Chapter 6. The heart and cardiovascular system

Chapter



6



The heart and cardiovascular system



aorta



pulmonary left atrial

artery

appendage



right



right

ventricle



Fig. 6.2 Most of the anterior surface of the

heart is formed by the right ventricle and

pulmonary artery. The tip of the left ventricle and

the left atrial appendage also appear on the left

border of the heart.



left



left

ventricle



Fig. 6.3 Computerised tomography scan of the heart showing the



140



position of the heart within the chest cavity. Viewed from below.



Fig. 6.4 A ‘corrosion cast’ of the chambers of the heart, made by

filling the chambers with wax or plastic and dissolving away the

muscle.



from the systemic veins and pumping it to the lungs. The

left heart, comprising the left atrium, mitral valve, left

ventricle, aortic valve and aorta, is a high pressure pump

receiving blood from the lungs and pumping it round the

body. In the early embryo, the heart forms as a simple

tube down the midline of the body. As the embryo grows,

the tube elongates more rapidly than the tissues around

it and thus develops a loop and a twist. It also becomes

divided into left and right chambers by the growth of a

partition or septum down the middle.

In the ninth week of gestation, the fetal heart rotates

in a clockwise direction until the right ventricle comes to

rest anteriorly behind the sternum. Most of the left

ventricle comes to lie posteriorly, apart from a small

portion of left ventricular muscle which forms the left

heart border when seen from the front and the extreme



tip or apex of the heart (Fig. 6.2). The way the heart is

situated within the chest cavity is also well demonstrated

on the computerised tomographic scan of the chest

shown in Figure 6.3. Note that the heart lies obliquely in

the chest and that its long axis, the planes of the interatrial

and interventricular septum, and the planes of the various

valves, are not aligned with any of the conventional

anatomical planes. The chambers of the heart can be

examined after death by injecting wax or plastic and

dissolving away the muscle (Fig. 6.4). They can also be

examined during life by injecting radio-opaque contrast

medium through catheters placed in the various chambers

of the heart and taking cine radiographs. By tilting the

x-ray tube and image detector appropriately, it is possible

to obtain detailed pictures of the full extent of the

ventricular cavities (Fig. 6.5).



Chapter



Structure and function



6



HEART MUSCLE

Ventricles



Fig. 6.5 Left ventricular cine-angiogram made by injecting radioopaque contrast medium into the heart through a catheter passed

via the femoral artery and aorta. The x-ray tube and image intensifier

are tilted into the ‘right anterior oblique’ position to outline the full

extent of the left ventricle.



Heart muscle or myocardium is a special type of muscle

that is extremely resistant to fatigue. As a result of the

higher pressures that it normally generates, the wall of

the left ventricle is much thicker than the wall of the right

ventricle. In a section taken through both ventricles, left

ventricular myocardium, including the intraventricular

septum, has a roughly circular outline with the right

ventricle appearing to be wrapped around one side of it

(Fig. 6.6). The muscle fibres of the heart are arranged in

a complicated spiral arrangement so that when they

contract (systole) not only is blood forced out of the

ventricles but the heart also elongates and rotates on the

fixed base provided by the attachment of the major blood

vessels. It is this movement that is felt as the beating of

the heart by a hand placed on the chest. The heart

normally lies in its own serous cavity, the pericardium,

which allows it to move without friction. Apart from

moving with each heart beat, the position of the

pericardium and the heart can be altered by the phase of

respiration or by rolling from one side to the other.

Atria

The atria of the heart are also muscular but are much

thinner walled than the ventricles (Fig. 6.7). They contract



Transverse (’short axis’) view of the heart

‘Long axis’ view of the heart



0.4–0.6 cm

right

ventricle



left

ventricle



0.8–1.5 cm

aorta



right

ventricle

wall



left

ventricle



septum



left

atrium



0.8–1.5 cm

0.2–0.3 cm



Fig. 6.6 ‘Short axis’ view of the heart. In the short axis or transverse

section, the thinner (low pressure) right ventricle is ‘wrapped around’

the left ventricle.



Fig. 6.7 Relative thickness of muscle in different parts of the heart.

141



Chapter



6



The heart and cardiovascular system

a fraction of a second before the ventricles and, in

doing so, they assist in the filling of the ventricles,

particularly when there is a need for increased cardiac

output. The atrial component of cardiac filling can

contribute up to 30% of cardiac output. Patients in whom,

as a result of disease, the atria are paralysed or are beating

out of synchrony with the ventricles are usually

comfortable at rest but may become short of breath on

exercise.

CARDIAC HYPERTROPHY AND DILATATION

Like any muscle, cardiac muscle responds to an increased

workload by growth. The heart responds in different

ways to pressure load and volume load. Pressure load is

caused by an increased resistance to ejection of blood

from the heart. The response to pressure load is cardiac

hypertrophy, initially without dilatation of the chamber

involved. For example, in aortic stenosis, the left

ventricular wall becomes excessively thickened but the

left ventricular cavity remains of normal size. Eventually,

when the pressure load is extreme or growth of the heart

muscle has outstripped its blood supply, failure of the

muscle occurs and the cavity begins to enlarge.

The heart responds to a volume load, for example, a

leaking mitral or aortic valve, an arteriovenous fistula or

left-to-right shunt, by both hypertrophy of the myocardium

and dilatation of the chamber involved. This is to

accompany the increased stroke volume that is required

to deal with the volume load. The chest radiograph shows

cardiac enlargement (Fig. 6.8) and this is also found on

echocardiography. Ventricular hypertrophy produces

characteristic electrocardiographic changes and it is

possible to identify the cardiac chamber involved from

the electrocardiographic appearances.



Fig. 6.8 Chest radiograph showing cardiac enlargement in response

to a volume load chronic mitral regurgitation (compare with Fig. 6.2).



142



HEART VALVES

There are four heart valves. They fall anatomically and

functionally into two groups: the inflow or atrioventricular

valves and the outflow or ‘semilunar’ valves. The tricuspid

and mitral valves separate right atrium and right ventricle

and left atrium and left ventricle, respectively. Both

develop from the endocardial cushions of the embryonic

heart and are composed of thin flexible leaflets that are

prevented from prolapsing back into the atrium when

the ventricle contracts by being attached by chordae

tendineae to specialised portions of ventricular muscle,

the papillary muscles (Fig. 6.9). The hydrodynamic

efficiency of the mitral and tricuspid valves is very high.

Their pliable edges smooth out eddies and turbulence in

blood flow and allow the rapid transfer of blood from

atrium to ventricle with a very small pressure differential.

The aortic and pulmonary valves develop from two spiral

ridges that divide the single great vessel leaving the

embryonic heart into aortic and pulmonary trunks. Each

normally has three cusps whose arrangement reflects

their embryonic origin (Fig. 6.10). As each cusp is shaped

like a half moon, they are sometimes called the semilunar

valves.

HEART SOUNDS

Closure of the heart valves at different stages of the

cardiac cycle gives rise to sounds that are readily audible

through a stethoscope. The sounds are normally described

as ‘lub-dup’. The first heart sound (‘lub’) is caused by

the closure of the mitral and tricuspid valves, and

the second heart sound, the rather higher pitched (‘dup’),

is caused by the closure of aortic and pulmonary

valves. The relationship between the heart sound, the

electrocardiogram and the arterial pulse wave is shown

in Figure 6.11. In children or in young adults, the



Fig. 6.9 Postmortem specimen showing attachment of valve cusps

to papillary muscles by chordae tendineae.



Chapter



Structure and function



6



Development of the aortic and pulmonary (semilunar) valves

pulmonary

artery

left

coronary

artery



right

coronary artery



primitive ‘trunk’ develops

four spiral ridges



spiral course

brings the

pulmonary artery

to cross in front

of the aorta



aorta



spiral ridges separate the aorta from the

pulmonary artery and also from cusps of

aortic and pulmonary valves



Fig. 6.10 The common ‘great vessel’ of the fetal heart is divided into aorta and pulmonary artery by the growth of the spiral ridges.



Differential diagnosis

Increased pressure load (afterload) on the heart



Pulse, heart sounds and ECG



Right ventricular pressure load



• Pulmonary valve stenosis

• Increased pulmonary vascular resistance

• chronic hypoxia

• chronic lung disease

• secondary to left heart failure

• Eisenmenger’s syndrome

• primary pulmonary hypertension



R



left ventricle

pressure



aortic pressure



Left ventricular pressure load



•

•

•

•

•

•



Aortic valve stenosis

Subaortic stenosis

Supravalvar aortic stenosis

Hypertrophic obstructive cardiomyopathy

Coarctation of the aorta

Systemic hypertension



first sound



second sound



T



second heart sound splits into two components during

inspiration (‘lub da-dup’) and comes together again in

expiration. This physiological splitting of the second heart

sound is the result of minor changes in the stroke volume

of left and right ventricles during the normal respiratory

cycle.

During inspiration, venous return to the right side of

the heart is increased, thus increasing right ventricular

stroke volume and delaying pulmonary valve closure. At

the same time, pooling of blood in the pulmonary veins

reduces filling of the left ventricle and makes aortic valve

closure slightly earlier than in expiration. The split may



P



Q S



P wave



QRS width



<0.12 s



<0.10 s



PR interval

<0.20 s



QT interval <0.42 s

at rate of 60 beats/min



Fig. 6.11 Relationship between heart sounds, electrocardiogram

and arterial pulse.



143



Chapter



6



The heart and cardiovascular system



Splitting of the second heart sound



Inspiration

Normal S

1



Wide, fixed

splitting S1



a2P2



spread of

electrical

activity

through

atria



Expiration

S1



S2



Atrial septal

a2 P2



S1



Electrical conduction in the heart



sinoatrial

node



left

atrium



a2 P2 defect



atrioventricular

node

Wide split

but varies

with inspiration



S1



Reversed

splitting S1



a2 P2



S2



S1



S1



a2 P2



P2 a2



Pulmonary

stenosis

right bundle

branch block



Hypertrophic

cardiomyopathy



fibrous ring

‘insulating’

ventricles

from atria



Fig. 6.12 Beat to beat variations in left and right ventricular stroke



right

bundle

branch



volume cause splitting of the second heart sound in phase with

breathing. Splitting of the second sound with inspiration is normal.

Other patterns may indicate cardiac abnormalities.



Fig. 6.13 Paths of the spread of electrical impulses in the heart

(note that there are no specific electrical pathways in the atria).



be widened by other factors that delay right ventricular

contraction, such as right bundle branch block or

pulmonary valve stenosis. Conversely, anything that

delays left ventricular contraction, such as left bundle

branch block, hypertrophic obstructive cardiomyopathy

or severe aortic stenosis, may so delay the aortic

component of the second heart sound that the normal

relationship is reversed and there is increasing splitting

of the second heart sound on expiration with the sounds

coming together on inspiration. This is known as

paradoxical splitting of the second heart sound. Finally,

in an atrial septal defect, there is a characteristically fixed

splitting of the second heart sound because the hole in

the intra-atrial septum means that left and right atrial

pressure remains equal throughout the respiratory cycle

(Fig. 6.12).



cells in other parts of the heart. The electrical impulse

spreads out from the sinoatrial node (Fig. 6.13) through

the cardiac muscle of the atria. The atria and the ventricles

are separated by a fibrous ring of tissue to which the

tricuspid and mitral valves are attached and which

does not support conduction of the cardiac impulse. The

only electrical pathway through this ring is through the

atrioventricular node, a localised area of specialised

conducting tissue lying between the tricuspid valve and

the aorta. There is a delay of 0.12–0.20s while the impulse

passes through the atrioventricular node, ensuring the

correct delay between atrial and ventricular contraction.

Once through the atrioventricular node, the electrical

impulse is rapidly conducted to ventricular tissue through

specialised conducting fibres which form the bundle of

His and its branches.



Electrical activity of the heart

The signal for contraction of each heart muscle cell is the

electrical depolarisation of its membrane. The electrical

signal is transmitted from cell to cell in an orderly way so

that under normal circumstances the heart contracts in

an orderly fashion. The physiological cardiac pacemaker

comprises a small group of cells in the sinoatrial node

situated close to where the right atrium joins the superior

vena cava. Normally, these cells undergo cyclical

repolarisation and depolarisation at a faster rate than

144



right

atrium



bundle of

His



left

bundle

branch



ELECTROCARDIOGRAM

The electrocardiogram (ECG) is an electrical and structural

map of the heart and is an invaluable aid to studying

normal heart rhythm and its disturbances. It works by

sensing and amplifying the very small electrical potential

changes between different points on the surface of

the body caused by the cyclical depolarisation and

repolarisation of the heart cells. Electrical potentials are

picked up by electrodes that are attached to the skin. The

points at which the electrodes are attached and the

conventional ways in which they are connected enable



Chapter



Cardiac arrhythmias



6



The ECG ‘complex’



The multilead ECG



electrical activity

from sinoatrial node

too small to detect

aVR



aVL



R



1

I



2

3 4



P



Q

S



T



III



II



1

2

3

4



P wave – atrial activation

PR interval – delay in conduction through AV node

QRS complex – ventricular activation

T wave – ventricular recovery



Fig. 6.15 Different parts of an ECG ‘complex’.

aVF



Fig. 6.14 How the ECG ‘looks at’ the heart from different

directions (a concept due to Goldberger and Wilson).



the ECG to ‘look at’ the heart from a sequence of different

directions (Fig. 6.14). The cycle of electrical changes

during a single heart beat is termed an ECG complex.

Different parts of the ECG complex reflect the activation

of different parts of the heart. The P wave signals atrial

activity and the QRS complex indicates ventricular activity

(Fig. 6.15).

In patients suspected of intermittent arrhythmias, the

ECG may be displayed as a continuous monitor trace

(Fig. 6.16). In patients outside hospital, the ECG can be

recorded continuously digitally for periods of 24–48 h

and then played back to analyse any rhythm disturbances.

This process is called ‘ambulatory ECG’ or ‘Holter

monitoring’. The ECG can be used to detect hypertrophy

of the different chambers of the heart (Fig. 6.17), abnormal

rhythms and cardiac damage.



Cardiac arrhythmias

Abnormalities of heart rhythm can be divided into those

in which the heart goes too slowly (bradycardia) and

those in which the rate is abnormally rapid (tachycardia).

Physiologically, heart rate can vary in a normal young

adult from 40 beats/min during sleep to 180 beats/minute

or more during vigorous exercise. The physiological

control of heart rate is due to a balance between

sympathetic nervous activity, which speeds the heart

rate, and vagal activity, which slows it down.

There are two principal mechanisms of arrhythmia

generation: automaticity and re-entry phenomena. The



Fig. 6.16 ECG trace displayed on a monitor at the nursing station

or bedside.



Differential diagnosis

Autonomic effects on the heart



Vagal tone (slows the heart)



• Increased in: children, athletes

• Stimulated by:

• carotid baroreceptors, pain, trauma (via

hypothalamus)

• ventricular stretch receptors (fainting reflex)

• Excessive in:

• malignant vasovagal syncope

• carotid sinus syncope

• Blocked by: atropine

Sympathetic tone (speeds up the heart)



• Increased by: fear, pain, hypovolaemia, heart failure,

physical activity

• Decreased: during sleep

• Blocked by: β-adrenoceptor blockers



145



Chapter



6



The heart and cardiovascular system



Effect of cardiac chamber hypertrophy on the ECG



right

atrium



left

atrium

P>3 mm



right atrial hypertrophy: tall ‘peaked’ P wave

e.g. pulmonary stenosis



left

atrium



right

atrium



P >0.12 s



left atrial hypertrophy: wide ‘M-shaped’ P wave

e.g. mitral stenosis



V2

V2 = deep

S wave



normal V1

V5



right ventricular hypertrophy



right ventricular

hypertrophy:

dominant

R wave in V1



V5 = large

R wave

left ventricular hypertrophy



also QRS 0.1 s

wide and

T wave inversion



Fig. 6.17 Electrocardiographic changes can be used to identify hypertrophy of the cardiac chambers.



latter comprises 90% of arrhythmias. Automaticity implies

normal conduction tissue or abnormal conduction

(ectopic) tissue that is repetitively firing faster than usual.

Re-entry phenomenon is described under tachycardia

below.



Heart block



BRADYCARDIA

Bradycardia may be caused by drugs, particularly βadrenoceptor blocking drugs (‘beta-blockers’); it may

also be a physiological finding in fit young athletes with

a high vagal tone. Extreme bradycardia may be caused by

heart block with failure of conduction of the electrical

impulse, most often as it passes through the atrioventricular

node or bundle of His (Fig. 6.18).



P



P

QRS



P



P



P



P



P



QRS



TACHYCARDIA

Ectopic beats

As all heart muscle and not only the sinoatrial node

exhibits the capacity for spontaneous depolarisation, it is

not uncommon to find an ‘ectopic focus’ of electrical

activity which can initiate extra beats out of time

with the normal cardiac cycle. These extra beats or

extrasystoles may be generated in the atrium or

ventricle. In otherwise healthy people, extrasystoles

are usually benign and harmless. Following myocardial

146



Fig. 6.18 Heart block is one cause of bradycardia; there is failure of

conduction of the electrical impulses from atrium to ventricle.



infarction or during a viral infection of the heart,

they may act as markers for metabolic damage and,

consequently, excessive irritability of the heart muscle

(Fig. 6.19).



Chapter



Cardiac arrhythmias



6



Sustained tachycardia

Ventricular and atrial extrasystoles



atrial

focus



ventricular focus

usually scarred

or injured

myocardium

R



R



R



atrial ectopic same shape

as normal complex

compensatory pause same

as normal RR interval



R



V



ventricular ectopic different

shape from normal complex

compensatory pause less

than normal RR interval



Fig. 6.19 Extrasystoles are caused by an ectopic focus of electrical

activity.



A persistent tachycardia may be caused by several ectopic

beats occurring in sequence (e.g. as the manifestation of

a particularly irritable ectopic focus). This is called a ‘focal

tachycardia’.

A more common mechanism for sustained tachycardia

is, however, the phenomenon of re-entry (Fig. 6.20). The

basic principle of a re-entry tachycardia is that there are

two alternative pathways for the conduction of the

electrical impulse; these pathways differ both in their

speed of conduction and their refractory period. Under

normal conditions, the cardiac impulse will be conducted

by both pathways but an exceptionally early beat may

find one pathway still refractory to conduction and

therefore the impulse will be conducted down the other

one alone. However, by the time it reaches the end of

this pathway, the other pathway will have recovered and

be able to conduct the impulse in the reverse direction.

This sets up the possibility of a ‘circus movement’ or

oscillation and the re-entry circuit can act as a focus for



Re-entry tachycardia



normal conduction

pathway via

atrioventricular

node



1



1



2



3



3

tachycardia



2



abnormal

conduction via

‘bypass tract’

(bundle of Kent)



conducting entirely

through bypass pathway

(longer refractory period,

fast conducting)



3



conducting entirely via

normal pathway (short

refractory period,

slow conducting)



4

4

1. Abnormal beats conducted through both normal (blue)

and accessory (red) pathways



conducting through both

normal and bypass

pathways



2. A premature atrial beat finds the red pathway refractory but is

conducted down the blue pathway

3. By the time the impulse reaches the ventricle, the red

pathway has recovered and now conducts rectogradely to

stimulate the atria and set up a re-entry tachycardia



Fig. 6.20 Mechanism of a re-entry tachycardia, based on the ‘paradigm’ of the Wolff–Parkinson–White syndrome. The left hand diagram

shows the ECG pattern produced when conduction is all along the bypass pathway, when it is all along the normal pathway and when it is

along both simultaneously.

147



Chapter



6



The heart and cardiovascular system

generating a tachycardia. This tachycardia may continue

until one of the pathways fatigues and cannot conduct

fast enough to maintain the circuit or until the process is

interrupted by an electrical stimulus which breaks the

circuit and re-establishes normal conduction (Fig. 6.21).

Fibrillation

The most extreme form of arrhythmia occurs when the

coordinated conduction of impulses between cells

completely breaks down and individual cells contract

haphazardly. This process is termed fibrillation. Atrial

fibrillation is common but not particularly hazardous



because the atrioventricular node acts as a ‘filter’,

preventing the ventricles from being stimulated at too

rapid a rate. Ventricular fibrillation is, however, rapidly

lethal because the rapidly contracting ventricles are

ineffective and unable to pump any blood into the

circulation. The only treatment for ventricular fibrillation

is to pass an artificial competing electric current through

the heart. This technique is referred to as defibrillation

and causes momentary extinction of all electrical activity,

allowing the whole system to reset (Fig. 6.22).



Blood supply to the heart

Terminating a re-entry tachycardia



Fig. 6.21 A critically timed extra stimulus can terminate a re-entry

tachycardia by making both pathways refractory.



Heart muscle needs a supply of blood to support both

its basal metabolic needs and the increased oxygen

requirements of exercise. The blood supply must be

capable of increasing to meet the heart’s demands during

exercise because heart muscle, unlike skeletal muscle, can

only work aerobically. The arterial blood supply to the

heart is provided by the right and left coronary arteries.

The right coronary artery supplies mainly the right

ventricle and the inferior surface of the left ventricle. It

divides at the end of its course into the posterolateral

branch and the posterior descending branch, which

supplies the posterior and lateral parts of the left ventricle

The left coronary has a common trunk (the left main

stem) which divides soon after its origin into the left

anterior descending coronary artery, which supplies

the interventricular septum, the anterior surface and the

apex of the left ventricle, and the circumflex coronary

artery, which supplies the lateral part of the left ventricle

(Fig. 6.23).



b



a

Fig. 6.22 A defibrillator (a). An electrical charge is built up within the machine and discharged through paddles applied to the

patient’s chest (b).

148



Chapter



Blood supply to the heart

LAD



6



LM



CA



LMCA



Cx



RCA



Cx

LAD



Fig. 6.23 Cine-angiograms to show (left and middle) the left coronary artery and (right) the right coronary artery (RCA) (Cx, left circumflex

artery; LAD, left anterior descending artery; LMCA, left main coronary artery).



The fetal circulation



pulmonary

artery



arterial

duct



aorta



Changes from fetal to adult circulation



pulmonary

artery



active constriction

of ductus

arteriosus



aorta



2

foramen ovale



left

atrium



right

atrium

1



right

ventricle



left

ventricle



1. Blood passes from

the right atrium to the

left atrium through

the foramen ovale

2. Blood passes from

the pulmonary artery

to the aorta through

the arterial duct



Fig. 6.24 In the fetal circulation, oxygenated blood from the

umbilical vein bypasses the liver through the ductus venosus; a

portion is shunted from the right to left atrium through the foramen

ovale and a further portion passes through the arterial duct.



In common with other arteries in the body, coronary

arteries are prone to atheroma which predisposes to

thrombosis and coronary artery occlusion. The clinical

features of coronary thrombosis and the myocardial

infarction are described later.

INTRACARDIAC SHUNTING

In the fetus, the placenta, rather than the lungs,

participates in respiratory gas exchange and the

unexpanded lungs offer a high resistance to blood flow.

Both sides of the fetal heart work to pump a mixture of

deoxygenated blood from the systemic veins and

oxygenated blood from the placenta into the aorta and

thus to the rest of the body. Blood entering in the right

atrium may pass either through the tricuspid valve into



fall in right

atrial pressure

closes valve

of foramen

ovale



left

atrium

right

atrium



right

ventricle



left

ventricle



Fig. 6.25 Changes that occur in the fetal circulation at birth. The

ductus arteriosus constricts and the fall in right arterial pressure as

the lungs expand closes the foramen ovale.



the right ventricle or through a hole in the intra-atrial

septum, the foramen ovale. Blood entering the right

ventricle is pumped into the pulmonary artery, with only

a small proportion of it entering the lungs. The remainder

passes via the ductus arteriosus into the aorta

(Fig. 6.24).

After birth, as the lungs inflate with air, intrapulmonary

vascular resistance of the lungs rapidly falls. The

subsequent fall in right atrial pressure and rise in left

atrial pressure creates a pressure change which forces the

valve-like foramen ovale to close and seals the interatrial

septum. At the same time, the ductus arteriosus constricts

and closes (Fig. 6.25). This separates the work of the right

and left sides of the heart and causes them to work in

series rather than in parallel. However, abnormalities in

the process of transition from fetal to adult circulation, or

149



Chapter



6



The heart and cardiovascular system



Examples of left to right shunts: atrial septal defect



pulmonary

artery



pulmonary

flow

murmur



pulmonary

artery



aorta



atrial septal

defect: shunt

from higher

pressure left

atrium to

right atrium



left

atrium

right

atrium



increased flow

at tricuspid

valve may

cause diastolic

murmur



aorta



left

atrium

right

atrium



right

ventricle



increased mitral

valve flow: may

cause diastolic

murmur

left

ventricle



left

ventricle

right

ventricle



dilated hyperdynamic

right ventricle



a



dilated

hyperdynamic

right ventricle



ventricular septal

defect: causes

loud pansystolic

murmur



b

Left to right shunt: persistent ductus arteriosus



pulmonary

artery



right to left shunt

through persistent

ductus arteriosus:

continuous murmur

below right clavicle



aorta



right

atrium



c



left

atrium



right

ventricle



Fig. 6.26 (a) Left to right shunt atrial septal defect. Blood passes

from the left to right atrium. The overall result is an increase in

pulmonary blood flow. (b) Left to right shunt: ventricular septal

defect. Blood passes from the high pressure left ventricle to the

lower pressure right ventricle. (c) Left to right shunt: persistent

ductus arteriosus. Blood passes from the high pressure aorta to the

lower pressure pulmonary artery.



the heart has to cope with the extra load of blood

shunted from the left. A two-to-one shunt means that

the output at the right side of the heart is twice that of

the left side of the heart and the increased workload

on the right side of the heart may lead to heart failure.

Alternatively, the excessively high blood flow through

the lungs may lead to irreversible damage to the

pulmonary vasculature and the development of

pulmonary hypertension. Examples of left to right

shunts are shown in Figure 6.26.

left

ventricle



anatomical defects in the partitions or ‘septa’ dividing the

right and left sides of the heart, may lead to short-circuits

or ‘shunts’.

Left to right shunt

A congenital or acquired defect in the interatrial septum,

interventricular septum or failure of closure of the

ductus arteriosus will produce a left to right shunt. Blood

follows the path of least resistance from the high pressure

left-sided chamber to the lower pressure right-sided

chamber. The result is that, instead of matching left

and the right sided cardiac outputs, the right side of

150



Left to right shunt: ventricular septal defect



Right to left shunt

If a septal defect or persistent ductus arteriosus is

combined with a further lesion that raises the pressure

on the right side of the heart then, instead of blood

flowing from the left-sided chamber to the right-sided

chamber, it will flow in the opposite direction, from the

right side of the heart to the left. The most common

example of congenital heart disease causing a right to

left shunt is Fallot’s tetralogy (Fig. 6.27) which is

physiologically equivalent to a ventricular septal defect

plus pulmonary valve stenosis. A right to left shunt can

occur when pulmonary vascular damage occurs in a

patient with a severe left to right shunt. The resistance of

the pulmonary arteries rises, resulting in increased

pressure on the right side of the heart and a reversal

of the shunt. This is called Eisenmenger’s syndrome

(Fig. 6.28).