Vital signs are vital: Focus on blood pressure

In the words of the renowned 19th-century German physician Johannes Müller, Stephen Hales' discovery of blood pressure was “more important than the discovery of blood.” Indeed, nearly 300 years after Hales wrote essays about his blood pressure experiments, hypertension is now the number one attributable risk for mortality throughout the world, according to the World Health Organization.

With every 20 mm Hg increase in systolic or 10 mm Hg increase in diastolic blood pressure, there is a doubling risk of mortality from both ischemic heart disease and stroke, the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) has reported. Happily, antihypertensive therapy reduces the incidence of stroke by 35% to 40%, myocardial infarction by 20% to 25%, and heart failure by 50%. It is therefore imperative that internists promptly recognize and correctly handle the various hypertensive situations that can present on an inpatient service.

The following 3 case-based scenarios offer some common and unusual presentations of hypertension in hospitalized patients.

Case 1

A 55-year-old obese man with a history of dyslipidemia, impaired fasting glucose and alcohol abuse is on his third day of hospitalization for treatment of chronic lower back pain refractory to oral therapy. His nurse alerts the on-call physician that the patient's blood pressure over the past 12 hours has been elevated (approximately 160/90 mm Hg). The physician reviews the patient's chart from his outpatient visits for the past year. He was seen on 3 separate occasions with his primary care physician, and the averages of 5 measurements on 2 separate occasions were 150/89 mm Hg and 155/92 mm Hg, respectively.

The initial step is to ensure that the patient's reported blood pressure readings are accurate. Blood pressure measurements should be obtained in both arms with an appropriate-size cuff and the bladder cuff covering 80% of the arm. Once the readings are verified, the hospitalist must consider secondary causes of hypertension. For instance, this patient's elevated readings could be secondary to nonsteroidal anti-inflammatory medications for back pain, alcohol abuse or withdrawal, poorly controlled back pain, or untreated sleep apnea.

Assuming these concerns have been addressed and dismissed, the hospitalist can conclude the patient meets the American Heart Association criteria for stage I hypertension. This is defined by the JNC 7 as an elevated blood pressure measured by an average of 2 or more seated blood pressure measurements at two or more office visits. The previous Joint National Committee guidelines defined optimal blood pressure as less than 120/90 mm Hg, pre-hypertension as 120-139/80-89 mm Hg, stage I hypertension as 140-159/90-99 mm Hg and stage II hypertension as 160-179/100-109 mm Hg.

However, the recently released JNC 8 guidelines did not define hypertension but set treatment thresholds at 150/90 mm Hg or greater in adults over age 60 without chronic kidney disease or diabetes mellitus, 140/90 mm Hg in adults over age 60 with chronic kidney disease or diabetes mellitus and 140/90 mm Hg in adults less than the age of 60 regardless of comorbidities.

The hospitalist should recommend lifestyle modifications before pharmacotherapy. The PREMIER trial noted that if the following 5 lifestyle modifications were implemented, the prevalence of hypertension and use of antihypertensive drugs were reduced:

• Weight loss (0.5 to 2 mm Hg drop in blood pressure per every 1 kg lost)
• Dietary sodium restriction to no more than 100 mmol daily
• Aerobic exercise for “most” days of the week
• Limitation of no more than 1 oz of ethanol in men and 0.5 oz of ethanol in women daily
• Vitamin D supplementation in patients with low or low-normal values.

If lifestyle modifications fail, ALLHAT demonstrated that diuretics are “unsurpassed in preventing cardiovascular complications of hypertension” and are well tolerated. Other agents may be useful in specific scenarios, as detailed in the JNC guidelines. These recommendations should be noted in the patient's dismissal summary for his or her primary care physician to further act upon in the ambulatory setting.

Case 2

A 36-year-old pregnant woman in her 29th week of gestation is hospitalized by her obstetrician to the general medical service for elevated blood pressure. Her current reading is 175/100 mm Hg. She had previously reported mild headaches (which have since resolved). She is otherwise asymptomatic. Serum complete blood count and electrolyte panel are unremarkable and her urine protein is 0.1 g/24 hours.

As with any case of severe hypertension, the hospitalist must first ascertain if there is any sign of end-organ damage and ask the patient about chest pain, headache or confusion. In this case, the patient is symptom-free. For pregnant patients in particular, the hospitalist should next obtain serum and urine studies to further evaluate for signs of end-organ damage or preeclampsia such as proteinuria (0.3 g or more in a 24-hour sample), acute kidney injury (creatinine greater than 1.5 mg/dL), hepatocellular injury (ALT greater than 2 times the upper limit of normal) and thrombocytopenia (<100,000/L). This patient's serologic studies are negative, and the urinalysis does not meet criteria for preeclampsia.

The hospitalist then must consider if this patient should be treated and if so, what is the safest yet most effective agent for her and her fetus. The American Congress of Obstetricians and Gynecologists has recommended initiating treatment for hypertension in the pregnant patient for systolic blood pressure greater than 160 mm Hg or diastolic blood pressure greater than 105 mm Hg. A 2007 Cochrane Database meta-analysis has revealed that treatment of mild-moderate hypertension (stage I hypertension) does not improve either maternal or fetal outcome. If the patient is diagnosed with stage II hypertension or greater, then pharmacologic therapy is indicated. Possible agents to consider are methyldopa, clonidine or labetalol. Labetalol, unlike other beta-blockers, does not decrease uteroplacental flow to a considerable extent and has been shown in randomized trials to be both safe and efficacious. Methyldopa and clonidine can also be considered. Hydralazine has been used in some instances but there is a risk of reflex tachycardia and hypotension. Unless the patient has been on chronic diuretic therapy, initiation of a diuretic is discouraged due to concerns for intravascular depletion. Angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers are contraindicated due to evidence of both fetal cardiac and renal malformations. Nitroprusside can be used in emergent situations but only for a brief period of time given concern for fetal cyanide poisoning.

Case 3

An 87-year-old man with Parkinson's disease and hypertension who takes amlodipine, 5 mg/d, is admitted for recurrent falls. His blood pressure seated is 137/76 mm Hg with a heart rate of 65 beats per minute (bpm), while upon standing his blood pressure is 105/65 mm Hg with a heart rate of 96 bpm. This change in vital signs is accompanied by presyncope. The initial plan is to discontinue his amlodipine, but then it is discovered that the patient's supine blood pressure readings during the night shift were 185/110 mm Hg.

The clinical scenario of supine hypertension and orthostatic hypotension (SH-OH) is often seen in patients with autonomic failure. The proposed pathophysiologic mechanism is impairment of noradrenergic neurotransmitters, which impedes arterial vasoconstriction and the compensatory increased chronotropy during postural change.

The diagnosis of SH-OH is often elusive in the clinical setting given that blood pressure readings are typically obtained with the patient seated. Studies have demonstrated that more than half of patients with orthostatic hypotension have supine hypertension. The diagnosis can be made bedside by measuring the patient's blood pressure after he or she has been supine for 5-10 minutes and then after he or she has stood motionless for 3-5 minutes with the arm positioned at heart level. If bedside orthostatic examination is negative but suspicion remains high, further evaluation with tilt-table testing is warranted.

Once the diagnosis is made, initial treatment measures include avoiding sudden postural change, large meals, lying supine during the day, and sleeping at an incline (in order to impede nocturnal natriuresis). Other options include application of an abdominal binder and lower-extremity compression stockings. Peripheral vasodilators, such as the amlodipine in this scenario, should be stopped. Alternative pharmacotherapy agents include transdermal nitroglycerin in the evenings or beta-blockers, which have been noted to improve the postural reflux that exacerbates orthostasis.

Conclusion

We have reviewed the appropriate means by which to measure blood pressure, diagnose hypertension and identify exacerbating factors. Understanding these tasks and both nonpharmacologic therapy and pharmacologic therapy is essential for the internist approaching the hospitalized patient with hypertension.