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Cardiovascular Physiology, 9e

Chapter 5: Cardiac Abnormalities

The student, through understanding normal cardiac function, diagnoses and appreciates the
consequences of common cardiac abnormalities:

Detects common cardiac arrhythmias from the electrocardiogram, identifies their physiological bases, and
describes their physiological consequences.

Lists 4 common cardiac valve abnormalities for the le! side of the heart and describes the alterations in
intracardiac and arterial pressures, flow patterns, and heart sounds that accompany them.

Identifies the consequences of similar valve abnormalities for the right side of the heart.

Recall that e"ective, e"icient ventricular pumping action depends on proper cardiac function in 5 basic
aspects. This chapter focuses on the abnormalities in 3 of these aspects: (1) abnormal cardiac excitation
and rhythmicity, (2) valvular stenosis (inadequate valve opening), and (3) valvular insu"iciency (incomplete
valve closure). Discussion of abnormalities in myocardial force production and cardiac filling is presented
in Chapter 11. The material presented here is an introduction to the more common cardiac electrical and
cardiac valve dysfunctions, with an emphasis on the primary physiological consequences of these
abnormal situations.


Many cardiac excitation problems can be diagnosed from the information in a single lead of an
electrocardiogram. The lead II electrocardiogram traces at the top of Figures 5–1 and 5–2 are identified as
normal sinus rhythms based on the following characteristics: (1) the frequency of QRS complexes is
approximately 1/s, indicating a normal beating rate; (2) the shape of the QRS complex is normal for lead II
and its duration is less than 120 ms, indicating rapid depolarization of the ventricles via normal conduction
pathways; (3) each QRS complex is preceded by a P wave of proper configuration, indicating sinoatrial (SA)
nodal origin of the excitation; (4) the PR interval is less than 200 ms, indicating proper conduction delay of
the impulse propagation through the atrioventricular (AV) node; (5) the QT interval is less than half of the R-
to-R interval, indicating normal ventricular repolarization; and (6) there are no extra P waves, indicating
that no AV nodal conduction block is present. The subsequent electrocardiographic tracings in Figures 5–1
and 5–2 represent irregularities commonly found in clinical practice. Examination of each of these traces
with the above characteristics in mind will aid in the di"erential diagnosis.

Figure 5–1.
Supraventricular arrhythmias.

Figure 5–2.
Ventricular arrhythmias.
The physiological consequences of abnormal excitation and conduction in the heart depend on
whether the electrical abnormality evokes a tachycardia, which will limit the time for cardiac filling
between beats; evokes a bradycardia, which is inadequate to support su"icient cardiac output; or
decreases the coordination of myocyte contraction, which will reduce stroke volume.

Supraventricular Abnormalities

Traces 2 through 6 below the normal trace in Figure 5–1 represent typical supraventricular
arrhythmias (i.e., originating in the atria or AV node). Supraventricular tachycardia (shown in trace 2 in
Figure 5–1 and sometimes called paroxysmal atrial tachycardia) occurs when the atria are abnormally
excited and drive the ventricles at a very rapid rate. These paroxysms o!en begin abruptly, last for a few
minutes to a few hours, and then, just as abruptly, disappear and the heart rate reverts to normal. QRS
complexes appear normal (albeit frequent) with simple paroxysmal atrial tachycardia because the
ventricular conduction pathways operate normally. The P and T waves may be superimposed because of
the high heart rate. Low blood pressure and dizziness may accompany bouts of this arrhythmia because
the extremely high heart rate does not allow su"icient diastolic time for ventricular filling.

There are 2 mechanisms that may account for supraventricular tachycardia. First, an atrial region,
o!en outside the SA node, may become irritable (perhaps because of local interruption in blood flow) and
begin to fire rapidly to take over the pacemaker function. Such an abnormal pacemaker region is called an
ectopic focus. Alternatively, atrial conduction may become altered so that a single wave of excitation does
not die out but continually travels around some abnormal atrial conduction loop. In this case, the
continual activity in the conduction loop may drive the atria and AV node at a very high frequency. This self-
sustaining process is called a reentry phenomenon and is illustrated in Figure 5–3. This situation may
develop as a result of abnormal repolarization and altered refractory periods in local areas of the
myocardium. Atrial flutter is a special form of tachycardia of atrial origin in which a large reentrant pathway
drives the atria at very fast rates (250–300 beats/min) and normal refractory periods of AV nodal tissue are
overwhelmed. Thus, ventricular rate is o!en some fixed ratio of the atrial rate (2:1, 4:1) with frequencies
o!en 150 to 220 beats/min. The electrocardiogram o!en shows a saw-tooth pattern of merged P waves
with intermittent normal QRS complexes.

Figure 5–3.
Normal and reentrant (circus) cardiac excitation pathways.

Conduction blocks occur at the AV node and generally represent impaired conduction through this
tissue. In a first-degree heart block (trace 3 in Figure 5–1), the only electrical abnormality is unusually slow
conduction through the AV node. This condition is detected by an abnormally long PR interval (>0.2 s).
Otherwise, the electrocardiogram may be completely normal. At normal heart rates, the physiological
e"ects of the first-degree block are inconsequential. The danger, however, is that the slow conduction may
deteriorate to an actual interruption of conduction.

A second-degree heart block (trace 4 in Figure 5–1) is said to exist when some, but not all, atrial impulses
are transmitted through the AV node to the ventricle. Impulses are blocked in the AV node if the cells of the
region are still in a refractory period from a previous excitation. In this situation, the primary problem is a
slower-than-normal conduction through the AV nodal region and thus the second-degree block is
aggravated by high atrial rates. In the second-degree block, some, but not all, P waves are accompanied by
corresponding QRS complexes and T waves. Atrial rate is o!en faster than ventricular rate by a certain ratio
(e.g., 2:1, 3:1, and 4:1). This condition may not represent a serious clinical problem as long as the
ventricular rate is adequate to meet the pumping needs.

In a third-degree heart block (trace 5 in Figure 5–1), no impulses are transmitted through the AV node. In
this event, some area in the ventricles—o!en in the common bundle or bundle branches near the exit of
the AV node—assumes the pacemaker role for the ventricular tissue. Atrial rate and ventricular rate are
completely independent, and P waves and QRS complexes are totally dissociated in the electrocardiogram.
Ventricular rate is very likely to be slower than normal (bradycardia) and is o!en slow enough to impair
cardiac output.

Atrial fibrillation (trace 6 in Figure 5–1) is characterized by a complete loss of the normally close synchrony
of the excitation and resting phases between individual atrial cells. Cells in di"erent areas of the atria
depolarize, repolarize, and are excited again randomly. Consequently, no P waves appear in the
electrocardiogram, although there may be rapid, irregular, small waves apparent throughout diastole. The
ventricular rate is o!en very irregular in atrial fibrillation because impulses enter the AV node from the atria
at unpredictable times. Fibrillation is a self-sustaining process. The mechanisms behind it are not well
understood, but impulses are thought to progress repeatedly around irregular conduction pathways
(sometimes called circus pathways, which imply a reentry phenomenon as described earlier and in Figure
5–3). However, because atrial contraction o!en plays a minor role in ventricular filling in resting
individuals, atrial fibrillation may be tolerated by some patients as long as ventricular rate is su"icient to
maintain the cardiac output. 1

Atrial flutter also represents a breakdown of the normal atrial conduction pathways but is less chaotic with
much of the atrial tissue being re-excited in sync with a single rapidly reverberating circus pathway. The
ECG o!en will look like the second-degree AV nodal block with a very rapid atrial rate (4:1 or more).

Ventricular Abnormalities

Traces 2 through 6 below the normal trace in Figure 5–2 show typical ventricular electrical
abnormalities. Conduction blocks called bundle branch blocks or hemiblocks (trace 2 in Figure 5–2) can
occur in either of the branches of the Purkinje system of the intraventricular septum, o!en as a result of a
myocardial infarction. Ventricular depolarization is less synchronous than normal in the half of the heart
with the nonfunctional Purkinje system. This results in a widening of the QRS complex (>0.12 s) because a
longer time is required for ventricular depolarization to be completed. The direct physiological e"ects of
bundle branch blocks are usually inconsequential.
Premature ventricular contractions (PVCs) (trace 3 in Figure 5–2) are caused by action potentials initiated
by and propagated away from an ectopic focus in the ventricle. As a result, the ventricle depolarizes and
contracts before it normally would. A PVC is o!en followed by a missed beat (called a compensatory pause)
because the ventricular cells are still refractory when the next normal impulse emerges from the SA node.
The highly abnormal ventricular depolarization pattern of a PVC produces the large-amplitude, long-
duration deflections on the electrocardiogram. The shapes of the electrocardiographic records of these
extra beats are highly variable and depend on the ectopic site of their origin and the depolarization
pathways involved. The volume of blood ejected by the premature beat itself is smaller than normal,
whereas the stroke volume of the beat following the compensatory pause is larger than normal. This is
partly due to the di"erences in filling times and partly to an inherent phenomenon of the cardiac muscle
called postextrasystolic potentiation. Single PVCs occur occasionally in most individuals and, although
sometimes alarming to the individual experiencing them, are not dangerous. Frequent occurrence of PVCs,
however, may be a signal of possible myocardial damage or perfusion problems.

Ventricular tachycardia (trace 4 in Figure 5–2) occurs when the ventricles are driven at high rates,
usually by impulses originating from a ventricular ectopic focus. Ventricular tachycardia is a very serious
condition. Not only is diastolic filling time limited by the rapid rate, but also the abnormal excitation
pathways make ventricular contraction less synchronous and therefore less e"ective than normal. In
addition, ventricular tachycardia o!en precedes ventricular fibrillation.

Prolonged QT intervals (the le! side of trace 5 in Figure 5–2) are a result of delayed ventricular myocyte
repolarization, which may be due to inappropriate opening of sodium channels or prolonged closure of
potassium channels during the action potential plateau phase. Although the normal QT interval varies with
heart rate, it is normally less than 40% of the cardiac cycle length (except at very high heart rates). Long QT
syndrome is identified when the QT interval is greater than 50% of the cycle duration. It may be genetic in
origin (mutations influencing various ion channels involved with cardiac excitability), may be acquired
from several electrolyte disturbances (low blood levels of Ca2+, Mg2+, or K+), or may be induced by several
pharmacological agents (including some antiarrhythmic drugs). The prolongation of the myocyte
refractory period, which accompanies the long QT syndrome, extends the vulnerable period during which
extra stimuli can evoke tachycardia or fibrillation. Patients with long QT syndrome are predisposed to a
particularly dangerous type of ventricular tachycardia called torsades de pointes (“twisting of points,” as
shown on the right side of trace 5 in Figure 5–2). This di"ers from the ordinary ventricular tachycardia in
that the ventricular electrical complexes cyclically vary in amplitude around the baseline and can
deteriorate rapidly into ventricular fibrillation.

In ventricular fibrillation (trace 6 in Figure 5–2), various areas of the ventricle are excited and contract
asynchronously. The mechanisms are similar to those in atrial fibrillation. The ventricle is especially
susceptible to fibrillation whenever a premature excitation occurs at the end of the T wave of the previous
excitation, that is, when most ventricular cells are in the “hyperexcitable” or “vulnerable” period of their
electrical cycle. In addition, because some cells are repolarized and some are still refractory, circus
pathways can be triggered easily at this time. Because no pumping action occurs with ventricular
fibrillation, the situation is fatal unless quickly corrected by cardiac conversion. During conversion, the
artificial application of large currents to the entire heart (via paddle electrodes applied across the chest)
may be e"ective in depolarizing all heart cells simultaneously, thus allowing a normal excitation pathway
to be reestablished.

Myocardial ischemia can also cause changes in the basic ECG pattern. In addition to potential alterations in
cardiac excitation and conduction described above, chronic inadequate coronary flow to the
subendocardium may cause T wave inversion, and ST segment depression. A more severe interruption of
coronary flow causing a transmural infarct will usually result in ST segment elevation.

1A real danger with atrial fibrillation lies in the tendency for blood to form clots in the atria in the absence

of the normal vigorous coordinated atrial contraction. These clots can fragment and move out of the heart
to lodge in small arteries throughout the systemic circulation. These emboli can have devastating e"ects
on critical organ function. Consequently, anticoagulant therapy is strongly recommended for patients in
atrial fibrillation.


Pumping action of the heart is impaired when the valves do not function properly. Abnormal heart sounds,
which o!en accompany cardiac valvular defects, are called murmurs. These sounds are caused by
abnormal pressure gradients and turbulent blood flow patterns that occur during the cardiac cycle. A
number of techniques, ranging from simple auscultation (listening to the heart sounds) to
echocardiography or cardiac catheterization, are used to obtain information about the nature and extent of
these valvular malfunctions.

In general, when a valve does not open fully (i.e., is stenotic), the chamber upstream of the valve has to
develop more pressure during its systolic phase to achieve a given flow through the valve. This increase in
“pressure” work will induce hypertrophy of cardiac muscle cells and thickening of the walls of that
chamber. When a valve does not close completely (i.e., is insu"icient), the regurgitant blood flow
represents an additional volume that must be ejected in order to get su"icient forward flow out of the
ventricle into the tissues. This increase in “volume” work o!en leads to chamber dilation but not to an
increase in wall thickness. 2

A second generality about valve abnormalities is that whenever there is an elevation in the atrial pressure
as a result of AV valve stenosis or regurgitation, this will result in higher pressures in the upstream capillary
beds. If capillary hydrostatic pressures are elevated, tissue edema will ensue with consequences on the
function of those upstream organs.

A brief overview of 4 of the common valve defects influencing le! ventricular function is given in Figure 5–4.
Note that similar stenotic and regurgitant abnormalities can occur in right ventricular valves with similar
consequences on right ventricular function.

Figure 5–4.
Characteristics of le! ventricular valve abnormalities: (AA) aortic stenosis, (B
B) mitral stenosis, (C
C) aortic
regurgitation (insu"iciency), and (DD) mitral insu"iciency.
Aortic Stenosis

Some characteristics of aortic stenosis are shown in Figure 5–4A. Normally, the aortic valve opens
widely and o"ers a pathway of very low resistance through which blood leaves the le! ventricle. If this
opening is narrowed (stenotic), resistance to flow through the valve increases. A significant pressure
di"erence between the le! ventricle and the aorta may be required to eject blood through a stenotic aortic
valve. As shown in Figure 5–4A, intraventricular pressures may rise to very high levels during systole, while
aortic pressure rises more slowly than normal to a systolic value that is subnormal. Pulse pressure is
usually low with aortic stenosis. High intraventricular pressure development is a strong stimulus for cardiac
muscle cell hypertrophy, and an increase in le! ventricular muscle mass invariably accompanies aortic
stenosis. This tends to produce a le!ward deviation of the electrical axis. (The mean electrical axis will fall
in the upper right-hand quadrant as shown in Figure 4–6.) Blood being ejected through the narrowed
orifice may reach very high velocities, and turbulent flow may occur as blood enters the aorta. This
abnormal turbulent flow can be heard as a systolic (or ejection) murmur with a properly placed
stethoscope. The primary physiological consequence of aortic stenosis is a high ventricular a!erload that is
caused by restriction of the outflow tract. This imposes an increased pressure workload on the le!

Mitral Stenosis

Some characteristics of mitral stenosis are shown in Figure 5–4B. A pressure di"erence of more than a
few millimeters of mercury across the mitral valve during diastole is distinctly abnormal and indicates that
this valve is stenotic. The high resistance mandates an elevated pressure di"erence to achieve normal flow
⋅ ⋅
across the valve Q = ΔP/R Q = ΔP/R . Consequently, as shown in Figure 5–4B, le! atrial pressure is
elevated with mitral stenosis. The high le! atrial workload may induce hypertrophy of the le! atrial muscle.
Elevated le! atrial pressure is reflected back into the pulmonary bed and, if high enough, causes
pulmonary congestion and “shortness of breath.” A diastolic murmur associated with turbulent flow
through the stenotic mitral valve can o!en be heard. The primary physiological consequences of mitral
stenosis are elevations in le! atrial pressure and pulmonary capillary pressure. The latter can cause
pulmonary edema and interference with normal gas exchange in the lungs (leading to shortness of breath).

Aortic Insu"iciency

Typical characteristics of aortic regurgitation (also known as insu"iciency or incompetence) are shown
in Figure 5–4C. When the leaflets of the aortic valve do not provide an adequate seal, blood regurgitates
from the aorta back into the le! ventricle during the diastolic period. Aortic pressure falls faster and further
than normal during diastole, which causes a low diastolic pressure and a large pulse pressure. In addition,
ventricular end-diastolic volume and pressure are higher than normal because of the extra blood that
reenters the chamber through the incompetent aortic valve during diastole. Turbulent flow of the blood
reentering the le! ventricle during early diastole produces a characteristic diastolic murmur. O!en the
aortic valve is altered so that it is both stenotic and insu"icient. In these instances, both a systolic and a
diastolic murmur are present. The primary physiological consequences of aortic insu"iciency are reduction
in forward flow out to the tissues (if the insu"iciency is severe) and increase in the volume workload of the
le! ventricle.

Mitral Regurgitation

Typical characteristics of mitral regurgitation (insu"iciency, incompetence) are shown in Figure 5–4D.
When the mitral valve is insu"icient, some blood regurgitates from the le! ventricle into the le! atrium
during systole. A systolic murmur may accompany this abnormal flow pattern. Le! atrial pressure is raised
to abnormally high levels, and le! ventricular end-diastolic volume and pressure increase. Mitral valve
prolapse is the most common form of mitral insu"iciency in which the valve leaflets evert into the le!
atrium during systole. The primary physiological consequences of mitral regurgitation are somewhat
similar to aortic insu"iciency in that forward flow out of the le! ventricle into the aorta may be
compromised (if the insu"iciency is severe) and there is an increase in the volume workload of the le!
ventricle. In addition, the elevated le! atrial pressure can also lead to pulmonary e"ects with shortness of

2A useful analogy is to compare the hypertrophied skeletal muscles of the weightli!er (doing isometric or

pressure work) to the nonhypertrophied but well-toned skeletal muscles of the long-distance runner (doing
isotonic or shortening work).

It might be useful for the student to be reminded that the heart is “simply” a pulsatile pressure-generating
pump producing one-way flow through a closed hydraulic system. There are many ways that this pump can
fail, and the information in this chapter just touches on the critical role of the excitation process (which sets
the “speed” of the pump) and the valves (that assure forward flow). Many of the physiological
consequences of abnormalities in these processes (i.e., inadequate output and lowered pressure) are easily
predicted from a basic consideration of fluid dynamics.


Cardiac arrhythmias can o!en be detected and diagnosed from a single electrocardiographic lead.

Physiological consequences of abnormal excitation and conduction in the heart depend on whether
the electrical abnormality limits the time for adequate cardiac filling or decreases the coordination of
myocyte contractions resulting in inadequate pressure development and ejection.

Supraventricular arrhythmias are a result of abnormal action potential initiation at the SA node or
altered propagation characteristics through the atrial tissue and the AV node.

Tachycardias may originate either in the atria or in the ventricles and are a result of increased
pacemaker automaticity, of spontaneously firing ectopic foci, or of continuous circular pathways setting up
a reentrant circuit.

Abnormal conduction through the AV node results in conduction blocks which may result in

Abnormal conduction pathways in the Purkinje system or in the ventricular tissue result in significant
QRS alterations.

Ventricular tachycardia and ventricular fibrillation represent severe abnormalities that are
incompatible with e"ective cardiac pumping.

Failure of cardiac valves to open fully (stenosis) can result in elevated upstream chamber pressure and
abnormal pressure gradients, congestion in upstream vascular beds, chamber wall hypertrophy, turbulent
forward flow across the valve, and murmurs during systole or diastole.

Failure of cardiac valves to close completely (insu"iciency, incompetence, regurgitation) can result in
large stroke volumes, abnormal pressure pulses, congestion in upstream vascular beds, turbulent
backward flow across the valve, and murmurs during systole or diastole.

5–1. You hear a systolic murmur that seems to be coming from the right side of the heart.

a. Which valve condition(s) might be the cause of this abnormal sound?

b. A finding of a right electrical axis deviation might support which of your possible diagnoses?

c. Would you expect your patient to have pulmonary congestion?

5–2. Which of the following arrhythmias might result in a reduced stroke volume?

a. paroxysmal atrial tachycardia

b. ventricular tachycardia

c. atrial fibrillation

d. ventricular fibrillation

e. third-degree heart block

5–3. Describe the primary pressure abnormalities across the cardiac valve that are associated with

a. aortic stenosis

b. mitral stenosis

5–4. You notice an abnormally large pulsation of your patient’s jugular vein, which occurs at about the
same time as heart sound, S 1 . What is your diagnosis?

5–5. What alteration in jugular venous pulsations might accompany third-degree heart block?

5–6. Given the following data, name the abnormal valve, predict the type of murmur that might be
detected, and whether pulmonary congestion might be present. Calculate the resistance to flow across this

Aortic pressures (systolic/diastolic) = 150/100 mm Hg

Le! ventricular pressures (systolic/diastolic) = 150/2 mm Hg

Le! atrial pressures (systolic/diastolic) = 50/32 mm Hg

Heart rate = 60 beats/min

Stroke volume = 50 mL/beat

5–7. Your 75-year-old male patient is alert with complaints of general fatigue. His heart rate = 90 beats/min
and arterial pressure = 180/50 mm Hg. A diastolic murmur is present. There are no ECG abnormalities
identified and mean electrical axis = 10 degrees. Cardiac catheterization indicates that LV pressure = 180/20
mm Hg and le! atrial pressure = 10/3 mm Hg (as peak systolic/end-diastolic). What abnormality is most
consistent with these findings?

5–8. Evaluation of your patient’s electrocardiogram shows that P waves occur at a regular rate of 90/min
and QRS complexes occur at a regular rate of 37/min. Which of the following is the most likely diagnosis?

a. supraventricular tachycardia

b. first-degree heart block

c. second-degree heart block

d. third-degree heart block

e. bundle branch block

5–9. An otherwise healthy, vigorous 74-year-old woman comes to your o"ice with complaints of having
recent episodes of intermittent dizziness and weakness associated with a feeling of fluttering and/or
pounding in her chest. Her blood pressure is 135/88 mm Hg and her overall pulse rate is about 80 beats per
minute with an irregularly irregular rhythm (i.e., no discernable pattern). What is the most likely diagnosis?
What will you do next?

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