Page 388 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

258 PART 3: Cardiovascular Disorders

inotropic agents and afterload reduction are generally not helpful and is often extremely useful in cardiogenic shock and should be consid-
may decrease blood pressure further. If conventional therapy of car- ered early as a support in patients who may benefit from later surgical
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diogenic shock aimed at improving systolic function is ineffective, then therapy. Cardiac transplantation and mechanical heart implantation are
increased diastolic stiffness should be strongly considered as the cause of considered when other therapy fails.
decreased pump function. Cardiac output responsiveness to heart rate is Filling pressures are optimized to improve cardiac output but avoid
another subtle clue suggesting impaired diastolic filling. Heart rate does pulmonary edema. Depending on the initial presentation, cardiogenic
not normally alter cardiac output (which is normally set by, and equal to, shock frequently spans the spectrum of hypovolemia (so fluid infusion
venous return) except at very low heart rates (maximally filled ventricle helps) to hypervolemia with pulmonary edema (where reduction in
before end diastole) or at very high heart rates (incomplete ventricular intravascular volume results in substantial improvement). If gross fluid
relaxation and filling). However, if diastolic filling is limited by tampon- overload is not present, then a rapid fluid bolus should be given. In
ade or a stiff ventricle, then very little further filling occurs late in dias- contrast to patients with hypovolemic or septic shock, a smaller bolus
tole. In this case, increasing heart rate from 80 to 100 or 110 beats/min (250 mL) of crystalloid solution should be infused as quickly as possible.
may result in a significant increase in cardiac output, which may be Immediately after infusion, the patient's circulatory status should be
therapeutically beneficial and also a diagnostic clue. reassessed. If there is improvement but hypoperfusion persists, then
further infusion with repeat examination is indicated to attain an ade-
Valvular Dysfunction Acute mitral regurgitation, due to chordal or papillary
muscle rupture or papillary muscle dysfunction, most commonly is quate cardiac output and oxygen delivery while seeking the lowest filling
pressure needed to accomplish this goal. If there is no improvement in
caused by ischemic injury. The characteristic murmur and the pres-
ence of large V waves on the pulmonary artery occlusion pressure trace oxygen delivery and evidence of worsened pulmonary edema or gas
exchange, then the limit of initial fluid resuscitation has been defined.
suggest significant mitral regurgitation, which is quantified by echocar-
diographic examination. Rupture of the ventricular septum with left-to- Crystalloid solutions are used particularly if the initial evaluation is
uncertain because crystalloid solutions rapidly distribute to the entire
right shunt is detected by Doppler echocardiographic examination or by
observing a step-up in oxygen saturation of blood from the right atrium extracellular fluid compartment. Therefore, after a brief period only
one-fourth to one-third remains in the intravascular compartment, and
to the pulmonary artery. Rarely, acute obstruction of the mitral valve by
left atrial thrombus or myxoma may also result in cardiogenic shock. evidence of intravascular fluid overload rapidly subsides.
Contractility increases if ischemia can be relieved by decreasing
These conditions are generally surgical emergencies.
More commonly, valve dysfunction aggravates other primary etiolo- myocardial oxygen demand, by improving myocardial oxygen supply
gies of shock. Aortic and mitral regurgitation reduces forward flow and by increasing coronary blood flow (coronary vasodilators, thrombo-
raises LVEDP, and this regurgitation is ameliorated by effective arteriolar lytic therapy, surgical revascularization, or intra-aortic balloon pump
counterpulsation), or by increasing the oxygen content of arterial blood.
dilation and by nitroprusside infusion. Vasodilator therapy can effect
large increases in cardiac output without much change in mean blood Inotropic drug infusion attempts to correct the physiologic abnormality
by increasing contractility (see Fig. 33-2). However, this occurs at the
pressure, pulse pressure, or diastolic pressure, so repeat Scv or cardiac
O 2
output measurement, or echocardiographic assessment is essential to expense of increased myocardial oxygen demand. Afterload is opti-
mized to maintain arterial pressures high enough to perfuse vital organs
titrating effective vasodilator doses. In contrast, occasional patients
develop decreased blood pressure and cardiac output on inotropic drugs (including the heart) but low enough to maximize systolic ejection.
When systolic function is reduced, vasodilator therapy may improve
such as dobutamine; in this case, excluding dynamic ventricular outflow
tract obstruction by echocardiography or treating it by increasing pre- systolic ejection and increase perfusion, even to the extent that blood
pressure rises. In patients with very high blood pressure, end-systolic
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load, afterload, and end-systolic volume is essential.
volume increases considerably so that stroke volume and cardiac output
Cardiac Arrhythmias Not infrequently, arrhythmias aggravate hypoperfusion decrease unless LVEDV and LVEDP are greatly increased; this sequence
in other shock states. Ventricular tachyarrhythmias are often associated is reversed by judicious afterload reduction.
with cardiogenic shock; sinus tachycardia and atrial tachyarrhythmias
are often observed with hypovolemic and septic shock. Specific therapy Right Ventricular Failure—Overlap With Obstructive Shock: Shock present-
of tachyarrhythmias depends on the specific diagnosis, as discussed in ing as low cardiac output, high venous pressures, and clear or ambiguous
Chap. 36. Inadequately treated pain and unsuspected drug withdrawal (concurrent pulmonary process) breath sounds is an important diagnostic
should be included in the intensive care unit differential diagnosis of challenge generally requiring urgent echocardiographic examina-
tachyarrhythmias; whatever their etiology, the reduced ventricular filling tion. This classic presentation of right heart failure must first be distin-
time can reduce cardiac output and aggravate shock. Bradyarrhythmias guished from cardiac tamponade (obstructive shock). Then the cause
contributing to shock may respond acutely to atropine or isoproterenol of right heart failure must be determined. Most commonly the cause is left
infusion and then pacing; hypoxia or myocardial infarction as the cause heart failure contributing to right heart failure, right heart failure due to
should be sought and treated. Symptomatic hypoperfusion resulting right ventricular infarction, or right heart failure due to increased right
from bradyarrhythmias, even in the absence of myocardial infarction or ventricular afterload—pulmonary artery hypertension. Increased
high-degree atrioventricular block, is an important indication for tem- right ventricular afterload then needs to be understood as acute, often
porary pacemaker placement that is sometimes overlooked. due to pulmonary embolism (obstructive shock), or acute on chronic
where inflammatory mediators, hypoxic pulmonary vasoconstriction,
Treatment of Left Ventricular Failure After initial resuscitation, which includes
consideration of early institution of thrombolytic therapy in acute coro- or high ventilator pressures may be the “acute” precipitants or contribu-
nary thrombosis and revascularization or surgical correction of other tors. Echocardiography is fundamental in distinguishing between all of
anatomic abnormalities where appropriate, management of patients the above scenarios.
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with cardiogenic shock requires repeated testing of the hypothesis Diagnosis and Management of Right Ventricular Failure With the above clinical pre-
of “too little versus too much.” Clinical examination is not accurate sentation, due to any of these underlying causes, volume resuscitation
enough; when the response to initial treatment of cardiogenic shock is is particularly problematic. Volume infusion increases right atrial and,
inadequate, repeated Scv or cardiac output measurement or repeated hence, right ventricular diastolic pressure. Excessive change in diastolic
O 2
echocardiographic exam may be required to titrate therapy. Therapy pressure gradient between right and left ventricles then shifts the inter-
for cardiogenic shock follows from consideration of the pathophysiol- ventricular septum from right to left. Importantly, right-to-left shift of
ogy illustrated in Figure 33-4 and includes optimizing filling pressures, the interventricular septum limits left ventricular filling and induces
increasing contractility, and optimizing afterload. Temporary mechanical inefficient and paradoxical septal movement during left ventricular
support using an intra-aortic balloon pump or a ventricular assist device contraction. As a result, stroke volume and cardiac output are reduced.

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