Page 425 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 37: Myocardial Ischemia 295

infarction such as substernal chest pain radiating to the arm, neck or jaw, inverted T waves that revert to upright—the so-called pseudonormaliza-
dyspnea, nausea, and diaphoresis. The vigilant clinician must therefore tion of T waves.
maintain a high index of suspicion and have a low threshold for obtain- The clinician must also be careful not to be fooled by electrocar-
ing a 12-lead ECG. diographic “imposters” of acute infarction, which include pericarditis,
The physical examination, although sometimes insensitive and non- J-point elevation, Wolff-Parkinson-White syndrome, and hypertrophic
specific, especially in the patient with multisystem illness or with cardiomyopathy. In pericarditis, ST segments may be elevated, but the
preexisting left ventricular dysfunction, may be helpful in confirming elevation is diffuse and the morphology of the ST segments in peri-
the diagnosis. Elevated jugular veins signal right ventricular diastolic carditis tends to be concave upward, while that of ischemia is convex.
pressure elevation, and the appearance of pulmonary crackles (in the Pericarditis may also be distinguished from infarction by the presence
absence of pulmonary disease) indicates elevated left ventricular filling of PR segment depression in the inferior leads (and also by PR segment
pressures secondary to depressed left ventricular function. A systolic elevation in lead aVR). 4
of the heart, representing contact of an ischemic dyskinetic segment of ■ SILENT ISCHEMIA
bulge occasionally can be palpated on the precordium near the apex
the left ventricle with the chest wall. During the ischemic episode, Recent interest has focused on “silent” myocardial ischemia, that is,
auscultation may reveal the presence of a fourth heart sound, indicative objective ECG evidence of myocardial ischemia that is not associated
of a noncompliant left ventricle. With extensive myocardial dysfunction, with angina or with anginal equivalents. Silent myocardial ischemia
5
a third heart sound may be present. A murmur of mitral regurgitation may be an incidental observation on a cardiac monitor or on a routine
attributable to papillary muscle dysfunction may also emerge. ECG, and consists of transient ST segment depression that may last
■ THE ELECTROCARDIOGRAM several minutes or even hours. The frequency of episodes of ST seg-
ment depression correlates with the severity of coronary artery disease
The electrocardiographic (ECG) abnormalities in myocardial ischemia in patients with known coronary artery disease or a history of angina.
vary widely and depend in large part on the extent and nature of coro- Decreased left ventricular function has been associated with episodes
6,7
nary stenosis and the presence of collateral blood flow to ischemic zones. of silent ST depression. In patients monitored with pulmonary artery
With acute total occlusion of a coronary artery, the first demonstrable (PA) catheters, silent ischemia may be manifested by increased pulmo-
ECG changes are peaked T waves changes in the leads reflecting the nary artery occlusion pressures, reflecting increased left ventricular
anatomic area of myocardium in jeopardy. As total occlusion continues, end-diastolic pressure (LVEDP). Echocardiography may demonstrate
there is elevation of the ST segments in the same leads. With continued transient wall motion abnormalities and diminished diastolic com-
occlusion, there is an evolution of ECG abnormalities, with biphasic and pliance. These signs of left ventricular dysfunction may precede ST
then inverted T waves. If enough myocardium is infarcted, Q waves, segment changes. 6,7
which represent unopposed initial depolarization forces away from the It is important to note that not all episodes of transient ST segment
mass of infarcted myocardium, which has lost electrical activity and depression are attributable to silent ischemia. Nevertheless, should this
no longer contributes to the mean QRS voltage vector may appear. The finding be observed on the cardiac monitor, especially in association with
formation of Q waves is accompanied by a decrease in the magnitude of transient elevation of left ventricular filling pressures, it is prudent to
the R waves in the same leads, representing diminution of voltage in the consider the possibility of myocardial ischemia as a potential factor com-
mass of infarcted myocardium. Indeed, loss of R wave voltage, revealed plicating the course of the critically ill patient, and to consider additional
by comparison with previous ECG tracings, may be the only ECG evi- diagnostic measures as above.
to note that QRS voltage can be affected by multiple factors, such as lead ■ CARDIAC BIOMARKERS
dence for the presence of permanent myocardial damage. It is important
placement, body position, QRS axis shifts, and pericardial and thoracic Measurement of enzymes released into the serum from necrotic myo-
abnormalities that may shield the electrical activity of the heart. These cardial cells after infarction can aid in the diagnosis of myocardial
conditions are frequently encountered in patients in the ICU and should infarction. The classic biochemical marker of acute myocardial infarc-
8
be taken into consideration in interpretation of Q waves and R waves. tion is elevation of creatine phosphokinase (CPK) levels. The CPK
Extension of an inferior MI to the posterior segment can be detected MB isoenzyme is found primarily in cardiac muscle, and only small
by enhancement of R waves in the anterior chest leads, since these forces amounts are present in skeletal muscle and brain. CK released from the
are now less opposed by posterior forces. True posterior infarction can myocardium begins to appear in the plasma 4 to 8 hours after onset of
be subtle, since the only signs may be prominent R waves, tall upright infarction, peaks at 12 to 24 hours, and returns to baseline at 2 to 4 days.
T waves and depressed ST segments in leads V and V . Involvement The magnitude of the increase in serum CK level and the rate at which it
1
2
of the right ventricle in inferior MI is also not readily detected on the rises and falls are a function of the total mass of myocardium affected, the
standard 12-lead ECG because of the small mass of the right ventricle extent and nature of coronary occlusion (eg, total or subtotal occlusion),
relative to the left ventricle and because of the positioning of the stan- the rate of washout from the infarcted myocardium, and the clearance
dard precordial leads away from the right ventricle. RV infarction may from the body. To be diagnostic for MI, the total plasma CK value must
be detected by ST elevation in recordings from right precordial leads, exceed the upper limit of normal, and the fraction consisting of the MB
particularly V . 3 isoenzyme must exceed a certain value (usually >5%, but depends on the
4R
Subtotal occlusion of an epicardial coronary artery may not result CK-MB assay used).
in ST elevation, but rather in ST depression or only T wave changes in A newer serologic test for the detection of myocardial damage
the leads reflecting the involved myocardium. These findings are less employs measurement of cardiac troponins. Troponin T and troponin I
8
specific for myocardial ischemia than ST elevation, as they may also be are constituents of the contractile protein apparatus of cardiac muscle,
caused by a myriad of factors besides ischemia, including cardioactive and are more specific than the conventional CPK-MB assays for the
drugs, in particular digoxin, and electrolyte disorders, in particular detection of myocardial damage. Their use is becoming more widespread,
hypokalemia. Left ventricular hypertrophy and acute left ventricular and has superseded the use of CPK MB in most settings. Troponins are
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pressure overload, as might occur in hypertensive crisis, may also result also more sensitive for the detection of myocardial damage, and troponin
in ST depression—the so-called strain pattern. Supraventricular tachy- elevation in patients without ST elevation (or in fact, without elevation
cardias have also been shown to result in ST depression, even in the of CPK-MB) identifies a subpopulation at increased risk for complica-
absence of coronary artery disease. In the presence of preexisting T-wave tions. Rapid point-of-care troponin assays, which have become available
abnormalities, ST segment, or T wave changes are even less specific for in the past few years, have further extended the clinical utility of this
ischemia. Ischemia may also be indicated by previously flattened or marker. Troponins may not be elevated until 6 hours after an acute

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