Management Of Hypertension

Hypertension results from an intense sympathetic "storm". Increased circulating catecholamines associated with rises in intracranial pressure produce marked hypertension as well as tachycardia and pronounced vasoconstriction. Electrocardiographic and enzyme changes indicative of myocardial ischemia have been documented during this phase. Acute left ventricular failure and pulmonary edema may result. Fortunately this period is usually self-limiting and requires no treatment.

If treatment is considered necessary, use of sodium nitroprusside, an agent with rapid onset and offset of action is recommended. In experimental studies, beta-blockers have also been used to abolish the hypertension seen during brain herniation. In the clinical setting, the short acting beta-blocker esmolol (Brevibloc) can be considered. The negative inotropic effects of esmolol are short-lived due to its short half-life and rapid disappearance from the circulation when the infusion is discontinued. A loading dose of 500 mg/kg over 1 minute is followed by an infusion of 50 mg/kg to the desired endpoint or 350 mg/kg.

Perfusion of the abdominal organs may suffer as a result of myocardial damage and low cardiac output during this phase. Poor cardiovascular function despite supportive therapy may preclude liver and pancreas recovery leading to wastage of abdominal organs. In this situation, rapid and timely transfer of the organ donor to the operating room, oftentimes without complete serological information allows procurement of the kidneys. Ultimately, cardiovascular collapse transforms a previous "heart-beating" donor into a potential "non-heart beating donor". To maximize organ retrieval all programs should have in place a protocol for the non-heart beating donor.

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