American heart journal
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American heart journal · Apr 1986
ReviewIschemia, resuscitation, and reperfusion: mechanisms of tissue injury and prospects for protection.
Since its introduction in 1960, CPR has evolved into a complex program involving not only the medical community but also the lay public. Currently, program activities include instruction of the lay public in basic life support techniques, development and deployment of emergency medical systems, recommendations for drug protocols for advanced cardiac life support and, most recently, introduction of new methods for tissue protection following resuscitation. After 25 years of experience, we are beginning to understand the pathophysiology of tissue ischemia during cardiac arrest and the interventions required to improve chances of survival and quality of life of the cardiac arrest victim. ⋯ A role for calcium antagonists in the treatment of postarrest encephalopathy has been demonstrated in animals and is currently undergoing clinical trials. Iron-dependent lipid peroxidative cell membrane injury may be important in the pathogenesis of postarrest encephalopathy. Animal studies suggest that the iron chelator deferoxamine may have a significant therapeutic role in the treatment of postarrest encephalopathy.
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American heart journal · Sep 1981
ReviewCombined vasodilator and inotropic therapy of heart failure: experimental and clinical concepts.
Vasodilators facilitate ventricular emptying by affording earlier onset of left ventricular (LV) ejection and increased stroke volume with achievement of a reduced end-systolic pressure and volume. Agents with positive inotropic properties increase stroke volume by shifting the end-systolic pressure-volume curve to the left through augmented force and velocity of contraction. With impedence reduction, improvement in pump performance occurs concomitant with reduced cardiac energy requirements (MVO2); positive inotropic agents most circumstances increase MVO2. ⋯ In clinical heart failure, nitroprusside alone lowers LV preload with a modest increase in cardiac output (CO); dopamine markedly increases CO with little fall in LV preload. In combination the two agents achieve the individual beneficial effects of each drug, and cardiac efficiency indices are improved. Thus combined vasodilator and inotropic therapy appears to have a sound physiologic rationale and clinically documented beneficial effect superior to either modality alone.