Postural Hypotension (Orthostatic Hypotension)

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Postural Hypotension is a symptom, not a condition.

This is colloquially known as a ‘head rush’ or ‘dizzy spell’, and is unsteadiness or LOC on standing from lying in those with inadequate vasomotor reflexes. It is defined as a fall in systolic BP of 20mmHg+ or a fall of diastolic BP by 10mmHg+ when an individual assumes a standing position.

 

Those at risk include:

  • The elderly
  • Those with autonomic neuropathy
  • Those on antihypertensive medications
  • Overdiuresis
  • Multi-system atrophy (MSA)

Postural hypotension is an important cause of falls and faints in the elderly.

 

Physiology

  • The symptom of orthostatic hypotension results from the gravity-induced pooling of blood in the lower extremities following a change in posture.
  • This pooling of blood compromises venous return, thus lowering cardiac output and subsequent arterial pressure.
  • This ultimately leads to insufficient perfusion of the upper body with blood.
  • In health, the blood pressure does not fall very much upon standing because the baroreceptor reflexis triggered.
  • This process is mediated by the autonomic nervous system. Carotid sinus baroreceptors are innervated by CN IX and the aortic arch baroreceptors are innervated by CN X.
  • Baroreceptors are stretch-sensitive mechanoreceptors. High blood pressure causes distension of blood vessel walls, which stimulates the baroreceptors to fire action potentials at a faster rate. This leads to inhibition of the sympathetic nervous system and activation of the parasympathetic nervous system.
  • In contrast, when blood pressure falls, blood vessel walls are less distended; this is recognised by the baroreceptors which stimulate sympathetic activation and parasympathetic inhibition, thereby triggering vasoconstriction and an increase in heart rate in order to elevate the blood pressure, press blood up into the body again, and avoid the ‘dizzy spells’ we have mentioned.
  • Secondary factors which cause a greater than normal fall in blood pressure are often responsible for orthostatic hypotension; factors such as hypovolaemia, sepsis, systemic vasodilatation or diuretics mean that the sudden change in blood pressure cannot be compensated for by the reflex.
  • Avoiding orthostatic hypotension relies on being able to maintain an adequate blood supply, which relies upon a heart strong enough to pump, arteries and veins which are able to constrict when necessary, and having enough blood and fluid within the vessels. Interruption in any of these can thus lead to problems.

 

Aetiology

  • Hypovolaemia:
    • Dehydration (vomiting, diarrhoea, fever, heat stroke)
    • Blood loss
    • Excessive use of diuretics
    • Vasodilators
    • Prolonged bed rest
    • Anaemia
  • Disease:
    • Addison’s disease
    • Atherosclerosis
    • Autonomic neuropathy
    • Diabetes (peripheral neuropathy may affect the autonomic nervous system and thereby interfere with the baroreceptor reflex)
    • Phaeochromocytoma
    • Parkinson’s disease
    • Heart disease
    • Hypopituitarism (low ACTH)
  • Medication:
    • Beta blockers (block the beta-adrenergic receptors in the body and prevent the heart rate from increasing, the heart from contracting as forcefully as is possible, and the dilatation of blood vessels)
    • Sildenafil (Viagra – works by dilating blood vessels and its effects are magnified if taken in conjunction with nitrites, so beware in patients with Angina!)
    • Tricyclic antidepressants
    • Monoamine oxidase inhibitors

Clinical Features

Upon moving from a sitting or lying to a standing position:

  • Lightheadedness
  • Weakness
  • Blurred vision
  • Syncope/LOC
  • Distortion in hearing
  • Seizures

 

These are the consequences of inadequate cerebral perfusion as a result of the blood pressure being too low. This may lead to a vasovagal episode to be stimulated, otherwise known as vasovagal/ neurocardiogenic syncope.

Vasovagal Syncope

  • Emotion, pain, fear, or standing for too long can stimulate reflex bradycardia +/- peripheral vasodilatation.
  • Excess activation of the parasympathetic system causes the heart rate to slow and blood vessels to dilate.
  • Onset is over seconds, and is preceded by nausea, pallor, sweating and closing in of visual fields (a phenomenon known as ‘pre-syncope’).
  • Patients may lose consciousness for ~2mins. This, as well as symptoms of dizziness occur due to the lowering of blood pressure and decrease of blood flow to the brain.
  • The vagus nerve that causes this response may also in some cases be triggered by micturition (especially in men) or by severe straining with constipation.
  • Brief clonic jerking of the limbs may occur (reflex anoxic convulsion due to cerebral hypoperfusion) but there is no stiffening or tonic àclonic sequence, and it can thereby be distinguished from a typical epileptic seizure of that nature.
  • Post-ictal recovery is rapid.

 

Diagnosis of Orthostatic Hypotension

  • Ensure patient has been lying down for at least 5 mins and is relaxed
  • Explain procedure and obtain consent
  • Take sitting or lying blood pressure with the arm supported at heart level, e.g. on a pillow
  • Leave the cuff in place and ask patient to stand
  • Allow the patient to stand for three minutes
  • Ensure their arm is once more supported at heart level and repeat blood pressure
  • Record results

 

Diagnose orthostatic hypotension if there is a drop in systolic BP of >20mmHg or a drop in diastolic BP of >10mmHg after standing for 3 minutes vs lying down.

Management

Conservative:

  • Lie down if feeling faint
  • Stand slowly (with escape route, e.g. a chair to fall back on)
  • Consider referral to a ‘falls clinic’
  • Manage any autonomic neuropathy
  • Increased water and salt ingestion can help
  • Physical measures such as leg crossing, squatting, elastic abdominal binders/stockings (must check dorsalis pedis pulse is present) and careful exercise may help
  • If prost-prandial dizziness, eat little and often and reduce carbohydrate and alcohol intake
  • Head-up tilt of the bed at night increases renin release, so decreases fluid loss and increases standing blood pressure

 

Medical:

  • Fludrocortisone (retians fluid). Monitor weight and beware if CCF or low albumin: oedema worsens.
  • Sympathomimetics e.g. midodrine or ephedrine. Can give pyridostigmine if detrusor under-activity too.

References

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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