http://surgerybook.net/

the precipitating event for the other. The hallmarks of the hemodynamic and neuroendocrine response

to systemic hypoperfusion from other causes are also typical of cardiogenic shock. Eliciting a history of

pre-existing cardiac disease, and physical findings such as pulmonary rales, cardiac murmurs, an S3

gallop, and jugular venous distention may be helpful. An electrocardiogram may detect significant

ischemia or other pathology. A chest radiograph may reveal bilateral pulmonary infiltrates typical of

cardiogenic edema, and cardio-specific serum tests (troponin I and creatine phosphokinase [CPK]) may

indicate myocardial damage.

Manifestations of cardiogenic shock develop as a consequence of failure of peripheral perfusion, the

associated adrenergic response, and the inability of the heart to accommodate blood returning from the

lungs and the periphery. In the absence of sepsis or tissue injury, however, there is not usually an

associated increase in the metabolic needs of the peripheral tissues. Sympathetic-mediated constriction

of the peripheral vasculature attempts to maintain central blood pressure and perfusion of cerebral and

coronary circulations. The clinical findings of cardiogenic shock may thus be similar to those of

hypovolemic shock because both involve induction of the adrenosympathetic response.

Table 9-2 Classification System and Causes of Shock

Diminished or ineffective contractile activity of the right or left side of the heart allows blood to

accumulate in the respective venous circulations. Shock from an acute left ventricular myocardial infarct

269

http://surgerybook.net/

occurs when more than 40% of the left ventricle is involved and may be present in approximately 20%

of Q-wave infarcts.30 Shock from an acute right ventricular myocardial infarct, on the other hand, is

rare and only occurs in approximately 10% of all inferior wall infarcts.31 Not only does the diagnosis of

each infarct vary, but also the treatment and support vary significantly.

Table 9-3 Hemodynamic Patterns in Shock

In any patient in shock, especially in those with compromised cardiac function, consideration should

be given to the institution of mechanical ventilation. The work of breathing can be considerable,

especially for the patient in a state of agitation or distress. Oxygen needs are decreased through

intubation and mechanical ventilation. In this manner, the patient can be comfortably sedated with a

secure airway; the work of breathing is undertaken by the ventilator, and gas exchange can be

optimized. If there is a tenuous balance between myocardial oxygen needs and availability, the balance

can thus be shifted in the patient’s favor.

Like other forms of shock, cardiogenic shock tends to be self-perpetuating. Myocardial perfusion

depends on the pressure gradient between the coronary artery and the left ventricle and the duration of

diastole. Both are compromised by the hypotension and tachycardia that characterizes this condition.

High-volume fluid resuscitation, sometimes necessary for treatment of other forms of shock, is poorly

tolerated and likely to be detrimental to an individual with the compromised myocardial function of

cardiogenic shock.

Extracardiac Obstructive Shock

4 A subset of patients with cardiogenic shock do not have intrinsic cardiac disease but have pump

failure due to extrinsic compression that limits diastolic filling and cardiac output. Cardiac tamponade,

tension pneumothorax, diaphragmatic herniation of abdominal viscera, mediastinal hematoma, and,

occasionally, positive-pressure mechanical ventilation may all precipitate cardiogenic shock by exerting

constricting pressure on the myocardium. The key to diagnosis and appropriate therapy is the physical

examination, supplemented by use of appropriate diagnostic modalities.

The classic physical findings of cardiac tamponade, Beck triad, are hypotension, muffled heart sounds,

and jugular venous distention. Unfortunately, these nonspecific clinical findings are seldom present

together. Elevated jugular venous pressure, noted by either physical examination or measurement of

CVP, although not specific for cardiac compression, is usually present. Pulsus paradoxus can be useful

for the diagnosis of cardiac tamponade. Although it may be caused by other conditions, it is virtually

always present in patients with tamponade.

Given the difficulty in evaluation of these patients, especially in combination with other shock states,

early diagnostic evaluation, both invasive and noninvasive, of cardiac function is warranted. Recent

guidelines suggest that any patient with concern for primary or secondary cardiac dysfunction should

undergo early ultrasound evaluation. This early evaluation not only evaluates the primary cardiac

function but also can lead to the early diagnosis and management of secondary causes of cardiac

dysfunction including cardiac tamponade and pulmonary embolism.

Table 9-4 Classification of Hemorrhagic Shock

270