1818 PART 6 Disorders of the Cardiovascular System

In a large study of patients with advanced heart failure, the presence

of a right atrial pressure >10 mmHg (as predicted on bedside examination) had a positive value of 88% for the prediction of a pulmonary

artery wedge pressure of >22 mmHg. In addition, an elevated JVP has

prognostic significance in patients with both symptomatic heart failure

and asymptomatic LV systolic dysfunction. The presence of an elevated

JVP is associated with a higher risk of subsequent hospitalization for

heart failure, death from heart failure, or both.

Assessment of Blood Pressure Measurement of blood pressure

usually is delegated to a medical assistant but should be repeated by

the examining clinician. Accurate measurement depends on body

position, arm size, time of measurement, place of measurement, device,

device size, technique, and examiner. In general, physician-recorded

blood pressures are higher than both nurse-recorded pressures and

self-recorded pressures at home. Blood pressure is best measured in

the seated position with the arm at the level of the heart and the feet

on the floor with the back supported, using an appropriately sized

cuff, after 5–10 min of relaxation. When it is measured in the supine

position, the arm should be raised to bring it to the level of the midright atrium. The length and width of the blood pressure cuff bladder

should be 80 and 40% of the arm’s circumference, respectively. A

common source of error in practice is to use an inappropriately small

cuff, resulting in marked overestimation of true blood pressure, or an

inappropriately large cuff, resulting in underestimation of true blood

pressure. The cuff should be inflated to 30 mmHg above the expected

systolic pressure and the pressure released at a rate of 2–3 mmHg/s.

Systolic and diastolic pressures are defined by the first and fifth Korotkoff sounds, respectively. Very low (even 0 mmHg) diastolic blood

pressures may be recorded in patients with chronic, severe AR or a large

arteriovenous fistula because of enhanced diastolic “run-off.” In these

instances, both the phase IV and phase V Korotkoff sounds should be

recorded. Blood pressure is best assessed at the brachial artery level,

though it can be measured at the radial, popliteal, or pedal pulse level.

In general, systolic pressure increases and diastolic pressure decreases

when measured in more distal arteries. Blood pressure should be measured in both arms, and the difference should be <10 mmHg. A blood

pressure differential that exceeds this threshold may be associated with

atherosclerotic or inflammatory subclavian artery disease, supravalvular aortic stenosis, aortic coarctation, or aortic dissection. Systolic leg

pressures are usually as much as 20 mmHg higher than systolic arm

pressures. Greater leg–arm pressure differences are seen in patients

with chronic severe AR as well as patients with extensive and calcified

lower extremity peripheral arterial disease. The ankle-brachial index

(systolic pressure in the dorsalis pedis and/or posterior tibial artery

divided by the higher of the two brachial artery pressures) is a powerful

predictor of long-term cardiovascular mortality.

The blood pressure measured in an office or hospital setting may

not accurately reflect the pressure in other venues. “White coat hypertension” (elevated clinic blood pressure and normal out of clinic blood

pressure) is defined by at least three separate clinic-based measurements >130/80 mmHg and at least two non-clinic-based measurements <130/80 mmHg in the absence of any evidence of target organ

damage. Individuals with white coat hypertension may not benefit

from drug therapy, although they may be more likely to develop sustained hypertension over time. Masked hypertension (normal or low

clinic blood pressure but elevated out of clinic blood pressure) should

be suspected when normal or even low blood pressures are recorded in

the office in patients with advanced atherosclerotic disease, especially

when evidence of target organ damage is present or bruits are audible.

Higher systolic blood pressures measured with a 24-h ambulatory

blood pressure device are associated with a higher risk of cardiovascular disease and all-cause death independent of blood pressures measured in the outpatient setting.

Orthostatic hypotension is defined by a fall in systolic pressure

>20 mmHg or in diastolic pressure >10 mmHg in response to assumption of the upright posture from a supine position within 3 min. There

may also be a lack of a compensatory tachycardia, an abnormal response

that suggests autonomic insufficiency, as may be seen in patients with

diabetes mellitus or Parkinson’s disease. Orthostatic hypotension is a

common cause of postural lightheadedness/syncope and should be

assessed routinely in patients for whom this diagnosis might pertain. It

can be exacerbated by advanced age, dehydration, certain medications,

food, deconditioning, and ambient temperature/humidity.

Arterial Pulse The carotid artery pulse occurs just after the

ascending aortic pulse. The aortic pulse is best appreciated in the

epigastrium, just above the level of the umbilicus. Peripheral arterial

pulses that should be assessed routinely include the subclavian, brachial, radial, ulnar, femoral, popliteal, dorsalis pedis, and posterior

tibial. In patients in whom the diagnosis of either temporal arteritis or

polymyalgia rheumatica is suspected, the temporal arteries also should

be examined. Although one of the two pedal pulses may not be palpable in up to 10% of normal subjects, the pair should be symmetric.

The integrity of the arcuate system of the hand is assessed by Allen’s

test, which is performed routinely before instrumentation of the radial

artery. The pulses should be examined for their symmetry, volume,

timing, contour, amplitude, and duration. If necessary, simultaneous

auscultation of the heart can help identify a delay in the arrival of

an arterial pulse. Simultaneous palpation of the radial and femoral

pulses may reveal a femoral delay in a patient with upper extremity

hypertension and suspected aortic coarctation. The carotid upstrokes

should never be examined simultaneously or before listening for a

bruit. Light pressure should always be used to avoid precipitation of

carotid hypersensitivity syndrome and syncope in a susceptible elderly

individual. The arterial pulse usually becomes more rapid and spiking

as a function of its distance from the heart, a phenomenon that reflects

the muscular status of the more peripheral arteries and the summation

of the incident and reflected waves. In general, the character and contour of the arterial pulse depend on the stroke volume, ejection velocity, vascular compliance, and systemic vascular resistance. The pulse

examination can be misleading in patients with reduced cardiac output

and in those with stiffened arteries from aging, chronic hypertension,

or peripheral arterial disease.

The character of the pulse is best appreciated at the carotid level

(Fig. 239-2). A weak and delayed pulse (pulsus parvus et tardus) defines

severe aortic stenosis (AS). Some patients with AS may also have a

slow, notched, or interrupted upstroke (anacrotic pulse) with a thrill

or shudder. With chronic severe AR, by contrast, the carotid upstroke

has a sharp rise and rapid fall-off (Corrigan’s or water-hammer pulse).

Some patients with advanced AR may have a bifid or bisferiens pulse,

in which two systolic peaks can be appreciated. A bifid pulse is also

described in patients with hypertrophic obstructive cardiomyopathy

(HOCM), with inscription of percussion and tidal waves. A bifid pulse

is easily appreciated in patients on intraaortic balloon counterpulsation

(IABP), in whom the second pulse is diastolic in timing.

Pulsus paradoxus refers to a fall in systolic pressure >10 mmHg with

inspiration that is seen in patients with pericardial tamponade but also

is described in those with massive pulmonary embolism, hemorrhagic

shock, severe obstructive lung disease, and tension pneumothorax.

Pulsus paradoxus is measured by noting the difference between

the systolic pressure at which the Korotkoff sounds are first heard

(during expiration) and the systolic pressure at which the Korotkoff

sounds are heard with each heartbeat, independent of the respiratory

phase. Between these two pressures, the Korotkoff sounds are heard

only intermittently and during expiration. The cuff pressure must be

decreased slowly to appreciate the finding. It can be difficult to measure pulsus paradoxus in patients with tachycardia, atrial fibrillation, or

tachypnea. A pulsus paradoxus may be palpable at the brachial artery

or femoral artery level when the pressure difference exceeds 15 mmHg.

This inspiratory fall in systolic pressure is an exaggerated consequence

of interventricular dependence.

Pulsus alternans, in contrast, is defined by beat-to-beat variability of

pulse amplitude. It is present only when every other phase I Korotkoff

sound is audible as the cuff pressure is lowered slowly, typically in a

patient with a regular heart rhythm and independent of the respiratory cycle. Pulsus alternans is seen in patients with severe LV systolic

dysfunction and is thought to be due to cyclic changes in intracellular

Physical Examination of the Cardiovascular System

1819CHAPTER 239

calcium and action potential duration. When pulsus alternans is

associated with electrocardiographic T-wave alternans, the risk for an

arrhythmic event appears to be increased.

Ascending aortic aneurysms can rarely be appreciated as a pulsatile

mass in the right parasternal area. Appreciation of a prominent abdominal aortic pulse should prompt noninvasive imaging with ultrasound

or computed tomography for better characterization. Femoral and/or

popliteal artery aneurysms should be sought in patients with abdominal aortic aneurysm disease.

The level of a claudication-producing arterial obstruction can often

be identified on physical examination (Fig. 239-3). For example, in a

patient with calf claudication, a decrease in pulse amplitude between

the common femoral and popliteal arteries will localize the obstruction to the level of the superficial femoral artery, although inflow

obstruction above the level of the common femoral artery may coexist.

Auscultation for carotid, subclavian, abdominal aortic, and femoral

artery bruits should be routine. However, the correlation between the

presence of a bruit and the degree of vascular obstruction is poor. A

cervical bruit is a weak indicator of the degree of carotid artery stenosis; the absence of a bruit does not exclude the presence of significant

luminal obstruction. If a bruit extends into diastole or if a thrill is present, the obstruction is usually severe. Another cause of an arterial bruit

is an arteriovenous fistula with enhanced flow.

The likelihood of significant lower extremity peripheral arterial

disease increases with typical symptoms of claudication, cool skin,

abnormalities on pulse examination, or the presence of a vascular bruit.

Abnormal pulse oximetry (a >2% difference between finger and toe

oxygen saturation) can be used to detect lower extremity peripheral

arterial disease and is comparable in its performance characteristics to

the ankle-brachial index.

Inspection and Palpation of the Heart The LV apex beat

may be visible in the midclavicular line at the fifth intercostal space

in thin-chested adults. Visible pulsations anywhere other than this

expected location are abnormal. The left anterior chest wall may heave

in patients with an enlarged or hyperdynamic left or right ventricle.

As noted previously, a visible right upper parasternal pulsation may be

suggestive of ascending aortic aneurysm disease. In thin, tall patients

and patients with advanced obstructive lung disease and flattened

diaphragms, the cardiac impulse may be visible in the epigastrium and

should be distinguished from a pulsatile liver edge.

Palpation of the heart begins with the patient in the supine position

at 30° and can be enhanced by placing the patient in the left lateral

decubitus position. The normal LV impulse is <2 cm in diameter and

moves quickly away from the fingers; it is better appreciated at end

expiration, with the heart closer to the anterior chest wall. Characteristics such as size, amplitude, and rate of force development should be

noted.

Enlargement of the LV cavity is manifested by a leftward and downward displacement of an enlarged apex beat. A sustained apex beat is a

sign of pressure overload, such as that which may be present in patients

with AS or chronic hypertension. A palpable presystolic impulse corresponds to the fourth heart sound (S4

) and is indicative of reduced

LV compliance and the forceful contribution of atrial contraction to

ventricular filling. A palpable third sound (S3

), which is indicative of

a rapid early filling wave in patients with heart failure, may be present

even when the gallop itself is not audible. A large LV aneurysm may

sometimes be palpable as an ectopic impulse, discrete from the apex

beat. HOCM may very rarely cause a triple cadence beat at the apex

with contributions from a palpable S4

 and the two components of the

bisferiens systolic pulse.

Right ventricular pressure or volume overload may create a sternal

lift. Signs of either TR (cv waves in the jugular venous pulse) and/or

pulmonary arterial hypertension (a loud single or palpable P2

) would

be confirmatory. The right ventricle can enlarge to the extent that

left-sided events are obscured. A zone of retraction between the right

ventricular and LV impulses sometimes can be appreciated in patients

with right ventricle pressure or volume overload when they are placed

in the left lateral decubitus position. Systolic and diastolic thrills signify

turbulent and high-velocity blood flow. Their locations help identify

the origin of heart murmurs.

■ CARDIAC AUSCULTATION

Heart Sounds Ventricular systole is defined by the interval between

the first (S1

) and second (S2

) heart sounds (Fig. 239-4). The first heart

sound (S1

) includes mitral and tricuspid valve closure. Normal splitting can be appreciated in young patients and those with right bundle

branch block, in whom tricuspid valve closure is relatively delayed. The

intensity of S1

 is determined by the distance over which the anterior

leaflet of the mitral valve must travel to return to its annular plane, leaflet mobility, LV contractility, and the PR interval. S1

 is classically loud

in the early phases of rheumatic MS and in patients with hyperkinetic

circulatory states or short PR intervals. S1

 becomes softer in the later

stages of MS when the leaflets are rigid and calcified, after exposure

to β-adrenergic receptor blockers, with long PR intervals, and with

LV contractile dysfunction. The intensity of heart sounds, however,

can be reduced by any process that increases the distance between the

stethoscope and the responsible cardiac event, including mechanical

ventilation, obstructive lung disease, obesity, pneumothorax, and a

pericardial effusion.

Aortic and pulmonic valve closure constitutes the second heart sound

(S2

). With normal or physiologic splitting, the A2

–P2

 interval increases

with inspiration and narrows during expiration. This physiologic interval will widen with right bundle branch block because of the further

delay in pulmonic valve closure and in patients with severe MR because

of the premature closure of the aortic valve. An unusually narrowly

split or even a singular S2

 is a feature of pulmonary arterial hypertension. Fixed splitting of S2

, in which the A2

–P2

 interval is wide and

does not change during the respiratory cycle, occurs in patients with a

S4

S4 S4

S4

S1

S1

S4

S1

S1

A2 S1

A2 A2

A2

P2

P2

A2

P2

P2

P2

A Dicrotic notch

C Dicrotic notch D Dicrotic notch

E Dicrotic notch

B Dicrotic notch

FIGURE 239-2 Schematic diagrams of the configurational changes in carotid pulse

and their differential diagnoses. Heart sounds are also illustrated. A. Normal. S4

,

fourth heart sound; S1

, first heart sound; A2

, aortic component of second heart

sound; P2

, pulmonic component of second heart sound. B. Aortic stenosis. Anacrotic

pulse with slow upstroke to a reduced peak. C. Bisferiens pulse with two peaks in

systole. This pulse is rarely appreciated in patients with severe aortic regurgitation.

D. Bisferiens pulse in hypertrophic obstructive cardiomyopathy. There is a rapid

upstroke to the first peak (percussion wave) and a slower rise to the second peak

(tidal wave). E. Dicrotic pulse with peaks in systole and diastole. This waveform may

be seen in patients with sepsis or during intraaortic balloon counterpulsation with

inflation just after the dicrotic notch. (Reproduced with permission from K Chatterjee,

W Parmley [eds]: Cardiology: An Illustrated Text/Reference. Philadelphia, Gower

Medical Publishers, 1991.)

1820 PART 6 Disorders of the Cardiovascular System

secundum atrial septal defect (ASD). Reversed or paradoxical splitting

refers to a pathologic delay in aortic valve closure, such as that which

occurs in patients with left bundle branch block, right ventricular pacing, severe AS, HOCM, and acute myocardial ischemia. With reversed

or paradoxical splitting, the individual components of S2

 are audible at

end expiration, and their interval narrows with inspiration, the opposite of what would be expected under normal physiologic conditions.

P2

 is considered loud when its intensity exceeds that of A2

 at the base,

when it can be palpated in the area of the proximal main pulmonary

artery (second left interspace), or when both components of S2

 can be

appreciated at the lower left sternal border or apex. The intensity of A2

and P2

 decreases with AS and pulmonic stenosis (PS), respectively. In

these conditions, a single S2

 may result.

Systolic Sounds An ejection sound is a high-pitched early systolic

sound that corresponds in timing to the upstroke of the carotid pulse.

It usually is associated with congenital bicuspid aortic or pulmonic

valve disease; however, ejection sounds are also sometimes audible in

patients with isolated aortic or pulmonary root dilation and normal

semilunar valves. The ejection sound that accompanies bicuspid aortic

valve disease becomes softer and then inaudible as the valve calcifies

and becomes more rigid. The ejection sound that accompanies PS

moves closer to the first heart sound as the severity of the stenosis

increases. In addition, the pulmonic ejection sound is the only rightsided acoustic event that decreases in intensity with inspiration. Ejection sounds are often heard more easily at the lower left sternal border

than they are at the base. Nonejection sounds (clicks), which occur

after the onset of the carotid upstroke, are related to MVP and may

be single or multiple. The nonejection click may introduce a murmur.

This click-murmur complex will move away from the first heart sound

with maneuvers that increase ventricular preload, such as squatting.

On standing, the click and murmur move closer to S1

.

Diastolic Sounds The high-pitched opening snap (OS) of MS

occurs after a very short interval after the second heart sound. The A2

–

OS interval is inversely proportional to the height of the left atrial–left

ventricular diastolic pressure gradient. The intensity of both S1

 and the

OS of MS decreases with progressive calcification and rigidity of the

anterior mitral leaflets. The pericardial knock (PK) is also high-pitched

and occurs slightly later than the OS, corresponding in timing to

the abrupt cessation of ventricular expansion after tricuspid valve

opening and to an exaggerated y descent seen in the jugular venous

waveform in patients with constrictive pericarditis. A tumor plop is

a lower-pitched sound that rarely can be heard in patients with atrial

myxoma. It may be appreciated only in certain positions and arises

from the diastolic prolapse of the tumor across the mitral valve.

The third heart sound (S3

) occurs during the rapid filling phase of

ventricular diastole. It can be a normal finding in children, adolescents,

and young adults; however, in older patients, it signifies heart failure.

A left-sided S3

 is a low-pitched sound best heard over the LV apex. A

right-sided S3

 is usually better heard over the lower left sternal border

and becomes louder with inspiration. A left-sided S3

 in patients with

chronic heart failure is predictive of cardiovascular morbidity and

mortality. Interestingly, an S3

 is equally prevalent among heart failure

patients with preserved and reduced LV ejection fraction.

The fourth heart sound (S4

) occurs during the atrial filling phase of

ventricular diastole and indicates LV presystolic expansion. An S4

 is

more common among patients who derive significant benefit from the

Major arteries Ankle-brachial index Ankle systolic pressures

Axillary a.

Right common

carotid a.

Left arm,

systolic pressure

in the brachial a.

Left ankle,

systolic pressure

in the posterior

tibial a. and the

dorsalis pedis a.

Brachial a.

Deep

brachial a.

Radial a.

Common iliac a.

Ulnar a.

Femoral a.

Popliteal a.

Posterior

tibial artery a.

Posterior

tibial artery a.

Anterior

tibial artery a.

Dorsalis pedis a.

Dorsalis

pedis a.

Deep femoral a.

FIGURE 239-3 A. Anatomy of the major arteries of the leg. B. Measurement of the ankle systolic pressure. The ankle-brachial index (ABI) is calculated by dividing the lower

of the two ankle pressures (i.e., the dorsalis pedis or posterior tibia) by the higher of the two arm pressures (i.e., left or right arm). Left and right ABIs should be recorded.

(Adapted from NA Khan et al: Does the clinical examination predict lower extremity peripheral arterial disease?. JAMA 295:536, 2006.)

Physical Examination of the Cardiovascular System

1821CHAPTER 239

atrial contribution to ventricular filling, such as those with chronic LV

hypertrophy or active myocardial ischemia. An S4

 is not present with

atrial fibrillation.

Cardiac Murmurs Heart murmurs result from audible vibrations

that are caused by increased turbulence and are defined by their timing

within the cardiac cycle. Not all murmurs are indicative of structural

heart disease, and the accurate identification of a benign or functional

systolic murmur often can obviate the need for additional testing in

healthy subjects. The duration, frequency, configuration, and intensity

of a heart murmur are dictated by the magnitude, variability, and duration of the responsible pressure difference between two cardiac chambers, the two ventricles, or the ventricles and their respective great

arteries. The intensity of a heart murmur is graded on a scale of 1 to 6;

a thrill is present with murmurs of grade 4 or greater intensity. Other

attributes of the murmur that aid in its accurate identification include

its location, radiation, and response to bedside maneuvers. Although

clinicians can detect and correctly identify heart murmurs with only

fair reliability, a careful and complete bedside examination usually can

identify individuals with valvular heart disease for whom transthoracic

echocardiography and clinical follow-up are indicated and exclude

subjects for whom no further evaluation is necessary.

Systolic murmurs can be early, mid, late, or holosystolic in timing

(Fig. 239-5). Acute severe MR results in a decrescendo early systolic

murmur, the characteristics of which are related to the progressive

attenuation of the LV to left atrial pressure gradient during systole

because of the steep and rapid rise in left atrial pressure in this context.

Severe MR associated with posterior leaflet prolapse or flail radiates

anteriorly and to the base, where it can be confused with the murmur

of AS. MR that is due to anterior leaflet involvement radiates posteriorly and to the axilla. With acute TR in patients with normal pulmonary artery pressures, an early systolic murmur that may increase in

intensity with inspiration may be heard at the left lower sternal border,

with regurgitant cv waves visible in the jugular venous pulse.

A midsystolic murmur begins after S1

 and ends before S2

; it is typically crescendo-decrescendo in configuration. AS is the most common

cause of a midsystolic murmur in an adult. It is often difficult to estimate the severity of the valve lesion on the basis of the physical examination findings, especially in older hypertensive patients with stiffened

carotid arteries or patients with low cardiac output in whom the

intensity of the systolic heart murmur is misleadingly soft. Examination findings consistent with severe AS would include parvus et tardus

carotid upstrokes, a late-peaking grade 3 or greater midsystolic murmur, a soft A2

, a sustained LV apical impulse, and an S4

. It is sometimes

difficult to distinguish aortic sclerosis from more advanced degrees

of valve stenosis. The former is defined by focal thickening and calcification of the aortic valve leaflets that is not severe enough to result

in obstruction. These valve changes are associated with a Doppler jet

velocity across the aortic valve of 2.5 m/s or less. Patients with aortic

sclerosis can have grade 2 or 3 midsystolic murmurs identical in their

acoustic characteristics to the murmurs heard in patients with more

advanced degrees of AS. Other causes of a midsystolic heart murmur

include pulmonic valve stenosis (with or without an ejection sound),

HOCM, increased pulmonary blood flow in patients with a large ASD

and left-to-right shunting, and several states associated with accelerated blood flow in the absence of structural heart disease, such as fever,

thyrotoxicosis, pregnancy, anemia, and normal childhood/adolescence.

The murmur of HOCM has features of both obstruction to LV outflow and MR, as would be expected from knowledge of the pathophysiology of this condition. The systolic murmur of HOCM usually can

be distinguished from other causes on the basis of its response to bedside maneuvers, including Valsalva, passive leg raising, and standing/

squatting. In general, maneuvers that decrease LV preload (or increase

LV contractility) will cause the murmur to intensify, whereas maneuvers that increase LV preload or afterload will cause a decrease in the

intensity of the murmur. Accordingly, the systolic murmur of HOCM

becomes louder during the strain phase of the Valsalva maneuver and

after standing quickly from a squatting position. The murmur becomes

A Normal

EXPIRATION INSPIRATION

S1 S2

A2 P2

B Atrial septal

defect

C Expiratory splitting

with inspiratory

increase (RBBB,

idiopathic dilatation PA)

D Reversed splitting

(LBBB, aortic

stenosis)

E Close fixed

splitting

(pulmonary

hypertension)

S1 S2

A2 P2

S1 S2

A2 P2

S1 S2

A2 P2

S1 S2

A2 P2

S1 S2

A2 P2

S1 S2

P A2 2

S1 S2

P A2 2

S1 S2

A2

P2

S1 S2

A2 P2

FIGURE 239-4 Heart sounds. A. Normal. S1

, first heart sound; S2

, second heart sound;

A2

, aortic component of the second heart sound; P2

, pulmonic component of the

second heart sound. B. Atrial septal defect with fixed splitting of S2

. C. Physiologic

but wide splitting of S2

 with right bundle branch block (RBBB). PA, pulmonary artery.

D. Reversed or paradoxical splitting of S2

 with left bundle branch block (LBBB).

E. Narrow splitting of S2

 with pulmonary hypertension. (Reprinted by permission from

Springer Nature: Springer-Verlag, Diagnosis of Heart Disease by NO Fowler, 1991.)

ECG

LVP

LAP

HSM

S1 S2

ECG

LVP

AOP

MSM

S1 A2

ECG

ECG

LVP AOP

EDM

S1 A2

S1 S2

LVP

LAP

PSM MDM

A B

FIGURE 239-5 A. Top. Graphic representation of the systolic pressure difference

(green shaded area) between left ventricle and left atrium with phonocardiographic

recording of a holosystolic murmur (HSM) indicative of mitral regurgitation. ECG,

electrocardiogram; LAP, left atrial pressure; LVP, left ventricular pressure; S1

, first

heart sound; S2

, second heart sound. Bottom. Graphic representation of the systolic

pressure gradient (green shaded area) between left ventricle and aorta in patient

with aortic stenosis. A midsystolic murmur (MSM) with a crescendo-decrescendo

configuration is recorded. AOP, aortic pressure. B. Top. Graphic representation of

the diastolic pressure difference between the aorta and left ventricle (blue shaded

area) in a patient with aortic regurgitation, resulting in a decrescendo, early diastolic

murmur (EDM) beginning with A2

. Bottom. Graphic representation of the diastolic

left atrial–left ventricular gradient (blue areas) in a patient with mitral stenosis with

a mid-diastolic murmur (MDM) and late presystolic murmurs (PSM).

1822 PART 6 Disorders of the Cardiovascular System

Impedance

Ao

LV

S1 S1

C C

M M

S2 S2

Contractility

Volume

FIGURE 239-6 Behavior of the click (C) and murmur (M) of mitral valve prolapse with changes in loading

(volume, impedance) and contractility. S1

, first heart sound; S2

, second heart sound. With standing (left side

of figure), volume and impedance decrease, as a result of which the click and murmur move closer to S1

. With

squatting (right), the click and murmur move away from S1

 due to the increases in left ventricular volume and

impedance (afterload). Ao, aorta; LV, left ventricle. (Adapted from RA O’Rourke, MH Crawford: Curr Prob Cardiol

1:9, 1976.)

softer with passive leg raising and when squatting. The murmur of AS is typically loudest in

the second right interspace with radiation into

the carotids, whereas the murmur of HOCM is

best heard between the lower left sternal border

and the apex. The murmur of PS is best heard

in the second left interspace. The midsystolic

murmur associated with enhanced pulmonic

blood flow in the setting of a large ASD is usually loudest at the mid-left sternal border.

A late systolic murmur, heard best at the

apex, indicates MVP. As previously noted, the

murmur may or may not be introduced by a

nonejection click. Differential radiation of the

murmur, as previously described, may help

identify the specific leaflet involved by the myxomatous process. The click-murmur complex

behaves in a manner directionally similar to

that demonstrated by the murmur of HOCM

during the Valsalva and stand/squat maneuvers

(Fig. 239-6). The murmur of MVP can be identified by the accompanying nonejection click.

Holosystolic murmurs are plateau in configuration and reflect a continuous and wide

pressure gradient between the left ventricle and

left atrium with chronic MR, the left ventricle

and right ventricle with a ventricular septal

defect (VSD), and the right ventricle and right

atrium with TR. In contrast to acute MR, in

chronic MR, the left atrium is enlarged and its

compliance is normal or increased to the extent

that there is little if any further increase in left

atrial pressure from any increase in regurgitant

volume. The murmur of MR is best heard over the cardiac apex. The

intensity of the murmur increases with maneuvers that increase LV

afterload, such as sustained hand grip. The murmur of a VSD (without

significant pulmonary hypertension) is holosystolic and loudest at the

mid-left sternal border, where a thrill is usually present. The murmur

of TR is loudest at the lower left sternal border, increases in intensity

with inspiration (Carvallo’s sign), and is accompanied by visible cv

waves in the jugular venous wave form and, on occasion, by pulsatile

hepatomegaly.

Diastolic Murmurs In contrast to some systolic murmurs, diastolic

heart murmurs always signify structural heart disease (Fig. 239-5). The

murmur associated with acute, severe AR is relatively soft and of short

duration because of the rapid rise in LV diastolic pressure and the

progressive diminution of the aortic-LV diastolic pressure gradient.

In contrast, the murmur of chronic severe AR is classically heard as a

decrescendo, blowing diastolic murmur along the left sternal border in

patients with primary valve pathology and sometimes along the right

sternal border in patients with primary aortic root pathology. With

chronic AR, the pulse pressure is wide and the arterial pulses are bounding in character. These signs of significant diastolic run-off are often

absent in the acute phase. The murmur of pulmonic regurgitation is also

heard along the left sternal border. It is most commonly due to pulmonary hypertension and enlargement of the annulus of the pulmonic valve.

S2

 is single and loud and may be palpable. There is a right ventricular/

parasternal lift that is indicative of chronic right ventricular pressure

overload. A less impressive murmur of PR is present after repair of tetralogy of Fallot or pulmonic valve atresia. In this postoperative setting, the

murmur is softer and lower-pitched, and the severity of the accompanying pulmonic regurgitation can be underestimated significantly.

MS is the classic cause of a mid- to late diastolic murmur, which is

best heard over the apex in the left lateral decubitus position, is lowpitched or rumbling, and is introduced by an OS in the early stages

of the rheumatic disease process. Presystolic accentuation refers to an

increase in the intensity of the murmur just before the first heart sound

and occurs in patients with sinus rhythm. It is absent in patients with

atrial fibrillation. The auscultatory findings in patients with rheumatic

tricuspid stenosis typically are obscured by left-sided events, although

they are similar in nature to those described in patients with MS.

“Functional” mitral or tricuspid stenosis refers to the generation of

mid-diastolic murmurs that are created by increased and accelerated

transvalvular diastolic flow, even in the absence of valvular obstruction, in the setting of severe MR, severe TR, or a large ASD with leftto-right shunting. The Austin Flint murmur of chronic severe AR is a

low-pitched mid- to late apical diastolic murmur that sometimes can

be confused with MS. The Austin Flint murmur typically decreases

in intensity after exposure to vasodilators, whereas the murmur of

MS may be accompanied by an OS and also may increase in intensity

after vasodilators because of the associated increase in cardiac output.

Unusual causes of a mid-diastolic murmur include atrial myxoma,

complete heart block, and acute rheumatic mitral valvulitis.

Continuous Murmur A continuous murmur is predicated on a

pressure gradient that persists between two cardiac chambers or blood

vessels across systole and diastole. The murmurs typically begin in systole, envelop the second heart sound (S2

), and continue through some

portion of diastole. They can often be difficult to distinguish from

individual systolic and diastolic murmurs in patients with mixed valvular heart disease. The classic example of a continuous murmur is that

associated with a PDA, which usually is heard in the second or third

interspace at a slight distance from the sternal border. Other causes of

a continuous murmur include a ruptured sinus of Valsalva aneurysm

with creation of an aortic–right atrial or right ventricular fistula, a coronary or great vessel arteriovenous fistula, and an arteriovenous fistula

constructed to provide dialysis access. There are two types of benign

continuous murmurs. The cervical venous hum is heard in children or

adolescents in the supraclavicular fossa. It can be obliterated with firm

pressure applied to the diaphragm of the stethoscope, especially when

the subject turns his or her head toward the examiner. The mammary

soufflé of pregnancy relates to enhanced arterial blood flow through

engorged breasts. The diastolic component of the murmur can be obliterated with firm pressure over the stethoscope.

Physical Examination of the Cardiovascular System

1823CHAPTER 239

Dynamic Auscultation Diagnostic accuracy can be enhanced

by the performance of simple bedside maneuvers to identify heart

murmurs and characterize their significance (Table 239-1). Except for

the pulmonic ejection sound, right-sided events increase in intensity

with inspiration and decrease with expiration; left-sided events behave

oppositely (100% sensitivity, 88% specificity). As previously noted,

the intensity of the murmurs associated with MR, VSD, and AR will

increase in response to maneuvers that increase LV afterload, such

as hand grip and vasopressors. The intensity of these murmurs will

decrease after exposure to vasodilating agents. Squatting is associated

with an abrupt increase in LV preload and afterload, whereas rapid

standing results in a sudden decrease in preload. In patients with MVP,

the click and murmur move away from the first heart sound with

squatting because of the delay in onset of leaflet prolapse at higher

ventricular volumes. With rapid standing, however, the click and

murmur move closer to the first heart sound as prolapse occurs earlier

in systole at a smaller chamber dimension. The murmur of HOCM

behaves similarly, becoming softer and shorter with squatting (95%

sensitivity, 85% specificity) and longer and louder on rapid standing

(95% sensitivity, 84% specificity). A change in the intensity of a systolic

murmur in the first beat after a premature beat or in the beat after a

long cycle length in patients with atrial fibrillation suggests valvular AS

rather than MR, particularly in an older patient in whom the murmur

of the AS may be well transmitted to the apex (Gallavardin effect).

Of note, however, the systolic murmur of HOCM also increases in

intensity in the beat after a premature beat. This increase in intensity

of any LV outflow murmur in the beat after a premature beat relates to

the combined effects of enhanced LV filling (from the longer diastolic

period) and postextrasystolic potentiation of LV contractile function.

In either instance, forward flow will accelerate, causing an increase

in the gradient across the LV outflow tract (dynamic or fixed) and a

louder systolic murmur. In contrast, the intensity of the murmur of

MR does not change in a postpremature beat, because there is relatively

little change in the nearly constant LV to left atrial pressure gradient or

further alteration in mitral valve flow. Bedside exercise can sometimes

be performed to increase cardiac output and, secondarily, the intensity

of both systolic and diastolic heart murmurs. Most left-sided heart

murmurs decrease in intensity and duration during the strain phase

of the Valsalva maneuver. The murmurs associated with MVP and

HOCM are the two notable exceptions. The Valsalva maneuver also

can be used to assess the integrity of the heart and vasculature in the

setting of advanced heart failure.

Prosthetic Heart Valves The first clue that prosthetic valve

dysfunction may contribute to recurrent symptoms is frequently a

change in the quality of the heart sounds or the appearance of a new

murmur. The heart sounds with a bioprosthetic valve resemble those

generated by native valves. A mitral bioprosthesis usually is associated

with a grade 1 to 2 midsystolic murmur along the left sternal border

(created by turbulence across the valve struts as they project into the

LV outflow tract) as well as by a soft mid-diastolic murmur that occurs

with normal LV filling. This diastolic murmur often can be heard only

in the left lateral decubitus position and after exercise. A high-pitched

or holosystolic apical murmur is indicative of pathologic MR due to a

paravalvular leak and/or intra-annular bioprosthetic regurgitation from

leaflet degeneration, for which diagnostic noninvasive imaging is indicated. Clinical deterioration can occur rapidly after the first expression

of mitral bioprosthetic valve failure. A tissue valve in the aortic position

is always associated with a grade 1 to 3 midsystolic murmur at the

base or just below the suprasternal notch. A diastolic murmur of AR is

abnormal in any circumstance. Mechanical valve dysfunction may first

be suggested by a decrease in the intensity of either the opening or the

closing sound. A high-pitched apical systolic murmur in patients with

a mechanical mitral prosthesis and a diastolic decrescendo murmur

in patients with a mechanical aortic prosthesis indicate paravalvular

regurgitation. Patients with prosthetic valve thrombosis may present

clinically with signs of shock, muffled heart sounds, and soft murmurs.

Pericardial Disease A pericardial friction rub is nearly 100%

specific for the diagnosis of acute pericarditis, although the sensitivity

of this finding is not nearly as high, because the rub may come and go

over the course of an acute illness or be very difficult to elicit. The rub

is heard as a leathery or scratchy three-component or two-component

sound, although it may be monophasic. Classically, the three components are ventricular systole, rapid early diastolic filling, and late

presystolic filling after atrial contraction in patients in sinus rhythm. It

is necessary to listen to the heart in several positions. Additional clues

to the presence of acute pericarditis may be present from the history

and 12-lead electrocardiogram. The rub typically disappears as the

volume of any pericardial effusion increases. Pericardial tamponade

can be diagnosed with a sensitivity of 98%, a specificity of 83%, and

a positive likelihood ratio of 5.9 (95% confidence interval 2.4–14) by

a pulsus paradoxus that exceeds 12 mmHg in a patient with a large

pericardial effusion.

The findings on physical examination are integrated with the symptoms previously elicited with a careful history to construct an appropriate differential diagnosis and proceed with indicated imaging and

laboratory assessment. The physical examination is an irreplaceable

component of the diagnostic algorithm and, in selected patients, can

inform prognosis. Educational efforts to improve clinician competence

eventually may result in cost saving, particularly if the indications for

imaging can be influenced by the examination findings.

■ FURTHER READING

Drazner MH et al: Value of clinician assessment of hemodynamics

in advanced heart failure: The ESCAPE trial. Circ Heart Fail 1:170,

2008.

Fanaroff AC et al: Does this patient with chest pain have acute

coronary syndrome? The Rational Clinical Examination Systematic

Review. JAMA 314:1955, 2015.

Fang JC, O’Gara PT: The history and physical examination. An

evidence-based approach, in Braunwald’s Heart Disease. A Textbook

of Cardiovascular Medicine, 11th ed, Zipes DP et al (eds). Philadelphia,

Elsevier/Saunders, 2019, pp 83–101.

TABLE 239-1 Effects of Physiologic Interventions on the Intensity of

Heart Murmurs and Sounds

Respiration

Right-sided murmurs and sounds generally increase with inspiration, except for

the PES. Left-sided murmurs and sounds are usually louder during expiration.

Valsalva Maneuver

Most murmurs decrease in length and intensity. Two exceptions are the systolic

murmur of HOCM, which usually becomes much louder, and that of MVP, which

becomes longer and often louder. After release of the Valsalva maneuver,

right-sided murmurs tend to return to control intensity earlier than do left-sided

murmurs.

After VPB or AF

Murmurs originating at normal or stenotic semilunar valves increase in the

cardiac cycle after a VPB or in the cycle after a long cycle length in AF. By

contrast, systolic murmurs due to AV valve regurgitation do not change or

become shorter (MVP).

Positional Changes

With standing, most murmurs diminish, with two exceptions being the murmur

of HOCM, which becomes louder, and that of MVP, which lengthens and often

is intensified. With squatting, most murmurs become louder, but those of HOCM

and MVP usually soften and may disappear. Passive leg raising usually produces

the same results.

Exercise

Murmurs due to blood flow across normal or obstructed valves (e.g., PS,

MS) become louder with both isotonic and submaximal isometric (hand grip)

exercise. Murmurs of MR, VSD, and AR also increase with hand grip exercise.

However, the murmur of HOCM often decreases with nearly maximum hand

grip exercise. Left-sided S4

 and S3

 sounds are often accentuated by exercise,

particularly when due to ischemic heart disease.

Abbreviations: AF, atrial fibrillation; AR, aortic regurgitation; HOCM, hypertrophic

obstructive cardiomyopathy; MR, mitral regurgitation; MS, mitral stenosis; MVP,

mitral valve prolapse; PES, pulmonic ejection sound; PR, pulmonic regurgitation;

PS, pulmonic stenosis; TR, tricuspid regurgitation; TS, tricuspid stenosis; VPB,

ventricular premature beat; VSD, ventricular septal defect.

1824 PART 6 Disorders of the Cardiovascular System

An electrocardiogram (ECG or EKG) is a graphical representation

of electrical activity generated by the heart. The signals, detected by

means of metal electrodes attached to the extremities and chest wall,

are amplified and recorded by the electrocardiograph device. ECG leads

(derivations) are configured to display the instantaneous differences in

potential between specific pairs of electrodes. The utility of the ECG

derives from its immediate availability as a noninvasive, inexpensive,

and highly versatile test. In addition to its use in detecting arrhythmias and myocardial ischemia, it may reveal findings related to lifethreatening metabolic disturbances or to increased susceptibility to

sudden cardiac arrest (see also Chaps. 306 and 408).

■ ELECTROPHYSIOLOGIC BACKGROUND

Depolarization of the heart is the initiating event for cardiac contraction. The electric currents that spread through the heart are produced

by three components: cardiac pacemaker cells, specialized conduction

tissue, and the heart muscle itself. The ECG records only the depolarization (stimulation) and repolarization (recovery) potentials generated by the “working” atrial and ventricular myocardium (see also

Chaps. 244 and 246).

The stimulus initiating the normal heartbeat originates in the sinoatrial (SA) node (Fig. 240-1), which possesses spontaneous automaticity. Spread of the depolarization wave through the right and left atria

induces contraction of these chambers. Next, the impulse stimulates

specialized conduction tissues in the atrioventricular (AV) nodal and

His-bundle areas; together, these two regions constitute the AV junction. The bundle of His branches into two main divisions, the right and

left bundles, which rapidly transmit depolarization wavefronts in a synchronous way to the right and left ventricular myocardium by way of

the Purkinje fibers. The main left bundle fans out into left anterior and

left posterior fascicle subdivisions. The depolarization wavefronts then

spread through the ventricular wall, from endocardium to epicardium,

triggering coordinated ventricular contraction. Since the cardiac depolarization and repolarization waves have directions and magnitudes,

they can be represented by vectors.

■ ECG WAVEFORMS AND INTERVALS

The ECG waveforms are labeled alphabetically, beginning with the

P wave, which represents atrial depolarization (Fig. 240-2). The

QRS complex represents ventricular depolarization, and the ST-T-U

complex (ST segment, T wave, and U wave) represents ventricular

240 Electrocardiography

Ary L. Goldberger

repolarization. The J point is the junction between the end of the QRS

complex and the beginning of the ST segment. Atrial repolarization

waveforms (ST-Ta

) are usually of too low in amplitude to be detected,

but they may become apparent in acute pericarditis, atrial infarction,

and AV heart block.

The QRS-T waveforms of the surface ECG correspond in a general

way with the different phases of simultaneously obtained ventricular

action potentials, the intracellular recordings from single myocardial

fibers (Chap. 244). The rapid upstroke (phase 0) of the action potential

corresponds to the onset of QRS. The plateau (phase 2) corresponds

to the isoelectric ST segment, and active repolarization (phase 3)

corresponds to the inscription of the T wave. Factors that decrease the

slope of phase 0 by impairing the influx of Na+ (e.g., hyperkalemia and

drugs such as flecainide) tend to increase QRS duration. Conditions

that prolong phase 2 or 3 (amiodarone, hypocalcemia) increase the QT

interval. In contrast, factors (e.g., hypercalcemia, digoxin) associated

with shortening of ventricular repolarization duration shorten the QT.

The hereditary short QT syndrome and its relationship to sudden cardiac arrest are discussed in Chap. 255.

The ECG is usually recorded on graph paper divided into 1-mm2

gridlike boxes. When the recording speed is 25 mm/s, the smallest

(1 mm) horizontal divisions correspond to 40 ms (0.04 s), with heavier

lines at intervals of 200 ms (0.20 s). Vertically, the ECG graph measures

the amplitude of a specific wave or deflection (1 mV = 10 mm with

standard calibration; the voltage criteria for hypertrophy mentioned

below are given in millimeters). There are four major sets of ECG

intervals: RR, PR, QRS, and QT/QTc

 (Fig. 240-2). The instantaneous

heart rate (beats per minute) can be computed from the interbeat (RR)

interval by dividing the number of large (0.20 s) time units between

consecutive R waves into 300 or the number of small (40 ms) segments

into 1500. The PR interval measures the time (normally 120–200 ms)

between atrial and ventricular depolarization, which includes the physiologic delay imposed by stimulation of cells in the AV junction area.

The QRS interval (normally 100–110 ms or less) reflects the duration

of ventricular depolarization. The QT interval subtends both ventricular depolarization and (primarily) repolarization times and varies

inversely with the heart rate. A variety of formulas have been proposed

for computing a rate-corrected QT, termed QTc

, but without formal

consensus. The classic “square root” formula (QTc

 = QT/√RR, computed

in second units) has been criticized for systematic errors at both lower

and higher heart rates. One alternative is the Framingham formula (given

here for units of milliseconds): QTc

 = QT + 0.154 (1000 – RR). The following upper normal limits (based on longest QT) have been proposed:

QTc

 of 460 ms in women and 450 ms in men. Lower limits are less well

defined. QT/QTc

 measurements, both visual and electronic, should be

assessed in light of inherent limitations in their precise determination

from standard ECGs waveforms.

Ventricular

myocardium

Purkinje

fibers

Left bundle

branch

Ventricular septum

Right bundle branch

His bundle

AV junction

Sinoatrial (SA)

node

AV node

RA

LA

LV

RV

FIGURE 240-1 Schematic of the cardiac conduction system. AV, atrioventricular;

LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

QRS

P

ST

T

U

PR interval

J

QRS interval

QT interval

FIGURE 240-2 Basic ECG waveforms and intervals. Not shown is the RR interval,

the time between consecutive QRS complexes.

Electrocardiography

1825CHAPTER 240

A Superior

Inferior

Right Left

+

– – –

–

–

–

+

+ + +

aVR + aVL

III aVF II

B Posterior

Right Left

+

+

+

+ + +

V6

V5

V4

V V3 V1 2

Anterior

–

–

–

–

– –

I

FIGURE 240-3 The six frontal plane (A) and six horizontal plane (B) leads provide a three-dimensional

representation of cardiac electrical activity.

Right axis deviation

Normal axis

Left axis deviation

–90°

–aVF –60°

–III

–30°

+aVL

0°

+I

+30°

–aVR

+60°

+II +90°

+aVF

+120°

+III

+150°

– aVL

180°

–I

–150°

+aVR

–120°

–II

Extreme axis deviation

FIGURE 240-4 The frontal plane (limb or extremity) leads are represented on a

hexaxial diagram. Each ECG lead has a specific spatial orientation and polarity. The

positive pole of each lead axis (solid line) and the negative pole (hatched line) are

designated by their angular position relative to the positive pole of lead I (0°). The

mean electrical axis of the QRS complex is measured with respect to this display.

V1

V3R

V4R

V2

V3

V4 V5 V6

FIGURE 240-5 The horizontal plane (chest or precordial) leads are obtained with

electrodes in the locations shown. Additional posterior leads are sometimes placed

on the same horizontal plane as V4

 to facilitate detection of acute posterolateral

infarction (V7

, midaxillary line; V8

, posterior axillary line; and V9

, posterior scapular

line). Right chest leads (V3

R–V6

R) may enhance detection of right ventricular

involvement in the context of inferior infarction.

■ ECG LEADS

The 12 conventional ECG leads are divided into two groups: six limb

(extremity) leads and six chest (precordial) leads. The limb leads

record potentials transmitted onto the frontal plane (Fig. 240-3A);

the chest leads record potentials transmitted onto the horizontal plane

(Fig. 240-3B).

The orientation and polarity of the frontal plane leads are represented on a hexaxial diagram (Fig. 240-4). The six chest leads are

obtained by exploring electrodes as shown in Fig. 240-5.

Each lead is analogous to a different video camera angle “looking” at the

same events—atrial and ventricular depolarization and repolarization—

from different spatial orientations. The 12-lead ECG can be supplemented with additional leads in special circumstances. For example,

right precordial leads V3

R to V6

R are useful in detecting evidence of

acute right ventricular ischemia. Bedside monitors and ambulatory

ECGs (e.g., Holter monitors, event recorders, patch electrode and other

medical wearable devices) usually employ only one or two modified

leads. The standard ECG leads are configured such that a positive

(upright) deflection is recorded in a lead if a wave of depolarization

spreads toward the positive pole of that lead, and a negative deflection

is recorded if the wave spreads toward the negative pole. If the mean

orientation of the depolarization vector is at right angles to a particular

lead axis, a biphasic (equally positive and negative)

deflection will be recorded.

GENESIS OF THE NORMAL ECG

■ P WAVE

The normal atrial depolarization vector is oriented

downward and toward the subject’s left, reflecting the

spread of depolarization from the sinus node to the right

and then the left atrial myocardium. Since this vector

points toward the positive pole of lead II and toward the

negative pole of lead aVR, the sinus-generated P wave

will be positive in lead II and negative in aVR. By contrast, activation of the atria from an ectopic pacemaker

in the lower part of either atrium or in the AV junction

region may produce retrograde P waves (negative in II,

positive in aVR). The normal P wave in lead V1

 may be

biphasic with a positive component reflecting right atrial

depolarization, followed by a small (<1 mm2

) negative component

reflecting left atrial depolarization.

■ QRS COMPLEX

Normal ventricular depolarization proceeds as a rapid, continuous

spread of activation wave fronts. This complex process can be divided

into two major sequential phases, and each phase can be represented

by a mean vector (Fig. 240-6). The first phase is depolarization of

the interventricular septum from the left to the right and anteriorly

(vector 1). The second results from the simultaneous depolarization of

the right and left ventricles; it normally is dominated by the more

massive left ventricle, so that vector 2 points leftward and posteriorly. Therefore, a right precordial lead (V1

) will record this biphasic

depolarization process with a small positive deflection (septal r wave)

followed by a larger negative deflection (S wave). A left precordial lead,

for example, V6

, will record the same sequence with a small negative

deflection (septal q wave) followed by a relatively tall positive deflection (R wave). Intermediate leads show a relative increase in R-wave

amplitude (normal R-wave progression) and a decrease in S-wave

amplitude progressing across the chest from right to left. The lead

where the R and S waves are of about equal amplitude is referred to as

the transition zone (usually V3

 or V4

) (Fig. 240-7).

The QRS pattern in the extremity leads may vary considerably

from one normal subject to another depending on the electrical axis

of the QRS, which describes the mean orientation of the QRS vector

with reference to the six frontal plane leads. Normally, the QRS axis

1826 PART 6 Disorders of the Cardiovascular System

ranges from −30° to +100° (Fig. 240-4). An axis more negative than

–30° is referred to as left axis deviation, and an axis more positive than

+90 to +100° is referred to as right axis deviation. Left axis deviation

may occur as a normal variant but is more commonly associated with

left ventricular hypertrophy, a block in the anterior fascicle of the left

bundle system (left anterior fascicular block or hemiblock), or inferior

myocardial infarction. Right axis deviation also may occur as a normal

variant (particularly in children and young adults), as a spurious finding due to reversal of the left and right arm electrodes, or in conditions

such as right ventricular overload (acute or chronic), lateral infarction,

dextrocardia, left pneumothorax, and left posterior fascicular block.

■ T WAVE AND U WAVE

Normally, the mean T-wave vector is oriented roughly concordant with

the mean QRS vector (within about 45° in the frontal plane). Since

depolarization and repolarization are electrically opposite processes, this

normal QRS–T-wave vector concordance indicates that repolarization

normally must proceed in the reverse direction from depolarization (i.e.,

from ventricular epicardium to endocardium). The normal U wave is a

small, rounded deflection (≤1 mm) that follows the T wave and usually

has the same polarity as the T wave. An abnormal increase in U-wave

amplitude is most commonly due to drugs (e.g., dofetilide, amiodarone,

sotalol, quinidine) or to hypokalemia. Very prominent U waves are a

marker of increased susceptibility to torsades de pointes (Chap. 246).

MAJOR ECG ABNORMALITIES

■ CARDIAC ENLARGEMENT AND HYPERTROPHY

Right atrial overload (acute or chronic) may lead to an increase in

P-wave amplitude (≥2.5 mm) (Fig. 240-8), previously referred to as

“P-pulmonale.” Left atrial overload typically produces a biphasic P wave

in V1

 with a broad negative component or a broad (≥120 ms), often

notched P wave in one or more limb leads (Fig. 240-8). This pattern,

historically referred to as “P-mitrale,” may also occur with left atrial

conduction delays in the absence of actual atrial enlargement, leading

to the more general designation of left atrial abnormality.

Right ventricular hypertrophy due to a sustained, severe pressure

load (e.g., due to tight pulmonic valve stenosis or certain pulmonary

artery hypertension syndromes) is characterized by a relatively tall

R wave in lead V1

 (R ≥ S wave), usually with right axis deviation

(Fig. 240-9); alternatively, there may be a qR pattern in V1

 or V3

R. ST

depression and T-wave inversion in the right to mid-precordial leads

are also often present. This pattern, formerly called right ventricular

“strain,” is attributed to repolarization abnormalities in acutely or

chronically overloaded muscle. Prominent S waves may occur in the left

lateral precordial leads. Right ventricular hypertrophy due to ostium

secundum atrial septal defects, with the accompanying right ventricular volume overload, is commonly associated with an incomplete or

complete right bundle branch block pattern with a rightward QRS axis.

Acute cor pulmonale due to pulmonary thromboembolism (Chap.

279), for example, may be associated with a normal ECG or a

variety of abnormalities. Sinus tachycardia is the most common arrhythmia, although other tachyarrhythmias,

such as atrial fibrillation or flutter, may

occur. The QRS axis may shift to the

right, sometimes in concert with the socalled S1

Q3

T3

 pattern (prominence of the

S wave in lead I and the Q wave in lead

III, with T-wave inversion in lead III).

Acute right ventricular dilation also may

be associated with slow R-wave progression and ST-T abnormalities in V1

 to V4

simulating acute anterior infarction. A

right ventricular conduction disturbance

may appear.

Chronic cor pulmonale due to obstructive lung disease (Chap. 296) usually

does not produce the classic ECG patterns of right ventricular hypertrophy

noted above. Instead of tall right precordial R waves, chronic obstructive

lung disease (emphysema) more typically is associated with small R waves in

– – –

–

–

–

2

1

+ + + +

+

+

V1 V2

V3

V4

V5

V6

C

V1

r

S

V1

RV LV

2

q

V6

R

B

V1

r

RV

LV

1 q

V6

A

FIGURE 240-6 Ventricular depolarization can be divided into two major phases,

each represented by a vector. A. The first phase (arrow 1) denotes depolarization

of the ventricular septum, beginning on the left side and spreading to the right. This

process is represented by a small “septal” r wave in lead V1

 and a small septal q

wave in lead V6

. B. Simultaneous depolarization of the left and right ventricles (LV

and RV) constitutes the second phase. Vector 2 is oriented to the left and posteriorly,

reflecting the electrical predominance of the LV. C. Vectors (arrows) representing

these two phases are shown in reference to the horizontal plane leads. (Reproduced

with permission from AL Goldberger et al: Goldberger’s clinical electrocardiography:

A simplified approach, 9th ed. Philadelphia, Elsevier/Saunders, 2017.)

I aVR

II

III

aVL

aVF

V1

V2

V3

V4

V5

V6

FIGURE 240-7 Normal electrocardiogram from a healthy male subject. Sinus rhythm is present with a heart rate of

75 beats per minute. PR interval is 160 ms; QRS interval (duration) is 80 ms; QT interval is 360 s; QTc

 (Framingham formula)

is 391 ms; the mean QRS axis is about +70°. The precordial leads show normal R-wave progression with the transition

zone (R wave ≈ S wave) in lead V3

.

Electrocardiography

1827CHAPTER 240

right to mid-precordial leads (slow R-wave progression) due in part to

downward displacement of the diaphragm and the heart. Low-voltage

complexes are commonly present, owing to hyperaeration.

Multiple voltage criteria for left ventricular hypertrophy (Fig. 240-9)

have been proposed on the basis of the presence of tall left precordial

R waves and deep right precordial S waves (e.g., SV1

 + [RV5

 or RV6

]

>35 mm). Repolarization abnormalities (ST depression with T-wave

inversions, formerly called the left ventricular “strain” pattern) also

may appear in leads with prominent R waves. However, prominent

precordial voltages may occur as a normal variant, especially in athletic

or young individuals. Left ventricular hypertrophy may increase limb

lead voltage with or without increased precordial voltage (e.g., RaVL +

SV3

 >20 mm in women and >28 mm in men). The presence of left atrial

abnormality increases the likelihood of underlying left ventricular

hypertrophy in cases with borderline voltage criteria. Left ventricular

hypertrophy often progresses to incomplete or complete left bundle

branch block. The sensitivities of conventional voltage criteria for left

ventricular hypertrophy are low in middle-age to older adults and may

be decreased further in obese persons and smokers, as well as with

right bundle branch block. ECG evidence for left ventricular hypertrophy is a major noninvasive marker of increased risk of cardiovascular

morbidity and mortality rates, including sudden cardiac death. However, because of false-positive and false-negative diagnoses, the ECG

is of limited utility in diagnosing atrial or ventricular enlargement.

More definitive anatomic and functional information may be provided

at increased cost by echocardiographic and other imaging studies

(Chaps. 241 and A9).

■ BUNDLE BRANCH BLOCKS AND RELATED PATTERNS

Intrinsic impairment of conduction in either the right or the left bundle system (intraventricular conduction disturbances) leads to prolongation of the QRS interval. With complete bundle branch blocks, the

widest QRS interval is ≥120 ms in duration; with incomplete blocks,

the QRS interval is between about 110 and 120 ms. The QRS vector

usually is oriented in the direction of the myocardial region where

depolarization is delayed (Fig. 240-10). Thus, with right bundle branch

block, the terminal QRS vector is oriented to the right and anteriorly

(rSR′ in V1

 and qRS in V6

, typically). Left bundle branch block alters

both early and later phases of ventricular depolarization. The major

QRS vector is directed to the left and posteriorly. In addition, the

normal early left-to-right pattern of septal activation is disrupted such

that septal depolarization proceeds from right to left as well. As a result,

left bundle branch block generates wide, predominantly negative (QS)

complexes in lead V1

 and entirely positive (R) complexes in V6

. Waveform patterns identical to those of left bundle branch block, preceded

by a sharp (but sometimes low amplitude) spike, are seen in most

cases of electronic right ventricular pacing due to the relative delay in

left ventricular activation. In contrast, biventricular pacing (cardiac

QRS in hypertrophy

V1

Main QRS vector

Normal

RVH

or or

V1

V6

V6

LVH

FIGURE 240-9 Left ventricular hypertrophy (LVH) increases the amplitude of

electrical forces directed to the left and posteriorly. In addition, repolarization

abnormalities may cause ST-segment depression and T-wave inversion in leads

with a prominent R wave. Right ventricular hypertrophy (RVH) may shift the QRS

vector to the right; this effect usually is associated with an R, RS, or qR complex in

lead V1

. T-wave inversions may be present in right precordial leads.

T

R′

r

S

V1

Normal

RBBB

LBBB

q

S

R

V6

T

FIGURE 240-10 Comparison of typical QRS-T patterns in right bundle branch block

(RBBB) and left bundle branch block (LBBB) with the normal pattern in leads V1

 and

V6

. Note the secondary T-wave inversions (arrows) in leads with an rSR′ complex

with RBBB and in leads with a wide R wave with LBBB.

RA

LA

Normal Right Left

II

V1

RA

RA

RA

RA

RA

RA

LA

LA LA LA

LA LA

V1

FIGURE 240-8 Right atrial (RA) overload may cause tall, peaked P waves in the

limb or precordial leads. Left atrial (LA) abnormality may cause broad, often

notched P waves in the limb leads and a biphasic P wave in lead V1

 with a prominent

negative component representing delayed depolarization of the LA. (Reproduced

with permission from MK Park, WG Guntheroth: How to Read Pediatric ECGs, 4th ed.

St. Louis, Mosby/Elsevier, 2006.)

1828 PART 6 Disorders of the Cardiovascular System

resynchronization therapy) usually produces a right bundle branch

morphology along with a wide R wave in lead aVR.

Bundle branch block may occur in a variety of conditions. In subjects without structural heart disease, right bundle branch block is seen

more commonly than left bundle branch block. Right bundle branch

block also occurs with heart disease, both congenital (e.g., atrial septal defect) and acquired (e.g., valvular, ischemic). Left bundle branch

block is often a marker of one of four underlying conditions associated

with increased risk of cardiovascular morbidity and mortality rates:

coronary heart disease (frequently with impaired left ventricular function), hypertensive heart disease, aortic valve disease (including after

transcatheter aortic valve replacement), and cardiomyopathy. Bundle

branch blocks may be chronic or intermittent. A bundle branch block

may be rate-related, not uncommonly occurring when the heart rate

exceeds some critical value.

Bundle branch blocks and depolarization abnormalities secondary

to artificial pacemakers not only affect ventricular depolarization

(QRS) but also are characteristically associated with secondary repolarization (ST-T) abnormalities. With bundle branch blocks, the

T wave is typically opposite in polarity to the last deflection of the QRS

(Fig. 240-10). This discordance of the QRS–T-wave vectors is caused

by the altered sequence of repolarization that occurs as a consequence

of altered depolarization. In contrast, primary repolarization abnormalities are independent of QRS changes and are related instead to

actual alterations in the electrical properties of the myocardial fibers

themselves (e.g., in the resting membrane potential or action potential

duration), not just to changes in the sequence of repolarization. Ischemia, electrolyte imbalance, and drugs such as digitalis all cause such

primary ST–T-wave changes. Primary and secondary T-wave changes

may coexist. For example, T-wave inversions in the right precordial

leads with left bundle branch block or in the left precordial leads with

right bundle branch block may be important markers of underlying

ischemia or other abnormalities. A distinctive abnormality simulating

right bundle branch block with ST-segment elevations in the right

chest leads is seen with the Brugada pattern (Chap. 255).

Partial blocks in the left bundle system (left anterior or posterior fascicular blocks or hemiblocks) generally do not prolong the QRS duration substantially but instead are associated with shifts in the frontal

plane QRS axis (leftward or rightward, respectively). Left anterior fascicular block (QRS axis more negative than –45°) is probably the most

common cause of marked left axis deviation in adults. In contrast, left

posterior fascicular block (QRS axis more rightward than +110–120°)

is extremely rare as an isolated finding and requires exclusion of other

factors causing right axis deviation mentioned earlier. Intraventricular

conduction delays also can be caused by factors extrinsic (toxic) to

the conduction system that slow ventricular conduction, particularly

hyperkalemia or drugs (e.g., class 1 antiarrhythmic agents, tricyclic

antidepressants, phenothiazines). Prolongation of QRS duration does

not necessarily indicate a conduction delay but may be due to preexcitation of the ventricles via a bypass tract, as in Wolff-Parkinson-White

(WPW) patterns (Chap. 249) and related variants.

■ MYOCARDIAL ISCHEMIA AND INFARCTION

(See also Chap. 275) The ECG is central to the diagnosis of acute and

chronic ischemic heart disease. Ischemia exerts complex time-dependent

effects on the electrical properties of myocardial cells. Severe, acute

ischemia lowers the resting membrane potential and shortens the

duration of the action potential. Such changes cause a voltage gradient

between normal and ischemic zones. As a consequence, current flows

between those regions. These currents of injury are represented on the

surface ECG by deviation of the ST segment (Fig. 240-11). When the

acute ischemia is transmural, the ST vector usually is shifted in the direction of the outer (epicardial) layers, producing ST elevations and sometimes, in the earliest stages of ischemia, tall, positive so-called hyperacute

T waves over the ischemic zone. With ischemia confined primarily to the

subendocardium, the ST vector typically shifts toward the subendocardium and ventricular cavity, so that overlying (e.g., anterior precordial)

leads show ST-segment depression (with ST elevation in lead aVR).

Multiple factors affect the amplitude of acute ischemic ST deviations.

Profound ST elevation or depression in multiple leads usually indicates

very severe ischemia. From a clinical viewpoint, the division of acute

myocardial infarction into ST-segment elevation and non-ST elevation

types is useful since the consistent efficacy of emergency (minutes to

hours) reperfusion therapy is limited to the former group; the evolving

indications for acute reperfusion therapy in non-ST elevation myocardial infarction are a focus of intensive investigation (Chap. 274).

Takotsubo syndrome may closely simulate the patterns of acute or

evolving ST-segment elevation or non-ST-segment elevation myocardial infarction (Chap. 273).

The ECG leads are usually more helpful in localizing regions of ST

elevation than non-ST elevation ischemia. For example, acute transmural anterior (including apical and lateral) wall ischemia is reflected

by ST elevations or increased T-wave positivity in one or more of the

precordial leads (V1

–V6

) and leads I and aVL. Inferior wall ischemia

produces changes in leads II, III, and aVF. “Posterior” wall ischemia

(almost always associated with lateral or inferior involvement) may

be indirectly recognized by reciprocal ST depressions in leads V1

 to

V3

 (thus constituting an ST elevation “equivalent” acute coronary

syndrome). Acute right ventricular ischemia usually produces ST

elevations in right-sided chest leads (Fig. 240-5). When ischemic ST

elevations occur as the earliest sign of acute infarction, they typically

are followed within a period ranging from hours to days by evolving T-wave inversions and often by Q waves occurring in the same

lead distribution. Reversible transmural ischemia, for example, due

to coronary vasospasm (Prinzmetal’s angina) may cause transient

ST-segment elevations without development of Q waves. Depending

on the severity and duration of ischemia, the ST elevations may resolve

completely in minutes or be followed by T-wave inversions that persist

for hours or even days. Patients with ischemic chest pain who present

with deep T-wave inversions in multiple precordial leads (e.g., V1

–V4

,

I, and aVL) with or without cardiac enzyme elevations typically have

severe obstruction in the left anterior descending coronary artery

(Fig. 240-12).

With infarction, depolarization (QRS) changes often accompany

repolarization (ST-T) abnormalities. Necrosis of sufficient myocardial

tissue may lead to decreased R-wave amplitude or abnormal Q waves

(even in the absence of transmural ischemia) in the anterior or inferior

leads (Fig. 240-13). Abnormal Q waves were once considered markers

of transmural myocardial infarction, whereas subendocardial infarcts

were thought not to produce Q waves. However, correlative studies

have indicated that transmural infarcts may occur without Q waves and

that subendocardial (nontransmural) infarcts sometimes may be associated with Q waves. Therefore, evolving or chronic infarcts are more

appropriately classified as “Q-wave” or “non-Q-wave” (Chap. A7).

V5

ST

ST

A B

ST

ST

V5

FIGURE 240-11 Acute ischemia causes a current of injury. A. With predominant subendocardial ischemia, the resultant ST vector will be directed toward the inner layer of

the affected ventricle and the ventricular cavity. Overlying leads therefore will record ST depression. B. With ischemia involving the outer ventricular layer (transmural or

epicardial injury), the ST vector will be directed outward. Overlying leads will record ST elevation.

Electrocardiography

1829CHAPTER 240

Loss of depolarization forces due to posterior or lateral infarction may

cause reciprocal increases in R-wave amplitude in leads V1

 and V2

 without diagnostic Q waves in any of the conventional leads. (Additional

leads V7

–V9

 may show acute changes.) In the weeks and months after

infarction, these ECG changes may persist or begin to resolve. Complete normalization of the ECG after Q-wave infarction is uncommon

but may occur, particularly with smaller infarcts. In contrast, ST-segment elevations that persist for several weeks or more after a Q-wave

infarct usually correlate with a severe underlying wall motion disorder,

although not necessarily a frank ventricular aneurysm.

The ECG has important limitations in both sensitivity and specificity in the diagnosis of acute and chronic ischemic heart disease.

Although a single normal ECG does not exclude ischemia or even

acute infarction, a normal ECG throughout the course of an acute

infarct is distinctly uncommon. Prolonged chest pain without diagnostic ECG changes therefore should always prompt a careful search for

other noncoronary causes of chest pain (Chap. 14). Furthermore, the

diagnostic changes of acute or evolving ischemia are often masked by

the presence of left bundle branch block, electronic ventricular pacemaker patterns, and Wolff-Parkinson-White preexcitation. However,

clinicians may also overdiagnose ischemia or infarction based on the

presence of ST-segment elevations or depressions; T-wave inversions;

tall, positive T waves; or Q waves not related to ischemic heart disease

(pseudoinfarct patterns). For example, ST-segment elevations simulating acute ischemia/infarction may occur with acute pericarditis

or myocarditis, including COVID-19 infections, as a normal variant

(including the typical “early repolarization” pattern), or in a variety of

other conditions (Table 240-1). Similarly, tall T waves do not invariably represent hyperacute ischemic changes but may also be caused

by normal variants, hyperkalemia, or cerebrovascular injury, among

other causes.

ST-segment elevations and tall, positive T waves are common findings in leads V1

 and V2

 in left bundle branch block or left ventricular

hypertrophy in the absence of ischemia. The differential diagnosis of

Q waves includes physiologic or positional variants, ventricular hypertrophy, acute or chronic noncoronary myocardial injury, hypertrophic

cardiomyopathy, and ventricular conduction disorders. Ventricular

hypertrophy, hypokalemia, drugs such as digoxin, and a variety of other

factors may cause ST-segment depression mimicking subendocardial

ischemia. Prominent T-wave inversion may occur with ventricular

hypertrophy, cardiomyopathies, myocarditis, and “stress cardiomyopathies” associated with takotsubo syndrome and cerebrovascular

injury (particularly intracranial bleeds), among others causes. Diagnostic confusion may also occur when nonischemic T-wave inversions

(“cardiac memory” effect) appear in normally conducted beats in

patients with intermittent wide QRS complexes, most commonly due

to ventricular pacing or to left bundle branch block.

■ METABOLIC FACTORS AND DRUG EFFECTS

A variety of metabolic abnormalities and pharmacologic agents alter

the ECG and, in particular, cause changes in repolarization (ST-T-U)

and sometimes QRS prolongation. Certain life-threatening electrolyte

disturbances may be diagnosed initially and monitored from the ECG.

Hyperkalemia produces a sequence of changes (Fig. 240-14), usually

beginning with narrowing and peaking (tenting) of the T waves.

Further elevation of extracellular K+ leads to AV conduction disturbances, diminution in P-wave amplitude, and widening of the QRS

interval. Severe hyperkalemia eventually causes cardiac arrest with a

A

B

ECG sequence with anterior Q-wave infarction

Early

Evolving

Early

Evolving

ECG sequence with inferior Q-wave infarction

I II III

I II III

aVR aVL aVF V2 V4 V6

aVR aVL aVF V2 V4 V6

FIGURE 240-13 Sequence of depolarization and repolarization changes with (A) acute anterior and (B) acute inferior wall Q-wave infarctions. With anterior infarcts, ST

elevation in leads I and aVL and the precordial leads may be accompanied by reciprocal ST depressions in leads II, III, and aVF. Conversely, acute inferior (or posterolateral)

infarcts may be associated with reciprocal ST depressions in leads V1

 to V3

. (Reproduced with permission from AL Goldberger et al: Goldberger’s cinical electrocardiography:

A simplified approach, 9th ed. Philadelphia, Elsevier/Saunders, 2017.)

V1 V2 V3 V4 V5 V6

FIGURE 240-12 Severe anterior wall ischemia (with or without infarction) may cause prominent T-wave inversions in the precordial leads and in leads I and aVL. This

pattern (sometimes referred to as Wellens T waves) is usually associated with a high-grade stenosis of the left anterior descending coronary artery.