In the past investigators have tried to increase forward blood flow in animal models of shock by using a-receptor blockers such as phentolamine, hydralazine, calcium antagonists, etc., even though amelioration of sympathetic vasoconstriction during hypoperfusion may be associated with maldistribution of blood flow and decreased oxygen extraction. Sometimes vasodilator therapy has been used as an adjunct to the treatment of low-flow shock of cardiogenic, obstructive, or septic origin in humans, in attempts to improve blood flow and tissue oxygenation. The main disadvantage of this treatment is that arterial blood pressure often falls further, even if cardiac output increases, and arterial oxygenation is reduced so that oxygen delivery may not increase. Hence, close monitoring of the hemodynamic and clinical response of an individual patient to the infusion of these drugs is needed to decide on their potential benefit.
Nitroprusside, nitroglycerin, phosphodiesterase inhibitors, and others, together with inotropic drugs, have been used to increase cardiac output during cardiogenic shock or after extensive cardiopulmonary surgery. Vasodilators are more often used to supplement standard therapy than as primary agents. Moreover, nitroprusside, rather than hydralazine, has been propagated as an adjunct for the emergency treatment of pericardial tamponade (before pericardiocentesis can be performed) after completion of fluid loading. Intravenous infusion of nitroglycerin has been studied as therapy for septic shock complicated by a relatively low cardiac output. However, the results of these studies suggest that the increase in cardiac output obtained with these drugs is modest at best.
Vasodilating prostaglandins such as epoprostenol and prostaglandin E . have been used in attempts to increase cardiac output, oxygen delivery, and oxygen uptake by the tissues during septic or traumatic shock, although the effects proved variable. A supply-dependent rise in oxygen uptake with a trial of these drugs may be associated with survival in some studies, but with mortality in others. This may primarily relate to differences in patient populations. A rise in oxygen delivery and uptake may sometimes be accompanied by a rise in oxygen extraction, suggesting improved microcirculatory blood flow with this type of drug (Silverman —— 1990).
Although some studies report favorable oxygenation and survival results with these drugs, others have found unchanged tissue oxygenation and outcome ( Silverman et— 1990). This has limited the widespread use of these drugs.
During reperfusion following ischemia, cells are overloaded with calcium and this is believed to contribute to reperfusion injury. Hence calcium antagonists have been studied in various models of shock and resuscitation for potentially protective effects on organ function. In clinical practice, there is no place for the routine use of calcium antagonists in situations associated with ischemia and reperfusion, even though the (cerebral) outcome of cardiac arrest, an extreme form of ischemia and reperfusion, was shown to be improved by the administration of the calcium antagonist nimodipine during prolonged cardiopulmonary resuscitation. Calcium antagonists are also used in solutions for preservation of organ transplants and in cardioplegic solutions for cardiac surgery. It has been suggested that 'controlled hypotension' decreases blood losses during anesthesia and surgery.
Finally, vasodilators are used in the management of subarachnoid hemorrhage. The aims is to reduce cerebral vasospasms and subsequent ischemic necrosis rather than lower arterial blood pressure, since the latter may adversely affect cerebral perfusion pressure. The drugs most commonly used for this purpose are the calcium antagonists such as nimodipine that can selectively dilate cerebral vessels. Adjunctive treatment with such drugs has been shown to improve neurological status and survival following subarachnoid hemorrhage.
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