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CHAPTER 3 Evaluation of the Patient With Cardiovascular Disease
23
harsh and shorter in duration. High-flow states such as those found in
patients with fever, during pregnancy, or with anemia may also lead to
midsystolic “flow” murmurs.
Holosystolic murmurs begin with S1 and end with S2; the classic
examples are the murmurs associated with mitral regurgitation and
tricuspid regurgitation. They may also occur with ventricular septal
defects and patent ductus arteriosus. Late systolic murmurs begin in
mid to late systole and end with S2. They can be characteristic of more
severe aortic stenosis and are also typical of murmurs associated with
mitral valve prolapse.
Diastolic murmurs are also classified by timing (i.e., early diastolic,
mid diastolic, and late diastolic). Early diastolic murmurs begin with
S2 and can result from aortic or pulmonic regurgitation; they are usually decrescendo in shape. Shorter and quieter murmurs typically represent an acute process or mild regurgitation, whereas longer-lasting
and louder murmurs are likely due to more severe regurgitation. Middiastolic murmurs begin after S2 and are usually caused by mitral or
tricuspid stenosis. They are low pitched and are often referred to as
diastolic rumbles. Because they are of low frequency, they are better
auscultated with the bell of the stethoscope. Similar murmurs can be
heard with obstructing atrial myxomas. Severe chronic aortic insufficiency can lead to premature closure of the mitral valve, causing a
mid-diastolic rumble called an Austin-Flint murmur. Late diastolic
murmurs occur immediately before S1 and reflect presystolic accentuation of the mid-diastolic murmurs resulting from augmented mitral
or tricuspid flow after atrial contraction.
Continuous murmurs begin with S1 and last though part or all of
diastole. They are generated by continuous flow from a vessel or chamber with high pressure into a vessel or chamber with lower pressure.
They are referred to as machinery murmurs and are caused by aortopulmonary connections such as a patent ductus arteriosus, AV malformations, or disturbances of flow in arteries or veins.
Other Cardiac Sounds
Pericardial rubs occur in the setting of pericarditis and are coarse, scratching sounds similar to rubbing leather. They are typically heard best at
the left sternal border with the patient leaning forward and holding the
breath at end-expiration. A classic pericardial rub has three components:
atrial systole, ventricular systole, and ventricular diastole. One might also
hear a pleural rub caused by localized irritation of surrounding pleura.
Continuous venous murmurs, or venous hums, are almost always present
in children. They can be heard in adults during pregnancy, in the setting
of anemia, or with thyrotoxicosis. They are heard best at the base of the
neck with the patient’s head turned to the opposite direction.
Prosthetic Heart Sounds
Prosthetic heart valves produce characteristic findings on auscultation.
Bioprosthetic valves produce sounds that are similar to those of native
heart valves, but they are typically smaller than the valves that they
replace and therefore have an associated murmur. Mechanical valves
have crisp, high-pitched sounds related to valve opening and closure.
In most modern valves such as the St. Jude valve, which is a bileaflet
mechanical valve, the closure sound is louder than the opening sound.
An ejection murmur is common. If there is a change in murmur or in
the intensity of the mechanical valve closure sound, dysfunction of the
valve should be suspected.
For a deeper discussion of this topic, please see Chapter 45,
“Approach to the Patient with Possible Cardiovascular Disease,” in
Goldman-Cecil Medicine, 26th Edition.
SUGGESTED READINGS
Agency for Healthcare Research and Quality, U.S. Department of Health and
Human Services: Total expenses and percent distribution for selected con-
ditions by type of service: United States, 2008. Medical Expenditure Panel
Survey: Household Component Summary Tables. Available at: http://
www.meps.ahrq.gov/mepsweb/data_stats/quick_tables_search.jsp?
component=1&subcomponent=0. Accessed August 5, 2014.
Calkins H, Shyr Y, Frumin H, et al: The value of the clinical history in the
differentiation of syncope due to ventricular tachycardia, atrioventricular
block, and neurocardiogenic syncope, Am J Med 98:365–373, 1995.
Go AS: The epidemiology of atrial fibrillation in elderly persons: the tip of the
iceberg, Am J Geriatr Cardiol 14:56–61, 2005.
Goldman L, Ausiello D: Cecil Medicine: part VIII. Cardiovascular disease,
Philadelphia, 2012, Saunders.
Heart Disease Fact Sheet. CDC Division for Heart Disease and Stroke Preven-
tion. https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_heart_
disease.htm.
Hirsch AT, Criqui MH, Treat-Jacobson D, et al: Peripheral arterial disease: detec-
tion, awareness, and treatment in primary care, JAMA 286:1317–1324, 2001.
Hoffman JI, Kaplan S, Liberthson RR: Prevalence of congenital heart disease,
Am Heart J 147:425–439, 2004.
National Heart, Lung and Blood Institute, National Institutes of Health.
Unpublished tabulations of National Vital Statistics System mortality data.
2008. Available at: http://www.cdc.gov/nchs/nvss/mortality_public_use_
data.htm. Accessed August 5, 2014.
National Heart, Lung and Blood Institute, National Institutes of Health,
Unpublished tabulations of National Hospital Discharge Survey, 2009.
Available at http://www.cdc.gov/nchs/nhds/nhds_questionnaires.htm.
Accessed August 5, 2014.
National Heart, Lung and Blood Institute. Unpublished tabulations of
National Health Interview Survey, 1965-2010. Available at: http://www.
cdc.gov/nchs/nhis/nhis_questionnaires.htm. Accessed August 5, 2014.
National Heart, Lung and Blood Institute, National Institutes of Health.
Morbidity and mortality: 2012 Chart book on cardiovascular, lung, and
blood diseases. Available at https://www.nhlbi.nih.gov/research/reports/
2012-mortality-chart-book.htm. Accessed September 26, 2014.
National Vital Statistics System, Centers for Disease Control and Prevention:
Mortality tables. Available at http://www.cdc.gov/nchs/nvss/mortality_
tables.htm. Accessed August 5, 2014.
Pickering TG, Hall JE, Appel LJ, et al: Recommendations for blood pressure
measurement in humans and experimental animals: part 1. Blood
pressure measurement in humans: a statement for professionals from
the Subcommittee of Professional and Public Education of the American
Heart Association Council on High Blood Pressure Research, Circulation
111:697–716, 2005.
4
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Diagnostic Tests and Procedures in the
Patient With Cardiovascular Disease
Esseim Sharma, Alan R. Morrison
ELECTROCARDIOGRAPHY
The electrocardiogram (ECG) is one of the most basic yet powerful
diagnostic tools in cardiovascular medicine. It is critical in the investigation of cardiac arrhythmias, myocardial infarction, and pericardial
disease, and may provide additional insight into a variety of other cardiac and noncardiac conditions.
The ECG is a simple and noninvasive procedure that makes use of
electrodes placed on the skin of the chest at specific locations in order
to measure the electrical activity of the heart. The output is a scroll of
wave forms represented as a temporal sequence of deflections on the
ECG (Fig. 4.1). The horizontal axis of the graph paper represents time,
and at a standard paper speed of 25 mm/second, which is also known
as the sweep speed, each small box (1 mm) represents 0.04 seconds,
and each large box (5 mm) represents 0.20 seconds. The vertical axis
represents voltage or amplitude (1 mm = 0.1 mV). Because the standard ECG demonstrates a 10-second window of time, the heart rate
can be calculated by simply counting the number of QRS complexes
and multiplying by 6. Alternatively, the heart rate can be estimated by
dividing the number of large boxes between complexes (i.e., R-R interval) into 300.
Lead Positioning
The standard ECG consists of 12 leads: six limb leads (I, II, III, aVR,
aVL, and aVF) and six chest or precordial leads (V1 to V6) (Fig. 4.2).
The limb leads view the electrical activity of the heart in the vertical
plane, while the precordial leads view the horizontal plane. The electrical activity recorded in each lead represents the direction and magnitude (i.e., vector) of the electrical force as seen from that lead position.
Electrical activity directed toward a particular lead is represented as an
upward (positive) deflection, and electrical activity directed away from
a particular lead is represented as a downward (negative) deflection.
Accurate lead placement is essential to reliable interpretation of the
ECG.
The limb leads consist of bipolar leads (I, II, and III) and unipolar or augmented leads (leads aVR, aVL, and aVF). The bipolar
leads represent electrical forces between the two leads, while augmented leads represent the electrical forces towards the lead. Lead I
measures electrical activity between the right and left arms (left arm
positive), lead II between the right arm and left leg (left leg positive),
and lead III between the left arm and left leg (left leg positive). A
vector perpendicular to the limb leads would be isoelectric. In aVR,
aVL, and aVF, the vector is positive if electrical forces are directed
toward the right arm for aVR, left arm for aVL, and left leg for aVF.
Taken together, the six limb leads form a frontal plane of 30-degree
arc intervals (Fig. 4.3).
The six standard precordial leads (V1 to V6) are attached to the
anterior chest wall and are also unipolar leads. Lead placement
should be as follows: V1: fourth intercostal space, right sternal border; V2: fourth intercostal space, left sternal border; V3: midway
between V2 and V4; V4: fifth intercostal space, left midclavicular
line; V5: level with V4, left anterior axillary line; V6: level with V4, left
midaxillary line.
Nonstandard lead configurations can be used in specific clinical scenarios. In patients where there is concern for right ventricular infarction, standard V1 and V2 leads are switched, and V3R to
V6R are placed at locations on the right chest wall in a mirror image
of the standard left-sided chest leads. Posterior leads may be used
to increase the sensitivity for diagnosing lateral and posterior wall
infarction or ischemia—areas that are often deemed to be electrically
silent on traditional 12-lead ECGs. To do this, six additional leads
are placed in the fifth intercostal space continuing posteriorly from
the position of V6. Shifting the right precordial leads (V1-V3) superiorly to the second intercostal space can be used to unmask Brugada
syndrome.
Electrocardiographic Intervals
In the normal heart, the electrical impulse originates in the sinoatrial
(SA) node, located superiorly in the right atrium, and is conducted
through the atria. Given that depolarization of the SA node is too weak
to be detected on the surface ECG, the first, low-amplitude deflection
on the surface ECG represents a summation atrial vector and is called
the P wave. The P wave has an electrical axis that moves in sum toward
the AV node, generally downward and to the left. The interval between
the onset of the P wave and the next rapid deflection (QRS complex) is
known as the PR interval. It primarily represents the time taken for the
impulse to travel through the atrioventricular (AV) node. The normal
PR segment ranges from 0.12 to 0.20 seconds. A PR interval greater
than 0.20 seconds defines first-degree AV nodal block.
After the wave of depolarization has moved through the AV node,
the ventricular myocardium is depolarized in a sequence of four
phases. The interventricular septum depolarizes from left to right.
This phase is followed by depolarization of the right ventricle and
inferior wall of the left ventricle, then the apex and central portions
of the left ventricle, and finally the base and the posterior wall of the
left ventricle. Ventricular depolarization results in a high-amplitude
complex on the surface ECG known as the QRS complex. The first
downward deflection of this complex is the Q wave, the first upward
deflection is the R wave, and the subsequent downward deflection
is the S wave. In some individuals, a second upward deflection may
occur after the S wave, and it is called R prime (R′). Normal duration
of the QRS complex is less than 0.10 second. Complexes longer than
0.12 seconds in duration are usually secondary to some form of interventricular conduction delay, including right or left bundle branch
block.
24
CHAPTER 4 Diagnostic Tests and Procedures in the Patient With Cardiovascular Disease
QT
QTob
25
The isoelectric segment after the QRS complex is the ST segment,
which represents a brief period during which relatively little electrical activity occurs in the heart. The junction between the end of the
QRS complex and the beginning of the ST segment is the J point. The
upward deflection after the ST segment is the T wave, which represents
ventricular repolarization. The QT interval, which reflects the duration
and transmural gradient of ventricular depolarization and repolarization, is measured from the onset of the QRS complex to the end of the
T wave. The observed QT (QTob) interval varies with heart rate, but for
rates between 60 and 100 beats/minute, the normal QT interval ranges
from 0.35 to 0.44 seconds. For heart rates outside this range, the QT
interval can be corrected (QTc) using the following formula (with R-R
interval in seconds):
c =
√
R−R interval
Importantly, patients with interventricular conduction delay due to
the presence of bundle branch blocks or pacing will have prolonged
QT intervals due to the dispersion of ventricular repolarization, which
0.2 sec
0.04 sec
R
T
P
1 mv
PR interval
QS
Fig. 4.1 Normal electrocardiographic complex with labeling of waves
and intervals.
ST
segment
QT interval
is not necessarily pathologic. Adjustment of the QT interval in these
cases remains controversial.
The TP segment is the isoelectric interval that follows the end of
the T wave and lasts till the beginning of the P wave. Because it represents an electrically silent portion of the ECG, the TP segment can
be used to measure excursions of other segments, such as the ST or
PR segments, to determine the presence of elevation or depression.
In some individuals, the T wave may be closely followed by a U wave
(0.5 mm deflection, not shown in Fig. 4.1), which can be seen for a
variety of reasons, including hypokalemia and central nervous system
abnormalities.
Axis
The cardiac axis refers to the overall direction of myocardial depolarization measured in the vertical plane and provides clinically useful
information. Though the axis can be calculated for any of the ECG
segments mentioned above, the mean QRS axis is the most clinically
useful.
Fig. 4.3 illustrates the axial reference system, a reconstruction of the
Einthoven triangle, and the polarity of each of the six limb leads of the
standard ECG. The normal QRS axis ranges from −30 to +90 degrees.
An axis more negative than −30 defines left axis deviation, and an axis
greater than +90 defines right axis deviation. Extreme axis deviation is
present when the mean QRS axis is between −90 and +180 degrees. A
positive QRS complex in leads I and aVF suggests a normal QRS axis
between 0 and 90 degrees.
While the precordial leads are not useful in determining cardiac
axis, they are helpful in determining the direction of cardiac activation in the horizontal plane. Normally, a small R wave occurs in
lead V1, reflecting septal depolarization, along with a deep S wave,
reflecting predominantly left ventricular activation. From V1 to V6,
the R wave becomes larger (and the S wave smaller) because the
predominant forces directed at these leads originate from the left
ventricle. The transition from a predominant S wave to a predominant R wave usually occurs between leads V3 and V4. A delay in this
transition is termed “poor R wave progression” and can be seen in
patients with prior anterior myocardial infarctions, among other
conditions. In patients with ventricular arrhythmias, the pattern of
S and R waves in the precordial leads is essential in localizing the foci
of the arrhythmia.
I
II
III
aVR
aVL
aVF
Fig. 4.2 Normal 12-lead electrocardiogram.
V1 V4
V2 V5
V3
V6
26 SECTION II Cardiovascular Disease
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i
o
n
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f
t
-
a
x
i
s
d
e
v
i
a
t
i
o
−60°
aVL
+60°
n
(
−
3
0
°
t
o
−
9
0
°
)
−30°
I
0°
)
°
0
9
+
o
t
°
0
3
−
+30°
(
n
o
i
t
a
i
v
e
d
s
i
x
a
o
N
−90°
−120°
)
°
0
−150°
9
−
o
t
°
0
9
−
+180°
e
d
s
i
x
a
t
h
g
i
+150°
R
aVR
+120°
aVF
+90°
II
III
Fig. 4.3 Hexaxial reference figure for frontal plane axis determination,
indicating values for abnormal left and right QRS axis deviations.
ABNORMAL ELECTROCARDIOGRAPHIC PATTERNS
Chamber Abnormalities and Ventricular Hypertrophy
Because of the downward and leftward vector direction, the P wave is
normally upright in leads I, II, and aVF, inverted in aVR, and biphasic in V1. Left atrial abnormality (i.e., enlargement, hypertrophy, or
increased wall stress) is characterized by a wide P wave in lead II (0.12
second) and a deeply inverted terminal component in lead V1 (able to
contain one small box or 1 mm2). Right atrial abnormality is identified
when the P waves in the limb leads are tall and peaked and at least 2.5
mm high and (able to contain two stacked small boxes).
Left ventricular hypertrophy may result in increased QRS voltage,
slight widening of the QRS complex, late intrinsicoid deflection, left
axis deviation, and abnormalities of the ST-T segments (Fig. 4.4A).
Multiple criteria with various degrees of sensitivity and specificity
for detecting left ventricular hypertrophy are available. The most frequently used criteria are given in Table 4.1.
Right ventricular hypertrophy is characterized by tall R waves in
leads V1 through V3; deep S waves in leads I, aVL, V5, and V6; and right
axis deviation (see Fig. 4.4B). The R wave is greater than 7 mm and the
R-S ratio is greater than 1 in lead V1. Other causes of a tall R-wave in
V1 must be excluded, including posterior wall myocardial infarction,
I aVR V1 V4
II aVL
III
aVF
V2 V5
V3 V6
A
I
II
aVR V1 V4
aVL
V2 V5
III
aVF
V3 V6
B
Fig. 4.4 (A) Left ventricular hypertrophy as seen on an electrocardiographic recording. Characteristic findings
include increased QRS voltage in precordial leads (i.e., deep S in lead V2 and tall R in lead V5) and downsloping
ST depression and T-wave inversion in lateral precordial leads (i.e., strain pattern) and leftward axis. (B) Right
ventricular hypertrophy with tall R wave in right precordial leads, downsloping ST depression in precordial
leads (i.e., RV strain), right axis deviation, and evidence of right atrial enlargement.
CHAPTER 4 Diagnostic Tests and Procedures in the Patient With Cardiovascular Disease
27
TABLE 4.1 Electrocardiographic
Manifestations of Atrial Abnormalities and
Ventricular Hypertrophy
Left Atrial Abnormality
P-wave duration ≥0.12 second
Notched, slurred P wave in leads I and II
Biphasic P wave in lead V1 with a wide, deep, negative terminal component
Right Atrial Abnormality
P-wave duration ≤0.11 second
Tall, peaked P waves of ≥2.5 mm in leads II, III, and aVF
Left Ventricular Hypertrophy
Voltage criteria
R wave in lead aVL ≥12 mm
R wave in lead I ≥15 mm
S wave in lead V1 or V2 + R wave in lead V5 or V6 ≥35 mm
Depressed ST segments with inverted T waves in the lateral leads
Left axis deviation
QRS duration ≥0.09 second
Left atrial enlargement
Right Ventricular Hypertrophy
Tall R waves over right precordium (R-to-S ratio in lead V1 >1.0)
Right axis deviation
Depressed ST segments with inverted T waves in leads V1 to V
Normal QRS duration (if no right bundle branch block)
Right atrial enlargement
3
TABLE 4.2 Electrocardiographic
Manifestations of Fascicular and Bundle
Branch Blocks
Left Anterior Fascicular Block
QRS duration ≤0.1 second
Left axis deviation (more negative than −45 degrees)
rS pattern in leads II, III, and aVF
qR pattern in leads I and aVL
Right Posterior Fascicular Block
QRS duration ≤0.1 second
Right axis deviation (+90 degrees or greater)
qR pattern in leads II, III, and aVF
rS pattern in leads I and aVL
Exclusion of other causes of right axis deviation (e.g., chronic obstructive
pulmonary disease, right ventricular hypertrophy)
Left Bundle Branch Block
QRS duration ≥0.12 second
Broad, slurred, or notched R waves in lateral leads (I, aVL, V5, and V6)
QS or rS pattern in anterior precordium leads (V1 and V2)
ST-T-wave vectors opposite to terminal QRS vectors
Right Bundle Branch Block
QRS duration ≥0.12 second
Large R′ wave in lead V1 (rsR′)
Deep terminal S wave in lead V
Normal septal Q waves
Inverted T waves in leads V1 and V
6
2
Wolff-Parkinson-White, right bundle branch block, muscular dystrophy, dextrocardia, and lead misplacement.
Interventricular Conduction Delays
The ventricular conduction system consists of two main branches, the
right and left bundles. The left bundle further divides into the anterior
and posterior fascicles. Conduction block can occur in either of the
major branches or in the fascicles (Table 4.2).
Fascicular block results in a change in the sequence of ventricular
activation but does not substantially prolong overall conduction time.
Left anterior fascicular block abnormality is identified when extreme
left axis deviation occurs (i.e., more negative than −45 degrees), when
the R wave is greater than the Q wave in leads I and aVL, and when the
S wave is greater than the R wave in leads II, III, and aVF. Left posterior
fascicular block is relatively uncommon but is associated with right
axis deviation (>90 degrees); small Q waves in leads II, III, and aVF;
and small R waves in leads I and aVL. Fascicular blocks can be seen in
conjunction with right bundle branch block (RBBB), and left or right
axis deviations can indicate concurrent left anterior or posterior fascicular blocks, respectively.
Complete bundle branch blocks cause QRS prolongation greater
than 120 milliseconds. A left bundle branch block (LBBB) can be
indicative of underlying coronary or myocardial disease—most
commonly fibrosis due to ischemic injury or hypertrophy. In LBBB,
depolarization proceeds down the right bundle, across the interventricular septum from right to left, and then to the left ventricle.
Characteristic electrocardiographic findings include a wide QRS
complex; a broad R wave in leads I, aVL, V5, and V6; a deep QS
wave in leads V1 and V2; and ST depression and T-wave inversion
opposite the terminal deflection of the QRS (Fig. 4.5A). Given the
abnormal sequence of ventricular activation and repolarization with
LBBB, many ECG abnormalities, such as Q-wave myocardial infarction (MI) and left ventricular hypertrophy, are difficult to evaluate.
Sgarbossa’s criteria can help to identify the presence of MI in the
setting of LBBB, though its sensitivity is limited. A new LBBB may
be a sign of an acute myocardial infarction in the correct clinical
setting (Fig. 4.6B).
With RBBB, the interventricular septum depolarizes normally from
left to right, as this depolarization depends on the left bundle. Thus,
the initial QRS deflection remains unchanged, and thus it is important
to note that ECG abnormalities such as Q-wave MI can still be interpreted. After septal activation, the left ventricle depolarizes, followed
by the right ventricle. The ECG is characterized by a wide QRS complex; a large R′ wave in lead V1 (R-S-R′); and deep S waves in leads I,
aVL, and V6, representing delayed right ventricular activation (see Fig.
4.5B). Ventricular repolarization is still abnormal, and secondary ST
and T wave changes will be present just as in LBBB. Although RBBB
may be associated with underlying cardiac disease, it is quite common
and may often reflect the fibrosis of aging.
Myocardial Ischemia and Infarction
Myocardial ischemia and myocardial infarction (MI) may be associated with abnormalities of the ST segment, T wave, and QRS complex. Myocardial ischemia primarily affects repolarization of the
myocardium and is often associated with horizontal or downsloping
ST-segment depression and T-wave inversion. These changes may
be transient, such as during an anginal episode or an exercise-related
stress, or they may be long-lasting in the setting of progressive angina
or MI. T-wave inversion without ST-segment depression can be a
nonspecific finding and must be correlated with the clinical findings
II
28 SECTION II Cardiovascular Disease
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A Left bundle branch block B Right bundle branch block
I
aVR
V
1
V
4
Diagnostic criteria for LBBB
QRS duration > 0.125 seconds
Broad R wave in I, aVL,V
Deep QS complex as in V1–V
T-wave inversion in lateral leads
Fig. 4.5 (A) Left bundle branch block (LBBB). (B) Right bundle branch block (RBBB). Criteria for bundle branch
blocks are summarized in Table 4.2.
II III II
aVL aVF aVR aVL aVF
V
2
V
5
5–V6
2
V
3
V
6
V
1
V
4
Diagnostic criteria for RBBB
QRS duration > 0.125 seconds
R > S in V
RSR in V
Deep wide S wave in I and V
1
1
V
2
V
5
6
II
V
3
V
6
to invoke ischemia or injury. Diffuse T-wave inversions across the precordial leads are often seen in patients with acute cerebral disease, such
as stroke or seizures.
ST-segment elevation of 2 mm or more in two or more contiguous
leads suggests more extensive myocardial injury, and in the right clinical presentation, is often considered to be an acute MI until proven
otherwise (Fig. 4.6A). Vasospastic or Prinzmetal angina may be associated with reversible ST-segment elevation without MI. ST-segment
elevation may occur in other settings not related to acute ischemia
or infarction. Persistent, localized ST-segment elevation in the same
leads as pathologic Q waves is consistent with a ventricular aneurysm.
Acute pericarditis is also associated with diffuse ST-segment elevation
across multiple contiguous and noncontiguous leads but is also associated with PR depression relative to the TP interval. Diffuse J-point
elevation in association with upward-coving ST segments is a normal
variant common among young men and is often referred to as early
repolarization.
A pathologic Q wave is one of the criteria used to diagnose MI.
Infarcted myocardium is impaired at conducting normal electrical
activity, and electrical forces are directed away from the surface electrode overlying the infarcted region, producing a Q wave on the surface ECG. A thorough understanding of contiguous leads allows for
identification of each region of the myocardium relative to the surface
lead, enabling the examiner to localize the area of infarction (Table
4.3). Pathologic Q waves are defined as follows: any Q wave 20 ms or
greater or QS complex in leads V2 to V3, or a Q wave 30 ms or greater
and 0.1 mV deep or greater or QS complex in leads I, II, aVL, aVF or
V4 to V6 in any 2 leads of a contiguous lead grouping (I, aVL, V6; V4
to V6; II, III, and aVF). Not all MIs result in the permanent formation
of Q waves. Small R waves can return many weeks to months after an
MI. Abnormal Q waves, or pseudoinfarction pattern, may be associated
with nonischemic cardiac disease, such as ventricular preexcitation,
cardiac amyloidosis, sarcoidosis, idiopathic or hypertrophic cardiomyopathy, myocarditis, and chronic lung disease.
Abnormalities of the ST Segment and T Wave
A number of drugs and metabolic abnormalities may affect the ST segment and T wave (Fig. 4.7). Hypokalemia may result in prominent U
waves in the precordial leads along with prolongation of the QT interval. Hyperkalemia may result in tall, peaked T waves. Hypocalcemia
typically lengthens the QT interval, whereas hypercalcemia shortens it.
A commonly used cardiac medication, digoxin, often results in diffuse,
scooped ST-segment depression. Cardiac pacing, LBBB, and RBBB
affect ventricular repolarization and alter the ST segment and T-wave.
Minor or nonspecific ST-segment and T-wave abnormalities may occur
in many patients and have no definable cause. In these instances, the
physician must determine the significance of the abnormalities based
on clinical findings.
Control
B
aVR aVL aVF V
V
V
V
V
V
III III
2 hours later
24 hours later
1
2
3
4
5
6
29
48 hours later
8 days later
6 months later
A
I
II
III
aVR V1 V4
aVL
aVF
V2 V5
V3 V6
V1
III
Fig. 4.6 (A) Evolutionary changes in a posteroinferior myocardial infarction (MI). Control tracing is normal.
The tracing recorded 2 hours after onset of chest pain demonstrated development of early Q waves, marked
ST-segment elevation, and hyperacute T waves in leads II, III, and aVF. A larger R wave, ST-segment depression, and negative T waves have developed in leads V1 and V2. These early changes indicate acute posteroinferior MI. The 24-hour tracing demonstrates further evolutionary changes. In leads II, III, and aVF, the Q
wave is larger, the ST segments have almost returned to baseline, and the T wave has begun to invert. In
leads V1 to V2, the duration of the R wave exceeds 0.04 seconds, the ST segment is depressed, and the T
wave is upright. (In this example, electrocardiographic changes of true posterior involvement extend past
lead V2; ordinarily, only leads V1 and V2 may be involved.) Only minor further changes occur through the 8-day
tracing. Six months later, the electrocardiographic pattern shows large Q waves, isoelectric ST segments,
and inverted T waves in leads II, III, and aVF and shows large R waves, isoelectric ST segment, and upright T
waves in leads V1 and V2, indicative of an old posteroinferior MI. (B) Electrocardiogram from a patient with an
underlying left bundle branch block (LBBB) who experienced an acute anterior MI. Characteristic ST segment
elevation and hyperacute T waves are seen in leads V1 through V6 and leads I and aVL despite the presence
of the LBBB. This is not always the case, and a patient with typical symptoms, an LBBB, and no definite
ischemic ST-segment elevations should be treated as if the individual is having a myocardial infarction or
acute coronary syndrome.
30 SECTION II Cardiovascular Disease
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TABLE 4.3 Electrocardiographic Localization of Myocardial Infarction
Infarct Location Leads Depicting Primary Electrocardiographic Changes Likely Vessel Involved
Inferior II, III, aVF RCA
Septal V1, V
Anterior V3, V
Anteroseptal V1 to V
Extensive anterior I, aVL, V1 to V
Lateral I, aVL, V5 to V
2
4
4
6
6
High lateral I, aVL CIRC
b
Posterior
Right ventricular
CIRC, Circumflex artery; LAD, left anterior descending coronary artery; RCA, right coronary artery.
a
This is a generalization; variations occur.
b
Usually in association with inferior or lateral infarction.
c
Usually in association with inferior infarction.
c
Prominent R in V
1
ST elevation in V1; more specifically, V4R in setting of inferior infarction RCA
Normal
LAD
LAD
LAD
LAD
CIRC
RCA or CIRC
a
Hyperkalemia
Hypokalemia
Hypercalcemia
Hypocalcemia
Hypothermia
Digitalis
Quinidine
Procainamide
Disopyramide
Phenothiazines
Tricyclic antidepressants
CNS insult
(e.g., intracerebral
hemorrhage)
Mild to moderate
(K = 5-7 mEq/L):
Tall, symmetrically peaked T
waves with a narrow base
More severe (K = 8-11 mEq/L):
QRS widens, PR segment
prolongs, P wave disappears;
ECG resembles a sine wave in
severe cases
ST depression
T- wave flattening
Large positive U wave, QT
prolongation due to U wave
Shortened QT interval due to a
shortened ST segment
Prolonged QT interval due to a
prolonged ST segment; T- wave
duration normal
Osborne or J waves: J-point
elevation with a characteristic
elevation of the early ST
segment. Slow rhythm, baseline
artifact due to shivering often
present.
ST depression
T- wave flattening or inversion
Shortened QT interval, increased U wave amplitude
Prolonged QT interval, mainly due
to prolonged T-wave duration
with flattening or inversion
QRS prolongation
Increased U-wave amplitude
Diffuse, wide, deeply inverted T
waves with prolonged QT
u
uT
Fig. 4.7 Metabolic and drug influences on the electrocardiographic recording. CNS, Central nervous system;
ECG, electrocardiogram.
AMBULATORY ELECTROCARDIOGRAPHIC
RECORDING
Ambulatory ECG monitoring allows clinicians to monitor and capture the presence and frequency of cardiac arrhythmias over a specified
period of time. Multiple types of ambulatory recording modalities are
available, and the decision to use one or the other largely depends on
the duration of surveillance required. Determination of the surveillance duration is influenced by many factors, including the frequency
of symptoms (daily, weekly, monthly, or longer), reason for the study
CHAPTER 4 Diagnostic Tests and Procedures in the Patient With Cardiovascular Disease
31
(i.e., quantifying arrhythmia burden vs. catching an arrhythmic event),
and severity of symptoms (lightheadedness vs. stroke).
A Holter monitor collects ECG data from two or three surface
leads on a recorder that the patient wears under their clothing, typically for 24 to 72 hours. The device stores all data over this period
of time. Patients are asked to write their symptoms in a diary, so that
symptoms can be correlated with the rhythm at that time. From these
recordings, algorithms analyze and identify abnormal strips for clinician review. Holter monitors are most useful for patients with frequent, daily symptoms, or for quantifying arrhythmic burden such
as frequent premature ventricular contractions. Electrocardiographic
devices are more recent innovations that also provide continuous
ECG recordings through small ECG sensors placed on the chest, usually over a period of two weeks, and can be used instead of Holter
monitors.
For patients with more infrequent symptoms, an event recorder
can be used to record data for up to a month. Like Holter monitors,
surface leads are placed on the chest and connected to a recording
device. Unlike Holter monitors, the device only maintains data for 30
to 60 second loops, after which it is erased. Data are only saved when
algorithms identify ECG abnormalities, or when patients press a button indicating the presence of symptoms. Therefore, patients must be
able to trigger the device. These data are usually uploaded to a monitoring center, where patients can be called for further questioning or
counseling.
Implantable loop recorders (ILRs) are small recording devices that
are implanted subcutaneously in the left parasternal chest wall. They
can record symptoms for up to two years. Like event recorders, data
are maintained on a loop, though for a much greater period of time
(about thirty minutes). Data are stored either automatically or through
a small magnetic activator that patients pass over the device. A device
programmer is then used to extract the data in the office. ILRs are especially useful in patients with rare but serious symptoms, or when quantifying arrhythmic burden, such as atrial fibrillation, may be critical to
informing the treatment plan.
In addition to clinician prescribed monitoring devices, there has
been a recent surge in the use of personal wearable devices such as
smartwatches that have the capacity to record and store single lead
ECG tracings. Some of these devices may even alert patients to the
presence of abnormal heart rhythms. Though the diagnostic utility of
these devices is unclear at this time, clinicians are likely to encounter
them at an increasing rate in practice, and abnormalities seen on these
devices may be used to prompt further investigation.
CHEST RADIOGRAPHY
Chest radiography is one of the most ubiquitous and commonly performed diagnostic tests in the world. It is an integral part of the initial evaluation and work-up for patients presenting with a number of
cardiovascular-related complaints, particularly chest pain, shortness
of breath, and postprocedural complaints involving cardiac devices.
Regardless of the clinical indication, chest radiography provides useful
information regarding cardiac structures that may provide additional
insight into a patient’s condition.
Routinely, chest radiography is performed in the posteroanterior
and lateral projections (Fig. 4.8). In the posteroanterior view, cardiac
enlargement may be identified when the transverse diameter of the
cardiac silhouette is greater than one half of the transverse diameter of
the thorax. The heart may appear falsely enlarged when it is displaced
horizontally, such as with poor inflation of the lungs or when the image
is taken in an anteroposterior projection, which magnifies the heart
shadow. The differential diagnosis for cardiac silhouette enlargement
on chest radiography includes cardiomegaly, pericardial effusion,
prominent epicardial fat pad, or an anterior mediastinal mass.
Left atrial enlargement is suggested when the left-sided heart border is straightened or bulges toward the left. Right atrial enlargement
may be confirmed when the right-sided heart border bulges toward
the right. Left ventricular enlargement results in downward and lateral
displacement of the apex. A rounding of the displaced apex suggests
ventricular hypertrophy. Right ventricular enlargement is best assessed
on the lateral view and may be diagnosed when the right ventricular
border occupies more than one third of the retrosternal space between
the diaphragm and thoracic apex.
The aortic arch and thoracic aorta may become dilated and tortuous in patients with severe atherosclerosis, long-standing hypertension, and aortic dissection. A widened mediastinum, which is defined
as a width of greater than 8.0 centimeters at the level of the aortic knob,
can be seen in acute aortic dissection, although it is not very sensitive
or specific for acute dissection.
Pulmonary venous congestion due to elevated left ventricular
end-diastolic pressure results in redistribution of blood flow in the
lungs and prominence of the apical vessels, which can be seen on chest
radiography. Transudation of fluid into the interstitial space may result
in fluid in the fissures and along the horizontal periphery of the lower
lung fields (i.e., Kerley B lines). As venous pressures further increase,
fluid collects in the alveolar space, which early on collects preferentially
in the inner two thirds of the lung fields, resulting in a characteristic
butterfly appearance.
Chest radiography is also used to evaluate device and lead positioning after implantation of defibrillators or pacemakers. The posteroanterior view helps to evaluate for device and lead integrity as well
as potential device placement complications such as pneumothorax.
A lateral view is necessary to evaluate ventricular lead positioning. In
the lateral view, a right ventricular lead will course anteriorly, while
a left ventricular lead will course posteriorly. The shape of the pulse
generator can help in determining the device manufacturer, which is
necessary to know for device interrogation.
ECHOCARDIOGRAPHY
Echocardiography is a widely used, noninvasive technique in which
sound waves are used to image cardiac structures and evaluate blood
flow. Transthoracic echocardiography is safe, simple, fast, and relatively inexpensive. It can provide a wealth of information on a
patient’s cardiovascular status, including ventricular function, valvular
function, chamber size, possible coronary artery disease, pericardial
disease, congenital heart disease, aortopathy, cardioembolic sources,
volume status, and hemodynamics, among many other things.
A piezoelectric crystal housed in a transducer placed on the
patient’s chest wall produces ultrasound waves. As the sound waves
encounter structures with different acoustic properties, some of the
ultrasound waves are reflected to the transducer and recorded. Steering
the ultrasound beam across a 90-degree arc multiple times per second creates two-dimensional imaging (Fig. 4.9). The development of
three-dimensional echocardiographic imaging techniques allows for
greater accuracy in measurements of chamber volumes and mass, as
well as the assessment of geometrically complex anatomy and valvular
lesions. Video 4.1 shows a three-dimensional image.
Doppler echocardiography allows assessment of the direction and
velocity of blood flow in the heart and great vessels. When ultrasound
waves encounter moving red blood cells, the energy reflected to the
transducer is altered. The magnitude of this change (i.e., Doppler shift)
is represented as velocity on the echocardiographic display and can
be used to determine whether the blood flow is normal or abnormal
32 SECTION II Cardiovascular Disease
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Fig. 4.8 Schematic illustration of the parts of the heart, outlines of which can be identified on a routine chest
radiograph. (A) Posteroanterior chest radiograph. (B) Lateral chest radiograph. Ao, Aorta; LA, left atrium; LV,
left ventricle; PA, pulmonary artery; RA, right atrium; RV, right ventricle.
RV
PE
LV
IVS
MV
PW
Ao
LA
A
Fig. 4.9 Portions of standard two-dimensional echocardiograms show the major cardiac structures in a para-
sternal long-axis view (A) and apical four-chamber view (B). Video 4.3 shows a moving image of a two-dimensional echocardiogram. Ao, Aorta; IVS, interventricular septum; LA, left atrium; LV, left ventricle; MV, mitral
valve; PE, pericardial effusion; PW, posterior left ventricular wall; RV, right ventricle. (Image courtesy Sheldon
E. Litwin, MD, Division of Cardiology, University of Utah, Salt Lake City, Utah.)
(Fig. 4.10). The velocity of a particular jet of blood can be converted
to pressure, allowing assessment of pressure gradients across valves
or between chambers. Color Doppler imaging allows visualization of
blood flow through the heart by assigning a color to the red blood cells
based on their velocity and direction (Fig. 4.11, Video 4.2). By convention, blood moving away from the transducer is represented in shades
of blue, and blood moving toward the transducer is represented in red.
Color Doppler imaging is particularly useful in identifying valvular
insufficiency and abnormal shunt flow between chambers. The use of
Doppler techniques to record myocardial velocities or strain rates can
aid in the assessment of myocardial function and hemodynamics.
Ultrasound contrast agents composed of microbubbles can be
used in patients who have poorly visualized cardiac structures, such
as obese patients or those with chronic lung disease. Ultrasound
contrast opacifies the endocardial cavity and aids in assessment of
cardiac function (Fig. 4.12). Video 4.3 shows a dynamic contrast
LV
RV
RA
LA
B
echocardiographic image. These contrast agents are also necessary in
the assessment of potential left ventricular thrombus. Agitated saline,
commonly referred to as “bubbles,” can be used to assess for intracardiac shunts.
Transesophageal echocardiography (TEE) allows two-dimensional
and Doppler imaging of the heart through the esophagus by having the
patient swallow a gastroscope mounted with an ultrasound crystal in
its tip. Given the proximity of the esophagus to the heart, high-resolution images can be obtained, especially of the left atrium, mitral valve
apparatus, and aorta. TEE is particularly useful in diagnosing left atrial
appendage thrombi, aortic dissection, endocarditis, prosthetic valve
dysfunction, and left atrial masses (Fig. 4.13, Video 4.4). TEE has been
used for decades intraoperatively during cardiac surgery, and it is now
being used with increasing frequency to guide percutaneous cardiac
procedures such as transcatheter aortic valve replacement, transcatheter mitral valve repair, and left atrial appendage occlusion.
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