Blood pressure (BP) is a variable with a continuous and unimodal variation. One can only consider normal and abnormal against the circumstances of the individual in question, with regard to age/sex, conditions in which it was measured, and other relevant factors.

Hypotension is therefore a BP that is much lower than usual and which may be causing symptoms such as dizziness or light-headedness. It is often defined as systolic 90/60 mmHg, but 100 mmHg may be more appropriate if the patient normally has hypertension.

Orthostatic (postural) hypotension

This is very common, especially in the elderly due to a number of underlying problems with BP control. The baroreflex mechanisms which control heart rate and vascular resistance decline with age (particularly in hypertensives) who thus display lability in blood pressure. They are particularly prone to postural hypotension, and the effects of drugs.

• It is defined as a drop in BP (usually >20/10 mmHg) within 3 minutes of standing.¹ Normal pooling of the blood in the lower limbs is not corrected for by the cardiovascular system on moving to a vertical position.²
• This is usually due either to a defective autonomic reflex arc, or hypovolaemia that can be the result of blood or fluid loss, diuretic or vasodilator therapy.
• Can also be associated with prolonged bed rest and drugs that affect reflex control of BP, including antidepressants, phenothiazide antipsychotics, levodopa, barbiturates, alcohol and vincristine.

Shy-Drager syndrome (now known as Multiple System Atrophy - MSA) and Bradbury-Eggleston syndrome (now known as Pure Autonomic Failure - PAF), are primary neuropathies that cause severe orthostatic hypotension as a result of widespread damage to the autonomic system:

• The condition is often worse in the morning and after food or exercise.
• It is associated with other signs of parasympathetic failure, e.g. dry mouth and eyes, impotence, loss of sweating and atonic bowel, bladder or stomach.
• In mild to moderate cases the patient presents with some or all of the following: feeling faint or dizzy, light-headedness, confusion and blurred vision.
• In more severe cases there may be a history of syncope or fits.

Acute hypotension

In the acute form it can be a serious clinical feature that may cause renal, cerebral and myocardial hypoxic damage. It is often associated with the different forms of shock including:

• Septic - Gram-negative septicaemia.
• Cardiogenic - following MI.
• Hypovolaemia - blood loss (haemorrhage), plasma loss (burns), dehydration (diarrhoea and/or vomiting), pooling of unavailable fluids (e.g. pancreatitis).
• Anaphylactic - type I IgE-mediated hypersensitivity reaction.
• Neurogenic - caused by trauma to spine or as an adverse effect of an epidural anaesthetic. Also, can result from pain or fear via reflex vagal stimulation.

• Vasodilatation - from antihypertensive drugs, heat exposure.
• Drugs such as: narcotic analgesics, alcohol, some antidepressants and anxiolytics.
• Cardiac dysfunction, e.g. arrhythmia, MI, aortic regurgitation, tamponade.
• Pulmonary embolism.
• Autonomic nervous system failure (systolic down ≥20 mmHg, diastolic down ≥10 mmHg inside 3 minutes of standing without increase in pulse rate).
• Micturition syncope.

Chronic hypotension

Primary acquired disease of the adrenals: Addison's disease (autoimmune adrenal failure). This is perhaps the best remembered cause of hypotension. Systolic BP is rarely >110 mmHg, symptoms of postural hypotension are common, and reactive hypoglycaemia after carbohydrates may masquerade as postprandial hypotension.
Note: secondary adrenal insufficiency does not cause hypotension, as aldosterone production is largely independent of the pituitary.

Vasovagal faints

• These are often associated with prolonged standing with resultant pooling of venous blood with reduced venous return to the heart. May be brief period of sweating and pre-syncope symptoms before collapse. Reduced cerebral perfusion causes loss of consciousness. Consciousness returns relatively quickly.
• When due to pain, emotional stress or site of blood, there is central reflex activation.
• Affects all age groups varying from infrequent attacks with an obvious trigger to frequent episodes with no apparent cause.
• Diagnosis is confirmed by tilt-table testing.

Postprandial hypotension

This is even more common than postural hypotension (30-40% elderly patients in residential homes) and mainly occurs in the elderly and those with autonomic neuropathy:³

• Cause is unclear but is associated with high carbohydrate meals.
• Defined as fall in BP (20 mmHg within 2 hours of a meal but usually occurs much sooner).
• Symptoms are same as those for postural hypotension.

Investigations

First-line investigation should include:

• FBC
• U & E
• Fasting glucose
• Pregnancy test (if patient unsure)
• ECG
• Echocardiogram - if suggested by history suggestive of cardiac problem
• Tilt table testing

Management

Postural hypotension

The key to managing this condition is individually tailored therapy. The goal of treatment is to improve the patient's functional capacity and quality of life, preventing injury, rather than to achieve a target BP.

• The patient (and carers) should be educated about the various factors that affect blood pressure and special aspects that have to be avoided, e.g. foods, habits, positions and drugs.
• Avoid triggers, e.g. high temperature environments.
• Review any medication being taken.
• Advise elderly on standing slowly, dorsiflexing the feet first and even crossing the legs whilst upright.
• Raising the head of the bed, which helps prevent diuresis and supine hypertension caused by fluid shifts.
• Initial intervention is to increase intravascular fluid volume by large daily salt intake, either added to food or as salt tablets:
  • Continue with this until weight increased by 1.3-2.3 kg; then can consider giving fludrocortisone, if necessary, to increase sodium retention. Dose is 0.1- 0.2 mg/day.¹
  • Can precipitate heart failure but peripheral oedema alone should not cause cessation of treatment.
• A morning dose of caffeine as coffee or tablet form can be effective.
• If symptoms still persist consider midodrine:
  • This is a peripherally acting alpha-1-adrenoceptor agonist. It increases BP via vasoconstriction.
  • It is recommended for mono- or combined therapy (with fludrocortisone) at an initial dosage of 2.5 mg orally two to three times daily, increasing gradually up to 10 mg three times daily.¹
  • Supine hypertension is a common (25%) adverse effect and may be severe. The last dose should be administered at least 4 hours before going to sleep and BP should be monitored.
  • Some patients become worse on midodrine and it is contraindicated in heart disease, renal failure, phaeochromocytoma and thyrotoxicosis.
  • Alternatives include dihydroxyphenylserine and octreotide.
• Physical counterpressure with compression hosiery, or whole-body inflatable suits may be required.

Acute hypotension

For detail see Resuscitation in Hypovolaemic Shock record.

• Check airways.
• Give O₂ by mask.
• Place patient head down.
• Administer IV fluids (0.9% saline) having excluded pulmonary oedema.
• Treat underlying cause.

Vasovagal faints

• Symptoms often resolve spontaneously
• Can try α-agonists, β2-blockers, disopyramide,⁴ hyoscine, ephedrine or antidepressants.
• If fails to respond to drugs, consider inserting pacemaker, especially if tilt testing shows large bradycardic response.⁵

Postprandial hypotension

• Patients need to take smaller, more frequent meals containing fewer sugars and starches.
• Lying down after meals needs to be balanced with risk of reflux.

Document references

1. EFNS guidelines on the diagnosis and management of orthostatic hypotension, European Federation of Neurological Societies (2006)
2. Merck Manual. Orthostatic Hypotension
3. O'Donovan D, Feinle C, Tonkin A, et al; Postprandial hypotension in response to duodenal glucose delivery in healthy older subjects. J Physiol. 2002 Apr 15;540(Pt 2):673-9. [abstract]
4. Abe H, Sumiyoshi M, Kohshi K, et al; Effects of orthostatic self-training on head-up tilt testing for the prevention of tilt-induced neurocardiogenic syncope: comparison of pharmacological therapy. Clin Exp Hypertens. 2003 Apr;25(3):191-8. [abstract]
5. Raj SR, Koshman ML, Sheldon RS; Outcome of patients with dual-chamber pacemakers implanted for the prevention of neurally mediated syncope. Am J Cardiol. 2003 Mar 1;91(5):565-9. [abstract]

Internet and further reading

• Current Medical Diagnosis & Treatment 2003. Eds. Tierney LM et al. Lange Medical Books.
• Oxford Handbook of Clinical Medicine, 4th Edition. Hope RA et al. Oxford University Press 1998.
• Oskarsson B, Quan D. Idiopathic Orthostatic Hypotension and other Autonomic Failure Syndromes; December 2006