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CHAPTER 35: Ventricular Dysfunction in Critical Illness 277

intrapulmonary shunt. Titrated morphine doses decrease venous tone
74
TABLE 35-5 Common Precipitating Factors of Acute on Chronic Heart Failure
and thereby decrease left ventricular filling pressures and improve
Poor compliance with medications pulmonary edema. In addition, morphine may make the patient less
Dietary indiscretion (salt load, alcohol) anxious, thereby decreasing whole-body oxygen demand. Nitrates are
Infection venodilators that serve to decrease left ventricular filling pressure and
mild arterial vasodilators, resulting in decreased afterload. Nitrates
Fever have the additional benefit of being coronary vasodilators.
High environmental temperature Afterload reduction is an important therapeutic intervention in patients
Effect of a new medication (β-blocker, calcium channel blocker, antiarrhythmic, with depressed left ventricular systolic contractility (= decreased slope of
nonsteroidal anti-inflammatory) the ESPVR, Fig. 35-1B). Because there is a decrease in the slope of the
ESPVR, small reductions in pressure afterload can result in improved ejec-
Arrhythmia (typically, new atrial fibrillation)
tion to smaller ESVs (Fig. 35-4). The reduction in ESV results in increased
Ischemia or infarction stroke volume and in substantially decreased end-systolic wall stress
Valve dysfunction (endocarditis, papillary muscle dysfunction) because, by the Laplace relation, wall stress is proportional to the product
of cavity pressure and radius. The decrease in wall stress reduces myocar-
Pulmonary embolism
dial oxygen demand. Afterload reduction in some critically ill patients may
Surgical abdominal event (cholecystitis, pancreatitis, bowel infarct) result in unacceptable hypotension. For this reason, it is best to start with
Worsening of another disease (diabetes, hepatitis, hyperthyroidism, hypothyroidism) an easily titratable medication with a very short half-life such as nitroprus-
side or, in the setting of ischemia, intravenous nitroglycerin (see Chap. 33).
Nitroprusside is infused at an increasing dose while the response of cardiac
output and blood pressure is measured repeatedly, so that an optimal dose
be the precipitant. Cardiac output may be depressed, so the kidneys are
hypoperfused. Activation of the renin-angiotensin axis accounts for avid resulting in maximum cardiac output with adequate perfusing pressures is
renal absorption of sodium and water, which may further worsen volume chosen. Nitroprusside and other nitrates are direct or indirect NO donors
overload. Vasopressin release increases water retention. Volume overload that cause vascular smooth muscle relaxation. Nitroprusside at larger
leads to elevated venous pressures with subsequent pulmonary edema doses can result in significant toxicity, with cyanide formation and methe-
due to elevated Pla and peripheral edema due to elevated systemic venous moglobinemia. When circulatory stability is achieved, other, longer-acting
pressures. There is an excessive reflex release of catecholamines leading to agents are substituted; angiotensin-converting enzyme inhibitors are par-
27,75
tachycardia and increased arterial tone, so arterial resistance rises. Increased ticularly useful, as are alternative drugs (see Table 35-3). Noninvasive
arterial resistance as afterload may be detrimental to left ventricular pump ventilation with positive airway pressures may improve oxygenation,
47,48
function. Coronary artery disease is common in this population, so decom- decrease dyspnea, and effectively reduce left ventricular afterload.
pensation may have followed an acute ischemic coronary event or coronary Inotropic or vasoactive agents are extremely useful in reversing depressed
ischemia may be precipitated by worsened congestive heart failure. systolic contractility, but routine use of inotropes is not indicated for heart
Dobutamine
failure because inotropic use may increase mortality rate.
46,76
■ CLINICAL FEATURES acts mainly on β -receptors and results primarily in increased ventricu-
1
Patients are often anxious, tachycardic, and tachypneic, with evidence lar contractility and in mild peripheral vasodilation. Doses from 2 to
15 µg/kg per minute are infused through a central venous line. Particularly
of hypoperfused extremities and possibly cyanosis. Jugular veins are in the presence of intravascular hypovolemia, the vasodilating effect of
distended, and hepatojugular reflux may be demonstrable on physical dobutamine may exceed its effect on increasing cardiac output, so blood
examination. An apical impulse lateral to the midclavicular line or farther pressure may decrease unacceptably. Dopamine has significant adverse
than 10 cm from the midsternal line is a sensitive but not specific indica- effects that should limit its use. Low-dose dopamine has been clearly
tor of left ventricular enlargement, whereas an apical diameter larger than shown not to be beneficial. At doses exceeding 10 µg/kg per minute,
3 cm indicates left ventricular enlargement. A sustained apical impulse dopamine is an α-agonist and therefore increases arterial resistance. The
73
suggests left ventricular hypertrophy or aneurysm. A third heart sound increased preload and afterload associated with dopamine are often unde-
or summation gallop is often present but may be obscured by increased sirable in treating decreased contractility. Milrinone and enoximone are
respiratory sounds. Pulse pressure is often reduced, so peripheral pulses phosphodiesterase inhibitors that increase contractility by increasing intra-
are “thready.” Crackles are heard in dependent lung fields but in severe cellular calcium during systole. These agents may also result in afterload
cardiac failure are heard in all zones. Wheezes and a prolonged expira- reduction and therefore may be particularly beneficial in short-term treat-
tory phase may be noted, suggesting edema surrounding the airways. ment of depressed contractility. The use of digoxin to increase contractility
Hepatomegaly, which may be pulsatile particularly with tricuspid valve is not generally helpful in the acute setting. In general, although positive
77
insufficiency, may be present and there is evidence of dependent edema inotropic agents improve contractility, they do so at the cost of increased
in the lower extremities and over the sacrum. myocardial oxygen demand and decreased efficiency of oxygen use and
Chest radiographic findings suggesting elevated left ventricular filling therefore may precipitate ischemia, arrhythmias, and other adverse out-
pressures include upper zone redistribution of vascular markings, septal comes. If acute decompensation leads to cardiogenic shock and recovery is
lines (Kerley B lines), loss of pulmonary vascular definition, perivascular anticipated after medical or surgical intervention, then intra-aortic balloon
and peribronchial cuffing, perihilar interstitial and then alveolar filling counterpulsation or other ventricular assist devices should be instituted
patterns, and pleural effusions. The cardiopericardial silhouette may be when afterload reduction and inotropic therapy are insufficient.
enlarged, suggesting enlarged cardiac chambers, and the azygos vein
may be enlarged, suggesting elevated Pra.
■ MANAGEMENT KEY REFERENCES

Therapy of acute-on-chronic heart failure initially aims to treat intra- • Andrew P. Diastolic heart failure demystified. Chest. 2003;124(2):
vascular overload and improve gas exchange. Therefore, the patient 744-753.
is positioned with the torso elevated at least 45°, and oxygen is admin- • Boyd JH, Kan B, Roberts H, Wang Y, Walley KR. S100A8 and
istered. Good intravenous access, optimally central venous, is estab- S100A9 mediate endotoxin-induced cardiomyocyte dysfunction
lished. Furosemide (20-40 mg initially, followed by increasing doses as via the receptor for advanced glycation end products. Circ Res.
required) induces a rapid diuresis. Even before diuresis is established, 2008;102(10):1239-1246.
furosemide reduces Pla by a venodilation effect and also reduces

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