Page 404 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

274 PART 3: Cardiovascular Disorders

■ INCREASED DIASTOLIC STIFFNESS as a result of increased CVP. Therefore, in the setting of increased
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In normal hearts and in hearts with depressed ventricular function, diastolic stiffness, any ischemia should be treated aggressively.
Nitrates increase coronary blood flow and decrease tone in the venous
increasing preload is an important mechanism of increasing cardiac
output. For hearts with normal systolic function, left ventricular end- capacitance bed, thereby reducing pericardial pressure; nitroprusside
also decreases diastolic stiffness.
diastolic filling pressures are often in the range of 0 to 10 mm Hg and
Increased intrathoracic or intrapericardial pressure is a common revers-
result in an adequate cardiac output. For hearts with depressed con- ible cause of apparent increased diastolic stiffness in critical illness.
tractility, higher filling pressures are usually required for an adequate
cardiac output. Therefore, there is no uniformly optimal filling pressure. Intrathoracic pressure is increased by positive-pressure mechanical
ventilation and more so by the addition of positive end-expiratory
Left ventricular function may be substantially impaired by increased
diastolic stiffness of the left ventricle—a shift up and to the left of the pressure (PEEP). Positive airway pressures and PEEP are variably trans-
mitted to the heart, depending on the distensibility of the lungs and chest
diastolic pressure-volume relation (Fig. 35-6). 19,55 This is a problem
whose importance is equal at least to depressed contractility in the wall. Increased intrathoracic pressure due to pneumothorax or massive
pleural effusion may tamponade the heart and thereby result in appar-
critically ill patient. Depressed systolic function reduces stroke volume
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because ESV increases; in contrast, increased diastolic stiffness reduces ent increased diastolic stiffness. Greatly increased intra-abdominal
pressure may elevate the diaphragm and similarly increase diastolic
stroke volume because EDV decreases. Increased diastolic stiffness
is a relatively frequent problem encountered in critically ill patients. stiffness. Pericardial pressure may be increased by pericardial effusion
and rarely by massive pneumopericardium. Because all these causes
It differs from depressed ventricular contractility because it is much
more difficult to treat and does not respond to conventional therapy of increased intra thoracic or intrapericardial pressure leading to appar-
ent increased diastolic stiffness are treatable, they must be identified or
of decreased left ventricular pump function. 56,57 In fact, in the absence of
an imaging study that demonstrates increased diastolic stiffness (small excluded early in critically ill patients.
Hypovolemic shock and septic shock may result in increased dia-
EDV in relation to the end-diastolic pressure [EDP]), the diagnosis of 63
increased diastolic stiffness is suggested by finding depressed ventricu- stolic stiffness. The increased diastolic stiffness associated with these
kinds of shock is associated with irreversibility of the shock state and
lar pump function unresponsive to fluid loading, afterload reduction, 64,65
and inotropic agents. Occasionally, the diagnosis of increased diastolic increased mortality rate. Infusion of catecholamines and calcium
may further contribute to increased diastolic stiffness by contraction
stiffness is suggested by the observation that cardiac output is unusually
sensitive to changes in heart rate. band formation. Hypothermia with body temperature falling below
35.8°C (95.8°F) also results in increased left ventricular diastolic stiff-
Chronic Causes: Chronic diseases that increase diastolic stiffness ness. This is a reversible phenomenon as temperature is increased. This
include concentric left ventricular hypertrophy due to hypertensive is an important consideration during massive fluid resuscitation and
cardiovascular disease, hypertrophic cardiomyopathy, and restrictive mandates resuscitation with warmed infusions.
myocardial diseases. In addition, diseases of the pericardium, including
constriction and effusion, and other processes that increase intra- Management of Diastolic Dysfunction: Whereas acute diastolic stiffness
thoracic pressure result in increased diastolic stiffness, as discussed due to ischemia, tamponade, and tension pneumothorax are readily
in Chap. 35. Concentric hypertrophy due to chronic hypertension is treated, acute therapy to reverse diastolic stiffness in the critical care
very common and may be an important contributor in combination setting is limited. Therefore, searching for an optimal filling pressure
with acute diseases depressing systolic function. 56,57 Hypertrophic that maximizes ventricular diastolic filling without resulting in sub-
cardiomyopathy results in increased diastolic stiffness and, in the stantial pulmonary edema is a critically important component of care
setting of hypovolemia, may also result in greatly increased afterload in these patients. In addition, hypovolemia and sepsis should be treated
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due to dynamic aortic outflow obstruction. Over a period of days aggressively and promptly, inotropic agents should be avoided or used
and months, β-blockers and calcium channel blockers may reduce at the smallest dose that results in the desired systolic or vascular
evidence of increased diastolic stiffness. More rapidly, these agents effect, hypothermia should be prevented and treated, and tachycar-
alleviate dynamic outflow obstruction in patients with hypertrophic dia or atrioventricular arrhythmias should be treated early (see below).
cardiomyopathy due to their negative inotropic effect. Restrictive Intrathoracic pressure is minimized by appropriate ventilator management
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cardiomyopathies include amyloidosis, hemochromatosis, sarcoid- and by decompressing surrounding compartments (pericardial, pleu-
osis, endomyocardial fibrosis, some glycogen storage diseases, and ral, and abdominal) when these cause cardiac tamponade.
res triction because of surgical correction of acquired and congenital
abnormalities. Amyloidosis is uncommon at age 40 but by age 90 has ■ SPECIAL EFFECTS OF ALTERED AFTERLOAD ON VENTRICULAR
a prevalence of 50%. FUNCTION IN CRITICAL ILLNESS
Clinical examination may show a Kussmaul sign, rapid x and y descents
in the jugular venous pressure waveform so that a and v waves are promi- An increase in afterload decreases left ventricular pump function because
nent, and a fourth heart sound. Hepatojugular reflux may be prominent stroke volume is reduced as a result of increased ESV (see Fig. 35-2).
because the increased venous return produced by this maneuver cannot In malignant hypertension, elevated aortic pressure results in decreased
be accommodated by the stiff heart. Diastolic ventricular pressure cardiac output and elevated left ventricular filling pressures leading
measurements may show a square root sign, which is a rapid early rise to pulmonary edema even if contractility is normal. Antihypertensive
in diastolic pressure to a relatively constant plateau. Echocardiographic therapy results in rapid improvement. When contractility is depressed,
evaluation may demonstrate rapid early diastolic filling to a relatively increased afterload may worsen cardiac function even more. This is
fixed diastolic diameter, similar to the square root sign, and increased particularly important in dilated cardiomyopathies, in which increased
myocardial echogenicity may be observed in amyloidosis. 59,60 afterload may be observed due to increased sympathetic tone, activation
of the renin-angiotensin-aldosterone axis, and abnormally increased
Acute Causes: As with diseases resulting in depressed left ventricular vascular smooth muscle tone.
systolic function, it is important to consider the acute, potentially Aortic valvular stenosis or dynamic obstruction of the aortic outflow
reversible causes of increased diastolic stiffness. Regional or global tract may also increase afterload and contribute to decreased left ventricu-
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ischemia results in delayed systolic relaxation. This change in diastolic lar pump function (see Chap. 41). Dynamic outflow tract obstruction is
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stiffness usually precedes depressed contractility because the sarco- most commonly due to hypertrophic cardiomyopathy. However, patients
plasmic reticulum calcium pump has a lower affinity for adenosine with preexisting concentric hypertrophy due to chronic hypertension who
triphosphate than do the contractile proteins. In addition, ischemia may have a decrease in intravascular volume may develop dynamic aortic out-
result in increased diastolic stiffness by increasing pericardial pressure flow tract obstruction with the classic findings of systolic anterior motion

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