SHOCK



Shock is acute severe circulatory failure. Re­gardless of etiology, shock is associated with marked reduction of blood flow to vital organs, and therefore profound arterial hypotension, im­paired mentation, and diminished urinary output usually occur. The common denominator of all four broad categories of shock (Table 3-8) is even­tual cellular damage and death. Shock may be di­vided into three stages. The first is a stage of “com­pensated hypotension”; that is, the fall in cardiac output or in delivery of cardiac output to the tis­sues stimulates a variety of compensatory mech­anisms that alter myocardial function and pe­ripheral resistance to maintain circulation to vital organs such as the brain and the heart. The clin­ical symptoms during this stage are minimal. In stage 2, the compensatory mechanisms for dealing with the low delivery of nutrients to the body are overwhelmed and tissue perfusion is decreased. Early signs of cerebral, renal, and myocardial in­sufficiency and of excessive sympathetic dis­charge are present. In stage 3, severe ischemia oc­curs along with damage to tissues by toxins, antigen-antibody reactions, or complement acti­vation. Especially prone to damage are the cap­illary endothelia in the kidneys, the liver, and the lungs. Ischemic damage to the gastrointestinal tract allows invasion by bacteria. Renal ischemia may lead to acute renal insufficiency. Damage to capillary endothelia throughout the body allows transudation of fluid and protein into the extra­cellular space, exacerbating hypotension. The severe acidosis and toxins released into the blood contribute to further myocardial depression.
The etiology of hypoperfusion is evident in car­diogenic and hypovolemic shock. Septic shock is most commonly caused by gram-negative bacte­rial infections but can occur with infections by other agents. The mechanism of shock appears to be related to the release of an endotoxin (part of the bacterial cell wall) that interacts with sub­stances from the blood and causes increased vas­cular permeability, intravascular coagulation, depression of myocardial contractility, and other adverse reactions. It is manifest by an abnormality in the distribution of blood flow to the tissues; that is, arteriovenous shunting of blood occurs and causes decreased delivery of nutrients to tis­sues despite an increase in cardiac output early in the course of the disease. Increased capillary permeability from the toxic products of infection allows fluid to leak into the interstitium, leaving the intravascular space relatively hypovolemic. Therefore, septic shock often involves the thera­peutic paradox of needing to administer large quantities of fluid to a patient who is massively edematous in order to maintain adequate filling pressures. The only definitive therapy for this syndrome is control of the infection, but tempor­izing therapy includes maintaining intravascular volume via fluid administration, often directed by hemodynamic monitoring. One must remember that myocardial dysfunction may be prominent in stage 3 of septic shock. “Leaky” pulmonary cap­illaries can cause pulmonary edema without my­ocardial dysfunction (noncardiogenic pulmonary edema or adult respiratory distress syndrome] in which left ventricular filling pressures are normal or low (see Chapter 22).
Signs and symptoms of shock are summarized in Table 3-9 and its management in Table 3-10. Invasive hemodynamic monitoring is often re­quired. Measurement of central venous pressure is sufficient in patients with known hypovolemic shock and good myocardial function; however, in patients with cardiac and lung disease, the central venous pressure may reflect poorly left ventric­ular filling pressures, and SwanGanz catheteri­zation to measure pulmonary arterial and pul­monary capillary wedge pressures should be used in the more critically ill patients.





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