Diagnosis and treatment of supine hypertension in autonomic failure patients with orthostatic hypotension

Abstract

Orthostatic hypotension is seen in various medical conditions. It can be secondary to medications or volume depletion. It can also be due to autonomic neuropathy secondary to other diseases, such as diabetes mellitus, or to primary degenerative processes of the autonomic nervous system. Orthostatic hypotension dominates the clinical picture of patients suffering from autonomic failure. Paradoxically, about one half of these patients also suffer from supine hypertension, which induces pressure natriuresis, worsening orthostatic hypotension. It also complicates the treatment of orthostatic hypotension. Supine hypertension is mediated by an increase in peripheral vascular resistance. This is due to residual sympathetic tone in patients with multiple system atrophy (Shy-Drager syndrome), but the cause is not known in patients with pure autonomic failure, who have increased vascular resistance despite very low levels or plasma norepinephrine and renin activity. The recent observation that patients with supine hypertension develop left ventricular hypertrophy suggests they should be treated. During the day, avoiding the supine position is often all that is required. Short-acting vasodilators (e.g., transdermal nitroglycerin) can be used during the night.

(c)2002 Le Jacq Communications, Inc.

Figures

Figure 1

Beat‐to‐beat finger blood pressure (FBP) and heart rate (HR) recording in a patient with pure autonomic failure. The blood pressure (BP) values were determined with a brachial BP cuff. One small box indicates a 7‐second interval. In the supine position, BP readings were in the hypertensive range. Respiratory sinus arrhythmia was almost completely abolished. When the patient stood up, BP decreased profoundly. There was no adequate compensatory increase in HR. In the first few minutes, the patient did not experience orthostatic symptoms despite the profound hypotension. After several minutes of standing, a further slight decrease in BP occurred. This decrease in BP exceeded the autoregulatory capacity of the brain, and the patient became severely symptomatic and had to sit. bpm=beats per minute

Figure 2

Frequency distribution of supine systolic (SBP, upper panel) and diastolic (DBP, lower panel) blood pressure in 117 primary autonomic failure patients. Patients were studied off medications and in sodium balance on a controlled diet containing 150 mEq/d sodium.

Figure 3

Diurnal variation in urine volume, creatinine clearance (Ccrea), and sodium excretion (Na+/crea) in patients with severe autonomic failure due to multiple‐system atrophy (MSA) and pure autonomic failure (PAF) (day: 8 a.m. to 8 p.m.; night: 8 p.m. to 8 a.m.). Ccrea was similar during the day and during the night. The urine volume and urinary sodium excretion were approximately two‐fold greater during the night than during the day. *p<0.05; **p<0.01

Figure 4

Average decrease in systolic blood pressure (δSBP) produced by 1 mg/min of the ganglionic blocker trimethaphan in patients with multiple‐system atrophy (MSA) and pure autonomic failure (PAF)

Figure 5

Change in systolic blood pressure (δSBP) with placebo and nitroglycerin patch (NTG) (left panel) or nifedipine (right panel) in autonomic failure patients. The medication was given at 8 p.m. (0 hours on the graph). The horizontal bar on the left panel indicates the time the patch remained on the skin. Compared to placebo, the maximal decreases in SBP were 36±10 mm Hg and 37 ±9 mm Hg 4 hours after the patch was applied or nifedipine was given, respectively. Supine SBP at 8 a.m., 2 hours after the nitroglycerin patch was removed, was similar with nitroglycerin and placebo. In contrast, the depressor effect of nifedipine was sustained throughout the observation period.

Figure 6

Comparison of the depressor effects produced by a standardized meal (Meal, 414 calories; n=16), transdermal nitroglycerin (NTG, 0.025–0.1 mg/hr; n=7), minoxidil (Minox, 2.5 mg p.o.; n=5), and hydralazine (Hydr, 50 mg p.o.; n=7). The maximal decrease in systolic blood pressure (?SBP) is presented in the y axis. Placb=placebo