Patients with elevated blood pressure (BP) in the intensive care unit (ICU) present with either a BP that threatens to cause imminent target organ damage (TOD) to vascular beds or a transient, usually more benign elevation in BP without threat of TOD.

Most organ beds can regulate the amount of blood flow they receive over a wide range of systemic pressures by autoregulation: OBF = OPPr/OVR, where OBF is organ blood flow, OPPr is organ perfusion pressure, and OVR is organ vascular resistance [11]. Small arteries and arterioles constrict or dilate in response to local myogenic effectors acting on the endothelium that respond to transmural (perfusion) pressure gradients. A decrease in OPPr leads to vasodilation; an increase in OPPr leads to vasoconstriction and limits pressure-induced damage when systemic pressure rises. The cerebral circulation can maintain perfusion with changes in MAP from about 60 to 150 mm Hg [11]. When MAP exceeds the usual autoregulatory range, breakthrough or loss of autoregulation occurs.

Sustained BP greater than the usual autoregulatory range leads to damage of the endothelial lining of capillaries and arterioles, resulting in leakage of plasma into the vascular wall. Fibrin deposition reduces lumen diameters and precipitates local edema and sclerosis. In patients with chronic hypertension, the loss of autoregulation typically occurs only at extremely elevated BPs, whereas in patients without any significant hypertension, in whom the protective autoregulation has not developed, edema and the consequent organ-specific symptoms can be seen with DBPs greater than 100 mm Hg [12].

When OPPr falls to lesser than the lower limits of autoregulation, organ ischemia and infarction may occur. Limits of critical perfusion pressure and tolerance to variation in OPPr vary among individuals. The elderly or patients with chronic hypertension tolerate an elevated MAP because of an upward shift in their cerebral autoregulation curve but have a diminished tolerance to hypotension with vessel functional and structural changes [12]. Patients without antecedent hypertension may develop a hypertensive crisis with acute conditions such as acute vasculitis, subarachnoid hemorrhage (SAH), unstable angina, or eclampsia at lower systemic BP.

Cerebral circulation is the most sensitive vascular bed to breakthrough and ischemia [13]. Cardiac perfusion tolerates a more pronounced drop in BP, even with underlying atherosclerotic disease, because myocardial oxygen demands decrease dramatically when pressures decrease. In organ beds such as the kidneys with antecedent atherosclerotic, acute BP changes are less tolerated and may worsen renal perfusion [4,5].

In most patients with hypertensive crises, the pathophysiologic abnormality is an increase in systemic vascular resistance (SVR), not an increased cardiac output (CO) (MAP = CO × SVR). The increase in SVR elevates BP, overrides local autoregulation, and leads to organ ischemia.

In the ICU, therapy must often begin before a comprehensive patient evaluation is completed. A systematic approach offers the opportunity to be expeditious and inclusive (Table 37.2).

A brief history and physical examination should assess the degree of TOD and rule out obvious secondary causes of hypertension. The history should include prior hypertension, other significant medical disease, medication use, compliance, recreational drugs use, and, most importantly, symptoms from TOD to neurologic, cardiac, or renal systems. Examination should verify BP readings in both arms, supine and standing, if possible and eliminate the rare but important finding of pseudohypertension due to extensive arterial calcification using Osler’s maneuver, which is performed by inflating the BP cuff to greater than the brachial systolic BP. A palpable radial or brachial artery, despite being pulseless, signifies a significantly stiff artery and the likely overestimation of the true BP [14]. Intra-arterial monitoring may be necessary to verify readings and monitor treatment. Also include direct ophthalmologic examination looking for hemorrhages, exudates, or papilledema; auscultation of the lungs and heart; and evaluation of the abdomen for masses or bruits and the peripheral pulses for bruits, masses, or deficits. Signs of neurologic ischemia include altered
mental status, headaches, nausea, and vomiting in addition to focal neurologic deficits. Ancillary evaluation should include electrolytes, blood urea nitrogen and creatinine, complete blood cell count with differential, or echocardiogram (ECG), chest radiograph, and assessment of recent urine output. As the patient’s condition stabilizes, further evaluation of unexplored reasons for the hypertensive crisis can be considered and pursued.

Most studies of hypertensive emergencies are either nonrandomized or suffer from (a) tremendous variation and inconsistency in definitions and cutoffs, (b) absence of important and long-term outcomes such as mortality, (c) being underpowered with wide confidence intervals, and (d) inconsistent reporting of adverse effects. Thus, treatment recommendations for hypertensive emergencies are not based on a large body of randomized controlled studies. One systematic review of hypertensive urgencies and emergencies studies found no evidence supporting any one agent over another. For hypertensive emergencies, nitroprusside, captopril, and clonidine were acceptable choices. For urgencies, a number of agents were used and effective [16]. A systematic review for the Cochrane collaboration, which included more recent studies, again failed to detect any specific agent or strategy that was superior to another. There was well-documented efficacy for BP reduction with nitrates (including nitroprusside), angiotensin-converting enzyme (ACE) inhibitors, diuretics, α-adrenergic antagonist, calcium channel blockers, and dopamine agonists [17]. Given this lack of data to guide therapy, how should we proceed?

The intensity of intervention must be determined by the clinical situation. In many situations, intubation, seizure control, hemodynamic monitoring, and maintenance of urine output can be as important as control of BP. Initial therapy should terminate ongoing TOD, not return BP to normal. Because cerebral circulation is the most sensitive to ischemia, the lower limit of cerebral autoregulation for each patient determines the initial goal. This floor is approximately 25% lesser than the initial MAP or a DBP in the range of 100 to 110 mm Hg [11]. Reasonable initial therapy is to decrease MAP by 25% with an agent that decreases SVR, considering the medical history, initiating events, and ongoing TOD [5]. Patients with acute left ventricular failure, myocardial ischemia, or aortic dissection require more aggressive treatment [18,19,20].

The decision to use oral or parenteral therapy depends on several factors. Atherosclerotic disease puts the patient at higher risk if therapy overshoots the mark. The answers to the questions in Table 37.3 guides the decision of parenteral versus oral therapy. Table 37.4 lists recommendations and precautions for therapeutic agents, and Table 37.5 lists proper dosing for each agent.

Once the patient is stable, additional diagnostic studies may proceed. An oral regimen can be started as the situation stabilizes. Because the ICU is an artificial environment, physicians should avoid attempts to normalize BP especially if large doses of medications are required. Further fine-tuning of BP to levels suggested by Joint National Committee VII [6] or the European Society of Hypertension/European Society of Cardiology guidelines for the management of hypertension [21] should occur once the patient resumes his or her usual diet, activity, and compliance at home.