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INTRODUCTION

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Perioperative hypertension can increase afterload and decrease left ventricular systolic function. Poorly controlled blood pressure can also result in increased bleeding and increased risk of cerebral and myocardial ischemia. For these reasons, intravenous vasodilator therapy is necessary to manage hypertension caused by increased systemic vascular resistance.

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Vasodilator drugs reduce the contraction of vascular smooth muscle cells through two general mechanisms, both of which reduce intracellular calcium concentrations. One, vasodilator drugs modulate the sympathetic nervous system by either decreasing the central sympathetic activity or by blocking peripheral adrenergic receptors. Two, they can also directly relax vascular smooth muscle. The magnitude of systemic blood pressure decrease by vasodilator therapy depends on preload, myocardial contractility, and compensatory reflexes.

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Systemic vasodilators, whether arterial or venous, have a number of potential physiologic side effects. Decreases in systemic vascular resistance and mean arterial pressure activate the baroreceptor reflex leading to tachycardia. To blunt this response, vasodilators are often administered concurrently with beta adrenergic receptor antagonists. Inhibition of hypoxic pulmonary vasoconstriction may cause hypoxemia in patients with underlying pulmonary disease or receiving one-lung ventilation. Coexisting pulmonary hypertension combined with systemic vasodilation may shunt blood through a patent foramen ovale and cause arterial hypoxemia. Dosing of vasodilators should be carefully titrated. Short-acting agents are preferable. Hypotension due to vasodilation may be aggravated by concurrent intraoperative hypovolemia or sympathectomy from regional anesthesia.

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DRUGS THAT BLUNT SYMPATHETIC NERVOUS SYSTEM ACTIVITY

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Alpha Adrenergic Receptor Antagonists

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Nonselective alpha adrenergic antagonists are most often used to manage hypertensive crises, such as that associated with pheochromocytomas. Blockade of the alpha-2 adrenergic receptor prevents increases in intracellular calcium, which then enables vascular smooth muscle relaxation in both arterioles and venules. Phentolamine is a reversible competitive antagonist of both alpha-1 and alpha-2 adrenergic receptors. Unlike phentolamine, which is given in IV form only, phenoxybenzamine is an oral alpha adrenergic antagonist used to manage pheochromocytoma-induced hypertension prior to resection. It has an elimination half-life of 18-24 hours. The vasodilation may cause reflex tachycardia, orthostatic hypotension, and nasal congestion.

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Alpha-2 Adrenergic Receptor Agonists

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Activation of presynaptic alpha-2 adrenergic receptors in the locus coeruleus results in decreased sympathetic outflow. The mechanisms include inhibition of adenylate cyclase, reduction in cyclic adenosine monophosphate (cAMP) levels, decreased intracellular calcium concentrations, and cellular hyperpolarization. Lower levels of catecholamines such as norepinephrine lead to peripheral arterial vasodilation. Parasympathetic, or vagal, activity predominates.

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Clonidine is a nonselective alpha adrenergic receptor agonist which is given orally and transdermally to manage preoperative hypertension. It preferentially binds to alpha-2 receptors but can still activate alpha-1 receptors. In contrast, dexmedetomidine is a much more selective alpha-2 agonist (1600:1) than clonidine, leading to a profound decrease in plasma catecholamines. It is an intravenous drug that has an elimination half-life of 1.5 hours and a more rapid onset (<5 minutes). Dexmedetomidine is used as a sedative-hypnotic, not an antihypertensive, although its sympatholytic properties may be helpful to reduce peripheral vascular resistance.

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DRUGS THAT RELAX VASCULAR ...

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