Clinica Cayanga Medical Resources

• Syncope
  Presentation
  Sequelae of syncope
  Incidence and mortality
  Differential diagnosis
• Palpitation

There are many other causes of repeated episodic events, often described by the patient as ‘blackouts'. The history is vital here and, apart from epilepsy, an important diagnosis to consider is hyperventilation in Da Costa's syndrome comprising the triad or left submammary stabbing pain, palpitation, and worrying awareness of breathing.

Electrical disturbances of cardiac function cause syncope either by reduction of the mechanical efficiency of the heart, or by complete interruption of cardiac activity due to asystole complicating atrioventricular block. Ventricular tachyarrhythmia, most commonly seen in coronary heart disease, can also cause syncope. Technical faults in pacing systems can result in asystole, due to sudden complete lack of pacing or, occasionally, very rapid pacing may occur. Inappropriate choice of pacing mode, mostly ventricular, may be associated with retrograde conduction to the atria causing them to contract during ventricular systole with regurgitation of blood into pulmonary veins. This has the effect of ventricular under filling and resultant low cardiac output known as pacemaker syndrome.

The neuroendocrine causes of syncope largely comprise
 1. cardioinhibition
 2. vasodepression.

Vasovagal syncope- is the most frequent and in many ways the best understood. Upright posture is an almost invariable feature, leading critically to the pooling of 500–1000 ml of blood in the lower limbs and to reduction in central blood volume. Susceptible people show higher than normal plasma concentrations of adrenaline and vasopressin prior to the attack. These cause vigorous left ventricular contraction and sensitization of left ventricular baroreceptors, respectively. Reduced cardiac filling on standing then triggers the sensitized baroreceptors to manifest a reflex that is appropriate in left ventricular dilatation—bradycardia and vasodilatation. In the context of low central blood volume this reflex is disastrous for the maintenance of blood pressure. In addition to the increased sensitivity of left ventricular baroreceptors, there is some evidence in sufferers of recurrent vasovagal attacks of an abnormal positive gain in the reflex at brainstem level. In the autonomic neuropathies the mechanism is different and results from a failure of the normal adaptations to the erect posture.

Presentation
True syncope is of sudden onset and brief duration, typically lasting less than 1 min. When it has been caused by structural cardiac or vascular causes, other symptoms may emerge; for instance in obstructive cardiac disease (classically aortic stenosis) it tends to occur on exertion. When the cause is a bradyarrhythmia, and in some of the neuroendocrine disturbances, sudden loss of consciousness tends to be devoid of warning, whereas, syncope due to tachyarrythmia is often heralded by palpitation and the vasovagal syndrome typically is preceded by tiredness, yawning, air hunger, boredom, nausea, and occasionally palpitation, which lead to dizziness and a rather gradual greying into syncope. Only a minority of vasovagal sufferers, usually older patients, give no history of prodrome.

Observers report striking pallor in syncope and often wonder if the patient is dead. Cyanosis supervenes in the second half of the first minute. There may be epileptiform movements and incontinence of urine (but rarely faeces). Recovery from cardiac causes is associated with a bright flush; episodes that are due to neuroendocrine causes do not end with a flush because of the longer time course of vasodepression.

Sequelae of syncope
Syncopal attacks may result in injury. They are also occasionally followed by a transient neurological defect which may lead to diagnosis of a transient ischaemic attack but unconsciousness is rarely associated with transient ischaemic attacks. The cause of neurological sequelae may be either systemic embolism from the left atrium in sinoatrial node disease or focal cerebrovascular disease giving a more persistent and severe perfusion defect than that experienced by the brain overall.

Incidence and mortality
It has been estimated that as many as 30 per cent of the population experience at least one episode in a lifetime and perhaps every individual is capable of fainting given unfavourable circumstances. More than 1 per cent of all emergency room attendance is reported to have been for syncope. The most common cause of these is vasovagal syncope, but in some 50 per cent of cases the cause remains undiagnosed. Unexplained syncope carries a much better prognosis for survival than cardiac syncope; one series has given the respective mortalities as 6 versus 30 per cent. Recurrent syncope, despite investigation and treatment of a probable cause, seems to carry an appreciable mortality and justifies detailed investigation including tilt testing and cardiac electrophysiological studies with ventricular extrastimulation to reveal a tendency to ventricular tachyarrhythmias.

Differential diagnosis
A challenge to the clinician is separation of syncope and epilepsy The value of the history from patient and observer cannot be overstated. The type or lack of warning, the sequence and timing of colour changes, the timing of convulsions and incontinence, the type of injury, the speed of recovery and the existence of pre-ictal amnesia are most important.