INITIAL TREATMENT OF SHOCK
Cardiovascular failure, or shock, can be caused by (1) depletion of intravascular volume, (2) compression of the heart or great veins, (3) intrinsic failure of the heart itself or failure arising from excessive hindrance to ventricular ejection, (4) loss of autonomic control of the vasculature, (5) severe untreated systemic inflammation, and (6) severe but partially compensated systemic inflammation. If the shock is decompensated, the mean arterial pressure or the cardiac output (more precisely, the product of the pressure and output) will be inadequate for peripheral perfusion; in compensated shock, perfusion will be adequate but at the expense of excessive demands on the heart. Depending on the type and severity of cardiovascular failure and on response to treatment, shock can go on to compromise other organ systems. This chapter discusses the cardiovascular and pulmonary disorders associated with shock.
Hypovolemic shock (shock caused by inadequate circulating blood volume) is most often caused by bleeding but may also be a consequence of protracted vomiting or diarrhea, sequestration of fluid in the gut lumen (eg, bowel obstruction), or loss of plasma into injured or burned tissues. Regardless of the etiology, the compensatory responses, mediated primarily by the adrenergic nervous system, are the same: (1) constriction of the venules and small veins in the skin, fat, skeletal muscle, and viscera with displacement of blood from the peripheral capacitance vessels to the heart; (2) constriction of arterioles in the skin, skeletal muscle, gut, pancreas, spleen, and liver (but not the brain or heart); (3) improved cardiac performance through an increase in heart rate and contractility; and (4) increased sodium and water reabsorption through the renin–angiotensin–aldosterone axis as well as vasopressin release. The result is improved cardiac filling, increased cardiac output (both directly by the increase in contractility and indirectly through increased end-diastolic volumes), and increased blood flow to organs with no or limited tolerance for ischemia (brain and heart).
The symptoms and signs of hypovolemic shock are many and can be caused either by the inadequate blood volume or by the compensatory responses. Some signs manifest themselves early, in mild forms of shock. Some present late and only in severe forms of shock. The goal is to recognize the early signs to prevent morbidity and mortality.
The most sensitive of the early signs of hypovolemic shock is diminished blood flow to the skin and subcutaneous tissues. This can be noted on casual assessment by noting difficulty with peripheral intravenous (IV) access or skin coolness, but is objectively assessed by documentation of capillary refill. This is best performed in the skin on the plantar surface of the foot, an area without pigmentation, with the color determined solely by the blood contained in the tissues. One begins by compressing the skin over the plantar surface of a toe with intense pressure, followed by milking of the blood ...