Orthostatic Hypotension - Clinical Tree

Questions

1 What physiologic responses prevent blood pressure from decreasing acutely when we stand?

After assuming the upright position, gravitational forces shift ∼700 mL of blood volume to the lower part of the body, mostly in the splanchnic vascular circulation. This fluid shift is detected by the baroreceptors in the carotid sinus and aortic arch This information is transmitted through the glossopharyngeal and vagus nerves to the nucleus tractus solitarii (NTS) in the medulla oblongata. These neurochemical stimuli trigger changes within the hypothalamus that upregulate sympathetic activity and downregulate parasympathetic activity of the heart. Subsequently, the heart rate (HR) increases and the vasculature in the peripheral and splanchnic beds constrict to maintain the cardiac output and prevent a decrease in blood pressure. In addition to the autonomic response, the renin-angiotensin-aldosterone system (RAAS) becomes activated, generating angiotensin II as a potent vasoconstrictor. The RAAS response time is delayed compared to sympathetic nervous system activation.

2 What is orthostatic hypotension?

Orthostatic hypotension (OH) describes a sustained reduction in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of 10 mm Hg within 3 minutes of standing or head-up tilt to at least 60 degrees on a tilt table. Such drops in blood pressure often cause dizziness, blurry or tunnel vision, fatigue, dull neck and shoulder pain, and increased fall risk. Symptoms improve when seated or in recumbent position. Importantly, OH is associated with reduced functional capacity and mortality in elderly patients ( Fig. 41.1 ).

Fig. 41.1, Tilt table testing consists of continuous heart rate and blood pressure measurements during 60-degree tilt on an adjustable table. In patients with autonomic failure, blood pressure does not respond to increases in heart rate during tilt. Orthostatic symptoms result.

3 How should blood pressure be measured to diagnose OH?

The most sensitive and precise measurements should be obtained during fasting conditions, early in the morning. Blood pressure and HR measurements should be taken after the patient has been lying supine for at least 5 minutes and twice more after standing at 1 and 3 minutes. If time precludes the acquisition of orthostatic vital signs, blood pressure and HR can be measured in the seated position and after standing. However, these measurements have low sensitivity to detect OH. Concomitant HR changes on standing provide additional information on the cardiovascular autonomic reflexes. Elevations in HR below 10 bpm during OH episodes should raise high suspicion for an autonomic neuropathy, and autonomic testing may be warranted.

4 Describe the most common causes of OH.

The most common cause of OH is polypharmacy. Medications, including alpha-1 blockers such as terazosin, prazosin, and tamsulosin, can predispose the patient to developing OH. In addition, tricyclic antidepressants, overuse of diuretics, and tizanidine (muscle relaxant) can also induce OH. Transient conditions such as dehydration (poor oral intake, vomiting, diarrhea, or blood loss) may also cause OH and are often accompanied by significant orthostatic tachycardia. Less common causes of OH include primary autonomic neuropathies such as pure autonomic failure, multiple system atrophy (MSA), and Parkinson disease. Secondary causes of autonomic neuropathies are diabetes mellitus, amyloidosis and autoimmune autonomic failure, and paraneoplastic syndromes.

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