Circulatory failure, or the inability of the heart to provide sufficient cardiac output to sat­isfy tissue metabolic requirements, is the most important and most common cause of altered pharmacokinetics during cardiac emergencies. Circulatory failure may result from decreased myocardial contractility, arrhythmias that allow insufficient time for diastolic filling or impair atrioventricular synchrony, circulatory stresses such as increased afterload or hypovolaemia, valvular dysfunction, tamponade, or a variety of less common insults.

Regardless of the aetiology, circulatory fail­ure elicits characteristic compensatory haemodynamic adjustments, mediated in large part by activation of the sympathetic nervous system [Peniel & Benowitz 1984; Benowitz & Meister 1978]. Enhanced sympathetic tone in­creases cardiac contractility and peripheral vas­cular resistance, both of which serve to main­tain arterial blood pressure. The increase in peripheral vascular resistance, however, is not uniform among different vascular beds.

Organs with high metabolic requirements such as the heart and brain exhibit autoregulation; despite sympathetic stimulation, the vessels in these or­gans remain relatively vasodilated as a result of the local effects of hypoxia, lactic acid or other products of anaerobic metabolism that accu­mulate when organ perfusion is reduced. Blood flow to the heart and brain tends to be pre­served, while vasoconstriction decreases blood flow in other organs such as the skin, muscles, and splanchnic organs.

Pathophysiology of Cardiopulmonary Resuscitation (CPR)

Cardiac output during cardiopulmonary resuscitation (CPR) is severely compromised; in humans the mean arterial pressure is less than 50% of normal (Chandra et al. 1981; McDonald 1981), and cardiac output in dogs is less than 30% of normal (Vorhees et al. 1980). Haemodynamic measurements are difficult to obtain in patients during CPR, but animal data suggest that changes in blood flow distribution are qualitatively similar to those observed with circulatory failure and spontaneous circulation.

Blood flow during CPR in anaesthetised, electrically fibrillated dogs is reduced to all organs, but is least reduced to the brain and next least to the heart (Vorhees et al. 1980). For the purpose of pharmacokinetic considerations, CPR and circulatory failure with spontaneous circulation can be considered to be similar, in that total cardiac output is reduced and the pattern of blood redistribution during promptly initiated CPR resembles that seen in circulatory failure.

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