677 Cardio

Lecture 9-HEART FAILURE 2
Lecture 14-SHOCK 38
Lecture 6-CARDIAC ARRHYTHMIAS 81
Lecture 7-CORONARY ARTERY DISEASE 120
Lecture 8-VALVULAR HEART DISEASES 165
DLA_Notes on HEART FAILURE 207
DLA_Notes on HYPERTENSION _ CO_VR 243
DLA_Notes on VALVULAR HEART DISEASES 278
DLA_Notes on CORONARY ARTERY DISEASE 324
DLA_Notes on ECG _ CARDIAC ARRHYTHMIAS 356
Pathophysiology Lecture 9
Topic: HEART FAILURE

Lecturer: Dr. S. Upadhya
1
Patient:
A 58-year-old man comes to the physician because of easy
fatigability and ankle-swells. He states that these
symptoms have developed slowly over the past 4 months.
He also states that he often has to get up at night either to
urinate or because of shortness of breath. There is no history
of chest pain. The patient was diagnosed to have
hypertension 2 years ago and he was given prescriptions for
antihypertensive medications. However, he never filled them
or followed up for BP monitoring.
Vital signs: Pulse 108 beats/min; Respiration 20 breaths/min;
Temperature 99ºF; BP 175/110 mmHg.
Physical examination: Pitting ankle edema, cold and clammy
skin, tender hepatomegaly. Audible S3 heart sound and
bilateral crackles in the lower lung fields.
2
Differential diagnosis:
❖Congestive heart failure

❖Renal failure
Most likely diagnosis is:

Congestive heart failure (CHF)
Reasons:
•Ankle edema (pitting type)
•Dyspnea in the night
•Cold and clammy skin
•Enlarged, tender liver
•Audible S3 3
Congestive Heart Failure (CHF)
Definition of CHF:
Inadequate pumping function of the heart,
leading to congestion and resulting in fluid
accumulation in the lungs and peripheral
tissues
The symptoms and signs depend on:

• Onset – acute/chronic
• Primary involvement of the side – left/right
ventricles or both
4
Congestive Heart Failure may start with:
Left Ventricular Failure (LVF)

Or
Right ventricular failure (RVF)
5
LEFT VENTRICULAR FAILURE (LVF)
Clinical Presentation:
❖Breathlessness (dyspnea) -
particularly when lying down (orthopnea)
or at night [paroxysmal nocturnal
dyspnea (PND)]
❖Blood-tinged sputum (hemoptysis)
❖Chest pain (occasional)
❖Fatigue, nocturia, and confusion 6
Etiology of LVF:
❖Inappropriate workloads placed on the LV:

-Volume overload (example: MR or AR)
-Pressure overload (example: systemic
hypertension)
❖Restricted filling of the LV (example: constrictive
pericarditis)
❖Myocardial loss - as in MI
❖Decreased myocardial contractility – as in
poisoning or infections
7
Pathophysiologic changes associated
with heart failure (HF):
❑Hemodynamic changes
❑Neurohumoral changes
❑Cellular changes
8
Hemodynamic Changes in HF
Heart failure can arise from:

• Systolic dysfunction
• Diastolic dysfunction
• Combination of both
In most patients, a combination of systolic

and diastolic dysfunction is responsible for
the symptoms of heart failure
9
Causes of Systolic Dysfunction
➢Coronary artery disease
➢Valvular heart disease
➢Hypertension
➢Aging
➢Dilated cardiomyopathy
10
Systolic dysfunction: Definition & Feaures
➢Pressure-volume relationship shows a

low ejection with a high or low ventricular
pressure during ejection
➢Reduction in the stroke volume (SV) & a

decrease in cardiac output (CO)
(CO = SV x HR)
➢Reduction in ejection fraction (EF).

11
Changes in left ventricular P-V loop in
Systolic Dysfunction:
Example: Patient with systemic hypertension

(Increase in afterload on LV)
Loop A: Normal
Left ventricular pressure
Loop B: Increased
afterload
•Increase in ventricular
A pressure during systole
B •Decrease in SV
•Increase in ESV
Left ventricular volume
12
Systolic Dysfunction:
Example: Patient with acute Myocardial Infarction
(Loss of myocardium)
Loop A: Normal
Loop B: Loss of myocardium
•Decrease in ventricular
pressure during systole
•Increase in ventricular
diastolic pr
•Decrease in SV
•Increase in ESV
13
Systolic dysfunction: Compensatory changes
To restore cardiac output, the heart responds with
the following compensatory mechanisms
(compensated heart failure):
i) Increase in preload (Frank-Starling relationship):

Ventricle operates at a larger end-diastolic
volume & pressure
ii) Release of catecholamines
iii) Cardiac muscle hypertrophy and ventricular
volume increase.
Limitation: When each of these mechanisms reach their

maximum physiological limits, heart failure becomes 14
uncompensated.
i) Compensated LV failure: SV is partially restored
by an increased preload (EDV) shown by the PV
loop C.
15
(Curve B: PV loop soon after loss of myocardium)
Frank-Starling relationship
Systolic contractile performance (represented by
stroke volume or CO) is proportional to preload within
the normal physiologic range
16
Diastolic dysfunction (also known as
HF with preserved systolic function or
HF with preserved EF)
17
Diastolic dysfunction: Definition & Features
• Ventricular filling is impaired during relaxation that

leads to a reduced ventricular volume and an
increased end-diastolic pressure.
•Diastolic pressure-volume curve is shifted to the
left, with an accompanying increase in ventricular
end-diastolic pressure.
•Contractility and ejection fraction (EF) remain
normal (Normal ventricular systolic function)
•Reduced LV filling with systemic symptoms of low
cardiac output
•Elevated left atrial pressure and pulmonary
congestion.
18
Diastolic Dysfunction:
abcd – PV loop before heart failure (control)
a’b’c’d’ – Change in PV loop due to failure
Pressure (mm Hg)
Diastolic Pressure-
Volume curve
Volume (mL) 19
Causes of diastolic dysfunction
❖ Increased stiffness (decreased

compliance) of the ventricle as in:
Hypertrophic cardiomyopathy, Restrictive
cardiomyopathy (amyloidosis, sarcoidosis),
Long-standing hypertension & coronary artery
disease, Valvular heart diseases with
elevated afterload.
❖ Reduced ventricular filling because of

pericardial disease: Constrictive pericarditis.
20
Neurohumoral Changes in Heart
Failure:
❖Increased sympathetic activity

❖Activation of Renin-Angiotensin-
Aldosterone System (RAAS)
❖Increased release of ADH
(vasopressin)
❖Release of cytokines and peptides
21
Neurohumoral Changes (continued):
Increased sympathetic activity:
• Occurs early in the heart failure

• Elevated plasma norepinephrine levels
• Increased cardiac contractility and rate
• Initially it may be helpful to improve SV but
continued effect leads to increased preload
and afterload which can worsen heart failure.
22
Neurohumoral Changes (Continued):
Activation of renin-angiotensin-aldosterone
system (RAAS):
• Reduced renal blood flow → Activation of RAAS.
• Consequence of continued hyperactivity of RAAS

initiates a vicious cycle:
Severe vasoconstriction combined with increased
plasma volume → Increased both preload & afterload
→ Further reduction in cardiac output → Further
reduction in glomerular filtration rate → RAAS
activation (cycle repeats)
23
Neurohumoral Changes (Continued):
Other cytokines/peptides in heart failure:
•The interleukins (ILs) – IL-1 accelerates myocyte

hypertrophy
•Tumor necrosis factor-α (TNF-α) – causes myocyte
hypertrophy and cell death (apoptosis)
•Endothelin – stimulates vasoconstriction in pulm
vasculature, myocyte growth, myocardial fribrosis
•B-type natriuretic peptide (BNP) – produces
natriuresis, diuresis, vasodilation, inhibition of renin
and aldosterone and inhibition of fibrosis.
24
B-type natriuretic peptide (BNP):
➢ Also known as brain natriuretic peptide

➢ Elevated when ventricular filling pressures
are high (myocyte stretching)
➢ Sensitive in patients with symptomatic heart
failure (due to systolic or diastolic dysfunction)
➢ Helpful in emergency department in the
diagnosis of acute decompensated heart failure
➢ Class I recommendation for both diagnosis
and prognosis of HF (American College of
Cardiology Foundation (ACCF)/American
Heart Association (AHA) guideline on HF).
25
Cellular Changes:
❖ Inefficient intracellular calcium
handling
❖ Adrenergic desensitization
❖ Myocyte hypertrophy
❖ Cell death (apoptosis)
❖ Myocardial fibrosis
The cellular changes in ventricular

myocardium in heart failure is
collectively known as ventricular
remodeling 26
Basis for clinical presentations in
patient with LVF
❖ Shortness of breath (dyspnea) of

different degree
27
Dyspnea in LVF: Hemodynamic Basis
Pulmonary congestion
produces dyspnea
by various ways
(Please refer
DLA notes)
28
Physical examination findings in LVF &
pathophysiological basis:
•Elevated respiratory rate and heart rate

↓ ↓
Shortness Sympathetic nerve
of breath stimulation
•Peripheral pulse may reveal “pulsus alternans”
Normal Pulsus alternans

29
Pale, Cold, and Sweaty Skin:
Pale & cold extremities is due to peripheral

vasoconstriction to maintain blood flow to the vital
organs
Sweating: Increased sweat gland activity as a part

of thermoregulation when body heat cannot be
dissipated through the constricted vascular bed of
the skin
30
Bibasilar Rales, Pleural Effusion:

• Fluid in the alveolar spaces (due to pulm
congestion) can be heard as rales in bilateral lower
lung fields.
• Increased capillary pressures can also cause fluid
accumulation in the pleural spaces
31
Sustained or Displaced Apical Impulse:
•When the apical impulse is felt throughout the
systole, it is sustained. Sustained impulse suggests
an increase in left ventricular mass/thickness due
to a high afterload (contraction against a high
pressure/resistance).
•When the left ventricular volume is increased
(↑preload), the apical impulse is displaced
downwards and laterally. Displaced impulse
suggests volume-overload failures.
32
Third Heart Sound (S3):
•S3 is a low-pitched sound that is heard during rapid

filling of the ventricle in early diastole.
•Increased end-systolic volume and pressure
characteristic of the failing LV, are responsible for the
prominent S3
•S3 is a consistent physical finding in CHF
•Heard best at the apex (Mitral area)
33
Fourth Heart Sound (S4):
•It is a low-pitched sound at the end of diastole that

corresponds to atrial contraction
•S4 can be heard if the ventricles are stiff
•Best heard laterally over the apex, particularly when
the patient is partially rolled over onto the left side
•S4 is commonly heard in any patient with heart
failure resulting from diastolic dysfunction or
Coronary Artery Disease (CAD)
34
Chest X-ray characterized by bat’s wing
density, cardiac enlargement in patient
with pulmonary edema due to LVF
35
P-V loop in progressive LVF
Curve A: Normal
Curve B: Immediate effect of reduced

contractility following AMI;
Compensation not started
Curve C: Compensated LV failure - SV is partially restored

due to increased preload
Curve D: Decompensated LV failure despite increase in
preload, SV remains low and heart is over stretched 36
Topic: PATHOPHYSIOLOGY OF SHOCK

1
Patient:
20-year old soldier is brought to the field hospital

with a profusely bleeding gun wound in the left
thigh
PE: Patient appears anxious and confused; The
skin is cold and wet; BP is 65/40 mmHg; HR is 144
beats/min; Pulse is weak and rapid
Lab: Hematocrit is decreased
Imaging: Arteriogram shows abrupt termination of
dye propagation in the left femoral artery.
The most likely diagnosis is:
Hypovolemic shock due to femoral artery bleed.
2
Pathophysiology of Shock
3
Definition of cardiovascular SHOCK:
An abnormality of the circulatory system in which

there is inadequate tissue perfusion because of a
relatively or absolutely inadequate cardiac output.
4
The causes and types of shock:
A. Hypovolemic shock:
Inadequate volume of blood to fill the vascular
system
B. Distributive shock (also called vasogenic or
low-resistance shock):
Increased size of the vascular system produced by
vasodilation in the presence of a normal blood
volume
C. Cardiogenic shock:
Inadequate output of the heart as a result of
myocardial abnormalities
D. Obstructive shock:
Inadequate cardiac output as a result of obstruction
of blood flow in the lungs or heart 5
A. Hypovolemic shock:
Conditions:
• Hemorrhage
• Trauma
• Surgery
• Burns
• Fluid loss due to severe vomiting or diarrhea
6
Physical findings in Hypovolemic Shock:
•Hypotension (systolic pressure <90)
•A rapid, low volume, thready pulse
•Cold, pale, clammy skin
•Intense thirst
•Rapid respiration
•Restlessness or Low activity
•Markedly decreased urine output
•Altered mental status
Do not rely on systolic BP as the main indicator of

shock. Compensatory mechanisms prevent a
significant decrease in systolic BP until the patient has
lost 30% of the blood volume. 7
Compensatory reactions activated by
Hypovolemic Shock:
•Vasoconstriction & consequences
•Tachycardia
•Venoconstriction
•Tachypnea – cause and benefit
•Increased movement of interstitial fluid into
capillaries
•Increased secretion of ADH
•Increased secretion of glucocorticoids
•Stimulation of renin-angiotensin-aldosterone
•Increased secretion of erythropoietin
•Increased synthesis of plasma proteins
8
Baroreceptor are mechanoreceptors
that detect arterial blood pressure (BP)
Increase in MAP
↓
Stretching of carotid sinus
and aortic arch
↓
Increased firing rate of
baroreceptors
↓
Action potentials travel
via IX CN and X CN
↓
Cardiovascular regulatory
centers in brain stem
9
Baroreceptor response to decrease in BP
Example : Hemorrhage Fall in arterial BP
Decrease in baroreceptor impulses to cardiovasc. regulatory centers
Increase in sympathetic nerve activity Increase in sympathetic nerve

& decrease in parasympathetic nerve activity to veins and arterioles
activity to the heart
Increase in heart rate and Increase in Vasoconstriction

increase in contractility venous return of arterioles
Increase in cardiac output Increase in

(CO = HR x SV) TPR
Increase in arterial BP
(MAP = CO x TPR) 10
Compensatory Mechanisms
Neurohormonal Activation
Most important hormones released to maintain
normal cardiovascular homeostasis during
hypovolemic shock include:
• Angiotensin II
• Epinephrine
• Norepinephrine
• Vasopressin (ADH)
• ACTH
• Aldosterone 11
Consequences of increased vasomotor
discharge during hypovolemic shock:
•Vasoconstriction is generalized, sparing only the
vessels of the brain and the heart
•Vasoconstriction in the skin - Coolness and pallor
•Vasoconstriction in the kidney – Drop in GFR.
This reduces water loss, but it reaches a point at
which nitrogenous products of metabolism
accumulate in the blood (prerenal azotemia). If
hypotension is prolonged, there may be severe
renal tubular damage, leading to acute renal
failure.
12
Reason for tachypnea and its importance in
hypovolemia:
•The fall in blood pressure and the loss of red cells
results in stimulation of the carotid and aortic
chemoreceptors → stimulation of respiratory
center→ Chemoreceptor reflex
•Stimulation of respiration increases thoracic
pumping and improves venous return
•Stimulation of respiration also increases
vasoconstrictor discharge
13
VICIOUS CYCLE-1 DURING SHOCK (Neural)
Fall in Blood Pressure
Cardiac depression &

peripheral vasodilation
Low cerebral
blood flow
Loss of
sympathetic tone
Ischemic brainstem depression

14
VICIOUS CYCLE-2 DURING SHOCK (Metabolic)
Inadequate bloodflow to organs
Cardiac depression
Tissue hypoxia
Metabolic acidosis
Lactic acid accumulation & fall in pH

15
CELLULAR DAMAGE BY HYPOPERFUSION IN SHOCK
16
Hypovolemic Shock becomes worse
when coexists with:
• Soft tissue trauma

• Acute lung injury
• Cerebral & myocardial injury
17
Traumatic Hypovolemic Shock (aka Crush
syndrome):
•Traumatic shock involves severe damage to

muscle, bone & connective tissues - as seen in
battle casualties and automobile accident victims
•Breakdown of skeletal muscle is a serious
additional problem because of:
•Large amounts of K+ enter the circulation,
•Myoglobinuria and acute renal injury,
•Free radicals generated at the sites cause
further tissue destruction (reperfusion-induced
injury).
18
Refractory Shock:
•The persistent shock reaches a state in which there
is no longer any response to vasopressor drugs
•Even if the blood volume is returned to normal,
cardiac output remains depressed
•Factors that make shock refractory are:
-Failure of precapillary sphincters to remain
constricted while postcapillary venules still remain
constricted. Therefore, blood flows into the
capillaries and remains there.
-Cerebral ischemia depresses vasomotor and
cardiac discharge, causing blood pressure to fall
and making the shock worse.
-Reduced myocardial blood flow.
19
B. Distributive shock:
Conditions:
• Anaphylaxis
• Sepsis
• Fainting (neurogenic)
•In distributive shock, most of the symptoms and

signs described under hypovolemic shock are
present
•Vasodilation causes the skin to be warm rather
than cold and clammy 20
Patient:
A 5-year-old girl is brought to the emergency
department because of dyspnea, swelling and
redness in her right forearm following a bee sting.
She has had a bee sting one month ago and her
reaction to the sting was a greater than normal
redness at the site of sting.
Vitals: Pulse is 126/min; Blood pressure is 80/50
mmHg and respirations are 30/min.
Physical examination shows a wheal of about a 3-cm
radius in her right fore arm, a swollen and stiff
abdomen, urticaria and angioedema over her arms,
abdomen, and thighs.
21
The most likely diagnosis is:
Anaphylactic shock (example of distributive

shock)
❑Septic shock
❑Neurogenic shock
22
Septic shock: a form of distributive shock
•Most common cause of death in ICUs in USA

•Initiated by release of bacterial toxins
•A complex condition that includes:
-Hypoperfusion resulting from loss of plasma into
the tissues ("third spacing")
-Reduced cardiac function resulting from toxins
that depress the myocardium
-Excess production of Nitric oxide and vasodilation
-Capillary endothelial damage and depletion of
intravascular volume
-Cellular hypoxia, lactic acidosis & multiorgan
failure 23
How to assess the type of shock?
•A patient is admitted with severe infection in

intensive care and is placed on a ventilator. He is
showing signs of hypoperfusion.
•He may be either in hypovolemic or in septic shock.
•Treatment of this patient requires definite diagnosis
of shock (Vasopressors could be catastrophic to a
hypovolemic patient; but are a valid treatment
choice in septic shock)
•Solution: Pulmonary artery catheterization (Swan-

Ganz catheter) and measurements of pressures
24
A comparison of readings obtained from a Swan-Ganz
catheter to distinguish hypovolemic & distributive shock
Type of shock CO SVR PWP CVP
Hypovolemic ↓ ↑ ↓ ↓
Distributive ↑ ↓↓ ↓ ↓
CO=Cardiac Output SVR=Systemic vascular resistance

PWP=Pulmonary wedge pressure CVP=Central venous pressure
↑ = Increase; ↓ = Decrease
25
C. Cardiogenic shock:
Conditions:
• Myocardial infarction
• Congestive Heart Failure
• Arrhythmias
26
Cardiogenic Shock: Pathophysiology
•Extensive infarction of LV (>30%)

•Impaired pumping of blood to myocardium
•Inadequate resting metabolic needs
•Positive feedback vicious cycle
•Congestion of the lungs and viscera resulting from
failure of the LV to put out all the venous blood
("congested shock“)
•The symptoms are:
Those of hypovolemic shock plus congestion of lungs
and viscera
•The incidence of shock in patients with myocardial
infarction is about 10%, and the mortality rate is 60–90%
27
A comparison of readings obtained from a Swan-Ganz
catheter in the three major categories of shock
Type of shock CO SVR PWP CVP
Hypovolemic ↓ ↑ ↓ ↓
Cardiogenic ↓ ↑ ↑ ↑
Distributive ↑ ↓↓ ↓ ↓
CO=Cardiac Output SVR=Systemic vascular resistance

PWP=Pulmonary wedge pressure CVP=Central venous pressure
↑ = Increase; ↓ = Decrease 28
X
↑PWP &
↑CVP
in cardiogenic
shock
29
D. Obstructive shock:
Conditions:
• Pulmonary embolism (massive)
• Tension pneumothorax
• Cardiac tamponade
• Cardiac tumor
30
Patient:
A 54 year old man develops sudden onset of
dyspnea and hypotension in the coronary care unit.
He was admitted five days back following an acute
MI. He is on thrombolytic agents.
PE: tachycardia; weak, thready pulse; tachypnea;
low BP; Pallor; cool, moist skin; mild cyanosis of lips
and fingers; He has significant pulsus paradoxus
(fall in arterial pulse is 16 mm Hg with inspiration);
Elevated JVP with absence of “y” descent
Auscultation of heart: Heat sounds are muffled
Auscultation of lungs: not significant
ECG: Low voltage waves
Imaging: Diastolic compression of the right ventricle;
31
pericardial effusion
The most likely diagnosis in patient is:
Cardiac tamponade
Other differentials:
➢Myocardial infarction
➢Pulmonary embolism
➢Tension pneumothorax
➢Constrictive pericarditis
Rupture of lateral and anterior free wall following

MI has high risk of Cardiac tamponade
32
Cardiac tamponade (an example of obstructive
shock):
• Sudden filling of the pericardial space with fluid
• Diagnosis:
Sudden onset of shortness of breath
Physical examination findings:
Three classic signs of Cardiac tamponade (Beck's
triad):
❑ Hypotension
❑ Elevated jugular venous pressure, and
❑ Muffled heart sounds
Additional finding: Pulsus paradoxus
33
Cardiac tamponade (an example of
obstructive shock):
Increase in intrapericardial pressure makes the

right ventricle to collapse first and left next.
34
Hemodynamics of Cardiac tamponade:
Sudden addition of fluid in the pericardial cavity

↓
Increase in intrapericardial pressure to the level of
the RA and RV pressures
↓
Right ventricle (RV) collapses first
↓
Reduced filling of the left ventricle
↓
Hypotension and shock.
35
Jugular Venous Pulse in Cardiac tamponade:
•JVP is elevated due to fluid in the cavity

•JVPulse tracing shows:
-Sharp and deeper “x” descent because high blood
pressure in JVP system fills the atrium when it is
relaxing.
-Absent “y” descent: as cardiac chamber is
strangulated, even after the opening of tricuspid
valve, blood cannot rapidly fall down due to high
pressure in ventricles.
Loss of the “y” descent associated with an
elevated JVP is diagnostic of Cardiac tamponade
36
Comparison of JVP tracings in Normal
and abnormal conditions
Pressure (mm Hg)
RV Constrictive Cardiac
Failure Pericarditis: Tamponade:
Rapid y descent Loss of
Makes v wave y descent
Normal prominent
37
Pulsus Paradoxus in Cardiac tamponade:
▪Arterial systolic blood pressure normally drops
about 5 mm Hg with inspiration.
▪Marked inspiratory drop in systolic blood
pressure (>10 mm Hg) is an important physical
finding in the diagnosis of cardiac tamponade
Arterial Pressure
Tracing
Reason: Ventricular Interdependence (“Zero-sum game”) &38

phase of breathing
The ECG findings in tamponade:
-Low voltage (amplitude) QRS complexes

-Electrical alternans (cyclic beat-to-beat
shift in the QRS axis)
Other causes of low voltage ECG:

-Chronic obstructive pulmonary disease
-Pleural effusion
-Pneumothorax
-Cardiomyopathy
-Obesity
39
Interaction between
CARDIAC OUTPUT and
VENOUS RETURN
40
Progressive course of the Heart Failure
Following an acute MI
C
A
B ●
D
41
Progressive course of Heart Failure
Following acute MI
Immediate effect of reduced contractility: (Point B)

There is a reduction in CO; This soon changes due to
the compensatory changes in the heart
Compensated failure: (Point C)
Blood volume expansion has partially restored the
CO by Starling’s mechanism; This gradually progresses
to massive volume expansion
Decompensated failure: (Point D)
As failure progresses, there is severe reduction in
contractility despite extreme increase in preload due
to overstretching of ventricle.
At this point, increase in preload is harmful to heart!
42
COMBINED GRAPH SHOWING CERTAIN CONDITIONS
Hypervolemia
Normal Blood Volume
Mild hypovolemia
with compensatory Increased Contractility
changes E
Cardiac Output Normal Contractility

N
or
Venous Return B
A Decreased Contractility
Hypovolemia Central Venous pressure
N: Normal
A: Hypovolemic shock
B: Cardiogenic shock with volume expansion
E: During exercise 43
Topic: EKG & CARDIAC ARRHYTHMIAS

1
Learning Objectives: Cardiology
Compare and contrast the clinical vignettes of cardiovascular

disorders listed in the next slide with reference to:
• Risk factors
• Etiology and pathogenic mechanism
• Altered morphology, physiology
• Signs and symptoms and basis for signs and symptoms
• Differential diagnosis
• Nutritional factors/aspects involved in the disease/disorder
• Prognosis, complications, mortality/survival
• Investigations (screening and confirmatory- list principles
involved and results expected)
2
List of cardiovascular disorders to be
covered in lectures
• Lectures 6: Cardiac Arrhythmias

• Lectures 7: Coronary Artery Diseases
• Lectures 8: Valvular Heart Diseases
• Lectures 9: Heart Failure
• Lectures 14: Shock
Each of the above lecture has a DLA posted in sakai

that has to be studied before attending the lectures.
Definition and Types of Arrhythmias
❖Arrhythmias are abnormal rhythms of

the heart
Classification:
❖Based on heart rate:
Bradyarrhythmias & Tachyarrhythmias
❖Based on site of origin:
Supraventricular & Ventricular
❖Based on mechanism:
Automatic, Triggered, or Re-entrant
arrhythmias 4
Clinical presentation of patients
with arrhythmias:
▪ Palpitation
▪ Lightheadedness
▪ Syncope
▪ Nonspecific presentations:
fatigue, dyspnea, or exertional
intolerance
5
Patient:
A 66-year-old man comes to the physician because

of an 8-month history of sudden onset of transient
loss of consciousness and postural tone. Each
episode lasts for about 10-15 seconds and he
recovers promptly without any resuscitative
measures. Episodes are often associated with
palpitations and lightheadedness.
PE: BP 95/56 mm Hg
Heart Rate - 44 beats/min, regular
JVP: shows prominent “a” waves
Rest of his physical examination is unremarkable
EKG: Number of P waves exceed that of QRS; P-R
interval-not measurable; Long R-R intervals. 6
Complete Heart Block
Other differentials are:

➢Sick sinus syndrome
➢Ventricular tachycardia
➢Aortic stenosis
➢Pulmonary stenosis
➢Postural hypotension
➢Vasomotor syncope
Presenting symptoms in this patient are:

Syncope, palpitations.
7
Diagnosis of cardiac arrhythmias:
❖The 12-lead electrocardiogram

❖Vagal maneuvers – carotid sinus massage
❖Electrophysiological (EP) studies - The ability to
trace specific pathways and map conduction
8
Normal Sinus Rhythm
P T
Q S
ECG findings:
•Rhythm – Regular (R-R interval same)
•Rate – 60 to100 beats/min
•QRS Duration - Normal
•P Wave - Visible before each QRS complex
•P-R Interval - Normal (<5 small Squares. Anything above
this would be 1st degree block)
•Indicates that the electrical signal is generated by the
sinus node and travelling in a normal fashion in the heart
9
Bradyarrhythmias:
TWO basic mechanisms for

bradyarrhythmias:
1. Reduced activity of the pacemaker

2. Conduction block
10
Common Bradyarrhythmias:
➢Sinus bradycardia-Reduced pacemaker activity
➢First-degree heart block

➢Second-degree heart block Conduction Block
➢Third-degree heart block
11
1st Degree AV Block
ECG findings:
•Rhythm – Regular
•Rate - Normal
•P wave-to-QRS ratio - 1:1
•P Wave rate - Normal
•P-R Interval - Prolonged (>5 small squares)
Mechanism: A conduction delay through the AV node but

all electrical signals reach the ventricles. This rarely causes
any problems by itself.
12
Example: Old age, Trained athletes.
2nd Degree Block – Mobitz Type 1 (Wenckebach)
Dropped QRS complex
P P P P P P P P
ECG findings:
•Rhythm - Regularly irregular
•Rate - Normal or Slow
•P:QRS ratio - 1:1 for 2,3 or 4 cycles then 1:0.
•P Wave rate - Normal but faster than QRS rate
•P-R Interval - Progressive lengthening of P-R interval until a
QRS complex is dropped
Mechanism: Gradual increase in refractoriness causes
conduction block of some; not all atrial impulses get through
13
to the ventricles at the AV node.
2nd Degree Block – Mobitz Type 2
Dropped QRS complex Dropped QRS complex
P P P P P P P P
ECG findings:
•Rhythm - Regular between the conducted beats
•Rate - Normal or Slow
•QRS Duration – Normal
•P:QRS ratio - 2:1, 3:1
•P-R Interval - Normal or prolonged but constant
Mechanism: Electrical excitation sometimes fails to pass
through the A-V node or bundle of His downwards.
Electrical conduction of the conducted beats is the same
always (hence have a constant P-R interval) 14
3rd Degree Block: Complete AV block
ECG findings:
•Rhythm - Regular
•Rate - Slow
•QRS Duration - Prolonged
•P Wave - Unrelated to QRS (AV dissociation)
•P-R Interval – Variation
Mechanism: No atrial impulses pass through the
atrioventricular node. Ventricles generate their own impulse
through an 'escape mechanism' from a focus somewhere
within the ventricle at a regular, slow rate. 15
Tachyarrhythmias:
THREE basic mechanisms for

Tachyarrhythmias:
1.Increased automaticity of pacemaker

2.Spontaneous depolarizations
3.Reentrant circuit – most common
16
Mechanism of Tachyarrhythmias:1.Increased
automaticity of the pace maker:
More rapid phase 4 depolarization of the action

potential of SA node leads to faster heart rate
With increased HR
Before increased HR
Phase 4
Examples: Sinus Tachycardia as in hyperthyroidism,
Anxiety, Pheochromocytoma and pulm embolism 17
300 150 Sinus Tachycardia
100
R R R
P T P T P T
ECG findings:
•Rhythm - Regular
•Rate - More than 100 beats per minute
•P-R Interval - Normal
•Origin: Impulse generating the heart beats are from
SA node, but at a faster pace than normal.
Occurs in: Exercise, stress, fright, fever 18
Mechanism of Tachyarrhythmias: 2.
Spontaneous depolarizations:
•If repolarization is delayed (longer plateau
period), spontaneous depolarizations
(EAD/DAD) can occur in phase 3 or phase 4 of
the ventricular/atrial action potential
•These depolarizations can repetitively reach
threshold and cause tachycardia
Ventricular EAD=Early Afterdepolarization

Action Potential DAD=Delayed Afterdepolarization19
Examples of tachyarrhythmias from
spontaneous depolarizations (EAD/DAD) are:
- Long QT syndrome: Due to several specific ion

channel defects
-Torsades de pointes
Class III antiarrhythmic drugs block K+ channels and

hence their toxicity may produce tachyarrhythmias
20
Long QT syndrome: Reduced function of potassium
channels leads to a prolonged plateau period, leading
to a prolonged QT interval
•These patients are prone

EKG T T’ to triggered activity
because of reactivation of
sodium and calcium
channels [early
Action afterdepolarizations (EAD)]
Potential
•Triggered activity in the
ventricles can lead to life-
threatening ventricular
arrhythmias 21
Torsades de pointes:
•A “twisting”, polymorphic ventricular
tachyarrhythmia
•Occurs in situations where the QT interval has
been prolonged
•The phrase "Torsades de Pointes" means
"twisting of the spikes", referring to the
characteristic appearance of the EKG
• Triggered arrhythmia may cause blackouts or
even sudden death.
22
23
Torsades de pointes is dangerous because it may
turn into fatal ventricular fibrillation (VF)
24
Mechanism of Tachyarrhythmias: 3.
Reentrant circuit:
▪Re-entry requires (i) an area of slow conduction
with unidirectional block, and (ii) an area of fast
conduction (two pathways in a region).
A- Block at slow tract & fast moves down
B- Slow moves retrograde in fast tract and
blocks the incoming next fast
C- Retrograde fast reenters in the slow tract
A B C 25
Examples of tachyarrhythmias due to Re-
entrant circuits:
▪Those originate in Atrium & known as

SupraVentricular Tachycardia (SVT):
Examples include, Atrial tachycardia, atrial
flutter and atrial fibrillation.
▪Those originate in Ventricle: Examples

include, Ventricular Tachycardia (VT),
Ventricular fibrillation.
▪Those have Atrio-Ventricular origin: Example,

as in Wolff-Parkinson-White syndrome 26
Commonly occurring
SVTs:
1. Atrial Tachycardia
1 2 (atrial rate: 150-250/min;
single focus)
2. Atrial Flutter
(atrial rate: 250-350/min;
single focus)
3. Atrial Fibrillation
(atrial rate: 350-600/min
3 & multifoci of origin)
27
Patient:
A 44-year-old man comes to the physician
because of occasional palpitations, shortness of
breath, dizziness and chest discomfort.
Physical examination:
Pulse: Irregularly irregular
JVP: absent “a” waves
Heart sounds: variable intensity S1
Lab:
EKG: Variable ventricular rate (80-180);
Indistinguishable P waves; PR interval not
measurable & Irregular RR intervals.
Blood: CK-MB normal
Chest X ray: Normal 28
Atrial Fibrillation (AF)
❖Atrial tachycardia
❖Atrial flutter
❖Ventricular tachycardia
❖Wolff-Parkinson-White syndrome
Most common complication of AF:

systemic thromboembolism
29
Atrial Fibrillation – an example of SVT
ECG findings:
•Rhythm - Irregularly irregular
•Heart Rate - usually 80-180 beats per minute
•QRS Duration - Usually normal
•P Wave - Not distinguishable as the atria are firing off
all over (absent or fibrillatory waves)
•P-R Interval - Not measurable
•Origin: Multiple sites within the atria are generating their
own electrical impulses, some of them pass through AV
node to ventricles, based on the refractoriness of the AVN.
This leads to irregular conduction of impulses to the
30
ventricles and hence generates an irregular pulse.
How do you differentiate
Supraventricular Tachycardia (SVT)
from Ventricular Tachycardia (VT)
Look at the QRS complex:

If the QRS complex is narrow or within
normal limits → SVT
If the QRS complex is wide → VT.
31
Narrow/Normal, QRS complex:
Indicates that depolarization of the ventricles must
be occurring normally over the specialized
conduction tissues and the arrhythmia must be
originating at or above the AV node.
Tachycardia with such QRS are - SVT
Wide QRS complex:

Indicates that ventricular depolarization is NOT
occurring normally over the specialized conduction
tissues
Tachycardia with such QRS are - VT
32
SVT: Narrow/normal QRS
VT: Wide QRS
33
Ventricular Tachycardia (VT)
ECG findings:
•Rhythm - Regular
•Rate - 180-190 Beats per minute
•QRS Duration – Prolonged (“wide QRS”)
•P Wave - Not seen
Mechanism: Abnormal tissues in the ventricle generate a
rapid heart rate and tachyarrhythmia.
Associated with a poor cardiac output.
34
Patient:
A 17-year-old boy comes to the physician because
of recurrent episodes of dizziness. During each
episode, he feels intense anxiety with palpitations
and breathlessness. He is asymptomatic in between
episodes; There is no h/o chest pain or syncope.
No abnormalities detected
Lab:
EKG: Short PR interval; wide QRS with a slurred
upstroke.
Blood: Normal; Chest X ray: Normal
35
Most likely diagnosis in this patient:
Wolff-Parkinson-White Syndrome
❖Atrial fibrillation
❖Atrial flutter
❖Syncope
❖Nodal re-entry tachycardia
❖Ebstein anomaly
Electrophysiological studies confirm presence

of a bypass tract (Bundle of Kent)
36
Wolff-Parkinson-White syndrome:
In WPW syndrome, the

Bundle of Kent (the Extra
Pathway) can “Complete the
Circuit” allowing Re-Entry
tachycardia
EKG at rest:
•Short PR interval
•Wide QRS
•Delta wave
(at arrow)
37
Ventricular Fibrillation (VF)
ECG findings:
•Rhythm - Irregular
•Rate - 300+, disorganized
•QRS Duration - Not recognizable
•P Wave - Not seen
•This patient needs to be defibrillated!!
-Disorganized electrical signals cause the ventricles to quiver
instead to contract in a rhythmic fashion
-Patient becomes unconscious as there in NO cardiac output
-This condition may occur during or after a myocardial infarct.
38
A Quick approach to Arrhythmias:
• First look at the heart rate:
>100 bpm = tachyarrhythmia
<60 bpm = bradyarrhythmia
• Secondly assess the origin of the arrhythmia:
If the QRS <120ms, then it is either a sinus arrhythmia,
supraventricular tachycardia or a junctional tachycardia.
If the QRS >120ms, it is either a ventricular tachycardia or
a supraventricular rhythm with additional bundle branch
block or an additional accessory AV pathway.
• Are there extra beats? → Ectopic (QRS without P)
39
Topic: CORONARY ARTERY DISEASE

1
Patient:
A 64-year-old man is brought to the emergency dept.
because of a 30 minute history of nausea, dyspnea
and crushing substernal chest pain. The pain
radiates to the left arm and is not relieved by rest.
Patient has a sedentary lifestyle, obesity,
hypercholesterolemia, type 2 diabetes mellitus.
PE: BP 100/60 mm Hg; rapid, low volume
pulse; diaphoresis; Bibasilar rales on chest
auscultation.
Laboratory findings:
EKG - Elevated of ST segment and inverted T waves
Blood biomarkers: ↑ CK-MB; ↑ Troponin T & I
Chest X ray: Bilateral mild pulm edema without
2
pleural disease or widening of the mediastinum.
Most likely diagnosis in patient:
Acute Myocardial Infarction
Other differential diagnosis:

❖ Gastroesophageal reflux disease
❖ Myocarditis
❖ Pneumothorax
❖ Pulmonary embolism
❖ Acute pancreatitis
❖ Anxiety
3
Clinical presentations of CAD include:
❖Silent ischemia
❖Angina pectoris
❖Acute coronary syndromes –
unstable angina and acute myocardial
infarction (MI)
❖Sudden cardiac death (SCD)
4
Anatomy of
Coronary Circulation
LCA
RCA LCX
Posterior descending
(postr interventricular) artery
Acute marginal
artery
LAD
Coronary Veins
5
Coronary Circulation:
LAD
territory RCA & LCX
territory
Septal
perfusion 6
Etiology of CAD:
•Atherosclerotic obstruction of the large
epicardial vessels - the most common cause
•Spasm of the coronary arteries
•Emboli
•Congenital abnormalities - rare cause
7
Atherosclerosis and Coronary artery Disease
•Large coronary vessels and epicardial

vessels are involved
•Most common sites: In areas exposed

to increased shear stresses such as
bending points and bifurcations
8
How Hypertension is a risk factor for CAD
& atherosclerosis?
Elevated blood pressure

↓
Increase in shear stress on the endothelium
↓
Infiltration of low-density lipoproteins (LDL) into
the subendothelial region
↓
Atherosclerosis
↓
Coronary artery disease (CAD)
9
Signs/Symptoms of CAD:
➢Chest Pain
➢Shortness of breath
➢Tachycardia
➢Fourth heart sound (S4)
➢Cardiogenic shock
10
Chest Pain:
•Chest pain is mediated by sympathetic afferent
fibers: T1-T5
•In the spinal cord, the pain impulses converge
with impulses from other somatic structures and
hence radiated to the chest wall, back, and arm
•The actual trigger for nerve stimulation is
adenosine. Blocking adenosine receptor (P1)
with aminophylline leads to reduced anginal
pain
11
Basis for clinical manifestations in CAD
Myocardial ischemia
Systolic dysfunction of Myocardial stiffness

LV ↓
↓ Diastolic dysfunction
Pulmonary congestion ↓
↓ Fourth Heart Sound (S4)
Shortness of breath
12
Clinical presentations of CAD:
❖Angina pectoris
❖Acute coronary syndromes (ACS)
13
Angina pectoris
•Typical angina is a syndrome defined by the
presence of three primary findings:
-Substernal chest discomfort/pain
-Aggravated by exertion or emotional
stress, and
-Relieved by nitroglycerine or rest
•Atypical angina: lacks one of the three main

characteristics
•If only the first feature is present, the discomfort
is more likely to be noncardiac in origin and is
often accompanied with conditions of the lungs,
esophagus, and chest wall 14
Pathophysiology of Angina:
Cellular ischemia occurs by

i) Increased myocardial O2 demand:
Eg: Thyrotoxicosis, Hypertrophy, High
afterload, High heart rate.
ii) Absolute reduction in O2 supply:

Eg: atherosclerosis and spasm.
iii) Combination of i & ii (eg:cocaine abuse)
15
Diagnosis of Angina pectoris:
•Typical symptoms
•ECG
•Stress testing with ECG or
imaging (echocardiographic or
nuclear)
•Coronary angiography for
significant symptoms or positive
stress test
16
ECG in angina:
ECG changes during an attack:

•T wave discordant to the QRS complex
•ST-segment depression
•Decreased R-wave height
ECG at rest:
• Normal at rest (30%)
•In the remaining 70%, the ECG shows
evidence of previous infarction, or hypertrophy.
17
ECG changes in angina pectoris
•Depression of ST segment; T wave inversion
Normal ECG
P T
S Patient’s ECG
ST segment
depression T wave inversion
J point
18
Location of lesion (ischemia/MI) by
observing changes in 12 lead ECG:
Inferior (diaphragmatic) wall: Lead II, III & aVF
Anterior wall/Anteroseptal: V1-V4
Lateral wall: Lead I, aVL, V5, V6
Right Ventricle: V1, V2 & V3
Septal wall : V1, V2

19
Lateral wall ischemia
20
Inferior & Lateral wall ischemia
21
Stress testing in angina:
• If a patient has a normal resting ECG and can
exercise, exercise stress testing with ECG is done
• A negative stress ECG usually rules out angina
pectoris and CAD; a positive result may or may not
represent coronary ischemia and indicates need for
further testing
• Nuclear imaging to assess LV function in response
to stress: identifies areas of ischemia, infarction,
viable tissue and, site and extent of myocardium at
risk.
22
Angiography in CAD:
• Gold standard for diagnosing CAD but is not
always necessary to confirm the diagnosis
• Indicated primarily to locate and assess
severity of coronary artery lesions
•Obstruction is assumed to be physiologically
significant when the luminal diameter is
reduced more than 70% of original
23
Acute Coronary Syndromes (ACS):
❖Unstable Angina (UA)

❖Non-ST elevation Myocardial Infarction
(NSTEMI)
❖ST-elevation Myocardial Infarction
(STEMI)
•These syndromes represent acute myocardial ischemia
•Most likely due to obstructive coronary artery disease
•All require early diagnosis and clinical management
•Produce potentially catastrophic complications,
including death
24
Unstable Angina
Characters of Chest pain in unstable angina:
-Occurs at rest
-Prolonged, lasting greater than 20 minutes
-Has been present in the past but has changed
in frequency, severity, or threshold needed to
bring on symptoms
-Refractory to nitroglycerin
25
Pathophysiology of Unstable Angina
•Plaque disruption & fissuring

•Platelet activation: adhesion, aggregation &
secretion
•Thrombotic occlusion
•Platelet release of vasoconstrictors such as
thromboxane A2 or serotonin that contribute to
further decrease in flow
26
Diagnosis of Unstable angina:
❖Characteristic chest pain
❖ECG: Variable patterns during an episode of

chest pain such as:
-Transient ST-segment elevation
-Transient ST-segment depression
-T-wave inversion
A normal ECG does not exclude the possibility that

chest pain is ischemic in origin!
27
Myocardial Infarction: causes
❖Atherosclerosis – most common

❖Other causes:
-Coronary emboli caused by endocarditis, mural
thrombi, prosthetic valves, or neoplasms;
-Inflammatory processes, including viral
infections (e.g., coxsackie B virus);
-Radiation-induced coronary stenosis;
-Congenital abnormalities in a coronary artery;
-Cocaine abuse.
❖Rare causes:
Hurler’s syndrome, homocystinuria, rheumatoid
arthritis, and systemic lupus erythematosus. 28
Pathophysiology of MI
Within 60 sec after coronary artery occlusion
↓
Myocardial oxygen tension in the affected cells
falls to zero
↓
Rapid shift to anaerobic metabolism in myocytes
↓
Lactic acid production
↓
Dysfunction in myocardial contraction and
relaxation.
If re-perfusion is not done, an irreversible injury
occurs.
29
Stages of Irreversible Myocardial Injury
❑Diffuse mitochondrial swelling

❑Damage to the cell membrane
❑Coagulation necrosis 18-72 Hours
❑Macrophage invasion
4-10 days
❑Soft tissue
❑Granulation tissue formation 10th day
❑Scar tissue 8 week
30
ST Elevation Myocardial Infarction
(STEMI):
WHO Criteria
❑ Clinical history of ischemic type
chest pain >20 minutes
❑ Changes in serial ECG tracings
❑ Rise and fall of serum cardiac
biomarkers
Must meet 2 out of 3 criteria
31
Physical Examination Findings in MI:
•General: Restless agitated, anguished facies,

clenched fist (Levine’s sign)
•Increased Heart rate and Respiratory rate
•Signs of hypoperfusion: low volume pulse, pale,
cold and clammy, ashen extremities
•Evidence of heart failure: Jugular venous
distention, crackles on lung exam, left ventricular
heave
•S3 and S4 gallops & murmurs
32
Evidences of MI
EKG Evidence for ischemia, injury &
loss of electrical function
Biochemistry Evidence of myocardial cell
death recovered from blood
Imaging Evidence for reduction of tissue
perfusion & abnormal wall
motion
Pathology Evidence of cell death
33
ECG changes in STEMI
Elevation of ST segment; pathologic Q wave
A B C D
A. Normal ECG prior to MI

B. During acute stage of MI: Marked ST elevation
C. After a few hours of MI: Pathologic Q waves,
less ST elevation and inverted T wave
D. After many days of MI: Pathologic Q wave alone
persists, indicating an old infarct. 34
Serial EKG changes in STEMI over the time
35
Acute lateral wall infarction (tracing obtained within a few
hours of onset of illness)
I aVL
V5 V6
There is striking hyperacute ST-segment elevation in

leads I, aVL, V5, and V6 and reciprocal depression in
other leads.
Artery most likely affected is : LCX artery 36
Acute Septal wall Infarction
Note the striking ECG changes in V2

The artery most likely affected is: LAD artery
37
Acute Anteroseptal Infarction
ECG changes in V1, V2, V3 & V4

Arteries involved: RCA and LAD artery
38
Acute Inferior wall MI
ECG changes in II, III and aVF

Artery involved: RCA/Post descending br
39
Biomarkers in acute MI
▪ Myoglobin
▪ MB isoenzyme of creatine kinase
(CK-MB)
▪ Cardiac troponin I (cTnI)
▪ Cardiac troponin T (cTnT)
40
Timing of Release of Various Biomarkers After Acute
Ischemic Myocardial Infarction
*Specific biomarker
for re-infarction
CKMB=MB isoenzyme of creatine kinase 41

Why cardiac Troponin-I and NOT Troponin-T is
an important biomarker?
•The cardiac isoform of TnI (cTnI) is unique in that it
has never been isolated from skeletal muscle
•cTnI appears to be uniformly distributed throughout
the atria and ventricles
•High specificity of cTnI for cardiac tissue makes it an
ideal biomarker of myocardial injury
•Although cTnI is 100% specific for cardiac injury, it is
not 100% specific solely for MI.
42
Non-ST-segment elevation MI
(NSTEMI, subendocardial MI):
▪Myocardial necrosis - evidenced by cardiac
markers in blood
▪Symptoms/signs similar to STEMI
▪Absent ECG changes
43
COMPLICATIONS OF ACUTE MI
➢ Cardiogenic shock
➢ Tachyarrhythmias including VF
➢ Bradyarrhythmias including heart block
➢ Left Ventricle failure & Pulmonary edema
➢ Right Ventricle failure if RV infarct
➢ Acute Mitral Regurgitation
➢ Rupture of interventricular septum
➢ Pulmonary embolism
➢ Cardiac rupture
➢ Dressler's syndrome
44
Conditions that can cause SHOCK in acute
MI:
•Obstruction in the LCA or LAD artery: severe LV
dysfunction.
•Necrosis of the septum: Ventricular septal defect.
•Rupture of the anterior free wall of LV from occlusion of
the LAD artery
•Rupture of the lateral free wall of LV from occlusion of
the left circumflex coronary artery
(Rupture of lateral/anterior wall leads to pericardial
effusion and cardiac tamponade)
•Rupture of the papillary muscles (posterior is most
affected due to single bl supply) produces severe mitral
regurgitation
Rupture of myocardial tissue usually occurs
4–10 days following acute infarction 45
Topic: VALVULAR HEART DISEASES

1
Classification of valvular heart disease
Dysfunctional cardiac valves can be:

Narrow (stenosis) or
Leaky (regurgitation/insufficiency)
The most common are:

❖Mitral stenosis (MS)
❖Mitral regurgitation (MR)
❖Aortic stenosis (AS)
❖Aortic regurgitation (AR)
2
Heart murmurs
Classification:
❖ Systolic – while the ventricle is contracting;
between S1 and S2
❖ Diastolic – while ventricle is filling;
between S2 and S1
❖ Continuous murmur
Pay attention on:

- Timing and duration
- Intensity (grade I to VI)
- Quality (blowing, harsh, rumbling)
- Radiation (to the neck, axilla, or back)
All diastolic and continuous murmurs are abnormal
and pathological 3
Phonocardiographic
Systolic Murmurs: representation
•An early systolic (or mid systolic) ejection
murmur:
-begins with S1 and ends before S2
-classically diamond-shaped (crescendo-
decrescendo)
•Pansystolic (holosystolic) murmur:

-begins with S1 and extend to S2
-classically high frequency, blowing in quality,
and relatively uniform in intensity
-all pansystolic murmurs are pathologic
•Late systolic murmur:

-occurs in the latter part of systole, well after S1
and end in or after S2
-all late systolic murmurs are pathologic 4
Examples for Systolic Murmurs:
Timing Example Heard best Radiation
Pansystolic Mitral Apex Axilla or
(holosystolic) regurgitation back
: VSD LLSB
Tricuspid LLSB Neck
regurgitation
Early systolic Aortic stenosis Second IS Neck
(Midsystolic): HOCM Apex, LLSB
Late systolic: Mitral valve Apex, LLSB
prolapse
LLSB=Lower left sternal border

HOCM=Hypertrophic obstructive cardiomyopathy
VSD=Ventricular septal defect; IS=Intercostal space 5
Examples for Diastolic Murmurs:
Timing Example Heard best

Early diastolic: Aortic Left sternal
(high pitched, Regurgitation border, third
decrescendo) intercostal
space
Middiastolic: Mitral stenosis Apex, with the
(low pitched) bell
Tricuspid stenosis Left sternal
border
All diastolic murmurs are pathological

6
Patient:
A 50 year old male presents with complaints of
substernal chest pain, which increases with
exertion, and shortness of breath which is
starting to limit his lifestyle. He has no risk factors
for coronary artery disease.
On Physical Exam you find the following:
▪Delayed carotid upstroke
▪Apical impulse is sustained but not displaced
laterally
▪An ejection systolic murmur in the second
intercostal space
ECG: Left axis deviation with high voltage QRS in
V4-V6 7
The most likely diagnosis:
Aortic stenosis
Other possible differentials:

➢Mitral regurgitation
➢Mitral valve prolapse
➢Hypertrophic Obstructive Cardiomyopathy
➢Myocardial Infarction
8
Aortic Stenosis (AS)
Causes of Aortic Stenosis:
Type Clinical presentation

Congenital* Patients below age 30
Rheumatic Patients age 30-70; Accompanying
AR and MS is frequent
Degenerative Patients above 70; Prevalent in
patients with diabetes or
hypercholesterolemia
*Bicuspid valve is the most common cause in USA

under all ages
9
Pathophysiology of AS:
Stenosed aortic valve increases afterload on the LV

↓
Increased LV pressure during systole
↓
Increased left ventricular wall thickness while the cavitary
radius remains relatively unchanged due to parallel
replication of sarcomeres producing
"concentric hypertrophy"
↓
Decrease in ventricular compliance
↓
Significant increase in left ventricular end-diastolic
pressure
10
Aortic stenosis: Hemodynamic changes
• Narrowing around the

aortic valve
• Aortic valve acts as
major resistance for
flow (afterload) during
ejection
• Left ventricular
pressure rises to very
high levels during
systole
• Left ventricular
hypertrophy
• Systolic murmur
appears 11
Pressure profile in
Aortic Stenosis
Pressure gradient
between LVP
and AP during
ejection
Systolic Murmur
Phonocardiogram 12
Physical examination in AS:
Palpation of the carotid pulse reveals a pulsus
parvus et tardus - both decreased (parvus) and
late (tardus) relative to the apical impulse
Auscultation:
-Midsystolic or earlysystolic murmur is heard,
loudest at the base of the heart, and often with
radiation to the sternal notch and the neck
-High-pitched aortic ejection click can be heard
just after the first heart sound (S1)
-Fourth heart sound (S4) is often present
13
CLINICAL CONDITIONS WITH ABNORMAL ARTERIAL
PULSE
• AS: pulsus parvus et

tardus or Anacrotic pulse
• AR: Water-hammer,
Bisferiens pulse
• HOCM: Bisferiens pulse
• CHF: Pulsus Alternans
• Cardiac Tamponade:
Pulsus Paradoxus
14
Hypertrophic obstructive cardiomyopathy
(HOCM):
•Subvalvular aortic stenosis due to severe
hypertrophy of the septum of the left heart
•Manifested by a systolic murmur noted on physical
examination
•Obstruction of outflow tract in this case is dynamic
•Greater obstruction occurs when preload is
decreased - Standing and Valsalva's maneuver
(both decrease venous return) and the murmur
becomes intense
•Both of these maneuvers cause a decrease in the
intensity of murmur in case of organic AS, because
less volume of blood flows across the stenotic
15
aortic valve
16
Aortic Regurgitation (AR)
Causes for AR:
•Endocarditis
•Rheumatic disease Valvular site
•Ankylosing spondylitis
•Congenital
Aortic site:
▪Aortic aneurysm
▪Heritable disorders of connective tissue - Marfan's
syndrome, Ehlers-Danlos syndrome, Osteogenesis
imperfecta
▪Inflammatory - Aortitis (Takayasu), Syphilis, Ankylosing
spondylitis, Rheumatoid arthritis and SLE
▪Aortic dissection 17
Pathophysiology of AR:
Regurgitant aortic valve produces a volume load

on the left ventricle
↓
Increased end diastolic volume and pressure
↓
Elongation and replication of sarcomeres in series,
leading to increased ventricular volume
↓
Enlarged ventricular cavity producing
"eccentric hypertrophy"
↓
Chronic AR leads to huge ventricular volumes
18
Comparison between the eccentric (volume
overload) and the concentric (pressure
overload) hypertrophy
19
Aortic regurgitation: Hemodynamic changes
❖An incompetent (leaky) aortic valve allows

blood to regurgitate from aorta to LV
during ventricular diastole
❖An elevated left ventricular end diastolic
volume and pressure (↑ preload)
❖Increased left ventricular and aortic
systolic pressures
❖Decreased aortic diastolic pressure
❖Widened aortic pulse pressure
❖Diastolic murmur appears.
20
Pressure profile in AR
•High LVP and AP

during systole
•Low AP during diastole
•High pulse pressure
Aortic pressure (AP)
Left atrial pressure

Left ventricular pressure (LVP)
Phonocardiogram Diastolic Murmur

21
Physical examination in AR: (i-iv)
i) Hyperdynamic (pounding) arterial pulses:

- A widened pulse pressure is responsible for
several characteristic peripheral signs
- Palpation of the peripheral pulse reveals a
sudden rise and then drop in pressure
(water-hammer or Corrigan's pulse)
- Head bobbing (DeMusset's sign)
- Rhythmic pulsation of the uvula (Müller's
sign)
- Arterial pulsation seen in the nail bed
(Quincke's pulse)
22
ii) Apical impulse:
Hyperdynamic and displaced laterally – due to
the increased volume and forceful contraction
of the left ventricle
iii) Soft S1 & S2:

S2 is soft due to improper closure
S1 is also soft because of early mitral valve
closure from elevated ventricular volume and
pressure.
23
iv) Auscultation for murmur in AR:
A high-pitched, blowing, decrescendo early

diastolic murmur heard best along the left sternal
border - due to regurgitant flow into left ventricle
(hall mark sign).
24
Mitral Stenosis (MS)
25
Pathophysiology of MS:
Mitral valve is narrow

↓
Insufficient blood flows to LV during ventricular
diastole ↓
Enlargement of LA with accumulated blood
↓
Elevated left atrial pressure during ventricular
diastole ↓
Elevated pulmonary venous pressure (pulm
wedge pressure) and pulmonary hypertension
↓
Right Ventricular Failure 26
Mitral stenosis: Hemodynamic changes
• Narrowing of mitral valve
reduces the amount of
blood that flows forward
through it
• The left atrium enlarges
and left atrial pressure
builds up
• There will be a pressure
gradient between left
atrium and left ventricle
throughout diastole
• Mid Diastolic murmur
appears 27
Pressure profile in MS
Pressure gradient
between LVP
and LAP throughout
ventricular filling
Diastolic Murmur
Phonocardiogram
28
i) Auscultation of heart:
• The characteristic murmur of MS is a low
pitched diastolic rumble in the apex
• Diastolic rumble occurs because of turbulent
flow across the narrowed mitral valve orifice
• In addition, an opening snap (OS) may be
heard before the diastolic rumble
• Opening snap is analogous to the ejection click
described for AS
• A2-OS interval is useful in determining the
severity of MS: “shorter the interval, greater
would be the severity of the disease”
29
ii) Auscultation of the lungs:
Reveals bilateral rales (crackles) because of

elevated pulmonary capillary pressure that
results in accumulation of intra-alveolar fluid
30
Mitral Regurgitation (MR)
31
• Most common cause of MR is Mitral valve

prolapse, followed by coronary artery disease
• Onset of MR may be acute or chronic
32
Pathophysiology of acute MR:
In acute mitral regurgitation, the sudden

volume overload on the LA and LV is not
compensated for by chamber enlargement
and hypertrophy
↓
Prominent atrial v waves with transmission of
this elevated LA pressure
↓
Elevated pressure in pulmonary capillaries
↓
Development of pulmonary edema
33
Pathophysiology of chronic MR:
Mitral valve fails to close properly during

ventricular systole
↓
Regurgitation of blood into the LA from the LV
occurs during systole
↓
Enlargement of LA and LV to accommodate
volume load
↓
Concomitant hypertrophy of the ventricular wall
↓
Increased diastolic filling of the left ventricle 34
MR: Hemodynamic changes
❖An incompetent (leaky) mitral valve allows
blood to regurgitate from LV to LA during
ventricular systole
❖An elevated left atrial volume and pressure
during ventricular systole
❖Left ventricular volume and also pressure
increase during ventricular diastole
❖There is no pressure gradient between LA
and LV throughout during ventricular filling
❖Systolic murmur appears
35
Mitral Insufficiency (Regurgitation)
Aortic pressure
Left ventricular pressure
An elevated LAP during

systole with no gradient
between LVP and LAP
during ventricular diastole
Left atrial pressure
Phonocardiogram Holosystolic Murmur

36
Physical Examination in MR:
i) Laterally displaced and Hyperdynamic
Apical Impulse:
Reason for lateral displacement - The
compensatory increase in left ventricular
volume and wall thickness
Reason for hyperdynamic - The ventricle now has
a low-pressure chamber (LA) into which to eject
blood
When mitral regurgitation develops suddenly, the
apical impulse is not displaced or
hyperdynamic, because the LV has not had
enough time for compensatory volume
increases to occur
37
ii) Holosystolic (pansystolic) Murmur:
•Regurgitant flow into the LA produces a high-

pitched murmur that is heard throughout systole
•The murmur begins with S1, continues to the S2
•Murmur is of constant intensity throughout systole
•Unlike the murmur of AS, there is no variation in
the intensity of the murmur as the heart rate
changes
•It is heard best at the apex and radiates to the
axilla
38
iii) Muffled S1 and S2:
The murmur often obscures the first and second

heart sounds
iv) Loud S3:
A third heart sound is heard in a patient with

severe MR or if heart failure is present
39
Mitral Valve Prolapse
• Incidence
– 1.0-2.0 % of population
– Female > Male (3:1)
• Clinical Presentation
– Asymptomatic
– Symptomatic
• Palpitations
• Arrhythmias
• Atypical Chest Pain
40
MVP-Physical Exam/Diagnosis
• Thin, young females
• Abnormalities:
– Associated skeletal abnormalities
• Auscultation:
– Mid-systolic click & late systolic murmur
– Systolic murmur becomes louder and
longer by Valsalva maneuver or on
standing (decreasing venous return)
Phonocardiogram: c=midsystolic click
41
Mitral Valve Prolapse
LA
LV
42
Directed Learning Activity in Cardiology
Topic: Basic Cardiac Physiology,

Left Ventricular Failure
Right Ventricular Failure
1
This DLA must be studied before
attending Lecture 8 on Heart
Failure
2
Normal Left ventricular pressure-volume loop
1 to 2 : Isovolumetric ventricular contraction
2 to 3 : Left ventricular ejection
3 to 4 : Isovolumetric ventricular relaxation
4 to 1 : Left ventricular filling
Aortic valve
closes(S2)
3 Aortic valve
opens
ESV 2
SV
Mitral valve Mitral valve
opens closes(S1)
4 1
EDV
3
ESPVR = End systolic pressure-volume relationship
4
An Index of myocardial contractility (inotropy)
Frank-Starling relationship
Systolic contractile performance (represented by
stroke volume or CO) is proportional to preload within
the normal physiologic range
5
Stroke Volume (SV)
•SV is the volume of blood ejected by each

ventricle in a beat
•It is the difference between end diastolic
volume and end systolic volume
SV = (EDV – ESV) ml per beat
•SV increases with an increase in EDV

•SV increases with a decrease in ESV
•When both increase in EDV and decrease in ESV
occur, SV increases maximally
6
Ejection Fraction (EF)
•EF is the fraction of end diastolic volume

that is ejected in one beat
SV
EF =
EDV
•It is an index of myocardial contractility

•Increase in EF indicates positive inotropic effect
•Decrease in EF indicates negative inotropic effect
7
Correlation between ECG waves, JVP waves
and Heart sounds during a cardiac cycle
EKG waves
JVP waves
First & Second Heart

Sounds 8
Causes of JVP waves:

a wave: atrial systole
c wave: Bulging of atrioventricular valve into atrial cavity during isometric
ventricular contraction
x descent: Downward movement of atrio-ventricular orifice during
ventricular ejection and drop in atrial pressure
v wave: atrial filling wave
y descent: atria emptying into ventricle when the a-v valve opens.
Correlation between Heart sounds (S1, S2, S3 &
S4) and ECG waves during phases of a cardiac
cycle
S1, S2 & S3 R
T
P
ECG
Q S
S1, S2 & S4
Systole Diastole
9
Directed Learning Activity (DLA):
Topic: LEFT VENTRICULAR FAILURE (LVF)
10
Explanation for dyspnea in patient
with LVF
❖ Shortness of breath (dyspnea) of

different degree is the most leading
patient presentation
❖ Causes for dyspnea is pulmonary
congestion originated by different
mechanisms
11
Dyspnea in LVF: Hemodynamic Basis
produces dyspnea
by various ways
(i-v in next 5 slides)
12
i) Shortness of Breath (Dyspnea):
Elevated pulmonary capillary pressures due to an

elevated left ventricular and atrial pressures
↓
pulmonary venous congestion and pulmonary
edema
↓
Stimulation of juxtacapillary J receptors resulting
in reflex shallow and rapid breathing.
Edema of the bronchial walls can lead to small

airway obstruction and produce wheezing known
as "cardiac asthma"
13
ii) Shortness of Breath (Dyspnea):
Replacement of air in the lungs by blood or

interstitial fluid
↓
Reduction of vital capacity, restrictive pulmonary
changes and closure of the small airways
↓
Increased “work of breathing” as the patient
tries to distend stiff lungs
↓
Respiratory muscle fatigue and dyspnea
14
iii) Shortness of Breath (Dyspnea):
Increased Pulmonary blood volume

↓
Ventilation-perfusion mismatch
↓
Widening of the alveolar-arterial O2 gradient,
hypoxemia and increased dead space
↓
Dyspnea
15
iv) Cause for Orthopnea:
From erect to recumbent position

↓
Blood pooling in the pulmonary circulation
coming from the extremities and abdomen
↓
Marked elevation in LV pressure
↓
Orthopnea
Patients usually learn to minimize orthopnea by

sleeping with the upper body propped up by two
or more pillows
16
v) Cause for Paroxysmal Nocturnal Dyspnea:
Changes during sleep such as:

-Reduced adrenergic support
-Increased vagal activity
-Normal nocturnal depression of resp center
Theses changes aggravate pulmonary pooling of

blood causing sudden onset of severe
respiratory distress at night called paroxysmal
nocturnal dyspnea (PND)
17
Directed Learning Activity (DLA):
Topic: RIGHT VENTRICULAR FAILURE (RVF)
18
Patient presentation:
A 64-year-old man with a 25-year history of chronic

obstructive pulmonary disease (COPD) comes to the
physician because of fatigue, exertional dyspnea and cough.
PE: Pulse 94/min, BP 170/92 mmHg.
He has barrel-shaped chest, labored respiration, bilateral
lower limb ankle edema, distended neck veins and
hepatojugular reflux.
Chest examination: bilateral, hyperresonant lung fields on
percussion
Cardiac examination: Right ventricular heave, Right sided S3
and S4; P2 component of S2 is loud; Systolic murmur heard
best at the right lower sternal border.
Abdominal examination: Tender hepatomegaly
19
Most likely diagnosis in this patient is:
Cor Pulmonale secondary to COPD
➢ Congestive (biventricular) heart failure
➢ Primary pulmonary stenosis
➢ Primary pulmonary hypertension
➢ Right ventricular infarction
Evidences of right ventricular failure (RVF)

secondary to pulmonary hypertension suggests
cor pulmonale
20
Cor pulmonale:
Condition characterized by enlargement

of right ventricle with failure as a sequel
of pulmonary disease
Pulmonary diseases:
-Pulmonary vascular diseases
-COPD
21
Right ventricular failure (RVF)
Causes:
-Secondary to LVF because of an increased
afterload placed on the right - most common
-Increased flow from a congenital shunt (ASD,
VSD) with pulm hypertension and increased right
ventricular afterload
-As a sequel of pulmonary diseases that cause
either pathological changes in pulm vasculature or
hypoxia-induced vasoconstriction
-Right ventricular ischemia or infarction.
22
Pathophysiology of RVF: The vicious cycle
23
How LVF possible in a patient with RVF:
High afterload on the right ventricle

↓
Increased RV pressure and volume
↓
Deviation of interventricular septum
towards the left ventricular chamber
↓
Insufficient filling of the left ventricle
↓
The bowing can be so severe that left ventricular

outflow can be partially obstructed. This phenomenon is
termed as "reversed Bernheim effect." 24
Clinical Presentation of RVF:
➢Shortness of breath
➢Pedal edema (pitting type)
➢Abdominal pain
25
Basis for shortness of breath in RVF:
i) Coexisting LVF → pulmonary edema → dyspnea
ii) Existing pulmonary diseases such as pulmonary

embolus, chronic obstructive pulmonary disease
iii) Congestion of the hepatic veins → ascites →

restricted diaphragmatic movements → dyspnea
iv) Reduced right-sided cardiac output → reduced

pulmonary blood flow and left-sided output →
Acidosis and hypoxia → air hunger (dyspnea)
26
Basis for Pedal Edema, Anasarca, Ascites:
Right ventricular failure

↓
Elevated right-sided pressure
↓
Accumulation of fluid in the systemic veins and
venous congestion
↓
Dependent edema (swelling of the feet and
legs), Generalized edema (anasarca), Ascites
(fluid in peritoneal cavity)
27
Basis for the Abdominal pain:
Right ventricular failure

↓
Elevated right-sided pressure
↓
Congestion of the systemic veins
↓
Venous congestion of the liver
↓
Distention of the liver capsule
↓
Right upper quadrant abdominal pain
28
Physical examination findings in RVF:
❖Elevated jugular venous pressure &

Hepatojugular reflux
❖Sustained systolic heave of the sternum (due
to right ventricular hypertrophy)
❖Right-sided S3 heard best at the left sternal
border
❖Additional signs of left ventricular failure
such as bibasilar rales (if the primary cause is
LVF)
29
Elevated Jugular Venous Pressure:
Elevated right atrial pressure indicates that the

fluid is accumulating in the venous system due
to a decreased right ventricular function
Other causes of elevated jugular pressures:

-Pericardial tamponade
-Constrictive pericarditis
-Massive pulmonary embolism
30
Measurement of Jugular venous pressure
45°
31
Hepatojugular reflux:
•Pressing on the liver for a short while

(approximately 5 sec) leads to displacement of
blood into the vena cava and an increase in
jugular venous pressure
•Sign of right ventricular failure
32
Clicker Time!
33
42-year-old woman has a heart rate=100 bpm; O2 content
of arterial blood=20 mL/dL; O2 content of pulm.arterial
blood=16 mL/dL; Oxygen consumption=300 mL/min. Her
Left ventricle PV loop is shown in the figure.
CO=SVxHR
=75x100
75 =7500
What is the cardiac out put of this woman?

A. 3500 mL/min
B. 4000 mL/min
C. 6500 mL/min
D. 7500 mL/min
0% 0% 0% 0%34 0%
E. 8000 mL/min
65-year-old man with a 20-year history of COPD
presents with chest pain and dyspnea. PE reveals
tachycardia, elevated JVP, positive hepatojugular
reflux and tender hepatomegaly. This patient is
most likely to have which of the following?
20% 20% 20% 20% 20%
A. Systemic hypertension
B. Left ventricular hypertrophy
C. Decreased right ventricular
preload
D. Decreased left ventricular
preload
E. Septal deviation towards right A. B. C. D. E.
ventricle 35
38-yr-old man with exertional dyspnea has a BP of 140/88 mm Hg and
a HR of 76 bpm. The steady state point at rest has been shown by
point, N.
20% 20% 20% 20% 20%
Which point on the graph indicates his cardiac

output during moderate exercise?
A. A
B. B
C. C
D. D A B C D E
E. E 36
Directed Learning Activity in
Cardiology
Topic: CARDIAC OUT, VENOUS

RETURN & HYPERTENSION
1
attending Lecture 14 on Shock
2
Physiology: Interaction between
CARDIAC OUTPUT and
VENOUS RETURN
3
Venous return (VR)
• Venous return is the amount of blood received by the
right atrium per minute
• In normal person, it is same as cardiac output (5 L/min)
• The pressure gradient between the right atrium and
the peripheral veins is the driving force for VR
• Higher the gradient, greater will be the venous return;
• Lower the gradient, less will be the venous return
• Factors that increase this gradient improve VR
• Factors that increase venous return are:
•Negative intrathoracic pressure
•Increase in total blood volume (preload)
•Contraction of skeletal muscles
•Increase in vascular tone of systemic veins
4
The vascular function curve
It is the plot between the venous return and right atrial pressure
•An inverse relationship exists
between RAP and VR in the
range 0 to 7 mm Hg of RAP
Venous return (L/min)
Normal
point
•No further increase in VR
occurs when RAP < 0 mm Hg
as veins collapse at negative
pressures
Mean circulatory pressure

or
Mean filling pressure
Right atrial pressure (mm Hg) 5

The effect of changing total blood volume on
vascular function curve
Increased blood volume:

• Curve moves upward & to RIGHT
• Mean circulatory pressure rises
N = Normal blood volume

N
Low blood volume:

• Curve shifts downward
& to the LEFT
• Mean circulatory
pressure falls
6
Cardiac function curve or Starling’s curve:
Reflects the contractile function of ventricle
Cardiac output (L/min)
Normal
Right atrial pressure (mmHg)
▪CO and VR are dependent on each other

▪Interaction between them is best understood by
combining the two function curves 7
Combining cardiac function curve and
Steady state point
Combining the two curves helps to predict the

changes in CO/VR under various conditions
8
Combining cardiac function curve and
Steady state point
Combining the two curves helps to predict the

changes in CO/VR under various conditions
9
The factors that alter the cardiac and
vascular function curves
Factor Curve that gets altered
•Change in myocardial Cardiac function curve

contractility
•Change in blood volume Vascular function curve
[C for C; V for V]
10
Effect of increasing myocardial contractility
on combined curves:
Positive inotropic agents

Eg:Sympathetic nerves,
digitalis
Normal
Increase in contractility
N’ ↓
Increase in cardiac output
N
↓
Decrease in RAP
↓
Increase in venous return
↓
Steady state point moves
upward & to the left
11
Effect of increasing total blood volume
on combined curves:
Increase in blood volume
↓
Increase in venous return
↓
Increase in RAP
↓
N’ Increase in cardiac output
↓
Steady state point moves
upward & to the right
N
Normal Increased blood volume:

Eg:Infusion of IV fluids
12
Pathophysiology of Hypertension
13
A 55-year-old male smoker with a history of high blood

cholesterol visits his family physician for a health
checkup.
His Blood Pressure records 180/120 mmHg.
Blood test: a high plasma renin activity.
Special test: Renal angiogram reveals a significant

asymmetric renal artery stenosis at the upstream
junction of the left renal artery and abdominal aorta
that reduces the entrance to the renal artery by 75%.
14
Systemic Hypertension due to renal artery

stenosis
Other differential:
➢Primary hyperaldosteronism
➢Cushing’s syndrome
➢Reninoma
➢Pheochromocytoma
15
Definitions:
•Hypertension (HTN) is a manifestation of
several diseases
•Hypertension is generally defined as an arterial
pressure greater than 120/80 mm Hg in adults
on at least three consecutive visits
•If the cause remains unknown, it is termed
essential hypertension or primary hypertension
•Hypertension in which the cause is known is
called secondary hypertension
•About 88% of population suffer from primary
hypertension 16
2017 Guideline: Categorization of High
Blood Pressure in Adults (American
College of Cardiology):
• Normal BP is defined as <120/<80 mm Hg;

• Elevated BP: 120-129/<80 mm Hg;
• Hypertension stage 1: 130-139 or 80-89
mm Hg, and
• Hypertension stage 2: ≥140 or ≥90 mm Hg.
http://www.acc.org/latest-in-cardiology/ten-points-to-
remember/2017/11/09/11/41/2017-guideline-for-high-blood-pressure-in-
adults
17
Isolated Systolic Hypertension (ISH):
• Systolic pr >160 mmHg, with a diastolic pr ˂90.

• Most common cause of HTN in elderly
• Primarily due to diminished arterial compliance
• Indicated by high pulse pressure.
18
Regulation of BP by Renin-angiotensin-
aldosterone mechanism
•Long term mechanism of regulation of BP

•The mechanism is mediated by hormones
•The mechanism regulates BP by regulating blood volume
•The activation of the system in response to a low BP
produces a series of responses to increase blood volume
Blood Cardiac Arterial

volume output BP
Blood volume is altered by altering salt and water in body

19
Regulation of arterial BP by
Renin-angiotensin-aldosterone mechanism
Retention of Salt and

Water increases plasma
volume, Cardiac output
and Blood Pressure
Increase in TPR and

Blood Pressure
20
Pathogenesis of HTN:
Recall Ohm’s law for systemic circulation:
(Mean arterial pressure – Rt. Atrial pressure) =

Total peripheral resistance X Cardiac output
Mechanisms causing hypertension:
❖Increased peripheral vascular resistance
❖Increased blood viscosity
❖Prolonged increase in cardiac output
❖Increased blood volume
21
COMMON CAUSES OF HYPERTENSION
➢Essential hypertension
➢Coarctation of aorta
➢Salt sensitivity
➢Renal abnormalities
➢Abnormalities of the RAAS
➢Disorders of adrenal gland
➢Neurological disorders
➢Nitric oxide deficiency
➢Insulin resistance
22
Coarctation of the Aorta:
•Congenital narrowing of the aorta distal to the

origin of the left subclavian artery
•Blood pressure is elevated in the arms, head, and
chest but lowered in the legs
•Because of low renal blood flow, plasma renin
level is increased
•Stimulation of Renin-angiotensin-aldosterone
system in a positive feedback manner
•Elimination of the constriction by resecting the
narrowed segment of the aorta usually cures the
condition
23
Site of coarctation
The pressure tracings from the thoracic and

abdominal aorta obtained from a 4-month-old
infant who exhibited dyspnea, difficulty feeding,
and poor weight gain
Physical examination reveals a weak femoral
pulse compared to the radial pulse with a radio-
femoral delay
Diagnosis: Coarctation of aorta. 24
Renal causes for hypertension:
▪ Constriction of one or both renal arteries
▪ Tumors of the renin-secreting juxtaglomerular
cells
▪ Ureteral obstruction: Increase in renal interstitial
pressure and stimulation of renin secretion
▪ Acute and chronic glomerulonephritis: a)
Activation of RAAS and/or b) ECF volume
expansion due to abnormal salt and water
handling by the kidneys.
▪Liddle's syndrome: a condition in which there is
abnormal Na+ retention due to over-activation of
the epithelial sodium channels (ENaC)
25
Liddle’s syndrome
•Young patient presenting with high BP

•H/O family members with early onset
severe hypertension
•Autosomal dominant transmission
•Suppressed renin
•Suppressed aldosterone
•Abnormality of epithelial sodium channels
(ENaC) in distal nephron
26
Adrenal Gland Disorders:
-Conn’s syndrome (primary hyperaldosteronism)
-Excess secretion of cortisol (Cushing’s syndrome)
-Hypersecretion of deoxycorticosterone (DOC) in
congenital adrenal hyperplasia
-Glucocorticoid remediable aldosteronism (GRA):
An autosomal dominant disorder in which ACTH
produces prolonged hypersecretion of aldosterone
as well as glucocorticoids. The genes encoding
aldosterone synthase and 11-hydroxylase are
identical and located close together on
chromosome 8. Suppression of ACTH by high dose
of glucodorticoids reduce BP in these patients.
-Pheochromocytoma-disorder of adrenal medulla. 27
HTN related to Insulin Resistance:
• Metabolic X syndrome: A combination of :

- Abdominal obesity,
- Hyperglycemia,
- Hypertriglyceridemia & Low HDL and
- Hypertension.
• Mechanism for HTN: Insulin resistance →

hyperinsulinemia → increased activity of the
sympathetic system→ hypertension
28
Clinical Presentation of HTN:
•Hypertension by itself does not produce symptoms
•Mostly it is discovered during routine screening or
when patients seek medical advice for its
complications
•The hypertensives present with:
-Myocardial infarction
-Congestive heart failure
-Strokes of thrombotic and hemorrhagic
origin
-Hypertensive encephalopathy - confusion,
disordered consciousness, and seizures
-Renal failure 29
Physical findings in HTN:
Observable changes are generally found only in
advanced cases. These include:
-Left ventricular hypertrophy and cardiac
enlargement and a loud S2
-Bruits in the renal artery on auscultation
-Hypertensive retinopathy - narrowed arterioles
seen on funduscopic examination; retinal
hemorrhages and exudates along with papilledema
30
FLOW CHART SHOWING COMPLICATIONS OF HYPERTENSION
31
CLICKER TIME!
32
Which of the following is True regarding
angiotensin II?
A. Secreted by macrophages
B. Directly increases preload
C. Directly increases
afterload on ventricles
D. Stimulates renin secretion
E. Stimulates adrenal
medulla
0% 0% 0% 0% 0% 0%
F. Directly acts on distal A. B. C. D. E. F.
nephron 33
63-yr-old woman comes because of headache and visual
disturbances of 8-month duration. Her blood pressure is
204/102 mm Hg. There is no evidence of stroke or transient
ischemic attack. Her serum studies show:
Low serum potassium and a high serum sodium. Serum
renin is 0.04 ng/mL (normal 1.8) and serum aldosterone is
72.4 ng/dL (normal 10).
Hypertension in this patient is most likely due to which of
the following?
A. Pheochromocytoma 20%
B. Renin secreting tumor of the kidney 20%
C. Primary hyperaldosteronism 20%
D. Renal artery stenosis 20%
E. Arteriosclerosis 20% 34
Pressure tracings from two different sites in the aorta of a
6-month-old infant is shown below. Which of the following
is increased in this infant?
Ascending Abdominal
aorta aorta
20% 20% 20% 20% 20%
A. Left ventricular stroke volume

B. Left ventricular wall thickness
C. Right ventricular wall thickness
D. Renal blood flow
E. Pulse pressure of femoral artery A. B. C. D. E.
35
Directed learning Activity (DLA)
Topic: VALVULAR HEART DISEASES
1
attending Lecture 8 on Valvular
Heart Diseases
2
Heart Sounds
Heart sounds are generated by:

✓ Opening and closing of the heart valves
✓ Turbulence in blood flow
✓ Vibrations in the support structures of the
heart
3
First Heart Sound (S1):
•Signals the beginning of ventricular

systole
•Generated by mitral and tricuspid valve
closure – M1T1
•Loudest over the apex
•Heard best by using the diaphragm of the
stethoscope
•The intensity of S1 is determined primarily
by:
-Valve mobility,
-Force of ventricular contraction &
-Velocity of valve closure 4
Variations of S1
Loud S1: Soft S1:
•Mitral stenosis •Mitral regurgitation

•Short PR interval •Long PR interval
•Tachycardia •Poor systolic function
•Hyperdynamic •Aortic/pulmonary
states regurgitation
S1 with varying intensity from beat to beat in

atrial fibrillation, reflecting variable
contractility
5
Second Heart Sound (S2):
•Generated by the closure of the aortic (A2)

and pulmonic (P2) valves, represented as
A2P2
•Best heard at the left upper sternal border
(over the base of the heart)
•A2 is the louder component and is audible at
all locations on the chest wall
•In normal, P2 is heard only at the upper left
sternal border and is always less audible than
A2 at this location
•Abnormalities of S2 are of 2 types:
-Alterations in intensity
6
-Alteration in timing of closure of valves
Variations of S2
Loud S2: Soft S2:
•Systemic hypertension •Aortic stenosis

•Pulm hypertension •Pulmonic stenosis
•Atrial septal defect •Aortic regurgitation
•Pulmonary regurgitation
7
Splitting of S2 (A2 P2):
•Normal split: A2P2 heard as two sounds during

deep inspiration and single during expiration
•Wide splitting of S2 (with normal respiratory

variation) occurs when P2 is delayed (e.g., Right
Bundle Branch block)
•Fixed splitting of S2 occurs when respiration-

induced changes in filling are similar in both
ventricles: e.g.,characteristic in atrial septal
defect (ASD)
8
Paradoxical splitting of S2 (P2 A2):
•Occurs in:
-Left Bundle Branch Block because of a delay
in left ventricular depolarization;
-Severe Aortic stenosis because of a delay in
closure of aortic valve.
•In paradoxical splitting, the interval from P2
to A2 shortens during inspiration (Note:
Normally the interval from A2 to P2 lengthens
during inspiration)
9
Diastolic Heart Sounds : S3 & S4
Ventricular gallop (S3):
•Occurs in early diastole; Corresponds to the end
of the rapid filling of the ventricle.
•Caused by interplay between ventricular filling
and existing ventricular (end-systolic) volume.
•Normal S3 is a low-frequency sound, best heard
at the apex (in case of LV_S3) or left lower sternal
border (in case of RV_S3).
•Pathologic S3 is associated with abnormally high
ventricular filling, low cardiac output, or a dilated,
poorly contractile ventricle.
•Hallmark sign of ventricular (heart) failure.
10
Diastolic Sounds: S3 & S4 (continued)
Atrial gallop (S4):
•A dull, low-frequency sound that precedes S1

•Best heard over apex with the bell of the
stethoscope in the left lateral position
•The S4 is attributed to forceful atrial
contraction to fill a noncompliant or stiff
ventricle (e.g., coronary artery disease).
•The S4 disappears in atrial fibrillation.
11
Continuous Murmur
Timing Condition Heard best

Continuous Left first and 2nd
murmur: Patent ductus intercostal
(systolic- arteriosus (PDA) spaces, Left
diastolic) sternal border
Phonocardiogram:
(SM=systolic murmur; DM=diastolic murmur) 12

Left ventricular
and aortic pressure
changes during a
normal cardiac cycle
Phonocardiogram
13
Clicker Time!
14
Which of the following sets of data mostly corresponds
to the figure below?
S1 S2 Ejection phase
A. 1 2 5,6
B. 2 4 6
C. 1 3 5,6
D. 1 3 6
E. 2 3 5 0% 0% 0% 0% 0%
1 2 2 4 1 3 1 3 152 3
5,6 6 5,6 6 5
Additional information
about valvular heart diseases
that are covered in lecture
16
Aortic stenosis (AS)
17
Pathogenesis of Aortic
Calcified valve
Stenosis:
Abnormal flow through valves

↓
Fibrosis and calcification
↓
Stenosis
•The normal aortic valve area: 3.5–4 cm2
•Critical aortic stenosis - when the area is < 0.8 cm2.
•Symptoms appear when a large systolic gradient between
the left ventricle and the aorta (> 150 mm Hg) occurs
18
Pressure profile in AS
19
Clinical Manifestations of AS and basis:
The three characteristic features of AS are:

Chest pain, Syncope & CHF
i) Chest pain (angina pectoris):

Mechanisms –
• coronary artery disease;
• increased oxygen demands because of
ventricular hypertrophy;
• decreased oxygen supply as a result of
excessive compression of the vessels;
• coronary artery obstruction from calcium
emboli arising from a calcified stenotic valve
20
ii) Syncope: Syncope is due to decreased
cerebral perfusion
Cause for syncope in AS –
•the fixed obstruction to out flow;
•transient atrial arrhythmias with loss of effective
atrial contribution to ventricular filling;
•arrhythmias arising from ventricular tissues
iii) Congestive heart failure (CHF):

•LVH→diastolic dysfunction of LV→progressive
increase in left ventricular end-diastolic pressure
→ elevated pulmonary venous pressure →
pulmonary edema→RVF
21
A 24-year-old man comes because of chest pain, dyspnea on

exertion and episodes of syncope while playing. His family
history is significant for similar illness in his brother who
died suddenly while playing.
Physical Examination: Double peaked pulse (bisferiens pulse),
Loud S4; A systolic murmur best heard between the apex and
left sternal border and radiates to the suprasternal notch.
The murmur increases by Valsalva but decreases by
squatting and passive leg raising.
Laboratory:
EKG: Left axis deviation due to LV hypertrophy
Echo: Asymmetrical septal hypertrophy with marked thickening
of the LV septal wall
22
Most likely diagnosis in patient:
Hypertrophic Obstructive Cardiomyopathy
(HOCM) or Idiopathic Hypertrophic Subaortic
Stenosis (IHSS)
➢Aortic stenosis
➢Restrictive cardiomyopathy
➢Glycogen storage diseases
➢Fabry disease
HOCM: an autosomal dominant disease, may

cause sudden death in young due to lethal
cardiac arrhythmias 23
Aortic regurgitation (AR)
24
A 45-year-old salesman is referred for evaluation of
a heart murmur. He had applied for a pilot’s license
and was denied because of the murmur. He is
asymptomatic and physically active. There is no
history of chest pain, dyspnea, or spells of syncope.
He has no family history of heart disease. He has
never had high blood pressure or diabetes, doesn’t
smoke, and takes no medications. He had suffered
from infective endocarditis when he was 40 year
old.
25
Physical Examination of the patient:
BP - 148/44 mmHg; Pulse - 78 bpm, reg;
Carotids: Very brisk with sharp collapse
Pulses are all very prominent and brisk; audible pulse
over the femoral arteries.
JVP: 5 with normal ‘a’ and ‘v’ waves
Lungs: Clear
Heart:
Palpation: Apical impulse is in the 6th intercostal space,
in the anterior axillary line.
Auscultation: S1 and S2 are soft;
An early diastolic blowing murmur, heard
best at the lower left sternal border;
An early systolic ejection murmur heard at
the upper right sternal border.
26
Aortic Regurgitation
➢Mitral stenosis
➢Pulmonary regurgitation
➢Tricuspid stenosis
➢Ventricular Septal defect
27
Pathology of AR:
❖Valvular cusp abnormality

❖Aortic dilatation
❖Aortic inflammation
❖Aortic tears with loss of commissural
support
28
Clinical presentation of patient with AR
and basis:
•Patient remains asymptomatic as the heart

responds to the volume load
•When the compensatory mechanisms fail,
symptoms appear
•Symptoms:
-Shortness of breath (due to pulm edema)
-Hypotension often with cardiovascular
collapse (low diastolic pressure)
29
Auscultation for murmurs in AR:
Three murmurs may be heard:
-A high-pitched, blowing, decrescendo early
diastolic murmur heard best along the left sternal
border - due to regurgitant flow into left ventricle
(hall mark sign).
-A crescendo-decrescendo, early systolic murmur
due to an increased stroke volume flowing across
the aortic valve, can be heard at the right upper
sternal border with radiation into the neck.
-Austin Flint murmur at the apex: a diastolic rumble
from regurgitant flow from the aortic valve
impinging on the anterior leaflet of the mitral valve
producing functional mitral stenosis 30
Mitral stenosis (MS)
31
Mitral Stenosis (MS)
Causes of MS:
Type Comments
a) Rheumatic: Most common
Narrowing results from fusion and
thickening of the commissures,
cusps, and chordae tendineae
b) Calcific: Usually causes mitral regurgitation
but can cause mitral stenosis
c) Congenital: Presents in infancy or childhood
d) Collagen- SLE and rheumatoid arthritis;
vascular: Rare cause of MS
32
Mitral Stenosis : Pathogenesis
• Scarring & fusion of mitral
valve apparatus
• Normal mitral valve area
(MVA): 4-6 cm2
• Mild mitral stenosis:
– MVA <2-2.5 cm2
– Minimal symptoms
• Mod mitral stenosis:
– MVA >1.5 cm2
– usually does not produce “Atrial” view of mitral
symptoms at rest
valve in a patient with
• Severe mitral stenosis rheumatic MS.
– MVA < 1.0 cm2
– produces symptoms at
33
rest (eg. dyspnea)
Pressure profile in MS
34
Clinical Manifestations of MS:
Clinically relevant mitral stenosis usually occurs
when the valve area decreases to less than 1 cm2
Symptoms:
i) Dyspnea and orthopnea – due to elevated LAP,
elevated pulm venous and capillary pressures
ii) Fatigue
iii) Hemoptysis
iv) Palpitations & Tachycardia - Increased left atrial
size predisposes to atrial tachyarrhythmias
v) Hoarseness of voice – Enlarged LA can impinge
on recurrent laryngeal nerve (Ortner's syndrome)
35
Atrial fibrillation (AF) is the most common
complication in MS:
•Abnormal enlargement leads to loss of organized

contraction of the left atrium and hence AF
•Thrombus in the left atrium is observed due to

stasis in LA (20% of patients with MS)
•Embolic events lead to neurologic symptoms

such as transient numbness/weakness of the
extremities, sudden loss of vision or stroke.
36
Mitral regurgitation (MR)
37
Causes for acute MR:

-Ruptured chordae tendineae as in infective
endocarditis; Trauma; Acute rheumatic fever
-Ruptured or dysfunctional papillary muscles as in
Ischemia; Myocardial infarction;Myocardial abscess
-Perforated leaflet as in infective endocarditis
38
Causes for Chronic MR:
-Inflammatory as in Rheumatic heart disease and

Collagen vascular disease
-Infection as in Infective endocarditis
-Degenerative as in Myxomatous degeneration of
the valve leaflets; Calcification of the mitral annulus
-Rupture or dysfunction of the chordae tendineae
or papillary muscles as in Infective endocarditis;
Trauma; Acute rheumatic fever; Myocardial
infarction
39
Variations in symptoms of Mitral Regurgitation (MR)
•The presentation of MR depends on how

quickly valvular incompetence develops
•Patients with chronic mitral regurgitation
develop symptoms gradually over time
•Common complaints in chronic MR include:
Dyspnea, easy fatigability, and palpitations
Dyspnea - due to pulmonary edema
Fatigue - due to decreased forward blood flow
to the peripheral tissues
Palpitations - due to atrial fibrillation
•Common complaints in acute MR include:
symptoms of left heart failure - shortness of
breath, orthopnea, and shock 40
Physiologic maneuvers in the
differential diagnosis of heart
murmurs (useful in
understanding clinical
vignettes in exams):
41
Physiologic maneuvers in the differential
diagnosis of heart murmurs and sounds
1. Respiration:
Right-sided murmurs typically increase with
inspiration, while left-sided murmurs generally are
louder during expiration (“RILE”)
2. Valsalva maneuver:
Most murmurs decrease in length and intensity
during the Valsalva maneuver
Two exceptions are - the systolic murmurs of
hypertrophic cardiomyopathy (HCM) & mitral
valve prolapse (MVP) – they become louder
42
3. Handgrip (isometric exercise):

Murmurs of MR , AR and VSD increase with
handgrip due to increase in afterload on LV
4. Transient arterial occlusion:

Transient external compression of both arms by
bilateral cuff inflation to 20 mmHg greater than
peak systolic pressure augments the murmurs of
MR, AR and VSD (due to increase in afterload on
LV)
This maneuver does not affect the murmurs due
43
to other causes
5. Positional changes:
i) Standing - Most murmurs diminish with
standing due to reduced preload. Exceptions:
the murmur of HCM & MVP become louder
ii) Passive leg raising - Most murmurs become
louder, while the murmurs of HCM and MVP
typically soften and may disappear due to
increased preload
44
Clicker Time!
45
Cardiac auscultation of a 44-year-old man shows
a heart murmur. A chest X-ray shows enlarged
right cardiac border but not the left. EKG shows
right axis deviation. What is the most likely
diagnosis? 20% 20% 20% 20% 20%
A. Aortic regurgitation
B. Aortic stenosis
C. Mitral regurgitation
D. Pulmonary stenosis
E. Tricuspid stenosis
A. B. C. D. E.
46
Directed Learning Activity in Cardiology
Topic: CORONARY ARTERY DISEASE
1
attending Lecture 7 on Coronary
Artery Diseases
2
54-year-old chronic smoker comes to the physician because
of a 9-month history of pain in the calf muscles by an half mile
walk associated with coldness and numbness in the legs. The
pain is relieved by rest. He also has erectile dysfunction.
Patient has a family history of hypercholesterolemia.
PE: BP 160/100 mm Hg; Low volume peripheral pulses in
both lower limbs; Loss of hair on dorsum of
feet; Atrophy of calf muscles; Bruits on femoral artery.
Lab: Elevated LDL and decreased HDL; elevated total serum
cholesterol
Angiogram: Narrowing of arterial lumens at multiple sites in
the aortoiliac region
Plain X ray: Irregular arterial calcifications in abdominal aorta
and iliac arteries
3
❖ Atherosclerosis
❖ Diabetic neuropathy
❖ Vasculitis
❖ Collagen vascular disease
The most likely diagnosis:

Atherosclerosis
Arterial biopsy: Fibrofatty plaque formation

with dystrophic calcification, atheroma.
Fibrous cap by smooth muscles and collagen
with necrotic lipid core and fibrous plaque 4
Pathophysiology of atherosclerosis
5
Sites of severe atherosclerosis in
order of frequency:
❖Abdominal aorta & iliac arteries

❖Proximal coronary arteries
❖Thoracic aorta, femoral and popliteal
arteries
❖Internal carotid arteries
❖Vertebral, basilar and middle cerebral
arteries
6
Pathogenesis of atherosclerosis:
Elevated LDL
••
•
• •
(γIFN)
7
❑Infiltration of low-density lipoproteins (LDL) into

the subendothelial region due to the shear stress
by flowing blood
❑Oxidation of LDL
❑Macrophages take up oxidized LDL through
receptors
❑Foam cell formation
❑Formation of fatty streaks
❑Oxidized LDL also has other deleterious
effects:
-stimulation of release of cytokines
-inhibition of NO production 8
❑Stimulation and movement of vascular smooth
muscle (VSM) cells from the media to the intima
❑Proliferation of VSM, lay down of collagen and
other matrix molecules
❑VSM cells also take up oxidized LDL and
become foam cells
❑Formation of atherosclerotic plaques
characterized by localized fibrous thickenings of
the arterial wall associated with lipid-infiltration
that may eventually calcify
❑Accumulation of lipid in foam cells is a key
event in the progression of atherosclerotic
lesions 9
❑As the atherosclerotic lesions age, T cells and
macrophages are attracted
❑The intercellular "soup" in the plaques contains
a variety of cell-damaging substances, including
ozone
❑As plaques mature, a fibrous cap forms over
them
❑The plaques with defective or broken caps are
most prone to rupture
❑The lesions alone may distort vessels &
obstruct the flow
❑Ulceration and rupture of plaques trigger
the formation of thrombi that obstruct flow 10
Relation to Dietary Cholesterol and
atherosclerosis:
❑Lowering plasma cholesterol slows the progress

of atherosclerosis – How?
❑Review the main pathways for the metabolism

of lipids
❑HDL is referred to as "good cholesterol" and
❑LDL is referred to as "bad cholesterol”
11
Pathways for metabolism of ingested lipids
Cholesterol
12
Summary of main pathways for the metabolism of
lipids:
•Dietary cholesterol and triglycerides (TGs) enter circulation
in the form of chylomicrons
•Under the influence of lipoprotein lipase, chylomicrons
release TGs to fat depots and muscles, and the resulting
chylomicron remnants are taken up by the liver
•The liver synthesizes cholesterol and packages it (along
with TGs) with specific proteins to form very low-density
lipoproteins (VLDL)
•VLDL enter the circulation and donate TGs to tissues
under the influence of lipoprotein lipase
•VLDL become cholesterol-rich intermediate-density
lipoproteins (IDL) and low-density lipoproteins (LDL)
13
when it loses TGs in tissues
Summary of main pathways for the metabolism of lipids
(continued from previous slide):
•The LDL supply cholesterol to the tissues for production of
cell membranes and the cholesterol as precursor for all
steroid hormones
•LDL are taken up by peripheral tissues as well as liver
•The oxidized LDL are taken up by macrophages and
smooth muscle cells in atherosclerotic lesions
•Liver releases high density lipoproteins (at this stage
called, nascent HDL) into circulation
•HDL takes up cholesterol from peripheral cells and
transport it to the liver where it is metabolized, keeping
plasma and tissue cholesterol low
14
Nutritional aspects of atherosclerosis:
❖Dietary supplementation of Vit B6, B12 & FA:
-Hyperhomocystinemia is associated with accelerated
atherosclerosis (about 7% population)
-Homocysteine is a significant source of H2O2 and
other reactive forms of oxygen, and thus, would
accelerate the oxidation of LDL
-Homocysteine is metabolized by enzymes that are
dependent on vitamin B6, vitamin B12, and folic acid
-Dietary supplementation of these vitamins reduces
plasma homocysteine, usually to normal.
❖Dietary antioxidant agents such as vitamin E, and β-
carotene has been used to inhibit oxidation of LDL.
❖Reducing saturated fatty acids and increasing
polyunsaturated fatty acids (PUFA)-Omega-3/6 fatty acids.
15
Clinical Manifestations of atherosclerosis:
➢Angina pectoris
➢Myocardial infarction
➢Thrombotic strokes
➢Aneurysmal dilation and rupture of the
abdominal aorta
➢Renovascular hypertension
➢Vascular insufficiency in the legs –
manifests as intermittent claudication and
gangrene
➢Intestine - clot formation and obstruction in
vessels supplying the intestines
16
Pathophysiology of
Coronary Artery Disease (CAD)
17
Anatomy of Coronary Circulation:
The right (RCA) and left (LCA) coronary arteries
arise in the root of the aorta just above the aortic
valve orifice
The coronary arteries (large and medium-sized) run
along the epicardial surface and send arterioles into
the myocardium
LCA: Quickly divides into the left anterior
descending artery (LAD) and Left circumflex artery
(LCX) arteries.
LAD: usually follows the anterior interventricular
groove and, in some people, continues over the
18
apex.
Coronary Perfusion in Right coronary
dominant individuals (85%):
LAD artery supplies:
•Anterior free wall of LV
•Anterior & major part of septum
•Apex
LCX artery supplies:
•Most of lateral free wall of LV
RCA supplies:
•Right ventricle
•Large part of Inferior wall
•Posterior wall of LV
•Posterior & minor part of septum
•SA node, AV node 19
In Left coronary dominant individuals
(15%):
The LCX supplies:

•Major part of Inferior wall
•Posterior wall of LV
•Apex
The remaining perfusion is same as

that in RCA dominance
20
Physiology of coronary circulation
•Coronary blood flow is maximum during ventricular
diastole and least during isovolumetric contraction
2 & 3: Ventricular systole
1 & 4: Ventricular diastole
2: Isovolumetric vent. contraction
3: Ventricular ejection
4: Isovolumetric vent. relaxation
1: Ventricular filling
•The coronary blood flow is mainly controlled by

local metabolic autoregulation
•Sympathetic stimulation does not produce
significant vasoconstriction in coronary vessels 21
Myocardial metabolism
•Myocardial metabolic requirement accounts for

7% of the body's resting oxygen consumption
•Myocardium cannot function anaerobically for
extended periods by building up an oxygen debt
•At rest the heart produces 70% of its ATP from
oxidation of fatty acids and 30% from oxidation
of carbohydrates
•During exercise, lactate becomes an important
substrate for the myocardial metabolism
22
A patient with myocardial ischemia may not
feel anginal pain because of:
Autonomic dysfunction of the afferent nerves

Examples: Patients with peripheral neuropathy or
transplanted heart
23
Pathogenesis of
Acute Coronary
Syndromes:
Plaque The integral role of
Fissure or platelets
Rupture
Platelet
Adhesion
Platelet
Activation
Platelet
Aggregation
Thrombotic
Occlusion
24
Platelet activation and pharmacological interventions
Epinephrine Collagen Arachidonic
ADP Acid
•Aspirin
Thrombin
•Ticlopidine •Heparin
•Clopidogrel •LMW Heparin
•Direct Thrombin
Activated Inhibitors
Platelet
IIb/IIIa
receptors •Abciximab Fibrin
Activated
Platelet
Activated
Another activated
Platelet
Platelet
25
Prinzmetal’s or Variant Angina: clues to
diagnosis
• A form of acute coronary syndrome caused by
coronary spasm
• Patients are usually younger, female, smokers, and
without other significant risk factors for coronary
artery disease
• Transient ST-segment elevation during chest pain
• Intermittent chest pain: often repetitive; usually at
rest; typically in the early morning hours & rapidly
relieved by nitroglycerine
• Patients often have manifestations of other
vasospastic disorders such as migraine headaches
and Raynaud's phenomenon
• Most attacks resolve without progression to MI
• Angiography shows no obstructions in vessels at
rest. 26
Conditions associated with
increased Cardiac Troponin-I
(cTnI) level
• Acute MI
• Congestive heart failure
• Unstable angina
• Myocarditis
27
Reason for Bradycardia in a patient with acute MI
•Occurs in inferior wall myocardial infarction (due

to occlusion of RCA)
•Reasons for bradycardia: i) Ischemia of AV node
and conduction defects, and/or ii) Vagus nerve
stimulation and conduction defects.
(Dysfunction of the SA node is rare because of
dual blood supply from both the right and the left
coronary arteries)
28
Certain key physical examination
findings in a patient with acute MI would
help to diagnose the associated
complications. The tables in next 3
pages list these combinations that are
commonly tested in exams.
29
Physical Findings Associated complication
Hypertension, High sympathetic tone (most

Tachycardia common in anterior MI)
Hypotension, AV nodal ischemia/High
Bradycardia vagal tone (Inferior wall MI)
Fast, slow or Atrial or ventricular
irregular pulse arrhythmias/Heart block
30
Physical Findings Associated
complication
S3 gallop, pulm rales, LV systolic dysfunction
pulsus alternans (signs of CHF if
dysfunction is >25%)
Hypotension, cool Cardiogenic shock
clammy skin, cyanotic,
altered mentation,
oliguria
Pericardial friction rub Pericarditis, Dressler’s
syndrome
(Postpericardiostomy
syndrome) 31
Physical Findings Associated
complication
Jugular venous distension, RV failure (RV
hypotension, RV S3, S4 infarction)
gallop, clear lungs
Harsh pansystolic murmur, Ventricular septal
at left lower sternal border rupture (septal MI)
Systolic murmur of MR Papillary muscle

rupture
32
Directed Learning Activity (DLA): Cardiology
Topic: ECG & CARDIAC ARRHYTHMIAS

Dr. S. Upadhya
1
attending Lecture 6 on Cardiac
Arrhythmias
2
Components of conducting system of the Heart
1. Sinoatrial node
3. Atrial internodal
pathways
2. Atrioventricular node
4. Bundle of His
5. Bundle branches
6. Purkinje fibers
The bundle of His normally forms the only electrical

connection between the atria and the ventricles 3
•AP originates at SA node
Sequence of spread •AP conducts to AV node

of cardiac action rapidly
•At the same time
potentials spreads over atria slowly
•AV delay occurs
•Spreads rapidly
over both the
ventricles from •Spreads rapidly
apex to base to the apex
through the through bundle
Purkinje fibers of His and
bundle branches
4
Certain basics of EKG/ECG:
The sites selected for ECG recording

Limbs: Right arm (RA), Left arm (LA), Left leg (LL)
•Leads connecting limbs are called “Limb leads”
•Leads kept on chest wall are called “Chest leads”
•Three lead systems are:
•Standard bipolar limb leads (3 in number):
Lead I, Lead II and Lead III
•Augmented unipolar limb leads (3 in number):
aVR, aVL and aVF
•Unipolar chest leads (6 in number):
V1, V2, V3, V4, V5 and V6
5
Clicker Time!
6
How many leads are present in a
conventional electrocardiograph?
A. 3 leads
B. 6 leads
C. 9 leads
D. 12 leads
E. 14 leads
0% 0% 0% 0% 0% 0%
F. 16 leads 3 6 9 12 14 16
leads leads leads leads leads leads
7
Genesis of EKG waves
SA node
P wave:
P
atrial
depolarization
wave
QRS complex:
•Ventricular
depolarization
wave
•Set of three waves
•Due to changing
direction of wave
of depolarization
in sequence
S
8
Genesis of ECG waves (continued)
•Ventricles remain in
depolarized state for
sometime before they
get repolarized
•No potential is recorded
•Corresponds to plateau
phase of ventricular AP
T wave: Ventricular repolarization wave
T T
9
Normal ECG waves, segments & intervals
Voltage
PR ST
segment QRS segment
interval
PR
interval QT interval
Time (sec)
10
Frontal Plane
▪Normal axis ranges

-30° and +110°
▪Less than -30° is
termed a left axis
deviation
▪Greater than +110°
is termed a right axis
deviation
11
Horizontal Plane
12
How to Calculate PR, QRS and QT intervals in
an ECG
PR interval = 0.04 x 4 = 0.16 sec (Normal: 0.12-0.20 sec)

QRS interval = 0.04 x 2 = 0.08 sec (Normal: 0.08-0.10 sec)
QT interval = 0.04 x 8½ = 0.34 sec (Normal: 0.32-0.43 sec)
13
Heart rate can be calculated from ECG
R-R interval
R-R interval gives one cardiac cycle length
60
Heart rate = ---------------------- beats per minute
R-R interval
60 60
Heart rate of above ECG = ----------- = -------- = 50 beats per minute
30x.04 1.2
14
What is the heart rate of this patient?
300 150 100 75 60
R-R interval
Lead II ECG
R-R interval = 23 boxes = 23x0.04 = 0.92 sec

Heart rate = 60/0.92 = 65 beats/min
R-R interval varies inversely with heart rate

15
Syncope in cardiac arrhythmias:
Bradyarrhythmias:
Sinus node disease, second- and third-degree
heart block and bradycardia associated with
pacemaker malfunction
Tachyarrhythmias:
Ventricular tachycardia, torsades de pointes,
Ventricular fibrillation and supraventricular
tachycardia
Patients with bradycardia often experience sudden loss of

consciousness without warning, whereas those with
tachyarrhythmias are more likely to describe palpitations
16
Action Potential of SA node (pace maker):
• Has got only three phases, 0, 3 & 4

• Has an unstable resting phase (phase 4)
called prepotential or pacemaker potential
which is responsible for automaticity of
the SA node
Membrane potential (mV)
Phase 0 Phase 3
Threshold
- 65
17
Mechanism of Bradyarrhythmias:
1. Reduced automaticity of the sinus node:
-Phase 4 of SA node action potential becomes

gradual
-Results in slow heart rate or pause
-If sinus node pacemaker activity ceases, the heart
will usually be activated at a slower rate by other
cardiac tissues with pacemaker activity (usually AV
node)
-Reduced sinus node automaticity occurs in
following conditions: Sleep, carotid sinus massage,
Vagal stimulation, Age, Hypothyroidism, Sinus
Bradycardia & drugs (beta-blockers, calcium
channel blockers) 18
Stimulation of Vagus (parasympathetic) nerve as an
example of bradyarrhythmia due to reduced
automaticity:
• On SA node: Decreases heart rate
• Known as negative chronotropic effect
• Mechanism: ACh binds with M2 receptors in SAN;
Decrease in rate of rise of phase 4 and hyperpolarization
of resting membrane potential lead to slow heart rate.
Normal heart rate
Heart rate after

parasympathetic
nerve stimulation
19
Mechanism of Bradyarrhythmias: 2. Conduction
block:
•The AV node and His bundle are the most

vulnerable sites for blocked conduction between
the atria and ventricles
•Atrioventricular block can occur:
-Increasing age
-Increased vagal input
-Congenital disorders: eg., muscular dystrophy and
tuberous sclerosis
-Acquired disorders: eg., sarcoidosis, gout, Lyme
disease, SLE, ankylosing spondylitis, and coronary
artery disease
20
Patient:
A 35-year-old man is referred to a cardiology clinic
for evaluation because of bradycardia.
Pulse: 40/min, regular BP: 90/46 mm Hg
JVP: Normal
Heart sounds: Normal S1 & S2 without any
murmurs, gallops
Lab:
EKG: Markedly prolonged RR intervals with HR of
40 beats/min; PR interval & QRS interval are within
limits.
Blood: Normal; Chest X ray: Normal
21
Most likely diagnosis in this patient:
Sinus Bradycardia
❖Hypothyroidism
❖Hypothermia
❖Digitalis toxicity
❖Beta-blocker toxicity
Physiological causes of Bradycardia:

-Increased vagal tone
-Sleeping
22
Sinus Bradycardia
ECG findings:
•Rhythm – Regular (constant RR intervals)
•Rate - less than 60 beats per minute (long RR int)
•P-R Interval - Normal
Examples: Trained athlets, High vagal tone, Inferior wall MI,

Hypothyroidism, Patient with raised intracranial tension &
Drug toxicity (Digitalis, Beta-blockers & Ca+2 channel
blocker) 23
Second degree Heart Block
Mobitz Type I or Wenchebach:
24
Examples of Supraventricular
Tachycardia (SVT):
1. Atrial tachycardia
2. Atrial flutter
3. Atrial fibrillation
25
A 46-year-old woman comes to the emergency

department because of sudden onset of
palpitations, lightheadedness, and shortness of
breath. These symptoms began approximately 2
hours ago.
PE: BP 95/70 mm Hg
Heart Rate - averages 170 beats/min, regular
Rest of her physical examination is unremarkable
EKG: rapid P waves; P-R intervals are short but

measurable; normal QRS complexes 26
Supraventricular Tachycardia (most likely

due to atrial tachycardia)
Other differentials are:

➢Ventricular tachycardia
➢Acute MI
➢Pulmonary embolism
27
Atrial tachycardia - an example of SVT
ECG findings:
•Heart Rhythm - Regular
•Heart Rate - 140-220 beats per minute
•QRS Duration - Normal (aka narrow)
•P Wave - Often buried in preceding T wave; may be negative
•P-R Interval - Depends on site of supraventricular pacemaker
•Other Features: Episodic or paroxysmal; Cardiac impulses
are NOT being generated by the sinus node. Impulses
originate from anywhere in the atria and pass through the
atrioventricular (AV) node. 28
Atrial Flutter – an example of SVT
ECG findings:
•P Wave - Replaced with multiple F (flutter) waves, usually at
a ratio of 2:1 (2F:1QRS) but sometimes 3:1
•P Wave rate - 300 beats per minute (range: 250-350)
•Heart Rhythm – Mostly Regular but may be irregular
•Heart Rate - Around 110 beats per minute (a fixed
relationship between P and QRS)
•QRS Duration - Normal (narrow)
•P-R Interval - Not measurable
•Other features: Episodic; Impulses originate anywhere other
than SA node; Variable AV block leads to irregular pulse. 29
Wolff-Parkinson-White syndrome: An Example
of Atrioventricular tachycardia
•An accessory atrioventricular connection is found
in approximately 1 in 1000 persons
•Part of the ventricle is "pre-excited" by the
accessory pathway before the normal conduction
via the AV node, the surface ECG shows a short
PR interval and a relatively wide QRS with a
slurred upstroke, termed a delta wave.
•If the accessory pathway recovers rapidly, the
normal cardiac impulse may travel in retrograde
fashion to the atria through this accessory
pathway and initiate a reentrant, atrio-ventricular
tachycardia (Patient feels palpitations at this
moment). 30
Two potential causes of tachyarrhythmia
with different mechanisms of genesis
Mechanism: Re-entrant circuit Spontaneous activity31

Clicker Time!
32
ECG of a 51-year-old woman with a 7-year history
of mitral stenosis is shown below. Which of the
following structures decide her heart beats?
A. SA node 0%
B. Atrial internodal pathways 0%
C. AV node 0%
D. Bundle of His 0%
E. Ventricular muscle 0% 33
What is the most likely diagnosis?
20% 20% 20% 20% 20%

A. First degree heart block
B. Second degree AV
block-type1
C. Normal sinus rhythm
D. Complete AV block
E. Second degree AV
block-type2 34

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Lecture 9-HEART FAILURE 2

Topic: HEART FAILURE

❖Congestive heart failure

Most likely diagnosis is:

The symptoms and signs depend on:

Left Ventricular Failure (LVF)

❖Inappropriate workloads placed on the LV:

Heart failure can arise from:

In most patients, a combination of systolic

➢Pressure-volume relationship shows a

➢Reduction in the stroke volume (SV) & a

➢Reduction in ejection fraction (EF).

Example: Patient with systemic hypertension

i) Increase in preload (Frank-Starling relationship):

Limitation: When each of these mechanisms reach their

• Ventricular filling is impaired during relaxation that

❖ Increased stiffness (decreased

❖ Reduced ventricular filling because of

❖Increased sympathetic activity

• Occurs early in the heart failure

• Reduced renal blood flow → Activation of RAAS.

• Consequence of continued hyperactivity of RAAS

•The interleukins (ILs) – IL-1 accelerates myocyte

➢ Also known as brain natriuretic peptide

The cellular changes in ventricular

❖ Shortness of breath (dyspnea) of

•Elevated respiratory rate and heart rate

•Peripheral pulse may reveal “pulsus alternans”

Normal Pulsus alternans

Pale, Cold, and Sweaty Skin:

Pale & cold extremities is due to peripheral

Sweating: Increased sweat gland activity as a part

Bibasilar Rales, Pleural Effusion:

Third Heart Sound (S3):

•S3 is a low-pitched sound that is heard during rapid

Fourth Heart Sound (S4):

•It is a low-pitched sound at the end of diastole that

Curve B: Immediate effect of reduced

Curve C: Compensated LV failure - SV is partially restored

Topic: PATHOPHYSIOLOGY OF SHOCK

20-year old soldier is brought to the field hospital

An abnormality of the circulatory system in which

Do not rely on systolic BP as the main indicator of

Decrease in baroreceptor impulses to cardiovasc. regulatory centers

Increase in sympathetic nerve activity Increase in sympathetic nerve

Increase in heart rate and Increase in Vasoconstriction

Increase in cardiac output Increase in

Fall in Blood Pressure

Cardiac depression &

Ischemic brainstem depression

Inadequate bloodflow to organs

Lactic acid accumulation & fall in pH

• Soft tissue trauma

•Traumatic shock involves severe damage to

•In distributive shock, most of the symptoms and

Anaphylactic shock (example of distributive

•Most common cause of death in ICUs in USA

•A patient is admitted with severe infection in

•Solution: Pulmonary artery catheterization (Swan-

Type of shock CO SVR PWP CVP

CO=Cardiac Output SVR=Systemic vascular resistance

•Extensive infarction of LV (>30%)

Type of shock CO SVR PWP CVP