Antihypertensives
in the ICU
Severe acute hypertension (defined as systolic
arterial pressure >180 mmHg and/or diastolic arterial pressure >110 mmHg) can result in end-organ damage and worse outcomes for patients in the intensive care unit.
Organ dysfunction seen with persistently elevated blood pressures include:
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Cardiovascular
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Acute Coronary Syndrome​
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Heart failure and pulmonary edema
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Aortic dissection
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Neurologic
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Stroke or Transient Ischemic Attack (TIA)​
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Acute encephalopathy
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Cerebral edema
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Retinal hemorrhage
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Renal
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Acute Renal Failure​
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To add to the complexity of management, there are a plethora of antihypertensive agents to choose from. Each agent is directed to the underlying contributing factors to the patient's hypertensive episode. Additionally, if the patient is in the surgical intensive care setting, there are likely other clinical factors related to their admitting diagnosis that will need to be taken into account, prior to choosing an antihypertensive strategy. A examples are patients with severe traumatic brain injuries, who will need tight management of their blood pressure to maintain acceptable cerebral perfusion pressures or management of hypertension s/p cardiac surgery when the myocardium is more vulnerable / irritable after bypass. It is for these reasons that a thorough history and physical exam is needed prior to choosing an intervention for hypertension in the surgical intensive care setting.
Antihypertensive Strategies

Salgado et al. Annals of Intensive Care 2013, 3:17
Mechanisms of Action
Beta-blockers: Block beta-1 receptors. Inhibit the effect of catecholamines on the heart. Heart rate decreases as does the force of contraction (contractility).
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Centrally acting agents: (e.g. clonidine) - suppress sympathetic stimuli outflow from the brain. Decreased catecholamines = decreased heart rate and contractility.
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Calcium Channel blockers: Inhibit the influx of calcium into smooth muscle cells of the vessel walls. Prevent contraction of vascular smooth muscle, resulting in vasodilation.
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Direct vasodilators: (e.g. hydralazine) - directly relax the vascular smooth muscles, causing vasodilation.
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Alpha-blockade: Block alpha-1 receptors on vascular smooth muscle, these block norepinephrine and epinephrine from causing vasoconstriction.
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ACE inhibitors: Block angiotensin-converting enzyme, reducing angiotensin II production and increases bradykinin, leading to vasodilation.
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Diuretics: reduce intravascular volume by diuresis. Usually an increased amount of sodium is excreted and water follows, thus decreasing the overall blood volume.
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Loop diuretics: work in the thick ascending limb of the loop of Henle
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Thiazide diuretics: Inhibit Na+ transport in the distal tubule.
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