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PatientPlus articles are written for doctors and so the language can be technical. However, some people find that they add depth to the articles found in the other sections of this website which are written for non-medical people.

Hypotension

Blood pressure 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 blood pressure that is much lower than usual, and which may be causing symptoms such as dizziness or lightheadedness. It is often defined as systolic 90/60 mmHg, but 100 mmHg may be more appropriate if the patient normally has hypertension.

A fall of 10-20 mmHg systolic, with increase in heart rate of >15 bpm on change of patient's position, indicates hypovolaemic cause rather than peripheral neuropathy or beta-blocker use.

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.

Other causes include:

  • 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

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

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 declines with age, particularly in hypertensives, who thus display lability in blood pressure, and are particularly prone to postural hypotension, and the effects of drugs.

  • Defined as a large drop in BP (usually >20/10 mmHg) on standing, where normal pooling of the blood in the lower limbs is not corrected for by the cardiovascular system on moving to a vertical position. 1
  • This is usually due to either 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, quinidine, 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 bowl, 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 blackouts (syncope) or fits.
Conditions producing orthostatic hypotension include:

Cardiac

Haematological

  • Pernicious anaemia

Endocrine

Neurological

Other

  • Pregnancy
  • Severe varicose veins
 

Vasovagal faints are often associated with prolonged standing with resultant pooling of venous blood with reduced venous return to the heart. Reduced cerebral perfusion causes loss of consciousness. 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.
Consciousness returns relatively quickly. May be brief period of sweating and pre-syncope symptoms before collapse.
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.2
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

Acute hypotension

  • 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,3 hyoscine, ephedrine or antidepressants.
If fails to respond to drugs, consider inserting pacemaker, especially if tilt-testing shows large bradycardic response.4

Orthostatic (postural) hypotension

  • 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, 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 Na retention. 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, can try propanolol or indomethacin.
  • Physical counterpressure with compression hosiery, or whole-body inflatable suits may be required.

Postprandial hypotension

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


Document References
  1. Merck Manual. Orthostatic Hypotension
  2. 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]
  3. 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]
  4. 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
Acknowledgements EMIS is grateful to Dr Hayley Willacy for writing this article. The final copy has passed scrutiny by the independent Mentor GP reviewing team. ©EMIS 2007.
DocID: 2303
Document Version: 20
DocRef: bgp1493
Last Updated: 13 Apr 2007
Review Date: 12 Apr 2009




















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