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CHAPTER 35: Ventricular Dysfunction in Critical Illness 275

of mitral valve leaflet, increased ejection velocities signifying increased Cardiac resynchronization therapy using biventricular pacing
gradients across the aortic outflow tract, and cavity obliteration at end improves cardiac function in patients having a decreased ejection frac-
systole. This appears to occur most commonly in elderly patients with tion, bundle branch block, and New York Heart Association class III or
previously treated hypertension. Volume infusion to reverse intravascular IV heart failure. 51,66 The role for resynchronization therapy in the critical
hypovolemia may prevent left ventricular cavity obliteration and outflow care setting has not been fully defined.
tract obstruction and thereby reduce ventricular afterload. It is important Arrhythmias including atrial fibrillation, atrial flutter, and ventricular
to identify outflow tract obstruction as the cause of increased afterload tachycardia should be immediately cardioverted if they are contributing
because this cause of increased afterload is worsened by conventional to a shock state. Otherwise, rapid heart rate due to atrial fibrillation is
afterload reduction therapy. slowed using β-blockers or second-line agents including calcium chan-
When afterload is reduced dramatically, or when intravascular nel blockers. Adenosine, verapamil, and maneuvers to increase vagal
volumes re expanded, the resulting high cardiac output state is sometimes tone may be useful in the diagnosis of tachyarrhythmias and in treating
called high-output cardiac failure. Actually, cardiac function still lies on a paroxysmal supraventricular tachycardia. Multifocal atrial tachycardia
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normal cardiac function curve, but the greatly increased venous return responds to correction of underlying pulmonary disease and to vera-
associated with low afterload results in high right- and left-side filling pamil or a class III antiarrhythmic agent. Ventricular dysrhythmias
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pressures with the appearance of right- and left-side congestion. This is contributing to altered hemodynamic function must be treated. Specific
particularly apparent in the presence of atrioventricular valvular stenosis, management of ventricular arrhythmias is detailed in Chap. 36.
which previously may have been occult. Causes of high-output failure
include anemia, arteriovenous fistulas, hepatic failure, Paget disease,
thyrotoxicosis, pregnancy, carcinoid syndrome, and renal cell carcinoma. MECHANISMS AND MANAGEMENT OF RIGHT
VENTRICULAR DYSFUNCTION
■ VALVULAR DYSFUNCTION Right ventricular pump function also depends on contractility, preload (the

The valves regulate preload and afterload and are therefore important diastolic pressure-volume relation), afterload, valve function, and heart rate
and rhythm. However, the right ventricle differs from the left ventricle, so
determinants of left ventricular pump function (see Chap. 41). In criti- the relative importance of each of these components is different. The left
cally ill patients, the effect of preexisting valvular disease may change with ventricle is well designed to generate high pressures. Its thick walls and
altered hemodynamics, or the extent of valvular disease may change small chamber volume result in manageable levels of wall stress despite
primarily. For example, aortic and mitral insufficiencies contribute to low high intracavitary pressures. The helical arrangement of muscle fibers
cardiac output at high ventricular filling pressures in critical illness, and changing from endocardium to epicardium in concentric layers results in
both respond quickly to afterload reduction. Moreover, mitral regurgita- a strong wall with an efficient distribution of wall stress. In contrast, the
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tion may worsen acutely due to increased EDV and expansion of the right ventricle is a thin-walled pump whose surface has a large radius of
mitral annulus. In contrast, mitral valve prolapse may worsen at low curvature so it is not suited as a high-pressure generator. Instead, the right
ventricular volumes due to hypovolemia. In high cardiac output states, ventricle functions as an excellent flow generator at low pressures. Right
previously insignificant mitral stenosis may result in a high Pla and pulmo- ventricular contraction moves sequentially from the apex to the pulmonary
nary edema. The gradient across the stenotic aortic valve may increase in outflow tract, giving it features of a peristaltic volume pump. During dias-
high-flow states and conversely decrease in low-flow states, so that, without tole, the right ventricle at normal diastolic pressure lies below its stressed
considering the flow across the valve, an incorrect judgment of the func- volume, a feature that allows it to accommodate a large filling volume
tional significance of the valvular disease may be made. Dysfunction of without an elevation in EDP. Because of these features, volume preload
prosthetic valves is important to identify and may be a surgical emergency. and, most importantly, pressure afterload become even more important
■ ABNORMAL HEART RATE AND RHYTHM determinants of right ventricular function than they are in the left ventricle.

Excessively fast or excessively slow heart rates limit cardiac output. ■ DECREASED RIGHT VENTRICULAR SYSTOLIC FUNCTION
Bradycardia is an important abnormal rhythm in a critically ill patient. Contractility of the right ventricle is decreased approximately to the same
First, it is important to determine whether hypoxemia, drugs such as extent as in the left ventricle by the many causes listed for the left ventricle
acetylcholinesterase inhibitors, or other reversible insults are the cause (see Tables 35-1 and 35-2). Occasionally, right ventricular contractility is
of bradycardia. In these cases, treatment consists of rapid reversal of the disproportionately reduced as in right ventricular infarction, arrhythmo-
cause. In other cases in which bradycardia is due to primary cardiac genic right ventricular dysplasia, Uhl anomaly, isolated right ventricular
disease, including myocardial infarction with involvement of the con- myopathy, and myopathy associated with uncorrected atrial septal defect.
ducting system, therapy is directed at increasing heart rate by other Right ventricle ischemia in the absence of coronary artery disease is very
means. Acutely, bradycardia may be treated with atropine and, if neces- important during critical illness. When afterload is elevated, the right
sary, by β-adrenergic agonist infusion titrated to heart rate response. ventricle responds along a preload-dependent right ventricular ESPVR, so
These temporizing measures allow placement of temporary or permanent right ventricular ESV increases. Right ventricular chamber pressures are
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pacemakers. In addition to the well-known indications for temporary increased, the radius of curvature is increased, and, hence, the wall stress
pacing after myocardial infarction, it should be recognized that in the thin right ventricular wall increases dramatically. Right ventricular
symptomatic bradycardia from any cause is an indication for pacing. myocardial oxygen demand increases proportionately. At increased right
Tachycardia at sufficiently high rates results in an inadequate diastolic ventricular pressures, the right ventricular intramural pressure increases,
filling time, so stroke volume is reduced because adequate diastolic fill- and hence, the gradient for right ventricular coronary blood flow
ing does not occur and the contribution to ventricular diastolic filling decreases. Oxygen supplied to the right ventricular myocardium may not
by the atria is less efficient, particularly during atrial fibrillation. An meet oxygen demand, so contractility decreases, further worsening right
end-diastolic gradient across the mitral valve develops at fast heart rates. ventricular function and leading to acute right ventricular failure. 71
Hypoxemia and acidosis encountered in critically ill patients are frequently
tachyarrhythmias. Hyperkalemia and hypokalemia, hypocalcemia, and ■ DISORDERS OF RIGHT VENTRICULAR PRELOAD,
associated with ventricular and, even more commonly, supraventricular
hypomagnesemia are common electrolyte disturbances associated with AFTERLOAD, VALVES AND RHYTHM
increased incidence of ventricular arrhythmias. Accordingly, manage- Increasing right ventricular EDV results in an increase in right ventricu-
ment of atrial and ventricular tachyarrhythmias involves correcting lar stroke volume, even though right ventricular EDP may not increase
these potential contributing abnormalities. much because, normally, EDV is below the right ventricular diastolic

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