Page 386 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

256 PART 3: Cardiovascular Disorders

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volume are nearly completely compensated for. Orthostatic decrease in DECREASED PUMP FUNCTION—CARDIOGENIC SHOCK
blood pressure by 10 mm Hg or an increase in heart rate of more than The diagnosis of decreased pump function as the cause of shock is made
30 beats/min may detect this level of intravascular volume reduction. by finding evidence of inappropriately low output (cardiac output) despite
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When approximately 40% of the intravascular volume is lost, sympa- normal or high input (right atrial pressure). Cardiac output is the most
thetic stimulation can no longer maintain mean systemic pressure, important “output” of the heart and is clinically assessed in the same way
resulting in decreased venous return and clinical shock. that perfusion was assessed during the urgent initial examination. Better
After sufficient time (>2 hours) and severity (>40% loss of intravas- estimates are later obtained using Scv , by thermodilution measure-
cular volume), patients often cannot be resuscitated from hypovolemic ment of cardiac output, and by echocardiographic examination. Right
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shock. This observation highlights the urgency with which patients atrial pressure or CVP is the most easily measured “input” of the whole
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should be resuscitated. Gut and other organ ischemia with systemic release heart and is initially assessed by examination of jugular veins and, after
of inflammatory mediators, a “no-reflow” phenomenon in microvascu- catheter insertion, by direct measurement. Left and right ventricular
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lar beds, and increased diastolic stiffness (see Fig. 33-3) contribute to the dysfunction can be caused by decreased systolic contractility, increased
pathophysiology. 34 diastolic stiffness, greatly increased afterload (including obstruction),
Shock after trauma is a form of hypovolemic shock in which a sig-
nificant systemic inflammatory response, in addition to intravascular valvular dysfunction, or abnormal heart rate and rhythm.
volume depletion, is present. Intravascular volume may be decreased Left Ventricular Failure: Acute or acute-on-chronic left ventricular failure
because of loss of blood and significant redistribution of intravascular resulting in shock is the classic example of cardiogenic shock. Clinical
volume to other compartments, that is, “third spacing.” Release of inflam- findings of low cardiac output and increased left ventricular filling
matory mediators results in pathophysiologic abnormalities resembling pressures include, in addition to assessment of perfusion, pulmonary
septic shock. Cardiac dysfunction may be depressed from direct damage crackles in dependent lung regions, a laterally displaced and diffuse
from myocardial contusion, from increased diastolic stiffness, from right precordial apical impulse, elevated jugular veins, and presence of a third
heart failure, or even from circulating myocardial depressant substances. heart sound. These findings are not always present or unambiguous.
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Shock related to burns similarly is multifactorial with a significant Therefore, echocardiography is helpful and often essential in establish-
component of intravascular hypovolemia and a systemic inflammatory ing the diagnosis. In some cases pulmonary artery catheterization may
response (see Chap. 123). assist in titrating therapy. Cardiogenic shock then is usually associated
Other causes of shock caused by decreased venous return include with a cardiac index lower than 2.2 L/m per minute when the pulmo-
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severe neurologic damage or drug ingestion resulting in hypotension nary artery occlusion pressure has been raised above 18 mm Hg. 37
caused by loss of venous tone. As a result of decreased venous tone,
mean systemic pressure decreases, thereby reducing the pressure gradi- Systolic Dysfunction As a result of a decrease in contractility, the patient pres-
ent driving blood flow back to the heart so that cardiac output and blood ents with elevated left and right ventricular filling pressures and a low
pressure decrease. Obstruction of veins owing to compression, throm- cardiac output. Mixed venous oxygen saturation may be well below 50%
bus formation, or tumor invasion increases the resistance to venous because cardiac output is low. The primary abnormality is that the relation
return and occasionally may result in shock. of end-systolic pressure to volume is shifted down and to the right (see
The principal therapy of hypovolemic shock and other forms of shock Fig. 33-4, upper panel) so that, at the same afterload, the ventricle cannot
caused by decreased venous return is rapid initial fluid resuscitation. eject as far (decreased contractility). It follows that pump function is also
Warmed crystalloid solutions are readily available. Colloid-containing solu- impaired, indicated by a shift down and to the right (see Fig. 33-4, lower
tions result in a more sustained increase in intravascular volume but there panel) so that at similar preloads cardiac output is reduced.
is currently no convincing evidence of benefit. The role of hypertonic Acute myocardial infarction or ischemia is the most common cause of
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saline and other resuscitation solutions is similarly uncertain. Alternatively, left ventricular failure leading to shock. The use of fibrinolytic therapy
transfusion of packed red blood cells increases oxygen-carrying capacity and early angioplasty or surgical revascularization has reduced the inci-
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and expands the intravascular volume and is therefore a doubly useful dence of cardiogenic shock to less than 5%. Infarction greater than 40%
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therapy. In an emergency, initial transfusion often begins with type-specific of the myocardium is often associated with cardiogenic shock ; anterior
blood before a complete cross-match is available. During initial resuscita- infarction is 20 times more likely to lead to shock than is inferior or pos-
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tion, the Early Goal-Directed Therapy protocol suggests that achieving a terior infarction. Details of the diagnosis and management of ischemic
hematocrit greater than 30% may be beneficial when Scv is less than 70%. heart disease are discussed in Chap. 37; other causes of decreased left
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However, after initial resuscitation, maintaining hemoglobin above 90 g/L ventricular contractility in critical illness are discussed in more detail in
(9 g/dL) does not appear to be better than maintaining hemoglobin above Chap. 35, and each may contribute to shock.
70 g/L (7 g/dL). After a large stored red blood cell transfusion, clotting Diastolic Dysfunction Increased left ventricular diastolic chamber stiffness
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factors, platelets, and serum ionized calcium decrease and therefore should contributing to cardiogenic shock occurs acutely during myocardial
be measured and replaced if necessary (see Chap. 89). ischemia, chronically with ventricular hypertrophy, and in a range of
Recognizing inadequate venous return as the primary abnormality of less common disorders (see Table 33-4); all causes of tamponade listed
hypovolemic shock alerts the physician to several commonly encoun- in Table 33-4 need to be considered in a systematic review of causes
tered and potentially lethal complications of therapy. Airway intubation of diastolic dysfunction. 40,41 Stroke volume is decreased by decreased
and mechanical ventilation increase negative intrathoracic pressures to end-diastolic volume caused by increased diastolic chamber stiffness.
positive values and thus raise right atrial pressure. The already low pres- Conditions resulting in increased diastolic stiffness are particularly
sure gradient driving venous return to the heart worsens, resulting in detrimental when systolic contractility is decreased because decreased
marked reduction in cardiac output and blood pressure. However, venti- diastolic stiffness (increased compliance; see Fig. 33-4, upper panel) is
lation treats shock by reducing the work of respiratory muscle, so ventila- normally a compensatory mechanism. Increased diastolic chamber stiff-
tion should be implemented early with adequate volume expansion. ness contributing to hypotension in patients with low cardiac output and
Sedatives and analgesics are often administered at the time of airway high ventricular diastolic pressures is best identified echocardiographi-
intubation, resulting in reduced venous tone because of a direct relaxing cally by small diastolic volumes.
effect on the venous capacitance bed or because of a decrease in circulat- Treatment of increased diastolic stiffness is approached by first con-
ing catecholamines. Thus, the pressure gradient driving venous return sidering the potentially contributing reversible causes. Acute reversible
decreases. Therefore, in the hypovolemic patient, these medications may causes include ischemia and the many causes of tamponade physiol-
markedly reduce cardiac output and blood pressure and should be used ogy listed in Table 33-4. Fluid infusion results in large increases in
with caution and with ongoing volume expansion. diastolic pressure without much increase in diastolic volume. Positive

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