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CHAPTER 33: Shock 259

Therefore, volume resuscitation must be judicious and is enabled by pressure, and organ system perfusion. Therefore, the goal of therapy is
repeat echocardiographic examination, specifically examining septal to accomplish this decompression as rapidly and safely as possible under
position and motion. ultrasound guidance. In patients who are hemodynamically stable, fluid
Early recognition of right versus left ventricular infarction as the infusion is a temporizing therapy that increases mean systemic pressure
cause of shock is important so potentially dangerous therapy, including so that venous return increases even though right atrial pressure is high.
systemic vasodilators, morphine, and β-blockers, are avoided. Right Excessive volume resuscitation worsens shock, as discussed above.
ventricular infarction is found in approximately half of inferior myo-
cardial infarctions and is complicated by shock only 10% to 20% of the ■ HIGH CARDIAC OUTPUT HYPOTENSION—SEPTIC SHOCK
time. Isolated right ventricular infarction with shock is uncommon Septic shock is the most common example of shock that may be
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and has a mortality rate ~50% comparable to left ventricular infarction caused primarily by reduced arterial vascular tone and reactivity, often
shock. Pulmonary crackles are classically absent. Therapy includes associated with abnormal distribution of blood flow. Septic shock
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infusion of dobutamine and volume expansion, although excessive accompanies severe infection from a wide variety of gram-positive,
volume can aggravate shock by shifting the intraventricular septum gram-negative, fungal, and viral pathogens and is a consequence of
from right to left. Because bradyarrhythmias are common and atrio- the endogenous inflammatory response induced by these pathogens.
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ventricular conduction is frequently abnormal, atrioventricular sequen- Induction of a similar endogenous inflammatory response by noninfec-
tial pacing may preserve right ventricular synchrony and often improves tious tissue injury (eg, pancreatitis, trauma) results in the same shock
cardiac output and blood pressure in shock caused by right ventricular state, now called distributive shock. Noninfectious distributive shock is,
infarction. Afterload reduction using balloon counterpulsation may by virtually all measures, the same as septic shock. Classical septic shock
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also be useful, as are early fibrinolytic therapy and angioplasty when is characterized by increased cardiac output with low SVR hypotension,
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indicated (see Chap. 37). manifested by a high pulse pressure, warm extremities, good nail bed
Pulmonary artery hypertension may contribute to right ventricu- capillary filling, and low diastolic and mean blood pressures. However,
lar ischemia, with or without coronary artery disease. In shock states septic shock is often initially associated with loss of intravascular volume
systemic arterial pressure is often low, and right ventricular afterload and therefore presents with combined hypovolemic and septic shock.
(pulmonary artery pressure) may be high owing to emboli, hypoxemic pul- Additional accompanying clues to a systemic inflammatory response
monary vasoconstriction, acidemic pulmonary vasoconstriction, sepsis, are an abnormal temperature and white blood cell count and differential
or ARDS. Therefore, right ventricular perfusion pressure is low leading and an evident site of sepsis.
to right ventricular ischemia and decreased contractility, which, in the Several pathophysiologic mechanisms contribute to inadequate organ
face of normal or high right ventricular afterload, results in right ven- system perfusion in septic shock. There may be abnormal distribution
tricular dilation with right-to-left septal shift. of blood flow at the organ system level, within individual organs, and
Approaches to right heart failure include verifying that pulmonary even at the capillary bed level. The result is inadequate oxygen delivery
emboli are present and initiating therapy with anticoagulation, fibrino- in some tissue beds.
lytic agents for submassive pulmonary embolism or shock, or surgical The cardiovascular abnormalities of septic shock (see Fig. 33-4) are
embolectomy as necessary. Pulmonary vasodilator therapy may be extensive and include systolic and diastolic abnormalities of the heart,
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useful in some patients if pulmonary artery pressures can be lowered abnormal arterial tone, decreased venous tone, and abnormal distribution
without significantly lowering systemic arterial pressures. Inhaled nitric of capillary flow leading to regions of tissue hypoxia. In addition, there
oxide, inhaled prostacyclins, sildenafil, and many other agents have may be a cellular defect in metabolism so that even cells exposed to
been variably successful. Measurements of pulmonary artery pressure, adequate oxygen delivery may not maintain normal aerobic metabo-
systemic pressure, cardiac output, and oxygen delivery before and after lism. Depressed systolic contractility illustrated as a rightward shift of
a trial of a specific potential pulmonary vasodilator are essential (see the end-systolic pressure-volume relation in Figure 33-5, upper panel,
Chap. 38). Hypoxic pulmonary vasoconstriction may be reduced by occurs in septic shock due to the systemic inflammatory response and
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improving alveolar and mixed venous oxygenation. More aggressive cor- an induced intramyocardial inflammatory response. Decreased sys-
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rection of acidemia should be considered in this setting. Adequate right tolic contractility associated with septic shock is reversible over 5 to 10
ventricular perfusion pressure is maintained by ensuring that aortic days as the patient recovers. Systolic and diastolic dysfunctions during
pressure exceeds pulmonary artery pressure.
sepsis that progress to the point that high cardiac output (hyperdynamic
Compression of the Heart by Surrounding Structures Compression of the heart circulation) is no longer maintained (normal or low cardiac output is
(cardiac tamponade) limits diastolic filling and can result in shock observed) are associated with poor outcome. 46
with inadequate cardiac output despite very high right atrial pressures. Decreased arterial resistance is almost always observed in septic
Diagnosis of cardiac tamponade can be made physiologically by using shock. Early in septic shock, a high cardiac output state exists with
pulmonary artery catheterization to demonstrate a low cardiac output normal or low blood pressure. The low arterial resistance is associated
in addition to elevated and approximately equal right atrial, right ven- with impaired arterial and precapillary autoregulation and may be due
tricular diastolic, pulmonary artery diastolic, and pulmonary artery to increased endothelial nitric oxide production and opening of potas-
occlusion pressures (particularly their waveforms). The diagnosis is sium adenosine triphosphate channels on vascular smooth muscle cells.
often best confirmed anatomically by using echocardiographic exami- Redistribution of blood flow to low-resistance, short time–constant
nation to demonstrate pericardial fluid, diastolic collapse of the atria vascular beds (such as skeletal muscle) results in decreased resistance to
and right ventricle, and right-to-left septal shift during inspiration. venous return, as illustrated in Figure 33-5 (lower panel) by a steeper
Septal shift during inspiration and increased afterload that accompany venous return curve. As a result, cardiac output may be increased even
decreased intrathoracic pressure during inspiration account for the when cardiac function is decreased (see Fig. 33-5, lower panel) because
clinically observed pulsus paradoxus. Although pericardial tampon- of decreased contractility (see Fig. 33-5, upper panel). Hypovolemia,
ade by accumulation of pericardial fluid is the most common cause of caused by redistribution of fluid out of the intravascular compartment
cardiac tamponade, other structures surrounding the heart may also and to decreased venous tone, can limit venous return during inad-
produce tamponade. Tension pneumothorax, massive pleural effusion, equately resuscitated septic shock.
pneumopericardium (rarely), and greatly elevated abdominal pressures Early institution of appropriate antibiotic therapy and surgical drain-
may also impair diastolic filling. age of abscesses or excision of devitalized and infected tissue is central to
Decreasing the pressure of the tamponading chamber by needle drain- successful therapy. Many anticytokine and anti-inflammatory therapies
age or surgical decompression of the pericardium, pleural space, and and inhibition of nitric oxide production have not been successful in
peritoneum can rapidly and dramatically improve venous return, blood improving outcome.

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