential part of management
❏ dissection may advance proximally to disrupt coronary blood flow or induce aortic valve incompetence,
or distally causing stroke, renal failure, intestinal ischemia or leg ischemia
❏ surgical repair
• operative repair involves replacement of the affected aorta with prosthetic graft
• CPB is required for repair of Type A dissections, and hypothermic circulatory arrest is often used
for transverse arch dissections and ascending aorta repairs
• aortic valve replacement and coronary reimplantation may be required for Type A aneurysms
that involve the aortic root
• Type B dissections can be medically managed unless expansion, rupture, or compromise of
branch arteries develops or HTN becomes refractory
❏ post-operative complications include renal failure, intestinal ischemia, stroke, paraplegia, and death
THORACIC AORTIC ANEURYSM
❏ etiology: medial degeneration, atherosclerosis, expansion of chronic dissections
• ascending aortic aneurysms
• symptomatic, expanding, > 5.5 cm in diameter, or greater than twice the size of the normal aorta
• aneurysms > 4.5 cm if operation is indicated for aortic regurgitation (annuloaortic ectasia)
• all acute type A dissections
• mycotic aneurysms
• transverse arch aneurysms
• ascending aortic aneurysms that require replacement that also extend into the arch
• acute arch dissections
• aneurysms > 6 cm in diameter
• descending thoracic aorta aneurysms
• symptomatic aneurysms
• aneurysms > 6 cm
• complicated type B dissections
❏ catheterization is indicated for patients > 40 years of age or if history of chest pain
(to diagnose coexistent coronary artery disease)
• ascending aortic aneurysms
• supracoronary interposition graft placement is performed if the aneurysm does not involve
the sinuses
• Bentall procedure (valved conduit) for patient's with Marfan's syndrome,
if the sinuses are involved or for annuloaortic ectasia
• transverse arch aneurysms
• Hemiarch repair if ascending aorta and proximal arch are involved (graft sewn to the
undersurface of the aorta to leave the brachiocephalic vessels attached to the native aorta)
• extended arch repair involves placement of an interposition graft and reimplantation
of a brachiocephalic island during a period of circulatory arrest (use retrograde
SVC perfusion and selective brachiocephalic perfusion to minimize cerebral complications)
• descending thoracic aorta aneurysms
• interposition graft placement
• to ensure spinal cord and kidney perfusion, consider using femoral-femoral bypass
(femoral artery and vein cannulation, with arterial blood pumped retrograde into
femoral artery for cephalad aortic blood flow)
TRAUMATIC AORTIC DISRUPTION
❏ this injury results from deceleration injury, and usually occurs just distal to the left subclavian artery
at the level of the ligamentum arteriosum
❏ chest radiograph findings include widened mediastinum, pleural capping, associated first and
second rib fractures, loss of the aortic knob, hemothorax, deviation of the trachea or NG tube,
and associated thoracic injuries (scapular fracture, clavicular fracture)
❏ definitive diagnosis is made by aortagram, but chest CT and TEE also aid in the diagnosis
❏ imperative that immediate life-threating injuries (i.e. positive diagnostic peritoneal lavage)
be treated prior to repair
❏ well-accepted therapeutic modality for the patient with end-stage heart disease
❏ majority of patients have ischemic (60%) or idiopathic (20%) cardiomyopathy,
with the minority having valvular or congenital problems
❏ world-wide overall 1 year survival is 79%, with an annual mortality rate of 4%,
and a 5 year survival approximately 60%
• end-stage heart disease (e.g. EF< 20%, nonbypassable CAD)
refractory to other surgical or medical management
• NYHA III-IV symptoms with maximal medical therapy and prognosis for 1 year survival < 75%
• no other major organ or systemic disease
• emotionally stable with social support
• medically compliant and motivated
❏ contraindications
• incurable malignancy
• major systemic illness
• irreversible major organ disease (e.g. renal, hepatic)
• active systemic infection (e.g. Hep C, HIV)
• emotional instability or acute psychiatric illness
• age > 70 years
• obesity
• irreversible pulmonary hypertension (PVR > 6 Wood units)
• severe COPD (FEV1 < 1 L)
• active drug addiction or alcoholism
❏ precardiac transplant assessment
• consultations: cardiology, cardiovascular surgery, respirology, transplant immunology, psychiatry,
psychology, dental surgery, social work, chaplaincy, transplant coordinator
• labs: group and screen, CBC, ESR, INR, PTT, lytes, BUN, creatinine, uric acid, glucose, cholesterol,
triglycerides, LFTs, protein electrophoresis, thyroid tests, stool analysis, urinalysis (24 hour)
• investigations: right and left heart catheterization, 2D Echo, ECG, PFTs, ABG, CXR, Abdo U/S,
antibody screen (HBV, HCV, HIV), HLA typing, anti-HLA antibodies, digoxin levels, antibody titres
(CMV, herpes simplex, EBV, toxoplasmosis)
❏ patients are optimized medically with diuretics, vasodilators (ACE inhibitors, hydralazine, B-blockers),
IABP, inotropes (digoxin), +/– LV assist device
❏ donor hearts are considered from patients up to age 50-55
❏ contraindications to heart donation
• major chest trauma
• known cardiac disease
• acute or chronic infection
• prolonged cardiac arrest
• HIV or Hep B/C positive
• systemic malignancy
❏ matching is according to blood type (ABO match is mandatory to avoid hyperacute rejection),
body size and weight (should be within 25%) and HLA tissue matching (if time allows)
❏ donor harvest
• the heart is inspected for evidence of coronary disease
• the SVC and IVC are clamped, the aorta is crossclamped, and
cold crystalloid cardioplegia is administered
• the heart is excised: as much SVC and IVC are preserved as possible, the pulmonary veins are divided,
the aorta is divided proximal to the crossclamp, and the distal main PA is divided
• the heart is bagged in cold saline and transported at 4-6ºC
❏ recipient operation
• the recipient is placed on CPB
• the diseased heart is excised leaving: a long cuff of SVC, a segment of low right atrium near the IVC,
the posterior wall of the left atrium, and the great vessels are incised just above the semilunar valves
• the donor heart is prepared by removing excess tissue
• the first suture line is started at the left atrial appendage of the donor heart and the free wall of the
left atrium is sewn and then the atrial septum
• the SVC and IVC are connected, followed by the pulmonary artery and then the aorta
❏ immediate postoperative management
• keep heart rate 75-90 (may need pacing)
• keep CVP low with diuretics to improve RV function
• treat high PA pressures with NO, nitroglycerin, milrinone, etc.
• support the RV with inotropes and afterload reducers for high PA pressures
• support LV if necessary (IABP, inotropes)
• treat coagulopathy aggressively
• monitor for, prevent and treat other organ system failure (renal, respiratory, hepatic, and neurological)
❏ immunosuppression
• the goal of immunosuppression is selective modulation of the recipient's immune response to
prevent rejection while maintaining defenses against infection and neoplasia, and minimizing toxicity
• immunosuppression protocols include rabbit anti-thymocyte serum (RATS), OKT3, azathioprine,
solu-medrol, cyclosporine, FK506 (tacrolimus) and mycophenolate mofetil (Cellcept)
CARDIAC TRANSPLANTATION . . . CONT.
❏ complications
• rejection
• the majority of transplant patients experience some form of
rejection, though less than 5% have hemodynamic compromise
• no noninvasive tests to detect rejection, and the gold standard
remains endomyocardial biopsies
• risk of acute rejection is greatest during the first 3 months after transplant
• infection
• bacterial and viral infections predominate, although fungal (Candida) and
protozoan (PCP, toxoplasmosis) are noted in 10% of patients
• fevers, rising WBC counts and abnormal CXR's must be aggressively evaluated
• allograft coronary artery disease
• approximately 50% develop graft CAD within 5 years of transplantation
• graft vasculopathy is the most common cause of late death following transplantation
• may reduce rate of graft CAD with diltiazem and statins
• malignancy
• develop in 15% of cardiac transplant recipients
• second most common cause of late death following transplantation
• cutaneous neoplams most common, followed by non-Hodgkin's lymphoma and lung cancer
• immunosuppressive medication side effects
• include hypertension (cyclosporine), hyperlipidemia (cyclosporine, steroids),
nephrotoxicity (cyclosporine), GI problems (steroids), osteopenic bone disease (steroids)
CONGENITAL HEART SURGERY

❏ the appropriate management of congenital heart disease is based on the precise identification
and pathophysiology of the patient's abnormality
❏ the appropriate diagnosis is achieved by
•
clinical assessement (cyanotic or acyanotic, presence of CHF)
•
CXR (increased/normal/decreased pulmonary blood flow)
•
ECG (normal or left axis deviation, RVH, LVH)
•
echocardiography (anatomy, shunts, valvular lesions, defects)
cardiac catheterization (O2 sats, shunt calculations, chamber pressures, septal defects,
•
orientation of great vessels)
❏ numerous congenital anomalies have been described (see Table 4)
Table 4. Common Congenital Heart Defects

I. Pure obstructive lesions
1. Pulmonic stenosis
2. Mitral stenosis
3. Aortic stenosis
4. Coarctation of the aorta
5. Interrupted aortic arch
II. Simple left-to-right shunts (acyanotic lesions with increased pulmonary blood flow)
1. Patent ductus arteriosus
2. Atrial septal defect
3. Ventricular septal defect
4. Endocardial cushion defect (AV canal)
5. Aortopulmonary window
III. Right-to-left shunts (cyanotic defects with decreased pulmonary blood flow)
1. Tetralogy of Fallot
2. Pulmonary atresia with ventricular septal defect
3. Pulmonary atresia with intact ventricular septum
4. Tricuspid atresia
5. Ebstein's anomaly
IV. Complex cyanotic defects (mixing defects)
1. Double outlet right ventricle
2. Univentricular heart (double inlet left ventricle)
3. Transposition of the great arteries
4. Total anomalous pulmonary venous connection
5. Truncus arteriosus
6. Hypoplastic left heart syndrome
V. Coronary artery congenital defects
1. Anomalous origin of coronary artery
2. Coronary artery fistula
3. Osteal stenosis
Adapted from Bojar RM. Manual of perioperative care in cardiac surgery, 3rd edition. Massachusetts: Blackwell Science Inc., 1999.

CONGENITAL HEART SURGERY . . . CONT.
PALLIATIVE PROCEDURES
❏ a Blalock-Taussig (BT) shunt involves an end-to-side anastomosis of the subclavian artery to the
ipsilateral PA and is used to increase pulmonary blood flow
❏ a modified Blalock-Taussig shunt (MBTS) uses a polytetrafluoroethylene (PTFE) tube graft as the shunt
between the subclavian artery and the ipsilateral PA
❏ a "central shunt" uses a short piece of PTFE graft to connect the ascending
aorta to the main PA (used to increase pulmonary blood flow)
❏ the bidirectional Glenn shunt entails an anastomosis between the SVC and the right PA,
thus providing blood flow to both pulmonary arteries (therefore "bidirectional")
❏ the Fontan operation is designed to deliver systemic venous blood to the
PA without the use of the (single) functioning ventricle
• the “hemi-Fontan” procedure involves the placement of a prosthetic patch inferior to the
SVC-RA junction and an anastomosis between the SVC-RA junction to the right PA
(the main PA is transected and oversewn), so that SVC blood flows directly to the
lungs (IVC blood continues to the single ventricle)
• the "modified" Fontan procedure consists of an anastomosis between the RA
and the PA (or the IVC and right PA after a Glenn Shunt), either directly or with a
nonvalved conduit (the main PA is transected and oversewn)
• the "lateral tunnel" Fontan procedure consists of a baffle tunnel between the IVC and SVC,
division of the SVC proximal to the cavoatrial junction, anastomosis of the proximal SVC
to the superior aspect of the right PA, and anastomosis of the distal SVC to the inferior surface of
the right PA (the main PA is transected and oversewn)
PURE OBSTRUCTIVE LESIONS

❏ pulmonic stenosis
• the critically ill infant with severe PS is usually cyanotic, with pulmonary blood flow provided
by the PDA
• indications for surgery: to increase pulmonary blood flow in critically ill infants;
severe PS and presence of symptoms in older infants or children
• surgical procedures: balloon valvotomy, surgical valvotomy, patch enlargement of right
ventricular outflow tract
❏ aortic stenosis
• may occur at 3 levels: subaortic (fibrous membrane or tunnel stenosis), valvar
(unicuspid or fusion bicuspid valve), or supravalvar (fibrous ridge or hypoplasia of ascending aorta)
• indications for surgery: infants with critical aortic stenosis (severe low output states, cyanosis by
right-to-left ductal shunting), older children with symptoms or peak gradient > 50 mmHg
• surgical procedures
• subaortic stenosis relieved by resection of fibrous membrane
or myectomy of hypertrophied ventricular septum
• valvular aortic stenosis relieved by percuateneous balloon valvotomy or valve replacement
• supravalvular aortic stenosis relieved by patch augmentation of ascending aorta
❏ coarctation of the aorta
• right-to-left shunting through the patent ductus arteriosus (PDA) provides perfusion to the
lower half of the body and may produce cyanosis
• indications for surgery: infants with severe coarctation and LV failure or ductal dependency,
older children with resting or exercise-induced hypertension or gradient > 30 mmHg
• surgical procedures: resection of coarct segment with end-to-end anastomosis, subclavian flap
procedure (augment narrowed segment with divided left subclavian artery), interposition tube
graft in adolescents and adults
❏ interrupted aortic arch
• systemic flow to distal aorta is dependent on ductal patency
(PGE1 may be required to maintain ductal patency)
• almost always an associated large subaortic ventricular septal defect (VSD)
• indications for surgery: within the first week of life
• surgical procedures: descending aorta is anastamosed to the ascending aorta and VSD is closed

SIMPLE LEFT-TO-RIGHT SHUNTS

❏ patent ductus arteriosus (PDA)
• can increase pulmonary blood flow and produce pulmonary vascular congestion
and LV volume overload
• patency may be critical to survival in neonates with complex heart disease by
providing pulmonary or systemic blood flow
• indications for surgery: PDA contributing to respiratory compromise or
persisting beyond 3rd month of life
• surgical procedures: transcatheter closure using intravascular coils, simple ligation, surgical division
❏ atrial septal defect (ASD)
• results in increased pulmonary blood flow and leads to pulmonary vascular congestion
and recurrent respiratory infections
• indications for surgery: should be closed by age 5 to avoid
pulmonary hypertension; in adults with evidence of left-to-right shunt
• surgical procedures: transcatheter closure, direct suture, use of pericardial or Dacron patch
❏ ventricular septal defect (VSD)
• occur most frequently in the membranous septum (80%)
• the child will present with pulmonary vascular congestion and
recurrent respiratory infections due to excessive pulmonary blood flow
• indications for surgery: repair should be performed by age 1 in all patients
with a significant shunt or LV volume overload
• surgical procedures: pulmonary artery banding (to reduce pulmonary blood flow if other associated
complex lesions), direct suture, patch closure, transcatheter closure (for muscular defects only)
❏ endocardial cushion defects (AV canal)
• defects resulting from deficiency of atrioventricular septum (common in Trisomy 21)
• indications for surgery: should be repaired by age 6 months to prevent development
of pulmonary hypertension
• surgical procedures: division of common AV valve + closure of ASD and VSD + creation
of separate mitral and tricuspid valves
❏ aortopulmonary window
• nonrestrictive communication between posterior aspect of ascending aorta and
main PA or right PA, causing CHF
• indications for surgery: soon after diagnosis is made
• surgical procedures: patch closure
RIGHT-TO-LEFT SHUNTS
❏ Tetralogy of Fallot
• hypoplasia of the right ventricular infundibulum producing a large nonrestrictive anterior VSD,
and overriding aorta, RV outflow tract obstruction and RVH
• hypoxic "tet" spell: intense cyanosis caused by increased right-to-left shunting
(infundibular spasm, increase in pulmonary vascular resistance or decrease in systemic
vascular resistance) that can lead to syncope, seizures and death
• indications for surgery: marked cyanosis, "tet" spells, severe RV outflow tract obstruction,
usually in first 2 years of life even if no symptoms
• surgical procedures: pulmonary valvotomy or pericardial patch enlargement of RV outflow tract
or RV-PA valved homograft conduit, + closure of VSD with Dacron patch
❏ pulmonary atresia with VSD
• extreme form of tetralogy of Fallot with no RV-PA connection (severe cyanosis)
• pulmonary blood flow dependent on PDA and from major aortopulmonary collateral arteries
• indications for surgery: severe cyanosis
• surgical procedures: systemic-to-pulmonary artery shunt as palliative procedure; definitive correction
(when distal pulmonary arteries are adequate size) by VSD closure with Dacron patch + RV-PA
homograft valved conduit
❏ pulmonary atresia with intact ventricular septum
• complete obstruction to RV outflow, producing severe cyanosis and survival dependent on
pulmonary blood flow through the PDA
• indications for surgery: indicated in infancy for profound cyanosis
• surgical procedures:
• if RV adequate size then MBTS or central shunt + RV outflow tract patch or pulmonary valvotomy
• if hypoplastic RV, then MBTS or central shunt and then Fontan procedure after 2 years of age
❏ tricuspid atresia
• characterized by complete absence of the tricuspid valve and varying degrees of RV hypoplasia
• the relative amounts of systemic and pulmonary blood flow and the patient's clinical presentation
depend on the orientation of the great vessels, the size of the VSD and the degree of
pulmonary stenosis
• indications for surgery: severe cyanosis in infancy, or progressive cyanosis or polycythemia before age 2
• surgical procedures: balloon atrial septostomy if restrictive ASD, PA banding to prevent
pulmonary vascular disease if large VSD, MBTS if severe cyanosis, bidirectional Glenn shunt
to improve pulmonary blood flow, Fontan operation definitive operation performed between ages 2-5

❏ Ebstein's anomaly
• congenital defect of the tricuspid valve in which the septal and
posterior leaflets are malformed and displaced into the RV
• the RA is massively enlarged, and an interatrial communication and
tricuspid regurgitation usually exist
• indications for surgery: severe cyanosis with polycythemia, progressive CHF, debilitating arrhythmias
• in newborns, consider closure of tricuspid valve + aortopulmonary shunt, or transplantation
• in older children, tricuspid valve repair or valve replacement + ASD closure
COMPLEX CYANOTIC DEFECTS
❏ double outlet right ventricle
• a complex spectrum of lesions in which one great artery and more than 50% of the other arise
from the RV, with LV outflow through a VSD
• classified by the location of the VSD - subpulmonic, subaortic, doubly committed
(lies beneath both valves), or noncommitted
• indications for surgery: progressive cyanosis, refractory CHF, palliative procedures to delay
definitive correction
• subaortic or doubly committed VSD: VSD enlargement + tunnel patch LV outflow into aorta
• subpulmonic VSD: VSD enlargement + tunnel patch LV outflow to PA + arterial switch procedure
• noncommitted VSD: VSD enlargement + tunnel patch LV outflow to aorta or
PA +/– arterial switch procedure
❏ univentricular heart (single ventricle)
• spectrum of anomalies in which the heart has only one effective pumping chamber
(usually hypoplastic RV)
• both AV valves are committed to the dominant chamber, giving rise to the name
“double inlet left ventricle”
• TGA is usually present, so the LV pumps directly into the PA and via the VSD into the aorta
• indications for surgery: palliative procedures for progressive cyanosis and to
prevent pulmonary vascular disease
• surgical procedures: PA banding to limit excessive pulmonary blood flow, MBTS for cyanosis
and diminished pulmonary blood flow, Fontan procedure after age 2
❏ transposition of the great arteries (TGA)
• characterized by the aorta arising anteriorly from the RV and the PA arising posteriorly
from the LV (D-TGA)
• survival depends on mixing by bidirectional shunting through an ASD, VSD, or PDA
• indications for surgery: most infants have severe cyanosis at birth
• initial palliation with balloon septostomy
• arterial switch operation - definitive repair involving reconnection of the aorta to the
LV outflow and the PA to the RV outflow, with translocation of the coronary arteries
to the new aorta
• Mustard procedure - removal of atrial septum and creation of pericardial baffle
that directs caval blood behind the baffle through the mitral valve into the LV
and eventually the PA
• Senning operation - involves mobilizing flaps of the atrial free wall and septum
to redirect flow in a manner similar to the Mustard procedure
• arterial switch operation is operation of choice since Mustard and Senning operations
are associated with RV dysfunction and atrial dysrhythmias
❏ total anomalous pulmonary venous connection
• characterized by all of the pulmonary veins draining into the right-sided circulation
(supracardiac - SVC or innominate vein, infracardiac - hepatic/portal vein or IVC,
intracardiac - coronary sinus or RA)
• often associated with obstruction at connection sites
• an ASD must be present to allow blood to shunt into the LA and then to the systemic circulation
• indications for surgery: severe cyanosis or CHF related to pulmonary venous obstruction
• supracardiac and infracardiac - anastomosis of the common pulmonary vein
to the posterior wall of the left atrium
• intracardiac - baffle placed in RA to redirect pulmonary venous flow through the ASD into the LA
❏ truncus arteriosus
• absence of the aortopulmonary septum resulting in a single great vessel arising from the
heart which gives rise to the aorta, PA and coronary arteries
• the truncal valve overlies a large VSD
• indications for surgery: repair within the first 6 months of life to
prevent development of pulmonary vascular disease
• surgical procedures: patch closure of the VSD + separation of the PA from the
aorta/truncus + closure of truncal incision + RV-PA homograft valved conduit

❏ hypoplastic left heart syndrome

• characterized by varying degrees of hypoplasia or atresia of the
mitral valve, LV, aortic valve, and aorta
• blood returning from the lungs is shunted through an ASD to the RA due to LA outflow obstruction
• blood flows from the PA through the PDA to the descending aorta to
provide systemic flow (therefore maintenance of ductal patency is critical)
• indications for surgery: urgent surgery once the diagnosis is made
• First stage (20-50% mortality): atrial septectomy + Norwood procedure (patch enlargement
of the ascending aorta and arch with homograft or pericardium, division of the PA and
closure of the distal PA, anastomosis of the enlarged neoaorta to the proximal PA,
and placement of a central shunt to provide pulmonary blood flow)
• Second stage (age 4-8 months): cavopulmonary anastomosis created between the SVC
and right PA (Glenn Shunt) + ligation of central shunt
• Third stage (age 2-3 years): modified Fontan procedure (IVC flow channeled into the right PA)
• the result is a RV that serves as the systemic ventricle, and pulmonary blood flow
is provided directly by systemic venous return
• heart transplantation is a therapeutic alternative to the Norwood procedure
VASCULAR - ARTERIAL DISEASES

ACUTE ARTERIAL OCCLUSION/INSUFFICIENCY
❏ due to embolus, arterial thrombosis or trauma. Time is of essence, after approximately 6 hours
(depending on collaterals), ischemia and myonecrosis is irreversible to limb
Embolus
❏ etiology
• cardiac is the source of 80-90% of embolic episodes; History of MI (< 3 months),
rheumatic heart disease, abnormal or prosthetic valves, A fib, MS, cardiomyopathy,
endocarditis, atrial myxoma
• arterial source – proximal arterial source such as aneurysm, atheroembolism
• paradoxical embolism with a history of venous embolus passing through intracardiac shunt
• other including a history of medications (oral contraceptives), previous emboli, neurologic / TIAs
❏ presentation
• sudden pain in lower extremity progressing within hours to a feeling of cold numbness,
loss of function and sensation
• no history of significant vascular claudication
• pulses are present in contralateral limb
• may have emboli to other locations (cerebral, upper limb, renal)
Arterial Thrombosis
❏ etiology
• it is important to differentiate thrombosis from embolism because the treatment for the
two may vary dramatically
• thrombosis usually occurs in a previously diseased (atherosclerotic) artery, congenital anomaly,
infection, hematological disorders and low flow rates (CHF)
❏ presentation
• gradual progression of symptoms; but may have an acute-on-chronic event
• progression to loss-of-function and sensory loss may be less profound than with acute embolus
• past history of claudication
• atrophic changes may be present
• contralateral disease may be present
Trauma
❏ etiology
• it is important to determine a history of arterial trauma, arterial catheterization,
intra-arterial drug induced injection, aortic dissection, severe venous thrombophlebitis,
prolonged immobilization, idiopathic
❏ symptoms
• symptoms (6 P’s)
• Pain: absent in 20% of cases because of prompt onset of anesthesia and paralysis
• Pallour: replaced by mottled cyanosis within a few hours
• Parasthesia: light touch goes first (small fibers) followed by
other sensory modalities (large fibers)
• Paralysis / Power loss: heralds impeding gangrene
• Polar (cold)
• Pulselessness
• do not expect all of the 6 P’s to be present and do not rely on pulses
• of the 6 P’s the most important are paralysis / power loss
• full cardiac exam including complete bilateral pulse examination
• atrophic skin and nail changes - longstanding arterial insufficiency
❏ investigations
• CXR, ECG, arteriography
❏ management
• immediate heparinization at 5000iu bolus and continuous infusion to maintain PTT > 60
• in the absence of power and sensation – need emergent re-vascularization:
(i) for embolus – embolectomy; (ii) for thrombus – bypass
• in the presence of power and sensation – need work-up – including angiogram:
(i) for embolus – embolectomy; (ii) for thrombus - bypass
• embolectomy: Fogarty catheter tied to fish embolus out of artery
• bypass: bypass occlusion allowing blood flow to resume to distal site
• identify and treat underlying cause
• continue heparin post-op, start warfarin post-op day 1 for 3 months
• re-perfusion phenomenon
• toxic metabolites from ischemic muscle ––> renal failure and multi-organ system failure
❏ complications
• beware compartment syndrome with prolonged ischemia; requires fasciotomy
❏ treatment of irreversible ischemia is amputation
❏ prognosis
• 12-15% mortality rate
• 5-40% morbidity rate (amputation)
CHRONIC ARTERIAL OCCLUSION / INSUFFICIENCY
❏ predominantly due to atherosclerosis (see Cardiology Chapter)
❏ risk factors
• major: smoking, hypertension, hypercholesterolemia, DM
• minor: hypertriglyceremia, obesity, sedentary, family history
• predominantly lower extremities
• femoropopliteal system > aortoiliac
• tandem lesions often present
• prevalence quoted at 1.5% <50 years old, 5% 50-65 years old, and 18% > 65 years old
❏ differential diagnosis
• osteoarthritis (OA) of the hip - worse in the A.M. and P.M. and varies from day-to-day
• neurogenic claudication – due to spinal stenosis; pain very similar, but relieved by rest
(longer than required for intermittent claudication) and requires a postural change for relief
• varicose veins – localized pain, typically less severe, after exercise and never occurs at rest;
related to the presence and site of varices
• claudication: 3 components
1.discomfort with exertion - usually in calves (cramping), but any exercising group
2.relieved by short rest - 2 to 5 minutes, and no postural changes necessary
3.reproducible - “claudication distance”
• 60-80% get better with conservative therapy, 20-30% stay the same, 5-10% get worse
• pulses: may be absent at some locations (document all pulses)
• signs of poor perfusion: hair loss, deformed nails, atrophic skin, ulcerations and infections
• other manifestations of atherosclerosis: CVD, CAD, Impotence
❏ investigations
• non-Invasive
• ankle-brachial index(ABI): measure brachial pressure bilaterally (use highest pressure)
and measure pressure at ankle. An abnormal ABI is defined as an index < 0.90.
Rest pain usually appears at an ABI < 0.3.
Problem: calcification of the artery may cause overestimation of ABI values.
Solution: Trans-cutaneous oxygen studies to measure tissue oxygenation
(30 mmHg necessary for primary wound healing). Doppler flow studies and
real-time Duplex scanning
• invasive
• arteriography: allows you to define site and size of occlusion as well as the
status of collateral flow. (Gold standard). Mainly a pre-operative planning tool
• digital subtraction angiography (DSA): electronically digitalizes x-ray signals and enhances image
❏ management
• conservative
• 70% of claudicants treated conservatively improve/unchanged, 5-10% develop gangrene
• modify risk factors
• exercise program to develop collateral circulation
• foot care (especially DM) - hygiene, cut nails carefully, treat sore/infection promptly
• drug treatment: ECASA, Plavix or Solaftizol (not yet available in Canada)
❏ surgical
• indications: claudication interfering with lifestyle, rest pain, pre-gangrene, gangrene
• endovascular – PTA
• arterial bypass grafts – aortoiliofemoral, axillofemoral, femoral popliteal, distal arterial.
Can use either in situ graft, reversed vein graft, umbilical vein graft or a polytetrafluoroethylene
(gortex) graft or dacron graft material
• amputation – for non-revascularizable limb
CRITICAL ISCHEMIA
❏ arterial compromise eventually leading to necrosis
• rest pain, night pain
• ulcerations, gangrene of toes
• pallor on elevation, dependent rubor, slow capillary refill
• decreased or absent pulses
• significant bruits may be heard (at 50% occlusion) – if stenosis severe, no bruit will be heard
• ABI < 0.5
❏ investigations
• as above
❏ management
• needs immediate surgery due to risk of limb loss
• initial procedures: transluminal angioplasty, laser, atherectomy and stents
❏ operations include
• inflow procedures for aortoiliac disease
• endarterectomy
• reconstructive procedures for superficial femoral artery occlusion
• profundoplasty
• femoropopliteal bypass
• aortoiliac or aortofemoral bypass
• axillofemoral bypass (uncommon)
ABDOMINAL AORTIC ANEURYSM (AAA)
❏ aneurysm: localized dilatation of an artery that is 2x normal diameter
• true aneurysm: wall is made up of all 3 layers of the artery
• false aneurysm: defect in arterial with aneurysmal sac composed of fibrous tissue or graft
❏ classification
• etiology: congenital
• Marfan syndrome, berry aneurysms acquired
• metabolic / endocrine
• degenerative
• inflammation / infection - syphilis
• neoplastic
• dissection
• shape:Fusiform (true aneurysms)
Saccular (false aneurysms)
• location: aortic
peripheral arteries
splanchnic
renal
❏ structure true or false
❏ inflammatory
❏ infected
❏ 95% of AAA’s are infrarenal
❏ incidence 4.7 to 31.9 per 100,000 person from 1951-1980
❏ the average expansion rate (80% of aneurysms) is 0.2cm/yr for smaller aneurysms (< 4 cm)
and 0.3-0.5 cm/yr for larger aneurysms (> 4-5 cm)
❏ may be associated with other peripheral aneurysms
❏ etiology
• cystic medial necrosis – likely due to enzymatic abnormalities in the aortic wall
• atherosclerosis
❏ high risk groups
• 65 years and older
• male:female = 3.8:1
• peripheral vascular disease, CAD, CVD
• family history AAA
❏ clinical presentation
• common
• 75% asymptomatic (often discovered incidentally)
❏ symptoms due to acute expansion or disruption of wall
• syncope, pain (abdominal, flank, back)
• uncommon
• partial bowel obstruction
• suodenal mucosal hemorrhage ––> GI bleed
• erosion of aortic and duodenal walls ––> aortoduodenal fistula
• erosion into IVC ––> aortocaval fistula
• distal embolization
❏ signs
• hypotension
• palpable mass felt at/above umbilicus
• pulsatile mass, in 2 directions
• bounding femoral pulses
• distal pulses may be intact

❏ investigations
• U/S (100% sensitive, able to measure up to +/– 0.6 cm accuracy); however, operator dependent, and
may not be possible with obese patients, excessive bowel gas or periaortic disease
• Aortogram (not useful because lumen may not change in size due to thrombus formation)
• CT (accurate visualization, determines size)
• MRI (very good imaging, but limited access)
• Doppler/Duplex (to rule out aneurysmal disease elsewhere in the vascular tree)
❏ treatment and prognosis
• decision to treat is based on weighing the risk of OR to disease complications (such as rupture)
• risk of rupture depends on
• size %/yr
• 4-5 cm – 2-3%
• 5-6 cm – 5-8%
• > 7 cm – 25-40%
• > 10 cm – 100%
• rate of growth (> 0.4 cm/yr)
• presence of symptoms, hypertension, COPD
• consider operate at > 5 cm since risk of rupture greater than or equal to risk of surgery
• mortality of elective repair = 2-3% (mostly due to MI)
• consider revascularization for patients with CAD before elective repair of CAD
• conservative
• reduce risk factors
• smoking
• HTN
• DM
• hyperlipidemia
• exercise
• watchful waiting if <4-5cm re-U/S q6mo
❏ surgery
•procedure
• laporotomy performed firm xyphoid process to symphis pubis
• aorta is dissected out
• distal clamp is placed onto aorta
• proximal clamp is placed onto aorta or common iliacs
• aneurysm opened
• removal of thrombis
• graft put into place: tube/bifurcation
• graft sewn into proximal site
• graft suture site tested
• graft sewn into distal site - last stitch not closed until integrity of anastomosis tested
• aorta wall sewn over graft
• indications for surgery
• ruptured
• symptomatic or rapidly expanding aneurysms
• asymptomatic aneurysms >5cm
• contraindications
• less than 1 year to live
• terminal underlying condition (cancer)
• overwhelming medical conditions
• recent MI, unstable angina, decreased mental acruity, advanced age
• early post-op complications
• myocardial ischemia
• arrhythmias
• CHF
• pulmonary insufficiency
• renal damage
• bleeding
• infection
• cord injury
• impotence
• late complications
• graft infection/thrombosis
• aortoenteric fistula
• anastomotic aneurysm
• infection

• post-op orders
• bedrest (24-48 hr)
• NPO
• NG ––> straight drainage, record drainage q12h +/– NG losses 1:1 q shift Ns with 10 mEq KCl/L
• Foley ––> straight drainage
• +/– PA line
• +/– arterial line
• routine post-op vitals q15min until stable then q1h
• routine CU ICU admission blood work
(includes CBC, lytes, BUN, Cr, PLT, PT, PTT, glucose)
• CXR on CUICU admission and daily until extubated
• ECG on admission q8h x 24 hrs and PRN after
• ABI’s/pedal pulses q1h x 4 h then q shift
• chest physiotherapy assessment and treatment
• weaning protocol as per CUICU portocol
• titrate FiO2 to keep PO2 > 90 mmHg or O2 sat > 95% c/c
• ventilation (if required) Vt 700 mL, FiO2 > 50% c/c, rate 12/min, PEEP 5 cm/H2)
to keep PaCo2 35-45 mmHg
• incentive spirometry when extubated
• epidural proticol if required
• IV’s: N/S or RL at 150 cc/hr x 24 hr; reassess at 24 hrs
• morphine 2-10 mg IV q1h PRN
• midazolam 2-4 mg IV q1h PRN max 20 mg/24hr
• dimenhydrinate 12.5-25 mg IV q4h PRN
• heparin 5,000U SC q12h for DVT prophylaxis start post-op
• sulcrote 1 gm NG q4h
• may require inotropic agents
• may require antiphypertensive agents
ABDOMINAL AORTIC DISSECTION
❏ Stanford Surgical Classification
• Type A: involves the ascending and aortic arch; requires emergency surgery
• Type B: involves the aorta distal to subclavian artery; emergency surgery only if
complications of dissection (require long-term follow-up to assess aneurysm size)
❏ male:female = 3-4:1
❏ predominantly older patients
❏ etiologic factors
• hypertension
• cystic medial necrosis (not atherosclerosis)
❏ associated factors
• Marfan's Syndrome
• coarctation of aorta
• congenital bicuspid aortic valve
❏ pathogenesis (usually in thoracic aorta)
• intimal tear ––> entry of blood separates media ––> false lumen
created ––> dissection often continues to aortic bifurcation
❏ symptoms and signs
• sudden searing chest pain that radiates to back
• asymmetric BPs and pulses between arms
• branch vessel "sheared off" – ischemic syndromes
• MI with proximal extension to coronary arteries
• "unseating" of aortic valve cusps
• new diastolic murmur in 20-30%
• neurologic injury - stroke (10%), paraplegia (3-5%)
• renal insufficiency
• lower limb ischemia
• cardiac tamponade - false lumen ruptures into pericardium
• hypertension (75-85% of patients)
❏ diagnosis and investigations
• CXR
• Pleural cap
• Widened mediastinum
• Left pleural effusion with extravasation of blood
• ECG - most common abnormality is LVH (90%)
• TEE, CT, aortography
❏ management
• sodium nitroprusside and B-blocker to lower BP and decrease cardiac contractility
• ascending aortic dissections operated on emergently
• descending aortic dissections initially managed medically
• 10-20% require urgent operation for complications


• pulsatile mass
❏ management
❏ prognosis

ANATOMY
❏ flow stasis
❏ surgery
• pregnancy
• estrogen use
• varicose veins


• most frequent site of thrombus formation is calf
• isolated calf thrombi often asymptomatic
• 30-50% are asymptomatic or minimal symptoms
• 20-30% extend proximally and account for most clinically significant emboli
• classic presentation < 1/3
• calf/thigh discomfort, edema, venous distension
• investigations (refer to PIOPED study for details)
• history and physical
• calf tenderness (if elicited on ankle dorsiflexion = Homan’s sign)
• wider circumference of affected leg
• fever POD #7-10
• clinical assessment incorrect 50% time, therefore must confirm by objective method
• non-invasive tests
• duplex doppler U/S
• 93% sensitive and 98% specific for symptomatic patients, decreased for asymptomatic patients
• detects proximal thrombi
• initial negative exam should be repeated 6-7 days later to detect proximal extension
• invasive testing
• ascending phlebography (venogram)
• the gold standard but costly
• detects distal and proximal thrombi
• complicated by contrast-induced thrombosis of peripheral veins (2-3%)
❏ management
• goals of treatment
• prevent formation of additional thrombi
• inhibit propagation of existing thrombi
• minimize damage to venous valves
• prevent pulmonary emboli (PE)
• 25% develop PE if untreated; 5% if treated
• aggressive medical management
❏ treated as outpatient
❏ fragment / low molecular weight heparin (LMWH)
❏ coumadin
❏ advantage: avoid hospitalization
• conservative medical management
• IV heparin, 5,000 U bolus + 1,000 U/hr to keep aPTT 2-2.5x control
• convert to warfarin 3-7 days after full heparinization; warfarin for 3-6 months
• risks of therapy - bleeding, heparin-induced thrombocytopenia, warfarin is teratogenic
• surgical
• venous thrombectomy - if arterial insufficiency with extensive iliofemoral thrombosis,
+/– venous gangrene
• inferior vena cava (IVC) (Greenfield) filter- inserted percutaneously, indications:
• recurrent PE despite anticoagulation
• contraindication to anticoagulation e.g. intra-cranial trauma
• certain operations for cancer, pulmonary embolectomy
• septic emboli refractory to combination antibiotic and anticoagulation
• "free-floating" thrombus loosely adherent to wall of IVC or pelvic veins
• IVC ligation, surgical clips - increases risk of venous insufficiency; rarely used
❏ DVT prophylaxis
• conservative
• minimize risk factors
• early ambulation, passive range of motion
• anti-embolism stockings
• pneumatic sequential compression devices
• elevation of limb
• medical prophylaxis
• optimize hydration to prevent hemoconcentration
• ECASA, warfarin, minidose heparin(5,000 U SC q8-12h) in high risk situations
❏ complications
• pulmonary embolus (PE)
• varicose veins
• chronic venous insufficiency
• venous gangrene
• phlegmasia cerulea dolens (PCD) - massive DVT with clot extension to iliofemoral
system and massive venous obstruction resulting in a cyanotic, immensely swollen,
painful and critically ischemic leg
• risk venous gangrene
• phlegmasia alba dolens (PAD) - as above with additional reflex arterial spasm
resulting in less swelling than PCD
• cool leg and decreased pulses
SUPERFICIAL THROMBOPHLEBITIS
❏ inflammation or thrombosis of any superficial vein
❏ etiology
• trauma
• association with varicose veins
• migratory superficial thrombophlebitis
• Buerger's disease
• SLE
• polycythemia
• thrombocytosis
• occult malignancy (especially pancreas)
• idiopathic
❏ a pulmonary embolus is rarely present with superficial thrombophlebitis
• pain and cord-like swelling along course of involved vein;
• most commonly involves long saphenous vein or its tributaries
• red, warm, indurated vein
❏ investigations
• non-invasive tests to exclude associated DVT (5-10%)
❏ treatment
• conservative
• bed rest and elevation of limb
• moist heat, compression bandages, mild analgesic,
anti-inflammatory and anti-platelet (e.g. ASA), ambulation
• surgical excision of involved vein indicated if conservative measures fail
• of suppurative thrombophlebitis - IV antibiotics and excise involved vein
❏ complications
• chronic recurrent superficial thrombophlebitis
VARICOSE VEINS
❏ distended torturous superficial veins due to incompetent valves in the deep,
superficial or perforator systems
❏ often greater saphenous vein with dilated tributaries
❏ can also occur in
• esophagus - esophageal varices
• anorectum - hemorrhoids
• scrotum - varicocele
❏ etiology
• primary
• most common form of venous disorder of lower extremity
• 10-20% of population
• inherited structural weakness of vein valves is main factor
• contributing factors
• age
• female
• oral contraceptive (OCP) use
• occupations requiring long hours of standing
• pregnancy
• obesity
• secondary
• result of increased venous pressure from deep-venous valvular insufficiency
and incompetent perforating veins
• malignant pelvic tumours with venous compression
❏ congenital anomalies
• acquired/congenital arteriovenous fistulae
• diffuse aching, fullness/tightness, nocturnal cramping
• aggravated by prolonged standing, end of day, premenstrual
❏ investigations
• patient standing: long, dilated and tortuous superficial veins along thigh and leg
• if ulceration, hyperpigmentation, indurated appearance think secondary varicose veins
• Brodie-Trendelenberg test (valvular competence test)
• while patient is supine, raise leg and compress saphenous vein at thigh; have patient stand;
if veins fill quickly from top down then incompetent valves; use multiple tourniquets to localize
incompetent veins

❏ management
• majority of symptoms relieved by elevation of leg and/or elastic stockings
• may require stripping (proceeding high ligation of saphenofemoral junction)
or sclerosing of veins if conservative management fails
• commonly a cosmetic problem
❏ prognosis
• natural history benign, slow with predictable complications
• almost 100% symptomatic relief if varicosities are primary
• generally good cosmetic results
• significant post-operative recurrence if followed long enough
❏ complications
• recurrent superficial thrombophlebitis
• hemorrhage - externally or into subcutaneous tissues
• ulceration, eczema, lipodermatosclerosis, hyperpigmentation
CHRONIC DEEP VENOUS INSUFFICIENCY

(POST PHLEBITIC SYNDROME, AMBULATORY VENOUS HYPERTENSION)
❏ late complication of DVT, often presenting several weeks to years post DVT
❏ etiology/pathogenesis
• recanalization of thrombosed veins with resulting damaged incompetent valves
• impairment of calf muscle pump, sustained venous hypertension
• pain (most common) relieved on recumbency and foot elevation
• pruritis
• aching fullness of leg, edema
• pigmentation - hemosiderin deposits
• varicose veins
• venous dermatitis
• ulceration (stasis dermititis) above medial malleolus
• venous ulcers are not painful as ischemic arterial ulcers where pain is worse with elevation
• arterial ulcers are often deep, extending through the fascia, with necrotic base whereas venous
ulcers are shallow
• venous ulcers are weeping (wet) and not well demarcated (opposite is true for arterial ulcers)
• positive Brodie-Trendelenberg
• investigations
• gold standard is ambulatory venous pressure measurement (rare)
• doppler U/S
• photoplethysmography
❏ management
• non-operative
• elastic compression stockings, leg elevation, avoid prolonged sitting/standing
• ulcers treated with zinc-oxide wraps (unna boot), split-thickness skin grafts, antibiotics, debridement
❏ operative
• if conservative measures fail, or if recurrent/large ulcers
• surgical ligation of perforators in region of ulcer, strip greater saphenous vein
LYMPHATIC OBSTRUCTION / LYMPHANGITIS

❏ inflammation of the lymphatic vessels (lymphangitis) secondary to ß-hemolytic streptococci
or staphylococci infection
• pain
• hyperemia along the affected lymphatic vessel
❏ management
• immobilization of affected limb
• antibiotic treatment
• should evidence of bacterial seeding be present, drainage may be required
❏ complication
• if the bacterial spread is not terminated at the lymphatic node, septicemia may result

VASCULAR - TRAUMA
PENETRATING (LACERATION)
❏ usually mechanism associated with fractures and dislocations that lead
to limb-threatening injuries
❏ etiology
• motor vehicle crash (MVC)
• gunshot wound
• loss of or relatively weak pulses
• expanding hematoma
• distal cyanosis
• pulsatile bleeding
• distal parasthesia
• polar extremity
• bleeding not controlled with direct pressure
• similar to acute arterial insufficiency
❏ investigations
• duplex doppler
• angiography if patient is stable
• intra-operative angiography if patient is not stable
❏ management
• vascular shunt
• repair damaged vessel
• repair associated orthopaedic injuries
❏ complications
• compartment syndromes – requiring surgical fasciotomy
• should the above not be performed within 6 hours of an ischemic limb, amputation is inevitable
BLUNT (CONTUSION, SPASM, COMPRESSION)

❏ usually mechanism associated with MVC or other direct non-penetrating Injuries
• similar to penetrating trauma
❏ investigations
• similar to arterial insufficiency
❏ management
• injuries are treated as in Arterial Insufficiency section

REFERENCES
www.acc.org – The American College of Cardiology (clinical guidelines, etc)
www.theheart.org – Cardiology Online (requires registration)
www.heartvalverepair.net – Heart Valve Repair Online
www.ctsnet.org – Cardiothoracic Surgery Network
Baue AE, Geha AS, Hammond GL, Laks H, Naunheim KS, eds. Glenn's thoracic and cardiovascular surgery: 6th edition.
Connecticut: Appleton & Lange, 1996.
Bojar RM. Manual of perioperative care in cardiac surgery, 3rd edition. Massachusetts: Blackwell Science Inc., 1999.
Cheng DCH, David TE eds. Perioperative care in cardiac anesthesia and surgery. Austin: Landes Bioscience, 1999.
Fuchs JA. Atherogenesis and the Medical Management of Atherosclerosis. In Vascular Surgery 4th edition, Robert B. Rutherford
Ed. 1995. WB Saunders Co., Toronto. pp 222-234.
Hallett JW Jr. Abdominal Aortic Aneurysm: natural history and treatment. 1992. Heart and Disease and Stroke. 1 (5): 303-8.
Harlan BJ, Starr A, Harwin FM. Illustrated handbook of cardiac surgery. New York: Springer-Verlag Inc., 1996.
Schmieder FA, Comerota AJ, Intermittent Claudication: magnitude of the problem, patient evaluation and therapeutic strategies.
2001. Am J Card 87 (12A): 3D-13D.

CARDIOLOGY
Dr. A. Woo
Stephen Juvet, Daniel Kreichman and Manish Sood, chapter editors
Katherine Zukotynski, associate editor
BASIC CLINICAL CARDIOLOGY EXAM . . . . . . 2 CARDIOMYOPATHIES . . . . . . . . . . . . . . . . . . . . . 32

Cardiac History Dilated Cardiomyopathy (DCM)
Functional Classification of Cardiovascular Disability Hypertrophic Cardiomyopathy (HCM)
Cardiac Examination Restrictive Cardiomyopathy (RCM)
Myocarditis
CARDIAC DIAGNOSTIC TESTS . . . . . . . . . . . . . 6
ECG Interpretation - The Basics VALVULAR HEART DISEASE . . . . . . . . . . . . . . .36
Hypertrophy and Chamber Enlargement Infective Endocarditis (IE)
Ischemia/Infarction Rheumatic Fever
Miscellaneous ECG Changes Aortic Stenosis (AS)
Ambulatory ECG (Holter Monitor) Aortic Regurgitation (AR)
Echocardiography (2-D ECHO) Mitral Stenosis (MS)
Coronary Angiography Mitral Regurgitation (MR)
Cardiac Stress Tests and Nuclear Cardiology Mitral Valve Prolapse
Tests of Left Ventricular (LV) Function Tricuspid Valve Disease
Pulmonary Valve Disease
Prosthetic Valves
ARRHYTHMIAS . . . . . . . . . . . . . . . . . . . . . . . . . . .12
Mechanisms of Arrhythmias PERICARDIAL DISEASE . . . . . . . . . . . . . . . . . . .45
Altered Impulse Formation Acute Pericarditis
Altered Impulse Conduction Pericardial Effusion
Other Etiologic Factors Cardiac Tamponade
Clinical Approach to Arrhythmias Constrictive Pericarditis
Bradyarrhythmias
Conduction Delays SYNCOPE . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .47
Tachyarrhythmias
Supraventricular Tachyarrhythmias (SVT’s) EVIDENCE-BASED CARDIOLOGY . . . . . . . . . . .48
Ventricular Tachyarrhythmias (VT’s) Congestive Heart Failure (CHF)
Pre-excitation Syndromes Ischemic Heart Disease (IHD)
Pacemaker Indications Atrial Fibrillation (A fib)
Pacing Techniques
COMMONLY USED CARDIAC . . . . . . . . . . . . . . .49
ISCHEMIC HEART DISEASE . . . . . . . . . . . . . . . .19 MEDICATIONS
Background ß-blockers
Angina Pectoris Calcium Channel Blockers (CCB)
Acute Coronary Syndromes Angiotensin Converting Enzyme (ACE) Inhibitors
Unstable Angina/Non ST Elevation Angiotensin II Blockers
Myocardial Infarction (MI) Diuretics
Acute ST Elevation MI Nitrates
Sudden Death Anti-Arrhythmic
Anti-Platelet
HEART FAILURE . . . . . . . . . . . . . . . . . . . . . . . . . .27 REFERENCES . . . . . . . . . . . . . . . . . . . . . . . . . . . . .52

Compensatory Responses
Systolic vs. Diastolic Dysfunction
Sleep-Disordered Breathing
High-Output Heart Failure
Acute Cardiogenic Pulmonary Edema
Cardiac Transplantation

BASIC CLINICAL CARDIAC EXAM
CARDIAC HISTORY
❏ coronary artery disease: chest pain (CP) (location, radiation, duration, intensity, activities associated with onset;
alleviating factors (associated with rest, NTG)
❏ heart failure: fatigue, presyncope
• left-sided symptoms: decreased exercise tolerance,
shortness of breath on extertion (SOBOE)/chest pain on exertion (CPOE)
• right-sided symptoms: paroxysmal nocturnal dyspnea (PND)/orthopnea, SOB at rest, ascites,
❏ Arrhythmia: presyncopal/syncopal episodes, palpitations
❏ Baseline function: exercise tolerance (# flights of stairs/blocks), need for nitroglycerin (NTG),
symptoms during low impact activities/daily activities (combing hair, showering) or at rest
FUNCTIONAL CLASSIFICATION OF CARDIOVASCULAR DISABILITY

Table 1. Canadian Cardiovascular Society (CCS) Functional Classification
Class Function
I ordinary physical activity does not cause angina; angina only with strenuous or prolonged activity
II slight limitation of physical activity; angina brought on at > 2 blocks on level (and/or by emotional stress)
III marked limitation of physical activity; angina brought on at ≤ 2 blocks on level

IV inability to carry out any physical activity without discomfort; angina may be present at rest
Table 2. New York Heart Association (NYHA) Functional Classification

Class Function
I ordinary physical activity does not evoke symptoms (fatigue, palpitation, dyspnea, or angina)
II slight limitation of physical activity; comfortable at rest; ordinary physical activity results in symptoms
III marked limitation of physical activity; less than ordinary physical activity results in symptoms
IV inability to carry out any physical activity without discomfort; symptoms may be present at rest
CARDIAC EXAMINATION
General Examination
❏ Skin – peripheral vs. central cyanosis, clubbing, splinter hemorrhages, Osler’s nodes, Janeway lesions
brownish-coloured skin – hemochromatosis
❏ Eyes – conjunctival hemorrhages, Roth spots, emboli, copperwire lesions, soft/hard exudates
Blood Pressure (BP)
❏ should be taken in both arms with the patient supine and upright
❏ be wary of calcification of the radial artery in the elderly as it may factitiously elevate BP (Osler’s sign)
❏ orthostatic hypotension - postural drop > 20 mm Hg systolic or > 10 mm Hg diastolic
• increased HR > 30 bpm (most sensitive - implies inadequate circulating volume)
patient unable to stand - specific sign for significant volume depletion
❏ pulse pressure(PP) (PP = systolic BP (SBP) - diastolic PB (DBP))
• wide PP: increased cardiac output (CO) (anxiety, exercise, fever, thyrotoxicosis, AR, HTN),
decreased total peripheral resistance (TPR) (anaphylaxis, liver cirrhosis, nephrotic syndrome, AVM)
• narrow PP: decreased CO (CHF, shock, hypovolemia, acute MI, hypothyroidism, cardiomyopathy),
increased TPR (shock, hypovolemia), valvular disease (AS, MS, MR), aortic disease
(e.g. coarctation of aorta)
❏ pulsus paradoxus (inspiratory drop in SBP > 10 mmHg ): cardiac tamponade, constrictive pericarditis,
airway obstruction, superior vena cava (SVC) obstruction, COPD (asthma, emphysema)
The Arterial Pulse
❏ remark on
• rate, rhythm, volume/amplitude, contour
• amplitude and contour best appreciated in carotid arteries
❏ pulsus alternans - beat-to-beat alteration in PP amplitude with cyclic dip in systolic BP;
due to alternating LV contractile force (severe LV dysfunction)
❏ pulsus parvus et tardus – slow uprising of the carotid upstroke due to severe aortic stenosis (AS)
❏ pulsus bisferiens – a double waveform due to AS + AR combined
❏ spike and dome pulse – double carotid impulse due to hypertrophic obstructive cardiomyopathy (HOCM)

BASIC CLINICAL CARDIAC EXAM . . . CONT.
Precordial Inspection
❏ observe for apex beat, heaves, lifts
Precordial Palpation
❏ apex - most lateral impulse
❏ PMI - point of maximal intensity
❏ location: normal at 5th intraclavicular space (ICS) at midclavicular line (≤10 cm from midline),
lateral/inferior displaced in dilated cardiomyopathy (DCS)
❏ size : normal is 2-3 cm in diameter, diffuse > 3 cm
❏ duration: normal is <1/2 systole (duration > 2/3 systole is considered sustained)
❏ amplitude (exaggerated, brief - AR, MR, L to R shunt)
❏ morphology (may have double/triple impulse in HOCM)
❏ abnormal impulses
• palpable heart sounds (e.g. S1 in MS, P2 = pulmonary artery (PA) pulsation, S3, S4)
• left parasternal lift (right ventricular enlargement (RVE), left atrial enlargement (LAE) ,
severe left ventricular hypertrophy (LVH))
• epigastric pulsation (RVH especially in COPD)
• thrills (tactile equivalents of murmurs) over each valvular area
Clinical Pearl
❏ Left parasternal lift - DDx - RVH (with pulmonary hypertension (HTN), LAE (secondary to
severe MR), severe LVH, rarely thoracic aortic aneurysm.
Auscultation - Heart Sounds
❏ S1
• composed of audible mitral (M1) and tricuspid (T1) components
• may be split in the normal young patient
❏ if S1 is loud
• short PR interval
• high left atrial (LA) pressure (e.g. early MS)
• high output states or tachycardia (diastole shortened)
❏ if S1 is soft
• first degree AV block
• calcified mitral valve (MV) (e.g. late MS)
• high LV diastolic pressures (e.g. CHF, severe AR)
• occasionally in MR
❏ if S1varies in volume
• AV dissociation (complete AV block, ventricular tachycardia (VT))
• AFib
❏ S2
• normally has 2 components on inspiration: A2 and P2
• normal splitting of S2 (A2 < P2) should vary with respiration
Exp. Insp.
S2 A2 P2 normal
• increased venous return to right side of heart with inspiration results in delayed closure of
pulmonary valve (PV) (widens split)
A2 P2 A2 P2 wide fixed splitting
• atrial septal defect (ASD)
S2 A2 P2 widened splitting (delayed RV or early LV emptying)
• right bundle branch block (RBBB), pulmonary HTN, MR, ventricular septal defect (VSD)
P2 A2 S2 paradoxical splitting (delayed LV or early RV emptying)
• left bundle branch block (LBBB), tight AS, systemic HTN, LV fib, paced rhythm,
tricuspid regurgitation (TR), Wolfe Parkinson White (WPW)
❏ soft S2
• aortic (A2) or pulomonic (P2) stenosis
❏ loud S2
• systemic (A2) or pulmonary HTN (P2)
❏ soft heart sounds
• low cardiac output
• obesity
• emphysema
• pericardial effusion ("muffled" = tamponade)
❏ S3 (see Figure 1): volume overloaded ventricle
• occurs during period of rapid ventricular filling
• low frequency - best heard with bell at apex
• causes
• may be normal in children and young adults (age < 30)
• LV failure (systolic dysfunction, acute MI)
• rapid ventricular filling (MR or high output states), RV S3 (TR, MS, RV failure)
• DDx - split S2, opening snap, pericardial knock, tumour plop
❏ S4 (Figure 1): pressure overloaded ventricle (decreased capacitance, increased contribution of
atrial kick to ejection fraction (EF))
• occurs during atrial contraction
• best heard with bell at apex
• always pathological (associated with diastolic dysfunction), ischemia (ventricular relaxation needs ATP),
hypertrophy (HTN, AS, HCM), RCM, RV S4 (pulmonary HTN, PS)
• DDx - split S1, ejection clicks, prolapse clicks
Extra Sounds
❏ opening snap - early-diastolic (see Figure 1) - MS (A2-opening snap (OS) interval shortens as MS worsens)
❏ ejection clicks (AS, PS)
❏ non-ejection mid-systolic clicks (mitral and tricuspid valve prolapse (MVP/TVP))
❏ pericardial (friction) rub: pericarditis, triphasic - ventricular systole, ventricular diastole and atrial systole
("scratchy" sound, like velcro)
❏ tumour plop
Auscultation - Murmurs
❏ Classification: timing (systolic/diastolic), location, radiation, intensity (grade murmurs I-VI), shape,
pitch (quality), variation with respiration or maneuvers
❏ presence or absence of accompanying thrills, association with extra heart sounds
Clinical Pearl
❏ Inspiration augments all right-sided murmurs and sounds, except pulmonary
ejection click.
❏ Expiration augments AR (heard best on full exhalation, sitting leaning forward).
❏ postural maneuvers
• left lateral decubitus (LLD) for MS, S3, S4
• squatting to standing position (MVP, hypertrophic obstructive cardiomyopathy (HOCM))
• passive leg elevation (MVP, HOCM)
Table 3. Maneuvers for Auscultation of Heart Murmurs
Maneuvers • Quiet inspiration • Transient arterial • Standing to squatting • Valsalva
• Sustained abdominal occlusion (using 2 • Passive leg elevation
pressure sphygmomanometers)
• Fist clenching
Physiological Effect 8venous return 8systemic arterial 8venous return 9venous return
resistance 8systemic arterial 8systemic arterial
resistance resistance
Effect on • 8right-sided •8left-sided murmurs • 9HCM • 9 AS

Intensity of the murmurs •8MR • 9MVP
Mummer •8TR •8VSD
•8PS
❏ systolic “ejection” murmurs (see Figure 1)

• diamond-shaped, crescendo-decrescendo
• outflow obstruction: AS, HOCM, PS
• high output or "flow" murmurs
• anemia
• thyrotoxicosis
• pregnancy
• arteriovenous fistula
• children
• fever
❏ pansystolic murmurs (see Figure 1)
• require a sustained pressure difference throughout systole
• MR
• TR
• VSD
❏ high-pitched diastolic decrescendo murmurs (see Figure 1)
• AR
• PR
❏ low-pitched diastolic murmurs (mid-diastolic rumble) (see Figure 1)
• MS
• TS
• severe AR may produce Austin Flint murmur
❏ high flow murmurs (result from 'relative' stenosis)
• MR, persistent ductus arteriosus (PDA), VSD (increased left atrial (LA) filling)
• ASD (increased right atrial (RA) filling)
❏ continuous murmurs (see Figure 1)
• PDA
• mammary souffle - goes away with pressure on stethoscope
• coronary arteriovenous fistula
• venous hum
• due to high blood flow in the jugular veins
• heard in high output states
S1 S2 S3 S1 S1 S2
S3 Pansystolic Murmur
S1 S2 S4 S1 S2 S1
S4 High Pitched Diastolic Murmur
S1 S2 OS S1 S2 OS S1
Opening Snap Low Pitched Diastolic Murmur
S1 S2 S1 S2 S1
Systolic Ejection Murmur Continuous Murmur
Figure 1. Heart Sounds and Murmurs
Jugular Venous Pulsations - JVP (see Figure 2)

❏ height of column of blood filling internal jugular vein, related to RA and RV filling and dynamics,
measured as X cm above sternal angle (ASA) (which lies 5cm above the RA; normal JVP is 2-4 cm ASA)
❏ distinguishing features of the JVP vs carotid impulse
• location - between heads of the sternocleidomastoid muscle, coursing towards angle of jaw
• multiple waveforms in normal patient
• non-palpable
• obliterated with pressure at base of neck
• soft, undulating quality
• changes with degree of incline and inspiration
(normally drops on inspiration)
• transient increase with abdominal pressure/Valsalva maneuver
• descents are clinically more prominent than waves at the bedside
❏ normal waveforms
• “a” wave = atrial contraction - precedes carotid pulse
• “x” descent = atrial relaxation
• “c” wave = bulging up of TV during RV systole (may reflect carotid pulse in neck)
• “x prime” descent = descent of base of heart during ventricular systole
• “v” wave = passive atrial filling against closed AV valve
• “y” descent = early rapid atrial emptying following opening of AV valve - occurs after carotid pulse felt

❏ pathological waveforms
• loss of "a" wave
• A fib, atrial standstill
• absent venous pulse
• RHF/CHF, SVC obstruction, cardiac tamponade
• giant "a" waves
• contraction of atrium against increased resistance
(RVH, PS, TS, pulmonary HTN) with every beat
• cannon “a” waves
• contraction of atrium against closed TV as in AV dissociation (AV dissociation, PVC);
not with every beat
• systolic venous pulsation (c-v waves)
• regurgitation of blood into venous system with ventricular contraction as in TR (rapid “y”)
• sharp "y" descent
• increased venous pressure as in constrictive pericarditis (“y”>”x” phenomenon)
❏ Hepatojugular reflux (HJR)
• positive response correlates better increased pulmonary capillary wedge pressure (PCWP)
(L-sided failure) than R-sided failure
• sustained > 4 cm rise in JVP with firm abdominal compression
• postivie response seen in TR, RV failure, pulmonary HTN, CHF, increased PCWP
❏ Kussmaul’s sign – a paradoxical rise in the JVP on inspiration
❏ differential diagnosis: constrictive pericarditis, right ventricular MI high venous pressure
a
x
c v
x1
y
Figure 2. Jugular Venous Pulsations
CARDIAC DIAGNOSTIC TESTS

ECG INTERPRETATION-THE BASICS
Key Features
❏ rate
❏ rhythm
❏ axis
❏ waves and segments
❏ hypertrophy and chamber enlargement
❏ ischemia/infarction
❏ miscellaneous
Rate
❏ each small box is 0.04 sec; each large box is 0.2 sec.
❏ if rhythm is regular, rate is obtained by dividing 300 by number of large squares between two R waves
❏ with irregular rhythms note the average ventricular rate over 10 seconds
❏ normal adult rate = 60-100 bpm
❏ bradycardia < 60 bpm
❏ tachycardia > 100 bpm
Rhythm
❏ ask four questions
• Are there P waves present?
• Are the QRS complexes wide or narrow?
• What is the relationship between the P waves and QRS complexes?
• Is the rhythm regular or irregular?
❏ definition of normal sinus rhythm
• has a P wave preceding each QRS complex, and a QRS after each P
• P wave axis is normal (negative in aVR and positive in II)
• PR interval is normal and constant
• P wave morphology is constant

CARDIAC DIAGNOSTIC TESTS . . . CONT.
Axis (see Figure 3)

❏ deviation - limb leads: normal = positive QRS in I and aVF
• axis is perpendicular to lead in which QRS is isoelectric
• QRS axis points toward ventricular hypertrophy and away from infarction
• see Ventricular Hypertrophy and Hemiblocks sections
❏ rotation - precordial leads: normally isoelectric QRS in V3, V4
• clockwise = isoelectric QRS in V5, V6
• counterclockwise = isoelectric QRS in V1, V2 (i.e. tall R wave in V1, see below)
–90º
Left Axis Deviation (LAD)
aVR –30º, aVL
–180º I
NORMAL
AXIS
III II
90º
Right Axis Deviation aVF
(RAD)
Figure 3. Axes of Electrocardiographic Limb Leads
Waves and Segments
❏ P wave - atrial depolarization, smooth contour, entirely positive or negative
❏ PR interval - rate dependent; reflects slowing of impulse through the AV node which is governed
by parasympathetic and sympathetic discharge
❏ QRS complex - ventricular depolarization; any Q wave in V1-3 is abnormal;
R wave increases in amplitude and duration through V1-V5;
S wave is largest in V2 and gets progressively smaller
❏ ST segment - above or below the baseline; point the QRS meets the ST segment is called the J point
❏ QT interval - should be < 1/2 of the RR interval
• interval is rate related (increased HR ––> decreased QT)
❏ T wave - ventricular repolarization
• normal = negative in aVR, flat or minimally negative in limb leads; otherwise positive
Q S
T
P U
P
DURATION 0.12 < 0.12

(seconds)
0.12-.20 ≤ 1/2 RR
Figure 4. ECG Waveforms and Normal Values

Illustration by Marc Dryer
HYPERTROPHY AND CHAMBER ENLARGEMENT

Right Ventricular Hypertrophy (RVH)
❏ QRS < 0.12 seconds, R/S ratio > 1 in V1, R/S ratio < 1 in V5 and V6, R > 7 mm in V1
❏ right axis deviation (RAD) (> 90º)
❏ Asymmetric ST segment depression and T wave inversion in V1 and V2 (RV strain pattern)
Left Ventricular Hypertrophy (LVH)
❏ S in V1 or V2 + R in V5 or V6 > 35 mm
❏ S in V1 or V2 or R in V5 or V6 > 25 mm
❏ R in aVL > 11 mm
❏ R in I + S in III > 25 mm
❏ left axis deviation (LAD) (> –30º) with slightly widened QRS
❏ asymmetric ST segment depression and T wave inversion (LV strain) leads I, aVL, V4-6
❏ left atrial enlargement (LAE)
Right Atrial Enlargement(RAE) (P Pulmonale)

❏ P wave > 2.5 mm (in height) in leads II, III or aVF
Left Atrial Enlargement (LAE) (P Mitrale)
❏ P wave duration > 0.11s best seen in leads I, II, aVL, V4-V6
❏ large, biphasic P wave in V1 with deep terminal component that is
at least one square wide (0.04 sec) and one square deep (1 mm)
❏ notched P with interpeak interval > 0.04 seconds in I, II or aVL
Clinical Pearl
DDx of tall R wave in V1
❏ RVH, Posterior MI, WPW, HCM (septal hypertrophy), Duchenne muscular dystrophy,
and dextrocardia.
ISCHEMIA / INFARCTION (see Figure 5)

During an ischemic event/acute MI, the ECG changes with time may include:
❏ ischemia: T waves invert at site of injury
❏ injury: ST segment elevation +/– tall peaked T waves, “hyperacute" T waves at area of injury,
with reciprocal ST segment depression
• acute MI = ST elevation in 2 or more contiguous leads in an arterial territory
❏ necrosis: Q waves develop: signifies completed transmural infarct
• significant if > 1 mm wide (> 0.04 seconds) or if > 1/3 the amplitude of QRS
• NOTE: Q waves are normally present in lead V1 and non-significant Q’s often present in lead III
DDx for ST Segment Changes
❏ elevation
• early repolarization (normal variant)
• acute MI
• post MI
• Prinzmetal's angina (coronary vasospasm)
• acute pericarditis
• ventricular aneurysm
• LBBB
❏ depression
• angina (ischemia)
• subendocardial infarction (non Q-wave MI)
• acute posterior wall MI (V1 and V2)
• LVH or RVH with strain
• digitalis effect (“scooping” or “hockey stick”)
• hypokalemia, hypomagnesemia
• LBBB, RBBB, WPW
T Wave
Acute Recent Old

days weeks-months months-years
(avg. 3-5) (avg. 2-6 months) (avg. > 6 months)
ST segment elevation T wave inversion Just significant Qs
Figure 5. ECG changes with Ischemia/Infarction
Illustration by Victoria Rowsell

Table 4. Areas of Infarction

Infarct Area Usual Involved Vessel Q waves
anteroseptal left anterior descending (LAD) V1, V2
anterior V3, V4
anterolateral I, aVL, V3-V6
extensive anterior I, aVL, V1 - V6
inferior right coronary artery (RCA) II, III, aVF
lateral* circumflex I, aVL, V5, V6
posterior RCA (accompanies inf. MI) V6, mirror image V1 and V2
circumflex (isolated post. MI)
right ventricle RCA (most often) V4R (V5R and V6R) (right sided chest leads)
*often no ECG changes because small infarcts and lateral wall is late in the depolarization (QRS complex)
Variations in Cardiac Vascular Anatomy

❏ Table 4 describes anatomy of "right-dominant" circulation (80%)
❏ compare with
• left-dominant circulation (15%)
• posteroinferior LV supplied by LCA
• balanced circulation (5%)
• dual supply of posteroinferior LV by RCA and LCA
left main coronary artery (LCA)
circumflex
right coronary left anterior descending (LAD)
artery (RCA)
septal perforator
obtuse marginal
acute marginal
diagonal
posterior
interventricular
Figure 6. Anatomy of the Coronary Arteries (right anterior oblique projection)
MISCELLANEOUS ECG CHANGES

Electrolyte Disturbances
❏ hyperkalemia
• peaked T waves, flat P, wide QRS, long PR interval, elevated ST segment
Illustrations by Pascale Tranchemontagne

❏ hypokalemia
• flattened T waves, U waves, ST depression, prolonged Q-T interval
Illustrations by Pascale Tranchemontagne

❏ hypocalcemia
• prolonged Q-T interval
❏ hypercalcemia
• shortened Q-T interval

Hypothermia
❏ prolonged intervals, sinus bradycardia, slow A fib
❏ beware of muscle tremor artifact
❏ Osborne or J wave deflection
Early Pericarditis
❏ early - diffuse ST segment elevation +/– "PR segment depression"
❏ early upright T waves
❏ later - isoelectric ST segment and T waves flat or inverted
❏ tachycardia
Low Voltages
❏ definition - total QRS height in precordial leads < 10 mm, limb leads < 5 mm
❏ DDx
• inappropriate voltage standardization
• pericardial effusion (e.g. tamponade)
• barrel chest (COPD), obesity
• hypothyroidism
• dilated cardiomyopathy, myocardial disease, myocarditis
• amyloidosis/infiltrative cardiomyopathy
Drugs
❏ Digoxin
❏ therapeutic levels may be associated with “Dig effect”
• T wave depression or inversion
• ST downsloping or “scooping”
• QT shortening +/– U waves
• slowing of ventricular rate in A Fib Illustration by Seline McNamee
❏ toxic levels associated with
• tachyarrhythmias (especially paroxysmal atrial tachycardia (PAT)) with conduction blocks
• PVC’s, bigeminy
• classic “regularization” of ventricular rate in A fib due to
complete AV dissociation
❏ Quinidine, phenothiazines, tricyclic antidepressants (TCA’s)
• prolonged QT interval, U waves
Other Cardiac Conditions
❏ hypertrophic cadiomyopathy (HCM)
• ventricular hypertrophy, LAD, septal Q waves
❏ Myocarditis
• conduction blocks, low voltage
Pulmonary Disorders
❏ chronic obstructive pulmonary disease (COPD)
• low voltage, RAD, poor R wave progression
• chronic cor pulmonale can produce RAE and RVH with strain
• multifocal atrial tachycardia (MAT)
❏ Massive pulmonary embolus (PE)
• sinus tachycardia and A fib are the most common arrhythmias
• RVH with strain, RBBB, SI, QIII, TIII (inverted T) (S1Q3 3)
T
AMBULATORY ECG (HOLTER MONITOR)

❏ 24-48 hr ECG recording with patient diary of symptoms to determine
correlation between symptoms and abnormalities
• indications 1. detect intermittent arrhythmias
2. relate symptoms to dysrhythmias
3. detect myocardial ischemia
ECHOCARDIOGRAPHY
❏ Two-dimensional (2-D) ECHO: anatomy - ultrasound (U/S) reflecting from tissue interfaces
• determines
• LV systolic ejection fraction (LVEF)
• chamber sizes
• wall thickness
• valve morphology
• pericardial effusion
• wall motion abnormalities
• complications of acute MI
❏ Doppler: blood flow – U/S reflecting from intracardiac RBCs
• determines blood flow velocities to estimate valve areas and determine intracardiac gradients
❏ Colour flow imaging determines:
• valvular regurgitation
• valvular stenosis
• shunts

❏ Transesophageal Echo (TEE)

• high quality images but invasive
• more sensitive for
• prosthetic heart valves
• to identify cardiac sources of systemic emboli, intracardiac thrombi, tumours,
debris within the aorta, valvular vegetations, and infective endocarditis
CORONARY ANGIOGRAPHY (see Cardiac and Vascular Surgery Chapter)
❏ technique: injection of radiopaque dye into coronary arteries via percutaneous femoral catheter
❏ information obtained: coronary anatomy, LVEF with ventriculography, hemodynamic indices
❏ Indications:
• Diagnosis: gold standard for detecting and quantifying CAD
• Prognosis: post-MI
• Guiding Therapy: e.g. CABG vs. PTCA vs. medical therapy
❏ complications (%): death (0.1), stroke (0.07), MI (0.07), other major (1.0-2.0), minor (10)
CARDIAC STRESS TESTS AND NUCLEAR CARDIOLOGY

❏ indications
• assessment of chest pain (detection of CAD)
• risk stratification post-MI
• preoperative screening and risk assessment
• assessment of response to therapy
• assessment of myocardial viability
❏ stressors
• physical stressors: treadmill or bicycle
• pharmacological stressors
• increased coronary flow: dipyridamole (Persantine), adenosine
• increased myocardial O2 demand: dobutamine (ß1-selective agonist)
❏ ischemia detectors
• ECG: observe for ischemic changes during stress
• ECHO: visualize myocardial effects of ischemia
• SPECT myocardial nuclear perfusion studies
• tracers infused during stress
• thallium-201 (201Tl, a K+ analogue)
• technetium-99 (99Tc)-labelled tracer (sestamibi = Cardiolyte)
• SPECT images of the heart obtained during stress and at rest 4h later
• fixed defect = impaired perfusion at rest and during stress (infarcted)
• reversible defect = impaired perfusion only during stress (ischemic)
• Other imaging techniques: PET, MRI, ultrafast CT, TEE (uncommonly used)
❏ ventricular function assessment (LVEF, RVEF, ventricular size and volume, wall motion anomalies, etc.)
• Radionuclide angiography (MUGA): 99Tc- radiolabelled RBCs
• ECHO
• Ventriculography
Table 5. Attributes and Limitations of Various Stress Tests

Factor Treadmill Test Stress Echo Nuclear Perfusion Radionuclide
(GXT) Angiography
Sensitivity 65-70% 90% 80-85% 80-85%
Specificity 65-70% 90% 90%
Localizing ischemia poor good good good
Additional info N/A rest & exercise rest LVEF, lung uptake, rest & exercise LVEF,
compared with GXT LVEF, plus all infarct size, LV size regional wall motion,
other echo LV volumes, RV function
parameters
Clinical or technical abnormal resting COPD, obesity obesity, attenuation arrhythmias
limitations ECG, pretest artifacts
probability very
important
Relative cost $ $$ $$$$ $$$
Modified from: Anon. Mayo Clinic Proceedings. 1996; 71:43-52.

Indication
Diagnostic and prognostic purposes? Localization of ischemia? Direct measurement of Vo2 max., timing
of cardiac transplanation, or selected
patients with unexplained dyspnea?
Able to exercise? Able to exercise? Able to exercise?
Yes No Yes Yes
Pharmacologic stress Cardiopulmonary exercise test

imaging
Normal findings on resting Exercise imaging study

ECG No Local expertise with the technique
Patient not taking digoxin? Primary question to be answered
Patient characteristics
Cost
Yes
Standard treadmill exercise test
Figure 7. Algorithm for test selection for an individual patient.

From: Anon. Mayo Clinic Proceedings 1996; 71;43-52.
ARRHYTHMIAS
MECHANISMS OF ARRHYTHMIAS
1. ALTERED IMPULSE FORMATION

❏ divided into two potentially arrhythmogenic processes:
❏ AUTOMATICITY = the ability of a cell to depolarize itself to threshold and, therefore, generate an
action potential
❏ cells with this ability are known as “pacemaker” cells
• SA node, purkinje cells throughout atria
• bundle of His, bundle branches
• purkinje cells in fascicles and peripheral ventricular conduction system
❏ automaticity is influenced by
• neurohormonal factors: sympathetic and parasympathetic
• drugs: e.g. Digoxin has vagal effect on SA and AV nodes but sympathetic effect
on other pacemaker sites
• local ischemia/infarction or other pathology
• blockage of proximal pacemaker (SA node) impulses which allows more distal focus to
control the ventricular rhythm
❏ TRIGGERED ACTIVITY = abnormal depolarization occurring during or after repolarization
• oscillations of the membrane potential after normal depolarization lead to recurrent depolarization
• prolonged QT interval predisposes (e.g. electrolyte disturbances, antiarrhythmic drugs)
• postulated mechanism of Torsades de Pointes

ARRHYTHMIAS . . . CONT.
2. ALTERED IMPULSE CONDUCTION

❏ re-entry
• phenomenon which requires parallel electrical circuit in which
two limbs have different refractory periods, e.g. AVNRT
❏ conduction blocks - partial or total
❏ ventricular pre-excitation
• congenital abnormality in which ventricular myocardium is
electrically activated earlier than by the normal AV nodal impulse
• e.g. bypass tract in WPW syndrome
OTHER ETIOLOGIC FACTORS
❏ increased LA size ––> increased risk of A fib
❏ bradycardia predisposes via temporal dispersion in refractory periods; e.g. tachy-brady syndrome
❏ hypoxia/acidosis lowers the threshold for V fib
❏ electrolyte disturbances, e.g.: hypokalemia, imbalances of Ca+2, Mg+2
❏ infection, e.g.: myocarditis or infective endocarditis (causing abscess and complete heart block)
❏ cardiomyopathies, degenerative disease, infiltration (e.g. sarcoid)
❏ ischemia, increased sympathetic tone
CLINICAL APPROACH TO ARRHYTHMIAS
ARRHYTHMIA
BRADYARRYTHMIA (< 60 BPM) CONDUCTION DELAY TACHYARRHYTHMIA (> 100 BPM)

• sinus bradycardia • AV nodal conduction blocks • IRREGULAR
• sinus arrest • 1º, 2º, 3º • A Fib
• escape rhythms • fascicular block • MAT
• junctional • bundle branch block • Atrial flutter (variable block)
• ventricular • frequent APBs, VPBs
• REGULAR
NARROW COMPLEX WIDE COMPLEX

• SVT • SVT with aberrancy (or BBB)
• Atrial flutter • ventricular tachycardia
• AVNRT
• WPW (retrograde conduction
through bypass tract)
Figure 8. Clinical Approach to Arrhythmias
BRADYARRHYTHMIAS
Presentation
❏ often asymptomatic
❏ symptoms can include dizziness, fatigue, dyspnea and presyncope or syncope
❏ effects of bradycardia depend on rate, and patient's co-morbid conditions (e.g. heart failure)
DDx
Sinus Bradycardia
❏ sinus rhythm at regular heart rate less than 60 bpm
❏ caused by excessive vagal tone: spontaneous (vasovagal syncope), acute MI (inferior),
drugs, vomiting, hypothyroidism, increased intracranial pressure (ICP)
❏ treatment: if symptomatic, atropine +/– electrical pacing (chronic)
Sinus Arrhythmia
❏ irregular rhythm with normal P wave and constant, normal PR interval
❏ normal variant - inspiration accelerates the HR; expiration slows it down
❏ pathological - uncommon, variation not related to respiration
Sinus Arrest or Exit Block
❏ sinus node stops firing (arrest) or depolarization fails to exit the sinus node (exit block)
❏ depending on duration of inactivity, escape beats or rhythm may occur
- next available pacemaker will take over, in the following order
• atrial escape (rate 60-80): originates outside the sinus node within the atria
(normal P morphology is lost)
• junctional escape (rate 40-60): originates near the AV node; a normal P wave is not seen
• may occasionally see a retrograde P wave representing atrial depolarization moving backward
from the AV node into the atria
• ventricular escape (rate 20-40): originates in ventricular conduction system
• no P wave; wide, abnormal QRS (ECG tracing)
❏ treatment: stop meds which suppress the sinus node (ß blockers, CCB, Digoxin); may need pacing

Sick Sinus Syndrome (SSS)

❏ includes above sinus node disturbances, when pathologic
• causes: structural SA node disease, autonomic abnormalities, or both
❏ bradycardia may be punctuated by episodes of SVT, especially A fib or atrial flutter (tachy-brady syndrome)
❏ treatment: pacing for bradycardia; meds for tachycardia
CONDUCTION DELAYS
AV Node Conduction Blocks
❏ look at the relationship of the P waves to the QRS complexes
❏ 1st degree - constant prolonged PR interval (> 0.2 seconds)
• all beats are conducted through to the ventricles
• no treatment required if asymptomatic
❏ 2nd degree (Mobitz) - not all P waves followed by QRS; distinguish Type I from Type II
• Mobitz Type I (Wenckebach) - due to AV node blockage
• progressive prolongation of the PR interval until a QRS is dropped
• treatment: none unless symptomatic; atropine
• Mobitz Type II - due to His-Purkinje blockage

• all-or-none conduction; QRS complexes are dropped at regular intervals (e.g. 2:1, 3:1, etc.)
with stable PR interval (normal or prolonged)
• risk of developing syncope or complete heart block
• treatment: pacemaker (ventricular or dual chamber)
❏ 3rd degree or complete heart block - no P wave produces a QRS response
• complete AV dissociation (atria and verntricles contracting independently;
may see P waves "marching through" QRS’s)
• can have narrow junctional QRS or wide ventricular QRS (junctional vs ventricular escape rhythm)
• rate usually 30-60 bpm
• may cause Stokes-Adams attacks: syncope associated with brief cardiac arrest
• treatment: pacemaker (ventricular or dual chamber)
Bundle Branch and fascicular Blocks

❏ RBBB, left anterior fascicle and left posterior fascicle should each be considered individually,
and combination (i.e. bifascicular) block S should also be noted
Bundle Branch Blocks (BBB)
❏ QRS complex > 0.12 seconds
❏ RBBB
• RSR' in V1 and V2 (rabbit ears), with ST segment depression
and T wave inversion
• presence of wide (or deep) S wave in I, V6
• widely split S2 on auscultation
❏ LBBB
• broad or notched monophasic R wave with prolonged
upstroke and absence of initial Q wave in leads V6, I and aVL,
with ST segment depression and T wave inversion RBBB
• large S or QS in V1
• paradoxically split S2 on auscultation
❏ note
• with BBB the criteria for ventricular hypertrophy become unreliable V1 V6
• with LBBB, infarction is difficult to determine
ARRHYTHMIAS
Hemiblock
. . . CONT.
❏ block of anterior or posterior fascicle of LBB
❏ anterior hemiblock
• normal QRS duration; no ST segment or T wave changes
• left axis deviation (> –45º), with no other cause present
• small Q in I and aVL, small R in II, III and aVF
❏ posterior hemiblock
• normal QRS duration; no ST segment or T wave changes
• right axis deviation (> 110 degrees), with no other cause present LBBB
• small R in I and aVL, small Q in II, III and aVF
TACHYARRHYTHMIAS
Presentation
❏ symptoms, when present, include palpitations, dizziness, dyspnea, chest discomfort, presyncope or syncope
❏ may precipitate CHF, hypotension, or ischemia in patients with underlying disease
❏ incessant untreated tachycardias can cause cardiomyopathy (rare)
❏ includes supraventricular and ventricular rhythms
DDx
1. SUPRAVENTRICULAR TACHYARRHYTHMIAS
❏ narrow (i.e., normal) QRS complex or wide QRS if aberrant ventricular conduction or pre-existing BBB
❏ aberrancy = intraventricular conduction delay associated with a change in cycle length
(i.e., with tachycardia); not normal pattern for the individual
Sinus Tachycardia
❏ sinus rhythm at a rate greater than 100 bpm
❏ Etiology: fever, hypotension, thyrotoxicosis, anemia, anxiety, hypovolemia, PE, CHF, MI, shock,
drugs (EtOH, caffeine, atropine, catecholamines)
❏ treatment: treat underlying disease; consider propranolol if symptomatic
Premature Beats
❏ Atrial Premature Beat (APB)
• single ectopic supraventricular beat originating in the atria
• P wave contour of the APB differs from that of a normal sinus beat
❏ Junctional Premature Beat
• a single ectopic supraventricular beat that originates in the vicinity of the AV node
• there is no P wave preceding the premature QRS complex, but a retrograde P wave may follow
the QRS if AV nodal conduction is intact
❏ treatment: none unless symptomatic; ß blockers or CCB
Atrial Flutter
❏ regular; atrial rate 250-350 bpm, usually 300
❏ etiology: IHD, thyrotoxicosis, MV disease, cardiac surgery, COPD, PE, pericarditis
❏ ventricular conduction is variable e.g. 2:1, 3:1, 4:1 block, etc.
❏ ECG: sawtooth inferior leads; narrow QRS (unless aberrancy)
❏ carotid massage (check first for bruits), Valsalva or adenosine:
increases the block (i.e. slows pulse), brings out flutter waves
❏ treatment
• rate control: ß blocker, verapamil, Digoxin
• medical cardioversion: procainamide, sotalol, amiodarone, quinidine
• electrical cardioversion: DC shock (@ low synchronized energy levels: start at 50 J)
Clinical Pearl
❏ Narrow complex tachycardia at a rate of 150 is atrial flutter with 2:1 block
until proven otherwise.
Multifocal Atrial Tachycardia (MAT)

❏ irregular rhythm; atrial rate 100-200 bpm; at least 3 distinct P wave
morphologies and 3 different P-P intervals present on ECG
❏ probably results from increased automaticity of several different atrial foci
❏ hence varying P-P, P-R, and R-R intervals, varying degrees of AV block
❏ common in COPD, hypoxemia, hypokalemia, hypomagnesemia, sepsis, theophylline or Digoxin toxicity
❏ if rate < 100 bpm, then termed a Wandering Atrial Pacemaker
❏ carotid massage has no effect in MAT
❏ treatment: treat the underlying cause; if necessary try metoprolol (if no contraindications)

Atrial Fibrillation (A fib)

❏ seen in 10% of population over 75 years old
❏ the majority of cardiogenic strokes and peripheral thromboembolic events occur in association with A fib
❏ Etiology: CAD, valvular disease, pericarditis, cardiomyopathy, PE,
HTN, COPD, thyrotoxicosis, tachy-brady syndrome, EtOH (holiday heart)
❏ irregularly irregular ventricular rate; narrow QRS unless aberrancy,
• undulating baseline; no P waves
❏ atrial rate 400-600 bpm, ventricular rate variable depending on AV node, around 140-180 bpm
❏ wide QRS complexes due to aberrancy may occur following a long short R-R cycle sequence
(“Ashman phenomenon")
❏ lose atrial contribution to ventricular filling (no “a” waves seen in JVP)
❏ carotid massage: may slow ventricular rate
❏ A fib resistant to cardioversion - significant LA enlargement, longer duration of A fib
❏ major issues to be addressed with A fib:
• Rate control (ventricular) – beta blocker, verapamil, digoxin
• Anti-coagulation (prevention of thromboembolic phenomenon)
• warfarin for paroxysmal or chronic A fib
• balance risk of bleeding 1%/year vs. risk of clot (warfarin reduces thromboembolic event rate
by 67% in nonrheumatic A fib)
• Cardioversion
• OK without anticoagulation within 48 hours of onset (by history) of A fib
• if > 48 hours after onset MUST anticoagulate at least 3 weeks prior to cardioversion
and 4 weeks after cardioversion
• alternate option is TEE prior to eraly electrical cardioversion to rule out clot (controversial)
• medical - sotalol, amiodarone, Class I agent if normal LV function
(e.g. IV procainamide, propafenone)
• electrical - synchronized DC cardioversion (Diltiazem)
• treat any etiology that can be identified
❏ Note – drug - refractory symptomatic A fib may be referred for AV node
ablation followed by permanent pacemaker insertion
Paroxysmal Supraventricular Tachycardia (PSVT)

❏ sudden onset regular rhythm; rate 150-250 bpm
❏ usually initiated by a supraventricular or ventricular premature beat
❏ common mechanisms are AV nodal reentry and accessory tract reentry
❏ atrioventricular nodal tachycardia (AVNRT) accounts for 60-70% of all SVTs
❏ retrograde P waves may be seen but are usually lost in the QRS complex
❏ treatment
• acute: Valsalva or carotid massage (check first for bruits), adenosine especially if associated
with WPW (adenosine is 1st choice if unresponsive to vagal maneuvers); if no response, try
metoprolol, digoxin, verapamil; DC shock if signs of cardiogenic shock, angina, or CHF
• chronic: ß blocker, verapamil, Digoxin, anti-arrhythmic drugs, EPS catheter ablation
2. VENTRICULAR TACHYARRHYTHMIAS
Premature Ventricular Contraction (PVC) or Ventricular Premature Beats (VPB)
❏ QRS width greater than 0.12 seconds, no preceding P wave, bizarre QRS morphology
❏ premature in the cardiac cycle, may be followed by a prolonged pause (compensatory)
❏ origin: LBBB pattern = RV site; RBBB pattern = LV site
❏ rules of malignancies with PVC’s
• frequent, (> 10/hour), consecutive (≥ 3 = VT) or multiform (varied origin)
• PVC’s falling on the T wave of the previous beat ("R on T phenomenon"):
vulnerable time in cycle with risk of VT or V fib )
❏ PVCs in isolation not treated, as risks not altered, no effect on mortality
❏ treatment: since no evidence to suggest that treatment decreased mortality,
PVCs are not usually treated
❏ consider ß blockers if symptomatic palpitations

Accelerated Idioventricular Rhythm

❏ benign rhythm - originates in terminal Purkinje system or ventricular myocardium
❏ represents a ventricular escape focus that has accelerated sufficiently to drive the heart
❏ Etiology: sometimes seen during acute MI (especially during reperfusion) or Digoxin toxicity
❏ regular rhythm, rate 50-100 bpm
❏ rarely requires treatment
❏ treatment: if symptomatic, lidocaine, atropine
Ventricular Tachycardia (VT)
❏ a run of three or more consecutive PVCs rate > 100 minute is called VT
❏ etiology
• note: only with memomorphic VT
• CAD with MI is most common underlying cause
❏ sustained VT (longer than 30 seconds) is an emergency, prestaging cardiac arrest and requiring
immediate treatment
❏ rate 120-300 bpm
❏ broad QRS, AV dissociation, fusion beats, capture beats, left axis deviation, monophasic or
biphasic QRS in V1 with RBBB, concordance V1-V6
❏ fusion beat
• occurs when an atrial impulse manages to slip through the AV node at the same time
that an impulse of ventricular origin is spreading across the ventricular myocardium
• the two impulses jointly depolarize the ventricles producing a hybrid QRS complex
that is morphologically part supraventricular and part ventricular
❏ capture beat
• occurs when an atrial impulse manages to “capture” the ventricle and get a normal QRS
❏ treatment (for acute sustained VT)
• hemodynamic compromise – DC cardioversion
• no hemodynamic compromise - DC shock, lidocaine, amiodarone,
type Ia agents (procainamide, guinidine)
Ventricular Fibrillation (V fib)
❏ medical emergency; pre-terminal event unless promptly cardioverted
❏ most frequently encountered arrhythmia in adults who experience sudden death
❏ mechanism: simultaneous presence of multiple activation wavefronts within the ventricle
❏ no true QRS complexes - chaotic wide tachyarrhythmia without consistent identifiable QRS complex
❏ no cardiac output during V fib
❏ refer to ACLS algorithm for complete therapeutic guidelines
Torsades de Pointes
❏ polymorphic VT - means "twisting of the points"
❏ looks like VT except that QRS complexes rotate around the baseline changing their axis and amplitude
❏ ventricular rate greater than 100, usually 150-300
❏ etiology: seen in patients with prolonged QT intervals
• congenital long QT syndromes
• drugs - e.g. Class IA (quinidine), Class III (sotalol), phenothiazines (TCAs), erythromycin
• electrolyte disturbances - hypokalemia, hypomagnesemia
• other - nutritional deficiencies
❏ treatment: IV magnesium, temporary pacing, isoproterenol and correct underlying cause
of prolonged QT, DC cardioversion if hemodynamic compromise present

Table 6. Differentiation of VT vs. SVT with Aberrant Conduction*

VT SVT
Clinical Clues
carotid massage no response may terminate
cannon “a” waves may be present not seen
neck pounding may be present not seen
ECG Clues
AV dissociation may be seen not seen
fusion beats may be seen not seen
initial QRS deflection may differ from same as normal
normal QRS complex QRS complex
axis extreme axis deviation normal or mild deviation
* if patient > 65, presence of previous MI or structural heart disease then chance of VT > 95%
PREEXCITATION SYNDROMES
Wolff-Parkinson-White (WPW) Syndrome
❏ bypass pathway called the Bundle of Kent connects the atria and ventricles
❏ congenital defect, present in 3:1.000
❏ criteria (delta wave)
• PR interval is less than 0.12 seconds
• wide QRS complex due to premature activation
• repolarization abnormalities
• delta wave seen in leads with tall R waves
• slurred initial upstroke of QRS complex
❏ the two tachyarrhythmias most often seen in WPW are PSVT and A fib
❏ carotid massage, vagal maneuvers, and adenosine can enhance the
degree of pre-excitation by slowing AV nodal conduction
❏ note: if wide complex A fib, concern is that anterograde conduction is occurring down a bypass tract;
therefore do not use agents that slow AV conduction (e.g. Digoxin) as may increased conduction
through the bypass tract and precipitate V fib. In WPW and A fib use IV procainamide
Lown-Ganong-Levine Syndrome
❏ the PR interval is shortened to less than 0.12 seconds
❏ the QRS complex is narrow and there is no delta wave
PACEMAKER INDICATIONS
❏ SA node dysfunction
• symptomatic bradycardia
❏ AV nodal - infranodal block
• Mobitz II
• complete heart block
❏ symptomatic carotid sinus hypersensitivity
PACING TECHNIQUES
❏ temporary: transvenous (jugular, subclavian, femoral) or external pacing
❏ permanent: transvenous into RA, apex of RV or both; power
source implanted under clavicle
• can sense and pace atrium, ventricle or both
• new generation = rate responsive, able to respond to physiologic demand
❏ nomenclature e.g. “VVIR”
V - chamber paced : ventricle
V - chamber sensed : ventricle
I - action : inhibit
R - rate responsive

ISCHEMIC HEART DISEASE (IHD)
BACKGROUND
Epidemiology
❏ commonest cause of cardiovascular morbidity and mortality
❏ male: female ratio
• = 2:1 with all age groups included (Framingham study)
• = 8:1 < age 40
• = 1:1 > age 70
• disparity due to protective effect of estrogen
❏ peak incidence of symptomatic IHD is from ages 50 to 60 in men and ages 60 to 70 in women
❏ spectrum of IHD/CAD ranges anywhere from asymptomatic to sudden death
Atherosclerosis and IHD
❏ atherosclerosis and thrombosis are by far the most important pathogenetic mechanisms in IHD
Major Risk Factors For Atherosclerotic Heart Disease
❏ smoking
• risk can be halved by cessation of smoking
❏ diabetes mellitus (DM)
• micro and macrovascular complications
❏ hypertension (HTN)
• depends on degree and duration
❏ family history (FHx)
• first degree male relative < 55 or first degree female relative < 60
❏ hyperlipidemia
Other Minor Risk Factors
❏ obesity
• > 30% above ideal weight
❏ sedentary lifestyle
❏ hyperhomocysteinemia
Preventative Measures
❏ smoking cessation
❏ tight glycemic control in diabetics
❏ BP control
• major reason for the recent decrease in IHD
❏ lipid-modifying therapy
❏ dietary measures e.g. mild alcohol consumption
❏ weight loss
❏ exercise improves weight, HTN, cholesterol and glycemic control
❏ family screening (high risk groups)
ANGINA PECTORIS
Definition
❏ symptom complex resulting from an imbalance between oxygen supply and demand in the myocardium
Pathophysiology of Myocardial Ischemia
O2 O2
Demand Supply
Heart Rate Length of Diastole
Contractility Coronary Diameter
Wall Tension Hemoglobin
SaO2
Figure 9. Physiological Principles
Etiology
❏ decreased myocardial oxygen supply
• atherosclerotic heart disease (vast majority)
• coronary vasospasm (variant angina= Prinzmetal’s Angina)
• severe aortic stenosis or insufficiency
• thromboembolism
• severe anemia
• arteritis (e.g. Takayasu’s syndrome, syphilis, etc.)
• congenital anomalies
❏ increased myocardial oxygen demand

• myocardial hypertrophy
• severe tachycardia
• severe hyperthyroidism
• severe anemia
DDx
❏ musculoskeletal (MSK) disease
• rib fracture
• intercostal muscle tenderness
• costochondritis (Tietze’s syndrome)
• nerve root disease (cervical radiculitis)
❏ gastrointestinal (GI) disease
• peptic ulcer disease (PUD)
• reflux esophagitis
• esophageal spasm and motility disorder (may be improved by NTG)
❏ pulmonary disease
• pulmonary embolism (PE)
• pneumothorax
• pneumonia
❏ cardiovascular (CV) disease
• aortic dissection (asymmetrical BP and pulses, new AR murmur)
• pericarditis
❏ Other
• intercostal neuritis (shingles)
• anxiety
❏ note
• careful history and physical required
• consider risk factors for each entity
• beware cardiac and non-cardiac disease may coexist
Diagnosis of Angina Pectoris
❏ history
• classically precordial chest pain, tightness or discomfort radiating to left shoulder/arm/jaw
• dyspnea or fatigue may present as "chest pain equivalents," especially in females
• associated with diaphoresis or nausea
• predictably precipitated by the "3 E's" Exertion, Emotion and Eating
• brief duration, lasting < 10-15 minutes and typically relieved by rest
• note: always list the presence or absence of the cardiac risk factors in a separate subsection
in the history (e.g., + FHx, + HTN, +DM, + smoking, - hypercholesterolemia)
❏ stress testing (see Cardiac Diagnostic Tests section)
Variant Angina (Prinzmetal’s Angina)
❏ vasospasm of coronary arteries results in myocardial ischemia
• may occur in normal or atherosclerotic vessels
❏ typically occurs between midnight and 8 am
❏ unrelated to exercise; relieved by Nitrates
❏ typically ST elevation on ECG (may be confused with acute MI)
❏ diagnose by provocative testing with ergot vasoconstrictors (rarely done)
Syndrome X
❏ patient has typical symptoms of Angina yet has normal angiogram
❏ may show definite signs of ischemia during exercise testing
❏ pathogenesis thought to be due to inadequate vasodilator reserve of coronary resistance vessels
❏ has better prognosis than patient with overt atherosclerotic disease
Medical Treatment
• decrease overall mortality
• decrease heart rate, contractility, and to a lesser degree, blood pressure (afterload)
• increase coronary perfusion
• avoid agents with intrinsic sympathomimetic activity (ISA) (e.g. Acebutolol) (these increase demand)
❏ nitrates
• used for symptomatic control
• no clear impact on survival
• decrease myocardial work and, therefore, oxygen requirements
through venous dilatation (decrease preload) and arteriolar dilatation (decrease afterload)
• dilate coronary arteries
• maintain daily nitrate-free intervals to try to prevent nitrate tolerance
❏ calcium channel blockers (CCB)
• variably decrease afterload, decrease heart rate and decrease contractility, produce coronary dilatation
❏ ECASA
• all patients
• decrease platelet aggregation
❏ lipid lowering

Coronary Artery Disease (CAD) Lipid Therapy
Trial Drug Dose CHD Event Reduction
primary WOSCOPS pravastatin 40 31%

prevention AFCAPS lovastatin 20-40 24%
secondary LIPID pravastatin 40 23%
prevention 4S simvastatin 20-40 34%
CARE pravastatin 40 24%
2000 Canadian Guidelines for Treatment of Dyslipidemia

Target Values
Level of Risk LDL TC:HDL Ratio Tryglycerides
(Definition)
Very High
(History of cardiovascular < 2.5 <4 <2
disease or 10 yr risk of CAD > 30%)
High
(10 yr risk of CAD 20-30%) <3 <5 <2
Moderate
(10 yr risk 10-20%) <4 <6 <2
Low
(10 yr risk < 10%) <5 <7 <3
Risk calculated based on Framingham data: dertermined by gender, age group, total cholesterol level, HDL level, SBP, history of smoking
❏ treatment strategy
• short acting nitrates on PRN basis to relieve acute attacks
and PRN prior to exertion
• be careful when combining ß blockers and verapamil/diltiazem
• both decrease conduction and contractility and may result in sinus bradycardia or AV block
• use nitrates and CCB for variant angina
low likelihood intermediate likelihood high likelihood
non-nuclear otherwise healthy poor surgical candidate

with multiple co-morbidities
+
– nuclear stress testing nuclear stress testing
–
– + +
medical follow-up cath medical follow-up
low risk high risk
medical management PTCA, CABG
Figure 10. Diagnostic Strategies in the Management of IHD
Indications for Angiography

❏ strongly positive exercise test
❏ significant, reversible defects on thallium scan
❏ refractory to medical therapy or patient unable to tolerate medical therapy
❏ unstable angina

Percutaneous Transluminal Coronary Angioplasty (PTCA)

❏ uses a balloon inflated under high pressure to rupture atheromatous plaques
❏ may be used as primary therapy in angina, acute MI, post-MI angina or in patients presenting
with bypass graft stenosis
❏ optimally used for proximal lesions free of thrombus and distanced from the origins of large vessel branches –
not in Left Main
❏ primary success rate is > 80%
❏ use of intracoronary stent is associated with a lower restenosis rate (compared with PTCA alone)
❏ complications (overall 3-5%)
• mortality < 1%
• MI 3-5%
• intimal dissection + vessel occlusion requiring urgent CABG
Surgical Treatment- Coronary Artery Bypass Grafting (CABG)
❏ indications - for survival benefit, or symptomatic relief of angina
• stable angina (survival benefit for CABG shown)
• left main coronary disease
• three-vessel disease with depressed LV function
• multi-vessel disease with significant proximal LAD stenosis
• unstable angina (see below)
• above indications or
• continuing angina despite aggressive medical therapy
• complications/failed PTCA
❏ comparison of CABG with PTCA
• studies: RITA, GABI, BARI, EAST, ERACI, CABRI
• highly select patient population - no left main disease and minimal LV dysfunction
• overall no difference in survival, but PTCA group had more recurrent
ischemia and required more interventions
• BARI, subset analysis - CABG superior in patients with DM and multi-vessel IHD
❏ predictors of poor outcome
• poor LV function (EF < 40%), history of CHF, NYHA III or IV
• previous cardiac surgery
• urgent/emergent case, preoperative IABP
• gender (relative risk for F:M = 1.6:1)
• advanced age (> 70), DM, co-morbid disease
❏ CABG operative mortality
• elective case < 1%
• elective case, poor LV function 1-3%
• urgent case 1-5%
• overall (1980-1990) 2.2%
❏ efficacy: > 90% symptomatic improvement in angina
❏ conduits and patency
• internal mammary (thoracic) artery 90% patency at 10 years
• saphenous vein graft 50% patency at 10 years
• radial/gastroepiploic/inferior 85% patency at 5 years
epigastric arteries (improving with experience)
ACUTE CORONARY SYNDROMES (ACS)

Spectrum of ACS
A. Unstable Angina
B. Acute Myocardial Infarcion
C. Sudden Death
A. UNSTABLE ANGINA/NON ST ELEVATION MI (NSTEMI)
Definition
❏ accelerating pattern of pain
• increased frequency
• longer duration
• occurring with less exertion
• less responsive to treatment (eg. require higher doses or more frequent doses)
❏ angina at rest
❏ new onset angina
❏ angina post-MI
❏ post-angiography
❏ post-CABG
❏ note that unstable angina is a heterogeneous group and can be divided into a higher and lower risk groups

Significance
❏ thought to represent plaque rupture and acute thrombosis with incomplete vessel occlusion
Diagnosis
❏ history
❏ ECG changes
• ST depression or elevation
• T wave inversion
❏ no elevation of cardiac enzymes
Management
❏ oxygen
❏ hospitalization/monitoring
❏ bed rest
❏ anti-anginal medications
• sublingual or IV nitroglycerine
• ß blockers are first line therapy
• aim for resting heart rate of 50-60
• CCB are second line therapy (use if ß blockers contraindicated, or if patient has refractory symptoms
despite aggressive treatment with ECASA, nitrates, and ß blockers)
• evidence suggests that they do not prevent MI or decrease mortality
• be cautious using verapamil/diltiazem with ß blockers
• use non-dihydropyridines if cannot use ß blockers otherwise may use amlodipine
or long-acting nifedipine if concomitant ß blockade
❏ ECASA
• 160-325 mg/day
❏ IV heparin or Plavix (GPIIB/IIIA inhibitor)
❏ angiography with view to potential PTCA or CABG – used to map areas of ischemia
❏ if aggressive medical management is unsuccessful
• may use intra-aortic balloon pump (IABP) to stabilize before proceeding
with revascularization – used to increase coronary perfusion during diasole
• proceed to emergency angiography and PTCA or CABG
B. ACUTE ST ELEVATION MYOCARDIAL INFARCTION (STEMI)

Definition
❏ syndrome of acute coronary insufficiency resulting in death of myocardium
Infarct Diagnosis Based on 2 of 3 - History, ECG, Cardiac Enzymes
❏ history
• sudden onset of characteristic chest pain for > 30 minutes duration
• may be accompanied by symptoms of heart failure (e.g. SOB, leg edema, etc.)
❏ ECG changes
• criteria: ST elevation of at least 1 mm in limb leads and 2 mm in precordial leads
• evolution of ECG changes in Q-wave MI
• 1st – abnormal T waves
• 2nd – ST-T elevations (hours post-infarct)
• 3rd – significant Q waves (hours to days post-infarct)
• 4th – inverted T waves, or may become flat or biphasic (days to weeks)
❏ cardiac enzymes
• follow CK-MB q8h x 3, Troponin q8h x 3
❏ cardiac Troponin I and/or T levels provide useful diagnostic, prognostic information and permit early
identification of an increased risk of mortality in patients with acute coronary syndromes
• Troponin I and T remain elevated for 5 to 7 days
❏ beware
• up to 30% are unrecognized or "silent" due to atypical symptoms
• DM
• elderly
• patients with HTN
• post heart-transplant (because of denervation)
❏ draw serum lipids within 24-48 hours because the serum values are unreliable after 48 hours,
but become reliable again 8 weeks post-MI

Patient Evaluation “unstable angina”
history • physical exam • ECG • enzymes
ST elevation non ST elevation
presumed acute MI sample enzymes
assess for positive enzymes negative enzymes

thrombolysis acute MI
unstable angina non cardiac chest pain
Figure 11. Diagnostic algorithm in acute IHD
Etiology
❏ coronary atherosclerosis + superimposed thrombus on ruptured plaque (vast majority)
• vulnerable "soft" plaques more thrombogenic
❏ coronary thromboembolism
• infective endocarditis
• rheumatic heart disease
• intracavity thrombus
• cholesterol emboli
❏ severe coronary vasospasm
❏ arteritis
❏ coronary dissection
❏ consider possible exacerbating factors
• see Angina Pectoris section
Plasma
Enzyme CK-MB
Level x
Normal
ISCHEMIC
HEART DISEASE
. . . CONT.
DAYS POST-MI
Figure 12. Cardiac Enzyme Profile in Acute MI
Further Classification of MIs

❏ Q wave
• associated with transmural infarctions, involving full thickness of myocardium
❏ non-Q wave
• usually associated with non-transmural (subendocardial) infarctions,
involving 1/3 to 1/2 of myocardial thickness
• in-hospital mortality from non-Q wave infarction is low (< 5%)
but 1 year mortality approaches that of Q wave infarction
Management
❏ goal is to minimize the amount of infarcted myocardium and prevent complications
❏ emergency room measures
• ECASA 325 mg chewed stat
• oxygen
• sublingual nitroglycerine
• morphine for pain relief, sedation, and venodilation
• ß blockers to reduce heart rate if not contraindicated

❏ thrombolytic therapy (see Table 7)

• benefits of thrombolysis shown to be irrespective of age, sex, BP, heart rate, or history of MI or DM
• indications for thrombolytic therapy
A. at least 0.5 hours of ischemic cardiac pain and
B. any of the following ECG changes thought to be of acute onset
• at least 1 mm of ST elevation in at least two limb leads
• at least 1 mm of ST elevation in at least two adjacent precordial leads or
• new onset complete BBB
C. presentation within 12 hours of symptom onset
• choice of thrombolytic agents include streptokinase and rt-PA
• patients having previously received streptokinase must
receive alternate agent due to development of immunity
❏ heparin
❏ PTCA, CABG
Long-Term Measures
❏ antiplatelet/anticoagulation therapy
❏ ECASA 325 mg daily
❏ nitrates
• alleviate ischemia but may not improve outcome
• start immediately and continue indefinitely if no contraindications
❏ CCB
• NOT recommended as first line treatment - Short Acting Nifedipine is contraindicated!
• Diltiazam and Verapamil are contraindicated in MI with associated LV dysfunction
❏ ACEI
• stabilize endothelium and prevent adverse ventricular remodeling
• symptomatic CHF
• reduced LVEF (< 40%) starting day 3 to 16 post-MI (SAVE trial)
• anterior MI
❏ lipid lowering agent (HMG-C0A reductase inhibitors or niacin)
• if total cholesterol > 5.5 or LDL > 2.6
❏ coumadin (for 3 months)
• for large anterior MI, especially if LV thrombus seen on 2D-ECHO
❏ see Figure 13 for post critical care unit (CCU) strategy
Table 7. Contraindications to Thrombolytic Therapy in AMI
Absolute Relative
• active bleeding • GI, GU hemorrhage or stroke within past 6 months
• aortic dissection • major surgery or trauma within past 2-4 weeks
• acute pericarditis • severe uncontrolled hypertension
• cerebral hemorrhage • bleeding diathesis or intracranial neoplasm
(previous or current) • puncture of a noncompressible vessel
• significant chest trauma from CPR
❏ Indications for Post-thrombolysis Heparin
• tPA used for thrombolysis
• Anterior MI
• Ventricular aneurysm
• Post-thrombolysis angina
• A fib
• Previous deep vein thrombosis (DVT), PE, or ischemic stroke
Prognosis
❏ 20% of patients with acute MI die before reaching hospital
❏ 5-15% of hospitalized patients will die
• risk factors
• infarct size/severity
• age
• co-morbid conditions
• development of heart failure or hypotension
❏ post-discharge mortality rates
• 6-8% within first year, half of these within first 3 months
• 4% per year following first year
• risk factors
• LV dysfunction
• residual myocardial ischemia
• ventricular arrhythmias
• history of prior MI
• resting LVEF is most useful prognostic factor

Table 8. Complications of Myocardial Infarction

Complication Etiology Presentation Therapy
Arrhythmia
(a) tachycardia sinus, AF, VT, VF early/late see Arrhythmia section
(b) bradycardia sinus, AV block early
Myocardial
Rupture
(a) LV free wall transmural infarction 1-7 days pericardiocentesis or surgery
(b) papillary muscle inferior infarction 1-7 days surgery
(MR) anterior infarction
(c) ventricular septum septal infarction 1-7 days surgery
(VSD)
Shock/CHF LV/RV infarction within 48 hours fluids, inotropes, IABP
aneurysm
Post Infarct Angina persistent coronary stenosis anytime aggressive medical therapy
multivessel disease PTCA or CABG
Recurrent MI reocclusion anytime see above
Thromboembolism mural thrombus in Q wave 7~10 days, heparin, warfarin
infarction up to 6 months
Pericarditis post-MI 1-7 days NSAIDs
(Dressler's) autoimmune (Dressler’s) 2-8 weeks NSAIDs, steroids
Acute MI Risk Stratification
Cardiogenic Shock ST Elevation or LBBB No ST Elevation

Acute Phase
(5% - 10%) and Presentation ≤ 12 hours and Presentation > 12 hours

(25% - 45%) (50% - 70%)
Thrombolysis
CCU Phase
? Rescue PTCA, CABS

No Reperfusion Reperfusion
(19% - 45%) (55% - 81%)
Non-Acute Risk Stratification

In-Hospital Phase
High-Risk (30% - 35%) Intermediate/Low-Risk

• prior MI (65% - 70%)
• CHF
• Recurrent Ischemia
• High-Risk Arrhythmia Non-invasive Stress Testing
Cardiac Catheterization
Ischemia or Normal Results
Poor Functional Status
Cardiac Catheterization No further testing at this time

••Please note that Echocardiography is done routinely post-MI.
It is controversial whether an EF < 40% is by itself an indication for coronary angiography.
Figure 13. Acute MI and Predischarge Risk Stratification

C. SUDDEN DEATH
Definition
❏ unanticipated, non-traumatic death in a clinically stable patient, within 1 hour of symptom onset
❏ immediate cause of death is
• V fib (most common)
• ventricular asystole
Significance
❏ accounts for ~ 50% of CAD mortalities
❏ initial clinical presentation in up to 20% of patients with CAD
Etiology
❏ primary cardiac pathology
• ischemia/MI
• LV dysfunction
• severe ventricular hypertrophy
• AS
• QT prolongation syndrome
• congenital heart disease
❏ high risk patients
• multi-vessel disease
• LV dysfunction
Management
Acute
❏ resuscitate with prompt CPR and defibrillation
Long Term Survivors
❏ identify and treat underlying predisposing factors
❏ IHD
• cardiac catheterization to evaluate cardiac anatomy, LV function and need for revascularization
❏ Holter monitoring
❏ electrophysiologic studies
Treatment
❏ antiarrhythmic drug therapy
• amiodarone, ß blockers
❏ surgery
• revascularization to treat ischemia
• map-guided subendocardial resection
• cryoablation, radiofrequency ablation
❏ implantable cardioverter-defibrillator
Prognosis
❏ 1 year mortality post-resuscitation 20-30%
❏ predictors of recurrent cardiac arrest in the "survivor" of sudden cardiac death
• remote MI
• CHF
• LV dysfunction
• extensive CAD
• complex ventricular ectopy
• abnormal signal-averaged ECG
HEART FAILURE
❏ overall, CHF is associated with a 50% mortality rate at five years
❏ see Colour Atlas R3 and R4
Definitions and Terminology
❏ inability of heart to maintain adequate cardiac output to meet the demands of whole-body metabolism
and/or to be able to do so only from an elevated filling pressure(forward heart failure)
❏ inability of heart to clear venous return resulting in vascular congestion (backward heart failure)
❏ either the left side of the heart (left heart failure) or the right side of the heart (right heart failure) or both
(biventricular failure) may be involved
❏ there may be components of ineffective ventricular filling (diastolic dysfunction) and/or emptying
(systolic dysfunction)
❏ most cases associated with poor cardiac function (low-output heart failure) but some are not due to intrinsic
cardiac disease (high-output heart failure; this is discussed separately below)
❏ CHF is not a disease itself - it is a syndrome involving variable degrees of both forward and backward
heart failure
Pathophysiology
❏ two components
• primary insults initiating the disease process
• compensatory responses which exacerbate and perpetuate the disease process in chronic heart failure
Primary damage
• myocyte loss
• overload
Necrosis, apoptosis Stretch
Pump dysfunction
• DIG
Neurohumoral activation Ventricular remodeling
• ACEI • dilatation
• hypertrophy
• ACEI Edema, tachycardia
• ß-blockers vasoconstriction, congestion
• Diuretics
Figure 14. Pathogenesis of CHF CHF
Clinical Pearl
❏ What are the five commonest causes of CHF?
• coronary artery disease (60-70%)
• idiopathic (20%) often in the form of dilated cardiomyopathy
• valvular (e.g. AS, AR and MR)
• HTN
• alcohol (may cause dilated cardiomyopathy)
Etiologies of Primary Insults

❏ consider predisposing, precipitating and perpetuating factors
❏ the less common causes of CHF
• toxic e.g. adriamycin, doxorubicin, radiation, uremia, catecholamines
• infectious e.g. Chagas disease(very common cause worldwide), Coxsackie, HIV
• endocrine e.g. hyperthyroidism, DM, acromegaly
• infiltrative e.g. sarcoidosis, amyloidosis, hemochromatosis
• genetic e.g. hereditary hypertrophic cardiomyopathy, Freidriech’s Ataxia
• metabolic e.g. thiamine deficiency, selenium deficiency
• peripartum
❏ precipitants (H-E-A-R-T F-A-I-L-E-D)
• H - HTN (common)
• E - endocarditis/environment (e.g. heat wave)
• A - anemia
• R - rheumatic heart disease and other valvular disease
• T - thyrotoxicosis
• F - failure to take meds (very common)
• A - arrhythmia (common)
• I - infection/ischemia/infarction (common)
• L - lung problems (PE, pneumonia, COPD)
• E - endocrine (pheochromocytoma, hyperaldosteronism)
• D - dietary indiscretions (common)
❏ it is important to differentiate an exacerbation due to a reversible
cause from progression of the primary disease for treatment and prognosis
COMPENSATORY RESPONSES IN HEART FAILURE
❏ cardiac response to myocardial stress
• pressure overload results in hypertrophy (e.g. HTN)
• volume overload results in cardiac dilatation (e.g. AR)
❏ systemic response to ineffective circulating volume
• activation of sympathetic nervous and renin-angiotensin systems result in
• salt and H2O retention with intravascular expansion
• increased increased heart rate and myocardial contractility
• increased afterload
❏ “compensated” heart failure becomes “decompensated” as cardiac and systemic responses overshoot
❏ treatments are directed at these compensatory overshoots
SYSTOLIC vs. DIASTOLIC DYSFUNCTION

Systolic Dysfunction (impaired ejection of blood from the heart)
❏ impaired myocardial contractile function
❏ hallmark is impaired stroke volume and/or ejection fraction
❏ symptoms predominantly due to decreased cardiac output
❏ examples
• MI
• myocarditis
• dilated cardiomyopathy
Diastolic Dysfunction (defect in ventricular filling)
❏ 1/3 of all patients evaluated for clinical diagnosis of heart failure have normal systolic function
(ejection fraction (EF))
❏ ability of LV to accept blood is impaired due decreased compliance
• transiently by ischemia
• permanently by severe hypertrophy (HTN, AS), infiltrative disease, MI (due to scarring) or HCM
❏ ischemia causes stiffness of LV because relaxation of myocardium is active and requires energy/ATP
• increased LV filling pressures produce venous congestion upstream
(i.e. pulmonic and systemic venous congestion)
❏ clues to diagnosis: S4, HTN, LVH on ECG/ECHO, normal-size heart on CXR, normal EF
❏ apex beat sustained but not displaced
• treatment: ß blockers, verapamil, diltiazem or ACEI
Table 9. Signs and Symptoms of L vs. R Heart Failure
Left Failure Right Failure
low cardiac output fatigue TR
(forward) syncope S3 (right-sided)
systemic hypotension
cool extremities
slow capillary refill
peripheral cyanosis
MR
Cheyne-Stokes breathing
pulsus alternans
S3
venous congestion dyspnea peripheral edema
(backward) orthopnea hepatomegaly
PND hepatic tenderness
basal crackles pulsatile liver
cough increased JVP
hemoptysis positive HJR
Kussmaul’s sign
SLEEP-DISORDERED BREATHING
❏ 45-55% of patients with CHF (systolic and diastolic heart failure) have sleep disturbances, which include
Cheyne-Stokes breathing, central and obstructive sleep apnea
❏ associated with a worse prognosis and greater LV dysfunction
❏ nasal continuous positive airway pressure (CPAP) is effective in treating Cheyne-Stokes respiration/sleep
apnea with improvement in cardiac function and symptoms
HIGH-OUTPUT HEART FAILURE
❏ a variety of factors may create a situation of relative heart failure by
demanding a greater than normal cardiac output for a variety of reasons
❏ rarely causes heart failure in itself but often exacerbates existing heart
failure or puts a patient with other cardiac pathology "over the edge"
❏ DDx: anemia, thiamine deficiency, hyperthyroidism, A-V fistula, Paget's disease of bone
Investigations
❏ work up involves assessment for precipitating factors and treatable causes of CHF
❏ blood work
• CBC (increased WBC - possible infectious precipitant;
decreased Hb - anemia as a precipitant/exaccerbating factor)
• electrolytes
• dilutional (hypervolemic) hyponatremia indicates end-stage CHF
• sign of neurohormonal activation and poorer prognosis
• hypokalemia secondary to high renin state
• BUN, Cr
• may be elevated due to prerenal insult
• be wary of ATN with diuretic therapy
❏ ECG
• chamber enlargement
• abnormal rhythms
• ischemia/infarction
❏ chest x-ray
• signs of pulmonary congestion
• peribronchiolar cuffing
• vascular redistribution
• Kerley B Lines
• interstitial pattern
• fluid in lung fissures
• alveolar filling if gross pulmonary edema
• also look for
• cardiomegaly (cardiac/thoracic (C/T) > 0.5)
• atrial enlargement
• pleural effusion
❏ echocardiography is the primary diagnostic method to determine
• EF (LV Grade I (EF = 60%), II (40-59%), III (21-39%), IV (= 20%)
• atrial or ventricular dimensions
• wall motion abnormalities
• valvular stenosis or regurgitation
❏ radionuclide angiography (MUGA) provides more accurate ejection fraction measurements
than echocardiography; however, it provides little information on valvular abnormalities
❏ myocardial perfusion scintigraphy (Thallium or Sestamibi SPECT)
• determines areas of fibrosis/infarct or viability
❏ angiogram in selected patients
Long-term Management of CHF
❏ short term goals of therapy are to relieve symptoms and improve the quality of life
❏ long term goal is to prolong life by slowing, halting, or reversing the progressive LV dysfunction
❏ treat the cause/aggravating factors
❏ symptomatic measures
• oxygen, bed rest, elevation of head of bed
❏ control of sodium and fluid retention
• sodium restriction (2 gm/d), requires patient education
• fluid restriction and monitor daily weights
• diuretics - for symptom control, mortality benefit demonstrated with spironolactone (RALES study)
• furosemide (40-500 mg/day) for potent diuresis
• metalozone may be used with furosemide to increase diuresis
❏ vasodilators
• goal is to arteriodilate (decrease afterload) and venodilate (increase preload),
thereby improving cardiac output and venous congestion
• in hospital, monitor response to therapy with daily weights and
measurement of fluid balance and follow renal function
• ACEI: standard of care (improves survival)
• all symptomatic patients
• all asymptomatic patients with LVEF < 35%
• post-MI setting if
• symptomatic heart failure
• asymptomatic LVEF < 40%
• anterior MI
• clearly shown to decrease mortality and slow progression in these settings
• hydralazine and nitrates
• second line to ACEI
• decrease in mortality not as great as with ACEI
• amlodipine
• may be of benefit in dilated cardiomyopathy
• angiotensin II receptor blockers e.g. losartan
• preliminary evidence suggests benefit
❏ inotropic support
• digitalis
• inhibits Na/K ATPase leading to decreased Na/Ca exchange and increased intracellular [Ca2+],
hence increasing myocardial contractility
• improves symptoms and decrease hospitalizations (DIG trial);
patients on digitalis glycosides may worsen if these are withdrawn
• no impact on survival
• excellent choice in setting of CHF with atrial fibrillation

❏ other agents
• ß blockers - recommended for functional class (FC) II-III patients
• should be used cautiously, titrate slowly because may initially worsen CHF
• postulated that these agents interfere with neurohormonal activation
• carvedilol confers survival benefit in FC II-III CHF
• metoprolol has been shown to delay time to transplant, decreased hospitalizations in dilated
cardiomyopathy and to decrease mortality (MERIT study)
• CCB (have equivocal effect on survival)
• antiarrhythmic drugs
• if required, amiodarone is drug of choice
• class I anti-arrhythmics associated with increased mortality in CHF
ACUTE CARDIOGENIC PULMONARY EDEMA
Definition
❏ left-sided backward heart failure leading to severe pulmonary congestion with extravasation of capillary fluid
into the pulmonary interstitium and alveolar space
❏ tachycardia, tachypnea, diaphoresis
❏ severe left-sided venous congestion
Management, use mnemonic "LMNOP"
❏ make sure to treat any acute precipitating factors (e.g. ischemia, arrhythmias)
❏ sit patient up with legs hanging down if blood pressure is adequate
❏ L - Lasix - furosemide 40 mg IV, double dose q1h as necessary
❏ M - Morphine 2-4 mg IV q5-10 minutes
• decreased anxiety
• vasodilation
❏ N - Nitroglycerine topical 2 inches q2h (or IV)
❏ O - Oxygen
❏ P - Positive airway pressure
• (CPAP or BiPAP) decreased need for ventilation and decreased preload
❏ other vasodilators as necessary in ICU setting
• nitroprusside (IV)
• hydralazine (PO)
• sympathomimetics
• potent agents used in ICU/CCU settings
• dopamine
• agonist at dopamine D1 (high potency), ß1-adrenergic (medium potency),
and α1-adrenergic receptors (low potency)
• "low-dose" causes selective renal vasodilation (D1 agonism)
• "medium-dose" provides inotropic support (ß1 agonism)
• "high-dose" increase systemic vascular resistance (SVR),
which in most cases is undesirable (α1 agonism)
• dobutamine
• acts at ß1 and α1 adrenoceptors
• selective inotropic agent (ß1 agonism)
• also produces arterial vasodilation (α1 antagonism)
• phosphodiesterase inhibitors (amrinone, Inocor)
• effects similar to dobutamine (inhibits PDE ––> cAMP ––>
inotropic effect and vascular smooth muscle relaxation (decrease SVR)
• adverse effect on survival when used as long-term oral agent
❏ inotropic support (dopamine, dobutamine) if necessary
❏ consider PA line to monitor capillary wedge pressure
❏ consider mechanical ventilation if needed
❏ rarely used but potentially life-saving measures
• rotating tourniquets
• phlebotomy
❏ indications - end stage cardiac disease (CAD, DCM, etc.)
• failure of maximal medical/surgical therapy
• poor 6 month prognosis
• absence of contraindications
• ability to comprehend and comply with therapy
❏ 1 year survival 85%, 5 year survival 70%
❏ complications: rejection, infection, graft vascular disease, malignancy

CARDIOMYOPATHIES
Definition
❏ intrinsic myocardial disease not secondary to CAD, valvular heart
disease, congenital heart disease, HTN or pericardial disease
❏ The diagnosis of any of the following mandates exclusion of the above conditions:
• dilated cardiomyopathy (DCM)
• restrictive cardiomyopathy (RCM)
• myocarditis
DILATED CARDIOMYOPATHY
Etiology
❏ idiopathic (risk factors: male, black race, family history)
❏ alcohol
❏ inflammatory (subsequent to myocarditis)
❏ collagen vascular disease: SLE, PAN, dermatomyositis, progressive systemic sclerosis
❏ infectious: post-viral (Coxsackie), Chagas disease, Lyme disease, Rickettsial diseases, acute rheumatic fever
❏ neuromuscular disease: Duchenne muscular dystrophy, myotonic dystrophy, Friedreich ataxia
❏ metabolic: uremia, nutritional deficiency (thiamine, selenium, carnitine)
❏ endocrine: thyrotoxicosis, DM
❏ familial
❏ peripartum
❏ toxic: cocaine, heroine, glue sniffing, organic solvents
❏ radiation induced
❏ drugs: chemotherapeutics (adriamycin)
Pathophysiology
❏ clinical manifestations
• CHF
• systemic or pulmonary emboli
• arrhythmias
• sudden death (major cause of mortality due to fatal arrhythmia)
Investigations
❏ 12 lead ECG
• ST-T wave abnormalities
• poor R wave progression
• conduction defects (e.g. BBB)
• arrhythmias
❏ chest x-ray
• global cardiomegaly (globular heart)
• signs of CHF
• 4-chamber enlargement
• depressed ejection fraction
• MR and TR secondary to cardiac dilatation
❏ endomyocardial biopsy: not routine, used to diagnose infiltrative RCM and myocarditis,
or to rule out a treatable cause
❏ angiography: selected patients
Natural History
❏ prognosis
• depends on etiology
• generally inexorable progression
• overall once CHF - 50% 5 year survival
• cause of death usually CHF or sudden death
• systemic emboli are significant source of morbidity
Management
❏ treat underlying disease - e.g. abstinence from EtOH
❏ treat CHF (see Heart Failure section), ß blockade (e.g. metoprolol, carvedilol)
and ACEI (+/– AII receptor inhibitors) to decrease remodeling
❏ anticoagulation to prevent thromboembolism (coumadin)
• absolute - A fib, history of thromboembolism or documented thrombus
• clinical practice is to anticoagulate if EF < 20%
❏ treat symptomatic or serious arrhythmias
❏ immunize against influenza and pneumococcus
❏ surgical therapy
• cardiac transplant - established definitive therapy
• LVAD
• volume reduction surgery (role remains unclear)
• cardiomyoplasty (latissimus dorsi wrap)

HYPERTROPHIC CARDIOMYOPATHY (HCM)

Pathophysiology
❏ defined as unexplained ventricular hypertrophy (not due to systemic HTN or AS). Histopathologic
features are myocardial fiber disarray, myocyte hypertrophy, and interstitial fibrosis
❏ cause is felt to be a genetic defect involving 1 of the cardiac sarcomeric proteins
(> 100 mutations associated with development of autosomal dominant inheritance)
• asymptomatic
• dyspnea
• angina
• presyncope/syncope- LV outflow obstruction or arrhythmia
• CHF
• arrhythmias
• sudden death (may be first manifestation)
Henodynamic Classification
❏ hypertrophic obstructive cardiomyopathy (HOCM): dynamic outflow tract (LVOT) obstruction
• either resting or provocable LVOT obstruction
❏ nonobstructive hypertrophic cardiomyopathy: decreased compliance and diastolic dysfunction
(impaired filling)
❏ complications: obstruction, arrhythmia, diastolic dysfunction
Hallmark Signs of HOCM
❏ pulses
• rapid upstroke pulse
• bifid pulse
• PMI: localized, sustained, double impulse, ‘triple ripple’ (triple apical impulse)
• normal or paradoxically split S2
• S4
• harsh, systolic, diamond-shaped murmur at LLSB or apex, enhanced by squat to standing or valsalva
(murmur secondary to LVOT obstruction and asociated mitral regurgitation)
Table 10. Factors Influencing Obstruction in Hypertrophic Cardiomyopathy
Increased Obstruction Decreased Obstruction
(decreased murmur) (decreased murmur)
inotropes, vasodilators, diuretics negative inotropes

hypovolemia vasoconstrictors
tachycardia volume expansion
squat to standing position bradycardia
Valsalva maneuver squatting from standing position
Amylnitrite inhalation sustained handgrip (isometrics)
Investigations
❏ 12 lead ECG
• LVH
• prominent Q waves or tall r wave in V1
• LVH - asymmetric septal hypertrophy (most common presentation)
• systolic anterior motion (SAM) of anterior MV leaflet
• resting or dynamic ventricular outflow tract obstruction
• MR (due to SAM and associated with LVOT obstruction)
• diastolic dysfunction
• LAE
• increased LV end-diastolic pressure
• variable systolic gradient across LV outflow tract
Natural History
❏ variable
❏ potential complications: A fib, VT, CHF, sudden death
❏ risk factors for sudden death
• most reliable
• history of survived cardiac arrest/sustained VT
• family history of multiple sudden deaths
• other factors associated with increased risk of sudden cardiac death (SCD)
• syncope
• VT on ambulatory monitoring
• marked ventricular hypertrophy
• prevention of sudden death in high risk patients
= amiodarone or implantable cardioverter defibrillator (ICD)

Management
❏ avoid extremes of excertion
❏ avoid factors which increase obstruction
❏ infective endocarditis prophylaxis for patients with obstructive HCM
❏ treatment of obstructive HCM
• medical agents
• ß blockers
•disopyramide
• CCB only used in patients with no resting/provocable obstruction
• patients with drug-refractory symptoms
• options
1. surgical myectomy
2. septal ethanol ablation
3. dual-chamber pacing
❏ treatment of ventricular arrhythmias - AMIO or ICD
❏ adult first-degree relatives of patients with HCM should be screened (physical exam, ECG, 2D-ECHO)
serially every 5 years
RESTRICTIVE CARDIOMYOPATHY (RCM)
Etiology
❏ infiltrative
• amyloidosis (especially in primary amyloidosis associated with light chain disease), sarcoidosis
❏ non-infiltrative
• scleroderma, idiopathic myocardial fibrosis
❏ storage diseases
• hemochromatosis (especially in DM, cirrhosis), Fabry's disease, glycogen storage diseases
❏ endomyocardial
• endomyocardial fibrosis (Africans), eosinophilic: Loeffler's endocarditis or eosinophilic
endomyocardial disease
• radiation heart disease
• pseudoxanthoma elasticum
• carcinoid syndrome (associated TV or PV dysfunction)
Pathophysiology
❏ infiltration of the myocardium ––> decreased ventricular compliance ––> diastolic dysfunction
• CHF - diastolic dysfunction predominates
• arrhythmias
Investigations
❏ 12 lead ECG
• low voltage
• non-specific, diffuse ST-T wave changes (no correspondence with vascular territory)
+/– nonischemic Q waves
❏ chest x-ray
• mild cardiac enlargement
• normal pericardium, normal or only slightly decreased systolic function,
impaired ventricular filling and diastolic dysfunction
• end-diastolic ventricular pressures
❏ endomyocardial biopsy to distinguish etiology (especially for infiltrative RCM)
Natural History
❏ depends on etiology
❏ generally poor prognosis
Management
❏ exclude constrictive pericarditis
❏ treat underlying disease
❏ supportive care
❏ treat coexisting CHF, arrhythmias
❏ anticoagulation
❏ consider cardiac transplantation - depending on etiology

MYOCARDITIS
❏ inflammatory process involving the myocardium (an important cause of dilated cardiomyopathy)
Etiology
❏ idiopathic
❏ infectious
• viral: Coxsackie virus B, Echovirus, Poliovirus, HIV, mumps
• bacterial: S. aureus, C. perfringens, C. diphtheriae, Mycoplasma, Rickettsia
• fungi
• spirochetal (Lyme disease – Borrelia burgdorferi)
• Chagas disease (Trypanosoma cruzi), toxoplasmosis
❏ acute rheumatic fever (Group A ß-hemolytic Streptococcus)
❏ drug-induced: emetine, doxorubicin
❏ collagen vascular disease: systemic lupus erythematosus (SLE), polyarteritis nodosa (PAN),
rheumatoid arthritis (RA), dermatomyositis (DMY)
❏ sarcoidosis
❏ giant cell myocarditis
❏ constitutional illness
❏ acute CHF
❏ chest pain - associated pericarditis or cardiac ischemia
❏ arrhythmias (may have associated inflammation of conduction system)
❏ systemic or pulmonary emboli
❏ sudden death
Investigations
❏ 12 lead ECG
• non-specific ST-T changes +/– conduction defects
❏ blood work
• increased CK, Troponin, LDH, and AST with acute myocardial necrosis
+/– increased WBC, ESR, ANA, rheumatoid factor, complement levels
❏ perform blood culture, viral titers and cold agglutinins for Mycoplasma
❏ chest x-ray
• enlarged cardiac silhouette
• dilated, hypokinetic chambers
• segmental wall motion abnormalities
Natural History
❏ usually self-limited and often unrecognized
❏ most recover
❏ may be fulminant with death in 24-48 hours
❏ sudden death in young adults
❏ may progress to dilated cardiomyopathy
❏ few may have recurrent or chronic myocarditis
Management
❏ supportive care
❏ restrict physical activity
❏ treat CHF
❏ treat arrhythmias
❏ anticoagulation
❏ treat underlying cause if possible

VALVULAR HEART DISEASE
❏ see Cardiac Surgery Chapter
INFECTIVE ENDOCARDITIS (IE)

Etiology
❏ Strep viridans (commonest, spontaneous bacterial endocarditis (SBE) on abnormal valve – prosthetic, MVP, etc.)
❏ Enterococcus (Group D strep, SBE)
❏ Staph aureus (enter through break in skin: IV drug abusers, usually rightsided, catheter-associated sepsis)
❏ Staphylococcus epidermidis (prosthetic valve)
❏ Strep bovis (underlying GI malignancy)
❏ others: gram-negative bacteria, Candida, HACEK organisms (Haemophilus species, Actinobacillus
actinomycetemcomitans, Cardiobacterium hominis, Eikenella, and Kingella), Pseudomonas (IV drug)
❏ frequency of valve involvement: MV >> AV > TV > PV
❏ risk of IE in various cardiac lesions (JAMA 1997;227:1794)
• high risk: prosthetic heart valves, previous IE, complex cyanotic congenital heart disease,
surgically constructed systemic to pulmonary shunts or conduits
• moderate risk: most other congenital cardiac malformations, acquired valvular dysfunction,
HCM, MVP with MR and/or thickened leaflets
Pathogenesis and Symptomatology
❏ usually requires source of infection, underlying valve lesion, +/– systemic disease/immunocompromised state
❏ portal of entry: oropharynx, skin, GU, drug abuse, nosocomial infection ––> bacteremia ––>
diseased valve/high flow across valve ––> turbulence of blood across valve ––>
deposition of bacteria on endocardial surface of valve
(vegetation = clump of fibrin, platelets, WBCs and bacteria) ––> endocarditis ––> septic embolization
❏ symptoms
• fever, chills, rigors
• night sweats
• 'flu-like' illness, malaise, headaches, myalgia, arthralgia
• dyspnea, chest pain
Signs
❏ fever, regurgitant murmur (new onset or increased intensity), constitutional symptoms, anemia
❏ signs of CHF (secondary to acute MR, AR)
❏ peripheral manifestations: petechiae, Osler's nodes ("ouch!" raised, painful, 3-15 mm, soles/palms),
Janeway lesions ("pain away!" flat, painless, approx. 1-2 cm, on soles/plantar surfaces of toes/palms/fingers),
splinter hemorrhages (especially on proximal nail bed, distally more commonly due to local trauma)
❏ CNS: focal neurological signs (CNS emboli), retinal Roth spots
❏ clubbing (subacute)
❏ splenomegaly (subacute)
❏ microscopic hematuria (renal emboli or glomerulonephritis) ± active sediment
❏ weight loss
Investigations
❏ blood work: anemia, uncreased ESR, positive rheumatoid factor
❏ serial blood cultures (definitive diagnosis)
❏ echocardiography (transesophageal > sensitivity than transthoracic)
• vegetations, degree of regurgitation valve leaflet perforation, abscess
• serial ECHO may help in assessing cardiac function
Natural History
❏ adverse prognostic factors
• CHF, Gram (–) or fungal infection, prosthetic valve infection, abscess
in valve ring or myocardium, elderly, renal failure, culture negative IE
❏ mortality up to 30%
❏ relapses may occur - follow-up is mandatory
❏ permanent risk of re-infection after cure due to residual valve scarring
Complications
❏ CHF (usually due to valvular insufficiency)
❏ systemic emboli
❏ mycotic aneurysm formation
❏ intracardiac abscess formation leading to heart block
❏ renal failure: glomerulonephritis due to immune complex deposition; toxicity of antibiotics

Management
❏ medical
❏ surgical
RHEUMATIC FEVER
Epidemiology
Etiology
Diagnosis
• major criteria
• pancarditis
• polyarthritis
• minor criteria
• polyarthralgia
• fever
plus
Clinical Features
Management
AORTIC STENOSIS
Etiology
❏ acquired
Definition
LV dysfunction
Pathophysiology
Symptomatology
Signs of AS
❏ pulses
• ejection click
Investigations
❏ 12 lead ECG
❏ chest x-ray
❏ ECHO
Natural History
Management
• IE prophylaxis
• AV replacement

AORTIC REGURGITATION (AR)

Etiology
❏ supravalvular (aortic root disease with dilatation of ascending aorta)
• atherosclerotic dilatation and aneurysm; cystic medial necrosis annuloaortic ectasia (Marfan syndrome);
dissecting aortic aneurysm; systemic HTN; (idiopathic Aortic root dilation); syphilis; connective tissue
diseases (ankylosing spondylitis, psoriatic arthritis, Reiter syndrome, rheumatoid aortitis)
❏ valvular
• congenital abnormalities (bicuspid AV, large VSD); connective tissue diseases (SLE, rheumatoid
arthritis, etc.); rheumatic fever (+/– associated AS); IE; myxomatous degeneration; deterioration of
prosthetic valve
❏ acute AR
• IE
• trauma
• acute rheumatic fever
• failed prosthetic valve
Pathophysiology and Symptomatology
❏ AR = blood flow from aorta back into LV (diastolic run-off)
❏ volume overload ––> LV dilatation ––> increased SV and more diastolic run-off
––> high SBP and low DBP (wide pulse pressure)
❏ LV dilatation combined with increased SBP ––> increased wall tension = pressure overload ––> LVH
• symptoms
• dyspnea/orthopnea/PND
• fatigue and palpitations (arrhythmias or hyperdynamic circulation)
❏ decreased DBP ––> decreased coronary perfusion; LVH ––> increased myocardial O2 demand
• symptoms
• syncope, angina (only if severe AR)
❏ usually symptomatic only after onset of LV failure (late in disease), LAE presents earlier onset of symptoms
Signs of chronic AR
❏ pulses
• increased volume, Waterhammer (bounding and rapidly collapsing)
• Bisferiens pulse - twice beating in systole; occurs inpresence of combined AS and AR
• de Musset's sign - head bobbing due to increased PP
• pistol-shot sounds over femoral artery (without compression)
• Traube’s sign: double sound heard with the stethoscope lightly applied over the artery
• Quincke's sign - pulsatile blushing of nail beds (nonspecific)
• Corrigan's pulse - visible carotid pulse
• Hill's test:- femoral-brachial SBP difference > 20 (greater differences correlate with more severe AR)
• Duroziez’s test: light proximal compression of femoral artery produces systolic-diastolic murmur over
femoral artery
• other - pulsating uvula (Mueller), liver (Rosenbach), pupil (Gandolfi), or spleen (Gerhard)
• heaving apex (hyperdynamic), displaced point of maximal impulse (PMI) (volume overload)
• S1 - soft in severe AR (early closure of MV)
• S2 - soft or absent (severe AR), may be loud if calcified
• S3 in severe AR (early LV decompensation)
• early diastolic decrescendo murmur (EDM) - high-pitched, at LLSB (cusp disease) or RLSB
(aortic root disease), length correlates with severity, best heard with patient sitting, leaning
forward on full expiration
• systolic ejection murmur (SEM) (physiologic, high flow murmur)- in aortic area
• Austin Flint murmur - diastolic rumble at apex, secondary to regurgitant jet on anterior MV leaflet
❏ acute AR - most of these signs are absent (SV not yet increased)
• patient usually presents in CHF, tachycardia, soft S1, soft or absent S2, short early diastolic murmur,
preclosure of MV (ECHO)
Investigations
❏ 12 lead ECG
• LVH, LAE
❏ chest x-ray
• LV enlargement, LAE, aortic root dilatation
❏ echocardiography (TTE)
• gold standard for diagnosis and assessment of severity of AR
• regurgitant jet from aorta into LV
• association of aortic leaflet morphology, LV size, LVF, aortic root size
• fluttering of anterior MV leaflet
• Doppler most sensitive
❏ radionuclide imaging
• serial resting and exercise EF (normal increased with exercise > 5%)
for serial monitoring of patients with asymptomatic severe AR
• sensitive sign of decreased LV function: failure to increase EF with exercise
• coronary angiography indicated if age > 40
• increased LV volume; CO normal or decreased (LV dysfunction); increased LVEDP

Natural History
❏ mild to moderate AR - few symptoms
❏ chronic progression to severe AR (may be asymptomatic more than 10 years)
❏ once symptomatic, prognosis is much worse
• mean mortality 4 years after onset of angina, 2 years after CHF
❏ severe acute AR - only 10-30% live more than 1 year after diagnosis
❏ late complications: arrhythmias, CHF, IE
Management
❏ asymptomatic
• follow with serial ECHO - assess LV size and function
• +/– afterload reduction: nifedipine, ACE inhibitors
• IE prophylaxis
❏ medical
• restriction of activities
• treat CHF (non-pharmacological, afterload reduction, Digoxin, and diuretics)
• acute AR: may stabilize with IV vasodilators before surgery
❏ surgical
• acute AR leading to LV failure - best treated surgically
• chronic severe AR - indications for surgery (generally operate prior to onset of irreversible
LV dysfunction):
• symptomatic patients with chronic severe AR
• progression of LV dilatation
• consider if poor LVEF (< 55%) at rest, or failure to increase EF with exercise (with serial MUGA
assessment)
• AV replacement
• mechanical, bioprosthetic, homograft, or sometimes pulmonary autograft
(Ross procedure) valve may be used
• valve repair (rare in AR)
• subcommissural annuloplasty for annular dilatation
MITRAL STENOSIS
Etiology
❏ congenital (rare)
❏ acquired
• RHD (most common) (especially developing nations; F > M):
❏ normal MV area = 4-6 cm2, hemodynamically significant MS with MV orifice < 2 cm2
❏ MS = LV inlet obstruction ––> LAE ––> increased LA pressure ––> increased pulmonary vascular resistance
––> increased right-sided pressure ––> right-sided CHF
• symptoms (2-5 year progression from onset of serious symptoms to death, slower progression
seen in the elderly)
• early: SOB/cough only with exertion or during high output states (fever)
• late: resting SOB/CP, activity limitation, orthopnea, hemoptysis
• complications: recurrent PE, pulmonary infections (bronchitis, pneumonia), LA thrombi
(systemic emboli: brain, kidney, spleen, arm)
• dyspnea (exertional, increased HR ––> decreased diastolic filling time ––>
increased LA pressure and pulmonary congestion)
• orthopnea/PND (increased venous return ––> increased LA pressure ––> pulmonary congestion)
• cough, hoarseness, hemoptysis
• palpitations (A fib secondary to LAE)
❏ LV inlet obstruction ––> fixed CO
• symptoms
• dyspnea
• fatigue
• low exercise tolerance
❏ atrial kick crucial - CO may decrease with A fib (loss of atrial kick), pregnancy, or tachycardia (shortened
diastolic filling period)
Signs of MS
❏ general examination
• mitral facies (mitral flush, pinched and blue facies),
• hepatic enlargement/pulsation, ascites, peripheral edema (all secondary to TR and RV failure)
❏ pulse
• +/– irregularly irregular (A fib), may be small volume
❏ JVP
• giant "a" waves (Pulmonary HTN, TS), "a" waves lost in A fib, elevated plateau (RV failure),
“v” waves (TR)
• apex - inconspicuous LV (tapping apex)
• palpable S1
• palpable P2 (in severe MS, pulmonary HTN)
• left parasternal lift (RV tap) palpable diastolic thrill at apex
• loud S1 (when valves are heavily calcified and not pliable ––> no closure of MV ( no S1)
• loud P2 (widely split S2)
• OS (lost if heavily calcified and not pliable), heard best in expiration at apex after P2
• mid-diastolic rumble (low pitch, heard with bell) - at apex, best in LLDB position and post-exercise
• a longer murmur and a shorter A2-OS interval (both caused by 8 LAP) correlate with worse MS
• presystolic accentuation of diastolic murmur due to atrial kick (lost with A fib)
• if pulmonary HTN present - loud P2, PR (Graham Steel murmur) associated murmurs: soft systolic apical
murmur (MR), Pansystolic murmur at LSB (TR)
❏ chest examination
• crackles (pulmonary congestion)
Investigations
❏ 12 lead ECG
• normal sinus rhythm/A fib, LAE (P mitrale), RVH (RAD)
❏ chest x-ray
• LA enlargement (LA appendage, double contour, splaying of carina), pulmonary congestion
(Kerley B lines), pulmonary hemosiderosis (diffuse nodularity) MV calcification, flattened
left heart border
❏ echocardiography (TTE)
• gold standard
• thickened calcified valve, fusion of leaflets, LAE, PAP, associated TR
• Doppler can estimate valvular area
❏ cardiac catheterization/ coronary angiography
• concurrent CAD in patients if age > 45 yr (males), > 55 yr (females)
Natural History
❏ symptoms arise > 15-20 years after initial rheumatic involvement of the valve,
followed by severe incapacitation (i.e. class IV NYHA symptoms) about 3 years later
❏ complications of A fib: acute respiratory decompensation; systemic and cerebral embolization
(often no evidence of residual atrial thrombus)
❏ other complications: IE, pulmonary hemorrhage, cardiac cachexia
Management
❏ avoid factors that increase LA pressure (tachycardia, fever, vigorous exercise, etc.)
❏ medical
• treat A fib (rate control, cardioversion)
• anticoagulation - if A fib or previous embolus
• IE prophylaxis
• diuretics and rate control (beta-blockers)
• MV area < 1.0 cm2 with symptoms
• NYHA class III or IV
• worsening pulmonary HTN
• IE
• systemic embolization
• unacceptable lifestyle limitations due to symptoms
• closed commisurotomy
• rarely performed in North America
• balloon valvuloplasty
• transthoracic echo (TTE) determines suitability for valvuloplasty
(based on morphology of leaflets and subchordal apparatus)
• open commisurotomy
• best procedure if valve amenable to repair
• all the above "turn the clock back" - re-stenosis will develop
• MV replacement
• if immobile leaflets/heavy calcification, severe subvalvular disease, MR
MITRAL REGURGITATION
Etiology
❏ annulus
• LV dilatation (CHF, DCM, myocarditis); mitral annular calcification; IE (abscess)
❏ leaflets
• congenital (e.g. clefts); myxomatous degeneration (MVP, Marfan’s); IE;
rheumatic heart disease; collagen vascular disease
❏ chordae
• trauma/tear; myxomatous degeneration; IE; acute MI
❏ papillary muscles and LV wall
• ischemia/infarction; rupture; aneurysm; HCM


❏ chronic MR = gradually increase flow across MV (into LA) during systole ––> progressive LAE ––>
decreased fraction of SV flows forward ––> LV dilatation (to decrease SV and maintain CO) ––>
increased LV wall tension ––> CHF
❏ "MR begets MR" - MR causes LV dilatation which in turn leads to annulus dilatation increased MR
• symptoms
• few symptoms initially (LAE generally can prevent an increase in PAP and the subsequent
pulmonary edema)
• later: dyspnea, PND/orthopnea, fatigue and lethargy
• palpitations
❏ acute MR = sudden onset of MV incompetence ––> increased LA pressure ––> increased PAP ––>
pulmonary edema ––> RV failure (acute onset CHF)
Signs of MR
❏ pulse
• quick and vigorous (unless LV failure)
• apex - displaced, hyperdynamic, enlarged due to LV dilatation
• +/– left parasternal lift (LA expands with MR), apical thrill
• S1 normal, soft, or buried in murmur
• S3 usually present
• holosystolic murmur - at apex, usually radiates to axilla, sometimes to base or back
(posteriorly directed jet)
• MR murmur secondary to mitral valve prolapse (MVP) - usually mid-systolic
• papillary muscle dysfunction - typically a late systolic whoop or honk
• mid-diastolic rumble - increase flow across valve (often no MS)
• severity - gauge by LV dilatation, S3, diastolic flow rumble
❏ A fib, CHF, pulmonary HTN develop late
❏ acute MR ––> CHF, S3 and S4 present; usually S1 and S2 normal with soft or absent murmur early in systole;
often a diastolic flow murmur
Investigations
❏ 12 lead ECG
• LAE, left atrial delay (bifid P waves), possible LVH
❏ chest x-ray
• LVH, LAE, pulmonary venous HTN
• etiology - flail leaflets, vegetations, etc.
• severity - regurgitant volume/fraction/orifice area
• LV function - increased LV/LA size; EF
• color flow mapping shows abnormal jet from LV to LA
• assess coronary arteries
• ventriculography - contrast fills LA to assess flow and chamber contours
• prominent left atrial "v" wave on Swan-Ganz
Management
❏ medical
• asymptomatic - serial echocardiograms to monitor progress
• IE prophylaxis
• symptomatic - decreased preload (diuresis) and decreased afterload (ACEI) for
severe LV dysfunction and MR in poor surgical candidate
❏ surgical
• acute MR - generally best managed surgically
• chronic MR - indications for surgery
• persistent symptoms (NYHA class II) despite optimal medical therapy
• onset of LV dysfunction or increased LV volume or size, even if asymptomatic
• valve repair for MR secondary to myxomatous degeneration
• preferred (low mortality), often technically difficult
❏ MV replacement
• if unable to repair MV
• attempt to conserve chordal structures/connections, correction of MR achieved
MITRAL VALVE PROLAPSE (MVP)
Etiology
❏ myxomatous degeneration of chordae and leaflets which are thickened, voluminous and redundant
(too big for the orifice)
❏ leaflets displaced into LA during systole
❏ 3-5% of population (F > M)
❏ alone, or with connective tissue diseases (e.g. Marfan’s)
❏ may be associated with pectus excavatum, straight back syndrome, and other MSK abnormalities
Symptoms
❏ click-murmur syndrome
❏ atypical chest pain (prolonged, non-exertional, stabbing)
❏ dyspnea, hyperventilation, anxiety, panic, palpitations, presyncope, fatigue - no causal relations or
mechanisms found
❏ +/– symptoms of MR
Signs of MVP
Clinical diagnosis based on presence of mid-systolic click +/– murmur
❏ mid-systolic click (tensing of redundant valve tissue, billowing of posterior leaflet in mid-systole)
❏ mid to late systolic murmur(regurgitation after prolapse of MV leaflets)
❏ maneuvers to change LV volume (exaggerate the disproportion of the valve with respect to the annulus) -
squat to stand, or Valsalva ––> decreased venous return, decreased ventricular filling ––>
earlier click and louder and longer murmur
Investigations
❏ 12 lead ECG
• nonspecific ST-T wave changes, PSVT, ventricular ectopy
❏ ECHO
• posterior systolic prolapse of MV leaflets into LA
• assess severity of MR
Natural History
❏ excellent prognosis (usually benign)
❏ risk of complications is most dependent on degree of MR
• progressive MR; severe MR (beware of ruptured chordae); IE; arrhythmias; thromboembolism;
sudden death
Management
❏ asymptomatic without MR - excellent prognosis (vast majority)
• follow-up q 3-5 years
❏ ß blockers - for palpitations, pain, anxiety
❏ anticoagulation - if systemic embolism
❏ for MR - IE prophylaxis, standard indications for MV repair/replacement
TRICUSPID VALVE DISEASE
Etiology
❏ TS: rheumatic, congenital, carcinoid syndrome, fibroelastosis
❏ TR: RV dilatation (commonest cause), IE (iv drug users), rheumatic, Ebstein anomaly,
AV cushion defects, carcinoid, tricuspid prolapse, trauma
Symptoms
❏ right heart failure
• fatigue
• pedal edema, abdominal pain (liver congestion), ascites
• dyspnea (may reflect right heart forward failure)
Signs
❏ carotid pulse: irregular if A fib and low volume
❏ JVP
• increased JVP
• prominent "a" waves in TS
• large “v” waves in TR ("cv" waves)
• positive HJR and Kussmaul's sign (rise in JVP with inspiration)
❏ precordial palpation for left parasternal lift (RV) in TR
• note: all right sided sounds are louder with inspiration, except a pulmonary ejection click
• TS: diastolic rumble in 4th left intercostal space (LICS)
• TR: holosystolic murmur along LLSB (Carvallo's murmur); may behave like an ejection murmur
• RV S3 along LLSB (with inspiration)
❏ abdominal examination
• hepatomegaly (congestion) with systolic pulsations from TR
• edema, ascites: 2º to fluid retention
Investigations
❏ 12 lead ECG
• TS: RAE
• TR: RAE, RVH, A fib
❏ chest x-ray
• TS: dilatation of RA without pulmonary artery enlargement
• TR: RA + RV enlargement
❏ ECHO
• diagnostic
Management
❏ supportive
• diuretics, preload reduction
• TV surgery usually determined by need for other interventions (e.g. MVR of r associated MS)
PULMONARY VALVE DISEASE
❏ much less commonly involved
Etiology
❏ pulmonary stenosis (PS): usually congenital; rheumatic uncommon; carcinoid
❏ pumonary regurgitation (PR): secondary to dilatation of valve ring
• pulmonary HTN (MS - most common, COPD, recurrent PE)
• rheumatic, IE
Symptoms
❏ chest pain, syncope, dyspnea, leg edema (RV failure and CHF)
Signs
❏ PS
• systolic murmur - maximum at 2nd LICS
• pulmonary ejection click; normal/loud/soft P2; right sided S4
❏ PR
• early diastolic murmur at base
• Graham Steel (diastolic) murmur at 2nd and 3rd LICS increasing with inspiration; no peripheral
stigmata of AR
Investigations
❏ 12 lead ECG
• RVH
❏ chest x-ray
• prominent pulmonary arteries if pulmonary HTN
• enlarged RV
❏ ECHO
• diagnostic - RVH, RV dilatation; PS or PR by Doppler
Management
❏ IE prophylaxis
❏ PR
• rarely requires treatment (well tolerated if systemic vascular resistance is normal)
• valve replacement may be required
❏ PS
• balloon valvuloplasty, depending on severity
PROSTHETIC VALVES
❏ bioprosthetic valves
• porcine heterograft, bovine pericardial, human homograft
• low incidence of thromboembolism, anticoagulation often not required (use ASA only),
ideal for those with contraindications to anticoagulation (pregnancy)
• degeneration of valve after 10 years on average
• higher failure rate in the mitral position
• contraindicated in children due to rapid calcification
❏ mechanical valves
• better predictability of performance and durability
• used preferentially if risk of reoperation is high
• always requires anticoagulation to prevent thromboembolism
• contraindications: bleeding tendency (e.g. peptic ulcer disease (PUD)),
pregnancy (Coumadin is teratogenic)
• target INR = 2.5-3.5
❏ post-op complications
• valve failure
• valve thrombosis (< 1%/year)
• valve degeneration
• IE (often < 1 year after surgery, Staph. epidermidis)
• bleeding problems due to anticoagulation (major: 1%/year)
• thromboembolism (2-5% per patient-year despite adequate anticoagulation)
• conduction abnormalities

PERICARDIAL DISEASE
ACUTE PERICARDITIS
Etiology
❏ idiopathic is most common: usually presumed to be viral
❏ infectious
• viral: Coxsackie virus A, B (most common)
• bacterial: Staph, Strep, septicemia
• TB
• fungal: histoplasmosis, blastomycosis
• protozoal
❏ post-MI: acute (direct extension of myocardial inflammation, 1-7 days), Dressler's syndrome
(autoimmune, 2-8 weeks)
❏ post-pericardiotomy (e.g. CABG), other trauma
❏ metabolic: uremia (common), hypothyroidism
❏ neoplasm: Hodgkin’s, breast, lung, renal cell carcinoma, melanoma
❏ collagen vascular disease: SLE, periarteritis, RA, scleroderma
❏ vascular: dissecting aneurysm
❏ infiltrative disease (sarcoid), drugs (e.g. hydralazine), radiation
Presentation
❏ diagnostic triad: chest pain, friction rub, and ECG changes
❏ chest pain - alleviated by sitting up and leaning forward, pleuritic, worse with deep breathing and
supine position
❏ pericardial friction rub - may be uni-, bi- or triphasic
❏ +/– fever, malaise
Investigations
❏ 12 lead ECG
• initially elevated ST in anterior, lateral and inferior leads +/– depressed PR segment, the elevation in the
the ST segment is concave upwards ––> 2-5 days later ST isoelectric with T wave flattening and inversion
❏ chest x-ray
• normal heart size, pulmonary infiltrates
• assess pericardial effusion
Management
❏ treat the underlying disease
❏ anti-inflammatory agents (NSAIDs, steroids if severe or recurrent); analgesics
Complications
❏ recurrences, atrial arrhythmias, pericardial effusions, tamponade, residual constrictive pericarditis
PERICARDIAL EFFUSION
Etiology
❏ two types of effusions:
• transudative (serous)
• CHF, hypoalbuminemia/hypoproteinemia, hypothyroidism
• exudative (serosanguinous or bloody)
• causes similar to the causes of acute pericarditis
• may develop acute effusion secondary to hemopericardium
(trauma, post MI myocardial rupture, aortic dessection)
❏ physiological consequences depend on type and volume of effusion, rate of effusion development, and
underlying cardiac disease
Symptoms
❏ none or similar to acute pericarditis
❏ dyspnea, cough
❏ extra-cardiac (esophageal/recurrent laryngeal nerve/tracheo-bronchial/phrenic nerve irritation)
Signs
❏ JVP: increased with dominant "x" descent
❏ arterial pulse: normal to decreased volume, decreased PP
❏ auscultation: distant heart sounds +/– rub
Investigations
❏ 12 lead ECG
• low voltage, flat T waves
❏ chest x-ray
• cardiomegaly, rounded cardiac contour (water bottle)
❏ ECHO (procedure of choice)
• fluid in pericardial sac
❏ pericardiocentesis
• establishes diagnosis
Management
❏ mild: frequent observation with serial ECHO, treat the cause, anti-inflammatory agents for inflammation
❏ severe: may develop cardiac tamponade
PERICARDIAL DISEASE . . . CONT.
CARDIAC TAMPONADE
❏ major complication of pericardial effusion
❏ cardiac tamponade is a clinical diagnosis
❏ high intra-pericardial pressure ––> decreased venous return ––> decreased diastolic ventricular filling ––>
decreased CO ––> hypotension + venous congestion
• symptoms
• tachypnea, dyspnea, shock
Signs
❏ “x” descent only, absent “y” descent
❏ hepatic congestion
Clinical Pearl
❏ Classic quartet: hypotension, increased JVP, tachycardia, pulsus paradoxus.
❏ Beck’s triad: hypotension, increased JVP, muffled heart sounds.
Investigations
❏ 12 lead ECG
• electrical alternans (pathognomonic variation in R wave amplitude), low voltage
❏ ECHO
• pericardial effusion, compression of cardiac chambers (RA and RV) in diastolic
• mean RA, LA, LV and RV diastolic pressures all high and equal
Management
❏ pericardiocentesis – ECHO-, ECG-guided
❏ pericardiotomy
❏ avoid diuretics and vasodilators (these decrease venous return to already under-filled RV ––>
decrease LV preload ––> decrease CO)
❏ fluid administration may temporarily increase CO
❏ treat underlying cause
CONSTRICTIVE PERICARDITIS
Definition
❏ chronic pericarditis resulting in fibrosed, thickened, adherent, and/or calcified pericardium
Etiology
❏ any cause of acute pericarditis may result in chronic pericarditis
❏ major causes are tuberculous, radiation-induced, post-cardiotomy, idiopathic
Symptoms
❏ dyspnea, fatigue, palpitations
❏ abdominal pain
Signs
❏ general examination - mimics CHF (especially right-sided HF)
• ascites, hepatosplenomegaly, edema
❏ increased JVP, Kussmaul's sign (paradoxical increase in JVP with inspiration), Friedrich's sign
(prominent “y” descent > “x” descent)
❏ pressures: BP normal to decreased, +/– pulsus paradoxus
❏ precordial examination: +/– pericardial knock (early diastolic sound)
Investigations
❏ 12 lead ECG
• low voltage, flat T wave, +/– A fib
❏ chest x-ray
• pericardial calcification, effusions
❏ CT/MRI/TEE
• pericardial thickening
• equalization of RV and LV diastolic pressures, RVEDP > 1/3 of RV systolic pressure
Management
❏ medical: diuretics, salt restriction
❏ surgical: pericardiectomy
Table 11. Differentiation of Constrictive Pericarditis vs. Cardiac Tamponade
Characteristic Constrictive Pericarditis Tamponade
JVP “y” > “x” “x” > “y”
Kussmaul’s sign Present Absent (JVP too high to see change)
Pulsus paradoxus 1/3 of cases Always
Pericardial knock Present Absent
Hypotension Mild-moderate Severe

SYNCOPE
Definition
❏ sudden, transient disruption of consciousness and loss of postural tone with spontaneous recovery
❏ usually caused by generalized cerebral hypoperfusion
Etiology
❏ cause of 50% of cases of syncope is unknown
❏ cardiac
• electrical
• tachycardia: VT, Torsades de pointes, SVT, rapid A fib
• bradycardia: sick sinus syndrome, 2º or 3º (Stokes-Adams attack) AV block
• pacemaker failure
• mechanical
• outflow obstruction: left-sided (AS, HOCM, MS, LA myxoma), right-sided
(PS, PE, pulmonary HTN)
• myocardial: CAD/MI, LV dysfunction
• other: tamponade
❏ extra-cardiac
• neurally mediated vasomotor
• vasovagal - the "common faint " (50%)
• situational/visceral: micturition/defecation syncope, cough syncope,
Valsalva, ocular pressure, etc.
• carotid sinus syncope
• psychiatric: somatization, panic, anxiety
• other: exercise, high altitude, drug-induced
• orthostatic hypotension: drug-induced (e.g. antihypertensives), venous pooling (postural, pregnancy),
autonomic neuropathy (primary: Shy-Drager, secondary: DM), hypovolemia (blood loss, diuresis),
pheochromocytoma
• neurological: vertebrobasilar TIA/stroke, subarachnoid hemorrhage,
cervical spondylosis, seizure, subclavian steal
• metabolic: hypoxia, hypoglycemia, hypocapnia
❏ history and physical examination are critical - reflect underlying pathology in 40-50%
(attention to cardiac and neurological exams) (see Neurology Chapter)
Table 12. Differentiation of Seizure vs. Syncope

Characteristic Syncope Seizure
Facial colour Pale Cyanotic

(lateral) tongue biting Rare Common
Aura No Sometimes
Nausea, diaphoresis Common before Uncommon
Level of concsciousness (LOC) Brief May be longer
Reoriention Within seconds Within minutes
Todd’s paralysis No Sometimes
Setting Rare when recumbent Anytime
Attacks Infrequent Repeated
Age Variable Younger (< 45)
CK Normal Increased
Positive EEG No Sometimes
Investigations
❏ directed by results of history and physical examination
❏ blood work: CBC, electrolytes, MgV, Ca+2, BUN, creatinine, glucose, ABG, CK-MB
❏ ECG
❏ ECHO
❏ carotid Doppler
❏ Holter monitor, loop Holter
❏ tilt-table testing
❏ electrophysiological study (EPS)

SYNCOPE . . . CONT.
Management
❏ treatment of underlying cause
SYNCOPE
Normal history History suggests cardiac Physical exam reveals Consider culprit
and physical exam disease; or physical orthostatic hypotension medications or
exam abnormal dehydration
Neurocardiogenic Cardiogenic syncope Normal neurologic exam Abnormal neurologic

syncope (ie. vasovagal) exam
Do tilt testing if recurrent 24 h monitoring Consider post-ganglionic Consider peripheral

automic insufficiency neuropathy, DM,
Shy-Drager Syndrome
Figure 15. Approach to the Patient with Syncope
EVIDENCE-BASED CARDIOLOGY
CONGESTIVE HEART FAILURE
❏ VeHEFT-I: Hydralazine/Isorbide Dinitrate decreases mortality in patients with CHF. (NEJM 1986; 314:1547)
❏ VeHEFT-II: Enalapril decreases mortality compared to Hydralazine/Isorbide Dintrate in patients with CHF.
(NEJM 1991; 325:303)
❏ CONSENSUS: Enalapril decreases mortality compared to placebo in severe CHF. (NEJM 1987; 316:1429)
❏ DIG TRIAL: Digoxin decreased rate of hospitalization, improves symptoms and exercise capacity, but has no
mortality benefit compared to placebo. (NEJM 1997; 336:525)
❏ PRAISE: Amlodipine has no mortality benefit over placebo in CHF, except decreases mortality in patients with
non-ischemic dilated CM (NEJM 1996; 335:1107)
❏ US-CARVEDILOL STUDY: Carvedilol is superior to placebo for morbidity and mortality in class II and
III heart failure (NEJM 1996;334:1349)
❏ MERIT: Metoprolol is superior to placebo for morbidity and mortality in class II and III heart failure
(Lancet 1999; 353:2001)
❏ RALES: Aldosterone antagonism with Spironolactone in addition to standard treatment decreases mortality in
patients with FC III-IV heart failure (NEJM 1999;341: 709)
ISCHEMIC HEART DISEASE
❏ GUSTO I: There is increased survival after acute MI in patients treated with rt-Pa and IV Heparin compared to
Streptokinase (NEJM 1993; 329:673)
❏ ESSENCE: Enoxaparin decreases mortality vs. unfractionated heparin in patients with unstable angina or
non-Q wave MI. (NEJM 1997; 337:447)
❏ PURSUIT: Integrelin (IIb/IIIa inhibitor) decreased mortality when given to patients with high risk unstable
angina (e.g. resting chest pain for >15 mins within last 24hrs + increases TnI/ECG changes) or non-Q wave MI,
and benefit increases if patients go for PTCA or CABG (Circulation 1996; 94:2083)
❏ BARI: subset analysis - CABG as an initial strategy has survival benefit over PTCA in diabetic patients
with multivessel disease (NEJM 1996;335:217)
❏ HOPE: Ramipril decreases rate of death, MI, and CVA in patients with CAD, Hx of CVD, PVD, or DM +1 other
cardiac risk factor, all who are not known to have any LV dysfunction. (NEJM 2000; 342:145)
ATRIAL FIBRILLAITON
❏ 5 RCT’s (SPAF-I, AFASAK, SPINAF, CAFA, BAATAF) level demonstrated 67% decrease in thromboembolic rate
in patients treated with coudamin in setting of nonrheumatic AF)

Table 13. Commonly Used Cardiac Therapeutics
DRUG CLASS EXAMPLES MECHANSIM OF INDICATIONS SIDE EFFECTS CONTRA-INDICATIONS
ACTION
ß-BLOCKERS • metoprolol, • Lowers myocardial • IHD • bradycardia • severe bradycardia, high-degree heart block
atenolol (ß1) O2 demand by 9 HR, • HTN • fatigue • caution in asthmatics (contraindicated if
• acebutolol BP and contractility • A Fib • dizziness severe asthma/bronchospasm)
(ß1, ISA) • stable class II to III CHF • nightmares, memory loss, depression, • caution in patients with peripheral claudication
• labetalol • SVT hallucinations phenomenon and Raynaud's
(α1, ß1, ß2) • depression of counterregulatory • caution in CHF
• carvedilol responses to hypoglycemia in diabetes
(α1, ß1, ß2) • +/– adverse effects on lipid profile
MCCQE 2002 Review Notes

and anti-oxidant) • bronchospasm
• sotalol (ß1, ß2, class III antiarrhythmic) • exacerbation of Raynaud's
phenomenon and claudication
• impotence
CALCIUM CHANNEL diltiazem see Table 15 • HTN • anorexia, nausea • sick sinus syndrome
BLOCKERS • 2nd line agent for IHD (1st line • edema • second or third degree AV block
(CCB) ß-blockers) • bradycardia • severe CHF
• SVT • CHF • AMI with CHF
• pregnancy
verapamil see Table 15 • HTN • bradycardia • sick sinus syndrome
• 2nd line agent for IHD (1st line • CHF • second or third degree AV block
ß-blockers) • constipation • severe CHF
• SVT • AMI (relative)
• diastolic dysfunction • pregnancy (relative)
• A Fib with bypass tract with
anterograde conduction
nifedipine see Table 15 • HTN • hypotension • NOTE evidence that short acting nifedipine is
• edema associated with increased mortality (AMI)
• flushing • severe AS
• dizziness • HCM
• headache • poor LV function
• pregnancy
• unstable angina or threatened MI in absence of
ß-blocker
ACE INHIBITORS captopril • peripheral vasodilator ––> • CHF (including post-MI) • dry cough (5-15% of patients) • bilateral renal artery stenosis
COMMONLY USED CARDIAC MEDICATIONS
enalapril afterload reduction with little change • HTN • hypotension • pregnancy (absolute)
ramipril in CO, HR or GFR • post-MI EF<40%) • hyperkalemia • documented angioedema 2º to ACEI
• also cause 9 in fluid volume • anterior MI • renal insufficiency
due to inhibition of aldosterone • angioedema (rare)
production • reversible neutropenia
• proteinuria
• membranous GN
• fatigue
ANGIOTENSIN II losartan (cozaar) • blocks angiotensin II receptor so • CHF • dizziness (< 2%) • bilateral renal artery stenosis
BLOCKER peripherally vasodilates and blocks • HTN • hypotension/syncope • pregnancy
aldosterone effects • renal dysfunction
Cardiology – C49
DRUG CLASS EXAMPLES MECHANSIM OF INDICATIONS SIDE EFFECTS CONTRA-INDICATIONS
ACTION
DIURETIC Furosemide • loop diuretic • acute pulmonary edema • hypokalemia • severe hypovolemia
• interferes with creation of • severe CHF • hypovolemia • severe hypotension
hypertonic medullary interstitium • refractory edema • azotemia • hypersensitivity to furosemide or sulfonamide
• diuretic effect within 1 hour after • hypercalcemia (use furosemide • hyperuricemia
C50 – Cardiology
oral administration, within 30 minutes with saline infusions) • hypochloremic metabolic alkalosis
after IV administration
NITRATES • sublingual/ patch/ IV • produce venous, arteriolar and • symptomaltic relief of angina • headaches • hypersensitivity
nitroglycerin coronary vasodilation • CHF in isosorbide • dizziness • active peptic ulcer
• isosorbide dinitrate dinitrate form (always combine • weakness
with hydralazine in CHF) • postural hypotension
• tolerance develops rapidly with
continuous use; maintain at least 8
nitrate-free hours per day
ANIT-ARRHYTHMIC Digoxin • Na+ – K+ – ATPase inhibitor causes 8 • A Fib • cardiac toxicity Absolute
intracellular Na resulting in exchange • CHF • AV blocks (e.g. Wenkebach, • high degree AV block
of Na+ for Ca2+ atrial tachycardia with block) • hypersensitivity
• 8 Ca2+ results in inotropic action, • tachycardias (eg VT
and cell stabilization atrioventricular Relative
• positive inotrope-increases force dissociation, accelerated • arrhythmogenic states (e.g.
contraction junctional rhythm) hypokalemia, acute MI, acute/chronic
• blocks AV node • bradyarrhythmias (e.g. sinus myocarditis, frequent PVCs, WPW
(decreased refractory period bradycardia, sinus arrest, with anterograde conduction down
and conduction time) and sinoatrial block) bypass tract, acute hypoxemia,
depresses SA node • regularization of R-R interval in A Fib chronic cor pulmonale , diastolic
• GI dysfunction in the absense of systolic
COMMONLY USED CARDIAC MEDICATIONS
• anorexia, nausea/vomiting dysfunction)

• CNS • risk of complete AV block/ bradycardia
• blurred or yellow vision • sick sinus syndrome
• headache • incomplete AV block
• weakness/apathy • HCM
. . . CONT.
• psychosis
ANTI-PLATELET ASA • cyclooxygenase inhibitor • acute MI • GI • hypersensitivity
• interferes with • Post-MI • nausea,vomiting, diarrhea • active peptic ulcer
platelet aggregation • Post CABG • dyspepsia, peptic ulcers
by impairing • Post PTCA • ototoxicity
production of • TIA/ CVA • tinnitus, vertigo, hearing loss
thromboxane A2 • hematological
• leukopenia, anemia
• purpura, thrombocytopenia
• bronchoconstriction
• impaired renal perfusion leading to
fluid retention
• dermatological or anaphylactic
hypersensitivity reactions
MCCQE 2002 Review Notes

COMMONLY USED CARDIAC MEDICATIONS . . . CONT.
Table 14. Beta-Blocker Actions

Clinical Effects Propranolol Atenolol Acebutolol Labetalol
ß-Activity non-selective ß1 ß1 non-selective
!-Activity N N N α1
ISA N N +++ +
Bronchoconstriction +++ + + ++
Orthostatic Hypotension – – – +++
Lipid Adverse Effects ++ ++ – +
CNS Adverse Effects +++ + ++ ++
CALCIUM CHANNEL BLOCKERS (CCB)

❏ major subtypes are represented by diltiazem (benzothaizepine), verapamil (phenylalkylamine)
and nifedipine (dihydropyridine)
❏ diltiazem and verapamil are strong cardiodepressants, whereas the dihydropyridines are strong vasodilators
Table 15. Calcium Channel Blocker Actions

Clinical Effects Diltiazem Verapamil Nifedipine
Coronary Vasodilator ++ ++ +++
Peripheral Vasodilator + ++ +++
Contractility <––> 9 <––>
Sinus Rate 9 9 8
AV Conduction 9 9 <––>
ANTI-ARRHYTHMIC DRUGS
1
2 slow Ca influx
++
MEMBRANE POTENTIAL
0
Na+ influx 3
threshold K+ efflux
4 Na+ influx
TIME
Figure 16. Representative Action Potential

COMMONLY USED CARDIAC MEDICATIONS . . . CONT.
Table 16. Antiarrhythmic drugs (Vaughn-Williams Classification)

Class Agent Indications Side Effects Mechanism of Action
Ia Quinidine SVT, VT Torsades de Pointes (all Ia) • moderate Na+
Procainamide diarrhea channel blockade
Disopyramide lupus-like syndrome • slows phase O upstroke
anti-cholinergic effects • prolongs repolarization
and thus slows conduction
Ib Lidocaine VT confusion, stupor, seizures • mild Na+
Mexiletine GI upset, tremor channel blockade
• shortens phase 3
repolarization
Ic Propafenone SVT, VT1 exacerbation of VT (all Ic) • marked Na+ channel
Flecainide A Fib2 negative inotropy (all Ic) blockade
Encainide bradycardia and heart block • markedly slows phase 0
(all Ic) upstroke
II Propranolol SVT, A Fib1 bronchospasm, negative • ß blockers

Metoprolol etc. inotrophy, bradycardia, AV block, • decreases phase 4
impotence, fatigue depolarization
III Amiodarone* SVT, VT photosensitivity, • blocks K channel

A Fib pulmonary toxicity, • prolongs phase 3
hepatotoxicity, repolarization and so
hyper/hypothyroidism prolongs the effective
refractory period
Sotalol SVT, VT , A Fib beta-blocker effects, Torsades de
Bretylium (IV) VT Pointes, hypotension
IV Verapamil SVT bradycardia, AV block • CCB

Diltiazem A Fib hypotension • slow phase 4
spontaneous
depolarization and so
slows conduction in
areas such as AV node
Amiodcrone hcs class I, II, III, IV, properties
❏ All anti-arrhythmics have potential to be pro-arrhythmic

❏ In the landmark CAST trial, two class Ic agents (encainide, flecainide)
prevented VPB’s post MI but significantly increased mortality
REFERENCES
Ischemic Heart Disease
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Rauch, U., et al. Thrombus Formation on the Atherosclerotic Plaques: Pathogenesis and Clinical Consequences. Annals of
Internal Medicine. 2001; 134: 224-238.
The Arterial Revascularization Therapies Study Group. Comparison of Coronary-Artery Bypass Surgery and Stenting for the
Treatment of Multivessel Disease. New England Journal of Medicine. 2001; 344:1117-1124.
Turpie, A. G. G. and Antman, E. M. Low-Molecular-Weight Heparins in the Treatment of Acute Coronary Syndromes. Archives of
Internal Medicine. 2001; 161: 1484-1490.
Yeghiazarians, Y., Braunstein, J. B., Askari, A., and Stone, P. H. Review Article: Unstable Angina Pectoris. New England Journal of
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Nuclear Cardiology
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Cardiovascular Notes - All in One File

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Cardiovascular Notes - All in One File

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Week

The Pericardium: (Coverings of the Heart)

Layers of the Heart Wall:

Chambers & Associated Great Vessels:

o 2 Ventricles (Inferior): [Vent = Underside]

2x SemiLunar (SL) Valves:

o The SinoAtrial (SA) Node:

o The Purkinje Fibres:

o Atrial & Ventricular Myocytes:

The Heart s Electrical A is

- 1. Atrial Systole/Ventricular Filling (Diastole):

o NB: Frank Starling Mechanism :

Relationship Between Flow, Pressure & Resistance:

Effects of Vasomotion on Rate & Velocity of Flow:

Factors Influencing Blood Pressure (Long Term):

Types of Blood Pressures:

Blood Vessel Structure:

Fluid Movements Across a Vessel:

ACUTE CARDIOGENIC PULMONARY OEDEMA

MCCQE 2002 Review Notes Cardiology – C31

Aneurysms (General Info):

CEREBRAL ANEURYSM (Congenital Berry Anerysms – See Sub-Arachnoid Haemorrhage Notes):

CVS24 – Cardiac and Vascular Surgery MCCQE 2002 Review Notes

MCCQE 2002 Review Notes Cardiac and Vascular Surgery – CVS25

CVS26 – Cardiac and Vascular Surgery MCCQE 2002 Review Notes

RUPTURED ABDOMINAL AORTIC ANEURYSM (RAAA)

VASCULAR – VENOUS DISEASE

MCCQE 2002 Review Notes Cardiac and Vascular Surgery – CVS27

- Revision of the Cardiac Cycle:

DDX #1 SUPRAVENTRICULAR TACHYCARDIAS:

- ATRIAL PREMATURE BEATS (APBs):

- ATRIAL FIBRILLATION (AF):

- PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT):

- TORSADES DE POINTES ( TWISTING OF THE POINTS ):

ESCAPE RHYTHMS (SINUS ARREST/EXIT BLOCK):

o 2. SECOND-DEGREE HEART BLOCK:

o 3. THIRD-DEGREE HEART BLOCK (AKA: COMPLETE HEART BLOCK):

- Class-II Antiarrh thmics 1-Blockers):

- Class-IV Antiarrhythmics (VG-Ca+ Channel Blockers):

CARCINOID HEART DISEASE:

CARDIOMYOPATHIES (“Heart Muscle Diseases”):

- (5. “STRESS CARDIOMYOPATHY”):

Review of Foetal Circulation:

CONGENITAL HEART DEFECTS:

- ATRIAL SEPTAL DEFECT (ASD):

DEEP VEIN THROMBOSIS “PHLEBOTHROMBOSIS” “THROMBOPHLEBITIS” :

RUPTURED ABDOMINAL AORTIC ANEURYSM (RAAA)

VASCULAR – VENOUS DISEASE

MCCQE 2002 Review Notes Cardiac and Vascular Surgery – CVS27

❏ signs and symptoms

What side is the Failure?

Management of Acute, Decompensated CCF:

- Aetiologies & Types:

Category Systolic (mmHg) Diastolic (mmHG) % Population

o +(If 2o Bacterial Endocarditis 2-6wks of High Dose IV Vancomycin)

INFECTIVE ENDOCARDITIS (IE)

C36 – Cardiology MCCQE 2002 Review Notes

C38 – Cardiology MCCQE 2002 Review Notes

Review of Coronary Anatomy:

LAD Apex, Anterior LV, Anterior 2/3 of IV-Septum

Degrees of Coronary Blockage:

*Ischaemia Vs. Hypoxia Vs. Infarction:

Regional Vs. Global Myocardial Ischaemia:

What Happens During Myocardial Ischaemia: