1. 
   

   What are the major causes of hypertension in hospitalized patients?

   
   
2. 
   

   What are the common hospital-acquired or iatrogenic causes that induce hypertension?

   
   
3. 
   

   What signs and symptoms should be assessed in the initial evaluation of a patient with reported hypertension?

   
   
4. 
   

   When should you lower blood pressure acutely?

   
   
5. 
   

   What are the risks associated with acutely lowering the blood pressure in the hospital?

The lifetime risk for the development of high blood pressure (BP) (systolic BP > 40 mm Hg), is 90%; half of patients age 60–70, and three quarters age 70–80 have hypertension. The prevalence of hypertension in the hospital setting has been reported to range from 50.5% to 72%.

The decision about whether to treat high BP in the hospitalized patient with antihypertensive agents is an important one, but it is not always straightforward. The definition of hypertension, goals for treatment, and benefits of therapy in reduction of cardiovascular morbidity and mortality have been well established in numerous clinical trials and widely disseminated to practicing physicians in evidence-based consensus documents. Unfortunately these goals do not necessarily apply to acutely ill patients. Thus the management of hypertension in the hospitalized patient should be highly individualized. There are few if any prospective trials regarding choice of antihypertensive medications in this setting. Recommendations are generally based on consensus opinion, customary use, extrapolation from animal models, and commonsense application of physiologic principles.

It is crucial not to reflexively order antihypertensive medications in all hospitalized patients with high BP and to recognize precipitating factors that commonly augment BP in the acutely ill and require a different approach. When treatment is initiated, it is important for the clinician to choose appropriate agents and optimal BP targets based on the underlying pathophysiology, acuity of the problem, and target end-organ damage. It is also important to capitalize on the opportunity to modify this traditional cardiovascular risk factor for patients who will likely benefit and thus reduce disparities in health care (Table 89-1).

Management of BP should take into consideration the basic principles:

• BP = cardiac output × vascular resistance.
  
• Cardiac output = heart rate × stroke volume.

The higher the heart rate (assuming no change in stroke volume, blood volume, blood viscosity, or peripheral resistance), the higher the BP. The autonomic nervous system predominantly mediates acute (instantaneous) changes in BP by inducing changes in heart rate, systemic vascular resistance, and venous tone. The feedback loop from mechanoreceptors in the carotid sinuses and aortic arch respond to acute fluctuations in BP, but in chronic essential hypertension, the set point rises, and a higher basal BP is tolerated. The renin-angiotensin-aldosterone system mediates chronic changes over days to weeks via the kidney. Low kidney perfusion, elevated sympathetic response, and other stimuli, common in the hospitalized patient, stimulate the release of renin. Angiotensin II increases both systolic and diastolic BP and signals the adrenal cortex to secrete aldosterone, which in turn increases the reabsorption of sodium from urine, sweat, saliva, and bowel. Catecholamines, especially epinephrine, from the sympathetic nervous system greatly affect BP. Binding of epinephrine to α1 receptors leads to vasoconstriction and increased peripheral vascular resistance, causing BP to rise. Binding to β1 receptors increases heart rate and cardiac output, which also raises BP. See Chapter 252, Hypertensive Urgencies.

A minority of patients may be admitted to the hospital with a primary diagnosis of hypertensive crisis. In a hypertensive emergency, a surge in BP is accompanied by end-organ damage. Hypertensive urgency, however, is an acute elevation in BP without end-organ damage. There is no BP threshold that defines a hypertensive crisis. Most patients have pressures that exceed 180/120 mm Hg, with diastolic BPs over 120 mm Hg being most strongly associated with end-organ damage. However, pregnant patients may develop target end-organ damage at significantly lower readings.

The hypertensive hospitalized patients have usually been admitted for other reasons and are incidentally noted to have hypertension due to monitoring of vital signs. There are many secondary factors that can acutely raise blood pressure in hospitalized patients (Table 89-2). The most common include stopping hypertensive medications because of failure to reconcile outpatient medications on admission, restriction of oral intake, volume expansion (often from crystalloid administration), the postoperative state, pain, anxiety, and withdrawal from alcohol, narcotics, or antianxiety/sedative drugs.

The first step is to determine whether the reported BP reading is a valid measure of intra-arterial BP. Many factors may affect the immediate accuracy of a BP measurement, including the device used (cuff size, leaky bulb, faulty aneroid device), the technique and bias of the examiner (positioning of the patient, placement of the cuff, inappropriately rapid deflation, excess bell pressure), and a noisy environment. Most errors overestimate the BP. In general, it is best to palpate the BP first to avoid underinflation in patients with an auscultatory gap. The BP should be checked in both arms.

Deviations from “normal” BP must be considered in the context of the patient’s chronic BP. A patient’s BP normally varies depending on the time of day, even from minute to minute, and typically decreases during sleep. Arterial monitoring has shown that the -systolic and diastolic BP also varies with the respiratory cycle and with each heartbeat. According to ambulatory BP monitoring, elderly patients are more likely to have wide fluctuations or lability of BP.

Patients with untreated or inadequately treated hypertension are prone to sudden elevations in BP and the development of hypertensive crises. Patients who develop a hypertensive crisis in settings other than chronic essential hypertension may develop end organ damage at lesser degrees of BP elevation, as they lack the vascular smooth muscle hypertrophy that provides some protection against the effects of uncontrolled hypertension. This is especially true for pregnant patients.

The next step is to obtain a history and physical examination along with basic tests (Table 89-3) to determine whether the patient has evidence of a hypertensive emergency and to determine the acuity of this patient’s hypertension and underlying precipitating factors.

Hypertensive emergencies are characterized by severe elevations complicated by evidence of impending or progressive target organ dysfunction. Examples include hypertensive encephalopathy, intracerebral hemorrhage, acute myocardial infarction (MI), acute left ventricular failure with pulmonary edema, unstable angina pectoris, dissecting aortic aneurysm, acute funduscopic changes and eclampsia.