Hypertensive crisis is a life-threatening situation caused by acute elevation of blood pressure. The rise in blood pressure is very rapid and thus overwhelms protective adaptive mechanisms in the arterioles which occur under physiological conditions. Endothelial damage results. Focal vessel wall ischemia, inappropriate constriction and dilatation of arterioles, and increase in vascular permeability develop and cause functional disturbances of the heart, central nervous system or kidneys. Without immediate treatment, irreversible organ damage results due to ischemia and hemorrhage. The goal of therapy is to lower blood pressure by 25% within one hour. Blood pressure should be maintained at this level for 24 hours. Thereafter, blood pressure may be reduced by an additional 25% or to 180/100 mm Hg. Initial reduction in blood pressure by 55% may provoke irreversible end organ ischemia and infarction although blood pressure still may be well above the normal range. Most frequently, hypertensive crisis is treated with sodium nitroprusside as it allows controlled reduction in blood pressure due to its very rapid onset but short duration of action. Cyanide toxicity may develop in patients treated with high doses of sodium nitroprusside or with renal or kidney failure. Other agents used may have disadvantages such as unpredictable antihypertensive effects (calcium channel blockers, angiotensin converting enzyme inhibitor [ACEI]), tachycardia (calcium channel blockers, phentolamine, dihydralazine) or reduced renal blood flow (betablocker, ACEI).