Cardiovascular System

Ammad Mahmood GUMSA Revision

Topics
Anatomy

Physiology
Heart sounds and ECG 5 min break!

Angina
Heart Failure Examination

Cardiac Anatomy

Cardiac Anatomy
Four chambers left and right atria and ventricles

Divided by:
Interatrial septum between atria Interventricular septum between ventricles Interventricular valves between atria and ventricles

The heart lies slightly to the left of the

mediastinum with RA to the right, RV at the front, LA to the left and LV at the back

Atria
When collapsed form flaps called auricles; inner

surface contains muscular ridges called pectinate muscles Right

Receives blood from: SVC head, neck, upper limbs, chest IVC rest of the trunk, viscera, lower limbs Cardiac veins drain into RA through the coronary sinus Interatrial septum contains a shallow depression

called the fossa ovalis at the site of the now closed foramen ovale
Left
Receives blood from the four pulmonary veins (2

Valves
Atrioventricular valves
Mitral valve (between LA and LV)

Tricuspid valve (between RA and RV)

Anchored by chordae tendinae which are attached to papillary

muscles in the ventricles prevents valve prolapse

Semilunar valves
Aortic valve (between LV and aorta) Pulmonary valve (between RV and pulmonary arteries) Closed by backflow of blood, prevented from prolapsing by the

valve leaflets supporting each other like the legs of a tripod. Also less movement of the base of the valve as it is not contracting
All valves have three leaflets or cusps except the mitral (or

bicuspid) valve which has two Purpose prevent backflow of blood

Ventricles
Large muscular chambers; left considerably larger than

right Distal end is the apex, proximal end the base Inner surface is covered by muscular ridges called trabeculae carnae Papillary muscles anterior and posterior in both ventricles. Septal papillary muscle only in RV for 3rd cusp The RV has a ridge called the moderator band which connects the conduction system of the heart to the anterior papillary muscle causing contraction of the muscle before ventricular contraction Contraction of the LV involves shortening of the distance between apex and base and shortening of its diameter Contraction of the RV pushes blood against the LV

Aortic sinuses
Sac-like dilations at the base of the aorta which

fill due to blood backflow closing the aortic valve and allowing entry of blood into the coronary arteries

Coronary Circulation

Cardiac Conduction System

Spontaneously initiates and distributes the

stimulus to contract to the cardiac muscle without neural/hormonal input Consists of:
Sinoatrial (SA) node Lies in posterior wall of RA, connected to AV node by internodal pathways Atrioventricular (AV) node Sole electrical connection between atria and ventricles, other conduction is prevented by the fibrous skeleton of the heart Conduction through AV node is delayed to allow atrial contraction to precede ventricular conduction Atrioventricular bundle, bundle branches and

Purkinje fibres
AV bundle (Bundle of His) extends towards apex and

branches into left and right bundle branches. Purkinje fibers extend from the apex back towards the base allowing

Cardiac Wall
Three layers:
Pericardium outer covering, parietal and visceral

(epicardium), cavity contains pericardial fluid Myocardium muscular layer Endocardium innermost layer lines the ventricles, simple squamous epithelium which is continuous with the great vessels

Cardiac Physiology

Cardiac Muscle Cells

Similar in structure to skeletal muscle except:
Cells are smaller, shorter and there is usually 1-2

nuclei T-tubules are short and broad, and only contact the SR, do not form triads Larger numbers of mitochondria as it depends mainly on aerobic metabolism Adjacent cells are joined by intercalated discs which provide a stronger mechanical, electrical and chemical connection
Cardiac muscle can be considered as a functional

syncytium ie a fused mass of cells

Cardiac action potentials

Resting state
K+ inside the cell, Na+ and Ca2+ outside, resting potential -90mV

Four stages of action potential Rapid Depolarisation AP brings membrane to threshold

opening Na+ channels and causing large Na+ influx and depolarisation Initial Recovery K+ channels open in response and cause small repolarisation Plateau Phase Influx of Ca2+ through L-type Ca channels opened by depolarisation balances the K+ outflow maintaining membrane potential at around 0mV Recovery as the Ca2+ channels slowly close the K+ outflow repolarises the cell

Excitation contraction coupling

In skeletal muscle the AP travels along the T-

tubules to the junction with the sarcoplasmic reticulum to cause Ca2+ release from the terminal cisternae In cardiac muscle the AP opens Ca2+ channels in the T-tubules themselves (the same channels responsible for the plateau phase) This Ca2+ then opens further Ca2+ channels in the sarcoplasmic reticulum causing a massive flow of Ca2+ into the cytosol This is called calcium-induced calcium release

Pacemaker potential
The cell membranes of certain cells in the

conducting system cannot maintain a resting potential and gradually depolarise back to threshold after each repolarisation The rate of spontaneous depolarisations varies across the conduction system, the fastest rate predominates:
SA node 80-100bpm (meaning heart is usually

under parasympathetic tone) AV node 40-60bpm Some cells in Purkinje network 20-40bpm

Pacemaker potential
There are four ion currents to consider:
IF current flow of Na+ into cell causing

depolarisation. Open as the cell repolarises as opposed to other channels K+ outflow causing repolarisation T-type Ca2+ channels open briefly during depolarisation to provide push towards threshold L-type Ca2+ channels open at threshold to cause large Ca2+ influx creating AP (role of Na+ in other cells)
Process is continuous after K+ has caused

repolarisation the IF current slowly depolarises the cell to activate T-type Ca2+ channels which bring the cell to threshold activating the L-type Ca2+ channels creating the AP and again activating the

Cardiac cycle
Four (overlapping) phases:
Atrial systole the ventricle has largely filled passively and is

topped up by contraction of the atria to the end-diastolic volume (EDV) Atrial diastole atria rests until next atrial systole Ventricular systole as it begins pressure in the ventricles exceeds that in the atria and the AV valves shut. There is a period of isovolumetric contraction rapidly increasing pressure inside the ventricle until it exceeds that in the aorta (/pulmonary arteries) and the blood is ejected. The volume ejected is the stroke volume and the percentage of the EDV it makes up is the ejection fraction (usually ~60%). Pressure in the ventricle then drops and as blood starts to backflow the semilunar valves shut this produces a small rise in arterial pressure knows as the dicrotic notch. The blood left in the ventricle is the end systolic volume (ESV) Ventricular diastole isovolumetric relaxation allowing pressure in the ventricle to fall below that in the atria opening the AV valves

Cardiovascular Physiology
Cardiac output

Stroke volume
Heart Rate Mean Arterial Pressure Total Peripheral Resistance Cardiovascular Response to Exercise

Cardiac output
Volume of blood the heart pumps in litres per

minute Calculated as heart rate x stroke volume (HRxSV) Average for adults is 5l/min (ie one blood volume) Can increase to 20-25l/min or even higher in athletes through changes in either heart rate

Heart rate (HR)

Normal HR is ~72bpm (under parasympathetic stimulation) Mechanisms for altering heart rate:
Sympathetic stimulation (noradrenalin acting on -adrenergic

receptors)
Increases the IF current to reach threshold faster Increases conduction through the conduction system

Increases contractility of the heart

Parasympathetic stimulation (Acetylcholine acting on

muscarinic receptors)
Opposite of the above

Increases permeability to K+ to hyperpolarise the membrane

further from threshold

Plasma adrenalin acting on -adrenergic receptors Changes in body temperature Other hormones eg noradrenalin, thyroxine Adenosine a metabolite released by cardiac myocytes

Stroke volume (SV)

Blood volume ejected with each beat usually

70ml Ejection fraction = stroke volume/EDV as a percentage Mechanisms for altering stroke volume:
Frank Starling mechanism Increase of EDV (ie venous return) increases SV. This is because sarcomeres are stretched further which increases the force of contraction. Unlike skeletal muscle, cardiac muscle at rest is not at the optimal length for contraction, it is on the rising phase of the relationship Sympathetic stimulation to increase contractility Stronger, quicker contraction and quicker relaxation at any given EDV

Mean Arterial Pressure (MAP)

Average blood pressure reflection of the

perfusion pressure of the major organs (except lungs) Normally between 70 and 110mmHg MAP = Cardiac output x Total peripheral resistance (COxTPR) TPR is the total amount of resistance to blood flow in the arterial system mainly controlled by arterioles MAP is maintained by various homeostatic mechanisms by altering CO and TPR eg if TPR decreases due to vasodilation in one area then either another area can vasoconstrict to increase TPR or CO can increase to maintain MAP

Total peripheral resistance

Can be altered by local or extrinsic controls affecting the

vascular tone in arterioles Local:

Active hyperaemia increased blood flow to metabolically

active tissues activated by release of mediators from the tissues eg CO2, H+, adenosine, hypoxia Flow autoregulation the rate of flow determines arteriolar tone ie increased flow causes vasodilation through stretch receptors Reactive hyperaemia extreme form of flow autoregulation caused by occlusion of proximal blood vessel Part of the inflammatory response
Extrinsic:
Sympathetic stimulation Hormones such as adrenalin, angiotensin II, vasopressin

(ADH)
Extrinsic controls may cause vasoconstriction (eg

adrenalin); local mediators produced due to metabolism then cause vasodilation helping to direct blood flow to the

Cardiovascular response to exercise

Even before exercise begins control centres in the brain activate

autonomic neurons feed-forward system Sympathetic stimulation causes vasoconstriction especially to abdominal organs Local mediators released due to metabolism cause vasodilation and increased blood flow to heart, skin, muscle etc CO increases due to increased venous return (Frank Starling mechanism) but mostly due to increased contractility due to sympathetic stimulation Overall TPR decreases, but the larger increase in CO means there is a small increase in MAP with a wider pulse pressure Chemo-, mechano- and baro-receptors feedback to the medullary cardiovascular centre to adjust the cardiac parameters as needed. Baroreceptors which would normally counter the rise in BP are reprogrammed upward Two types of exercise:
Dynamic eg running cause small increase in MAP as lots of areas

vasodilate

Factors which limit exercise

VO2 the capacity of the circulatory system to

deliver oxygen to the tissues. At VO2MAX more blood can be oxygenated by the lungs but cannot be delivered by the heart. This is because CO cannot increase any further as at the upper limits of HR the time for ventricular filling is too short Respiration respiration rate and depth increase greatly in exercise but pO2, pCO2 and pH only change in heavy exercise Muscle mass Age Cardiac disease

Cardiac Investigations

Cardiac Examination

Heart sounds
Major heart sounds are caused by closure of the

valves Four heart sounds:

S1 closure of the AV valves S2 closure of the semilunar valves S3 blood flowing into ventricles S4 atrial contraction

Murmurs
Heart murmurs are caused by turbulent blood

flow eg due to stenosis, regurgitation or can be physiological Murmurs to know about at this stage are the murmurs of the left heart valves:
Systolic Aortic Stenosis, Mitral Regurgitation Diastolic Aortic Regurgitation, Mitral Stenosis

Murmurs should be described in terms of site,

grade, systolic/diastolic, radiation, duration and character If you want to hear what they are like: www.youtube.com/user/Drparth2008 Other murmurs include innocent murmurs of childhood and murmurs caused by congenital

ECG
Tracing of the electrical activity of the heart

through skin electrodes Standard 12 lead ECG uses 10 physical leads to produce 12 separate signals which are used for analysis

ECG components
P wave atrial depolarisation
Absent in atrial fibrillation

QRS complex ventricular depolarisation

widened in problems in the conduction system eg bundle

branch block
T wave ventricular repolarisation
Inverted in many conditions eg post MI

PR interval
prolonged in heart block

ST segment
Elevated or depressed in myocardial ischaemia

QT interval
Prolonged in some rare conditions

ecgpedia.org

Other investigations
Imaging
CXR mostly for heart failure Echocardiography ultrasound used to examine

heart, can look at valves, wall motion, calculate ejection fraction MRI with contrast (gadolinium) Angiography
Exercise testing
Exercise tolerance test ECG recording during

exercise on treadmill or exercise bike. Bruce protocol (speed and incline increase every 3 minutes) is used Cardio-pulmonary testing calculation of VO2

5 min break..

Clinical Cardiology

Atherosclerosis
Pathological process affecting arterial wall; responsible for

many common diseases Involves a number of pathological processes eg inflammation, and hyperlipidaemia Steps:
Shear stress damages the endothelium of the artery allowing it to

take up LDL which is oxidised Monocytes bind to the endothelium and enter it to become macrophages. These express scavenger receptors allowing them to uptake the oxidised LDL becoming foam cells These are lead down in the tunica intima forming fatty streaks T cells are stimulated by the oxidised LDL to release cytokines causing smooth muscle cells to proliferate and migrate from the tunica media to the tunica intima An atherosclerotic plaque is now formed which develops a fibrous

Images from Robbins Pathological Basis of Disease

Atherosclerotic Diseases
Carotid arteries
Strokes (cerebral infarct), TIA

Coronary arteries
Angina, ACS

Renal arteries
Renal artery stenosis, hypertension

Mesenteric arteries
Ischaemic colitis

Aorta
Aortic aneurysms

Limb arteries
Intermittent claudication, critical limb ischaemia

Angina Pectoris
Occurs when an atherosclerotic plaque causes stenosis

(but not occlusion) of coronary arteries meaning the myocardial demand for oxygen via blood cannot be met during periods of exercise eg physical exertion, following a heavy meal (increased blood supply to gut), or in cold weather (peripheral vasoconstriction increases TPR) Coronary arteries particularly at risk, especially harmful as cardiac tissue relies mainly on aerobic respiration An inadequate oxygen supply and inadequate removal of metabolites leads to ischaemia causing lactic acidosis and build-up of other toxic metabolites Sensory nerves are stimulated, possibly by adenosine released by ischaemic myocardium causing chest pain

Causes
Atherosclerotic risk factors:
Non-modifiable Age Male gender Family history Ethnicity (South Asian etc) Modifiable Hyperlipidaemia Hypertension Smoking Diabetes Obesity Poor diet, sedentary lifestyle

Investigation
Diagnosis is most often clinical

Tests:
ECG Exercise ECG Coronary angiography Myocardial perfusion scans eg thallium scan

Treatment
Medication
Antiplatelets eg Aspirin or Clopidogrel
Prevent thrombosis

ACEI eg Ramipril
Counteract RAA system, reduce blood pressure and other effects

Statin eg Simvastatin
Reduce cholestrol

Nitrates eg GTN, ISMN

Metabolised to nitric oxide which causes venodilation mainly

reducing preload and reducing myocardial demand

-blockers eg Atenolol
Counteract sympathetic effects discussed earlier to reduce

myocardial demand
Calcium channel inhibitors eg Verapamil
Reduce contrctility of the heart and block vasoconstriction to

reduce myocardial demand

Potassium channel openers eg Nicorandil
Hyperpolarise membranes causing vasodilation

Treatment
Risk factor reduction
Smoking cessation, adjust diet and lifestyle, lose

weight, control diabetes, control blood pressure and cholestrol

Intervention
Angioplasty and stenting
CABG

Heart Failure
Definition complex syndrome resulting from any

structural or functional cardiac disorder which disables the heart from acting as a pump and maintaining circulation Causes coronary artery disease, hypertension, valvular disease, cardiomyopathies, lung disease (cor pulmonale) Preload the tension the ventricular walls have developed at the end of diastole before contraction
Increased by increasing venous return and vice versa Estimated as the EDV. An increase in EDV will increase the

SV (Frank Starling Mechanism) to give the same ESV regardless of EDV

Afterload the tension the heart must generate to

overcome TPR
Increased in hypertension and ventricular dilation, decreased

in LVH

Pathology
Can be thought of in terms of:
Left heart failure - systolic and diastolic dysfunction Systolic impaired contractility and increased afterload lead to reduced ejection fraction and increased pressure in the heart causing pulmonary congestion Diastolic abnormal ventricular relaxation eg due to fibrosis of the heart following MI; leads to systemic and pulmonary congestion Right heart failure Most commonly due to left heart failure which increases the afterload of the right ventricle

Important to consider the compensatory

mechanisms activated by heart failure:

Frank Starling mechanism Neuro-hormonal alterations Ventricular hypertrophy and remodelling

Frank Starling Mechanism

As mentioned as the EDV increases due to

incomplete emptying causing the SV to subsequently increase This is initially beneficial however when the EDV increases to the point where SV cannot increase further to compensate the LV pressure rises. This rise is transmitted through the LA to the lungs causing pulmonary congestion

Neurohormonal alterations
3 main components Autonomic nervous system:
Increased sympathetic and decreased parasympathetic

stimulation to help increase CO and maintain BP

Renin-Angiontensin-Aldosterone system
Causes vasoconstriction and increases circulating volume to

maintain BP
Antidiuretic hormone
Promotes water retention to increase blood volume & BP

Others include ANP, BNP and endothelins These mechanisms initially help but eventually become

pathological:
Increased blood volume and venous return cause pulmonary

congestion Vasoconstriction increases afterload and impairs SV and CO Increased metabolic demand on the heart Sustained sympathetic stimulation causes down-regulation of adrenergic receptors and increases inhibitory G-proteins causing a negative inotropic response

Ventricular hypertrophy & remodelling

Eccentric remodelling
Occurs due to chronic volume overload (eg aortic

regurgitation), myocytes elongate causing ventricular hypertrophy and dilation

Concentric remodelling
Occurs due to chronic pressure overload (eg

hypertension), myocytes thicken causing ventricular hypertrophy only

Wall stress = pressure x radius / 2x wall thickness

Initially hypertrophy reduces wall stress (because

of increased wall thickness) Dilation increases wall stress due to increased radius Eventually there is pressure overload causing

Signs and symptoms

Symptoms caused by vascular congestion and

failure to adequately perfuse tissues Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, nocturnal cough Fatigue and weakness Impaired urine output during day and nocturia Dulled mental state Peripheral oedema and weight gain due to increased venous pressure Tachycardia, tachypnoea and sweating due to sympathetic stimulation

Investigations
Clinical diagnosis

CXR shows pulmonary congestion and

cardiomegaly ECG Echocardiogram Bloods cardiac enzymes, BNP Other imaging or biopsies dependent on cause of heart failure

Treatment
ACEI eg ramipril
Reduce vasoconstriction (reduced ATII) and prevent

increase in blood volume (reduced aldosterone) causing decreased preload and afterload Also blocks remodelling effect of angiotensin Can substitute with angiotensin receptor blockers eg losartan
Diuretics eg frusemide, eplerenone,

spironolactone
Loop diuretics eg frusemide used to clear oedema

by inhibiting NaCl reabsorption at the thick ascending loop of Henle Potassium sparing diuretics eg eplerenone,

Treatment
-blocker eg atenolol
Must be started at a low dose and titrated up, counteracts effects of

chronic sympathetic stimulation

Digoxin
Antagonises the Na+/K+ pump to increase intracellular Na+; through

the Na+/Ca2+ exchanger this causes increased intracellular Ca2+ Has a positive inotropic effect on the heart to increase CO and also has indirect effect to increase vagal activity No effect on mortality but helps with symptoms Toxicity is common causing ectopic beats and heart block
Other positive inotropes such as IV dobutamine can be used

short term in very sick patients but may increase mortality

Treatment
Treat underlying cause of the heart failure eg

hypertension, coronary artery disease Device therapy

Pacemakers CRT ICD

Heart transplantation

Cardiac Examination

 Wash hands, introduce, consent, position

General inspection comfortable? breathless?

Hands clubbing, nail changes, temperature,

cyanosis Pulse rate, rhythm, volume, character Face xanthelassma, central cyanosis Neck JVP, carotid pulse Praecordium
Inspection scars, chest deformities Palpation apex beat, thrills, heaves Auscultation four areas aortic, pulmonary,

tricuspid, mitral
To finish my examination.
BP

Lung bases

Questions?