Simple fainting (Benign Vasovagal Syncope)
Simple fainting, also known as Benign Vasovagal Syncope, is the commonest cause of syncope in all age groups. It occurs most frequently in young adults. It rarely presents for the first time in older people.
Attacks are precipitated by recognised triggers such as fear, severe pain, sight of blood etc.. Prior to losing consciousness the individual often experiences warning symptoms such as lightheadedness, nausea, ringing in the ears, receding and echoing sounds, darkening of vision, sweatiness (hot or cold) and generalised weakness. These symptoms last for several seconds before consciousness is lost (if it is lost). Onlookers will notice extreme pallor, and often sweatiness. The pulse will be very weak and slow.
When sufferers pass out they fall down (unless this is impeded) and, when in this position, effective blood flow to the brain is immediately restored, allowing the person to regain consciousness.
Management is by avoidance of triggers. Should warning symptoms occur, prompt squatting may prevent progression to loss of consciousness.
Injury is unusual following Vasovagal Syncope.
Autonomic Mediated Syncope
Autonomic Mediated Syncope (Vasovagal Syncope, Neurally Mediated Syncope, Neurocardiogenic Syncope, Malignant Vasovagal Syncope) may present for the first time at any age. It often occurs when upright, though can occur when sitting. It rarely occurs when lying. There often are no precipitating circumstances though attacks are more likely to occur in certain situations, for example during a large meal in a warm restaurant, when watching a production in a hot theatre, when flying in an aircraft, or after prolonged standing.
The onset may be abrupt or associated with prodromal fatigue, weakness, nausea, sweating, pallor, visual disturbance, abdominal discomfort, headache, pins-and-needles, lightheadedness or vertigo. Presyncope may last for seconds or minutes. This prodromal phase may be absent in older individuals.
If syncope ensues, the individual usually lies still while unconscious, though occasionally s/he may convulse briefly. (Prolonged convulsions, blue face, or tongue biting at the time of collapse, and prolonged confusion and aching muscles afterwards help distinguish a true primary seizure from one secondary to vasovagal syncope. Sleepiness and urinary incontinence are of less value in making the distinction).
On recovery of consciousness following syncope the person may complain of nausea, clamminess, lightheadedness, headache and malaise and may be unable to stand up for several minutes. Full recovery may take some hours. There is a significant incidence of injury associated with vasovagal syncope. Interestingly, co-existing heart disease is rare.
The exact mechanism of Autonomic Mediated syncope is not completely understood. One popular theory is that syncopal episodes may be due to inappropriate activation of stretch receptors (detectors) in the left ventricle (largest chamber of the heart). Normally, on standing upright about 500-1000 mls of blood is displaced by gravity from the chest to the lower limbs. Most of this change occurs in the first 10 seconds. In addition, with prolonged standing, about 700 ml of plasma leaks out off capillaries. As a consequence of the gravitational pooling and reduction in plasma volume the return of venous blood to the heart is reduced and blood pressure drops. Corrective mechanisms are triggered. The heart begins to beat more rapidly, the heart muscle contracts more vigorously and the blood vessels around the body constrict. These changes help restore the blood pressure to normal.
However, in patients with Autonomic Mediated Syncope it is thought that the vigorous muscle contractions may inappropriately activate over-sensitive stretch receptors in the left ventricular wall.
Normally these receptors are activated only if the pressure in the heart is too high. Activation triggers corrective mechanisms that act to increase vagal tone, thus slowing the heart rate, and reducing sympathetic tone, thus lowering the blood pressure. Unfortunately, in Autonomic Mediated Syncope the blood pressure is already too low and the corrective mechanisms triggered by the stretch receptors simply exacerbate the situation creating a vicious cycle which leads to a dramatic slowing of the heart rate and a precipitous fall in the blood pressure with syncope ensuing. (See Flow diagram)
Although this theory sounds very plausible, there is no hard evidence to support it. In fact, recent evidence appears to refute it. Increasingly it is thought that the problem lies with the control centres in the brain, rather than with the stretch receptors in heart muscle.
Further Information
Patients in the UK have a legal duty to inform the DVLA about any condition likely to affect their ability to drive safely. You can contact the DVLA:
By phone. DVLA drivers’ medical enquiries: Telephone: 0300 790 6806
Monday to Friday, 8am to 5:30pm. Saturday, 8am to 1pm
By email. You can email DVLA to tell them about your driving and medical issues.
By post:
Drivers’ Medical Enquiries
DVLA
Swansea
SA99 1TU
Where the individual concerned is uncertain about the need to contact the DVLA, he/she should seek advice from their GP or relevant specialist or contact the DVLA directly for advice. Failure to notify their insurance company may also affect the validity of his/her insurance. This includes life insurance and health insurance as well as car insurance.
When a patient contacts the DVLA, he/she may be informed that they may continue to drive (Section 88 of the Road Traffic Act) whilst investigations are being undertaken provided they have not been advised to cease doing so by their GP and/or specialist (and have actively sought that opinion) and hold a valid driving license.
The doctor’s duty is to advise his/her patient when they should cease to drive and notify the DVLA. Where the doctor is uncertain he/she should consult “Assessing fitness to drive – a guide for medical professionals.“
Doctors may consult with the DVLA Medical Advisors on an anonymous case basis OR on a named basis with the individual’s permission OR when there is evidence that an individual continues to drive despite being advised that he/she is unfit to do so. The GMC has produced specific guidelines on this aspect.
DVLA guidelines for syncope are constantly updated. The latest guidelines (February 2020) can be found here – see pages 21 – 26.
Orthostatic (postural) hypotension is defined as a drop of 20 mm Hg in systolic blood pressure and 10 mm Hg diastolic blood pressure on standing, associated with typical symptoms.
It is absolutely critical to establish a reproducible supine blood pressure before checking standing blood pressure. Otherwise an incorrect diagnosis may be made. Lying BP should therefore be repeated until a reproducible reading is obtained. Standing BP and heart rate should then be measured immediately on standing, at 1 minute, 2 minutes, 3 minutes and 5 minutes.
Symptoms of orthostatic hypotension may include lightheadedness, darkening of vision, and inability to remain upright. Patients may also complain of so-called Coat Hanger pain. This is caused by reduced oxygen supply to muscles in the neck and shoulder girdle.
Orthostatic hypotension may be caused by:
Volume depletion e.g. by excessive sweating without adequate fluid replacement
Anaemia e.g. because of blood loss
Drugs:
• anti heart failure drugs
• anti hypertensive drugs
• anti Parkinson’s disease drugs
• anti depressant drugs
Autonomic neuropathy
Non-drug treatment of Orthostatic hypotension (With thanks to Professor Chris Mathias, Imperial College London):
Correct:
• hypovolaemia
• anaemia
Avoid:
• drugs likely to lower blood pressure
• standing up quickly
• straining at stool
• hot baths
• large meals – especially refined carbohydrate rich food
• excessive alcohol
• prolonged standing
• severe exertion
Introduce:
• Head-up sleeping – raise the head of the bed by 10º
• small frequent meals
• increased salt intake
• judicious exercise
• counter physical manoeuvres
Consider:
• Compression stockings
• abdominal binders
• anti-gravity suit if very symptomatic and all else fails
• oral water ingestion – 400 mls significantly increases BP in autonomic failure
Drug treatment of Orthostatic hypotension:
Volume expanders:
Fludrocortisone – low dose, starting with 50 mcg note increasing the dose gradually every six weeks to a maximum of 200 mcg or 300 mcg note if required
Flurbiprofen – a Non Steriodal Anti Inflammatory Drug may be used in conjunction with Fludrocortisone to enhance fluid retention
Adrenoreceptor agonists:
Midodrine – post-ganglionic alpha agonist.
Ephedrine – beta agonist. Use with care tds with last dose early evening
Specific targeting:
Octreotide – for post-prandial hypotension
Desmopressin – with Fludrocortisone if nocturnal polyuria
Erythropoietin – for refractory anaemia in renal failure
For more information on Syncope please do not hesitate to get in touch with Dr Deering through our appointments page.
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