Syncope

(Date of publication 19 March 2004)

We are all familiar with the unfortunate Victorian heroine who falls to the ground when confronted by something unexpected and deeply shocking, such as the sight of a naked male chest. However, emotional stress is only one of many different causes of fainting, or syncope.

A brief outline of the clinical picture is given on the American Heart Association site; essentially, syncope consists of a transitory loss of consciousness and posture, usually associated with a temporarily insufficient flow of blood to the brain. According to the British Heart Foundation the condition is surprisingly common, affecting 30% of adults at some point in their lives and accounting for up to 6% of attendances at Accident and Emergency Departments.

Syncope may be neurally-mediated, or a consequence of cardiac arrhythmia or a physical obstruction to bloodflow. The most common type is vasovagal syncope, also known as neurocardiogenic or vasodepressor syncope, when the brain fails to regulate the body’s blood pressure and heart rate adequately. The basic mechanism involved is explained here . People of all ages who are otherwise healthy can be affected by this benign disorder, but it is particularly frequent in young women. Victims are almost always standing and before fainting generally experience a range of symptoms including nausea, sweating, rapid heartbeat and dizziness, which last anywhere from a few seconds to a few minutes. Once fainting occurs, the patient should be allowed to lie down, with legs elevated, until completely recovered.

A Tilt Table Test may be used to ascertain whether vasovagal syncope is responsible for fainting episodes. The patient lies down on a special table with belts and a footrest, an intravenous line is inserted, a sphygmomanometer cuff placed and ECG leads attached. Once the patient has been belted to the table, it is tilted upright to a 60-80° angle for approximately 45 minutes. If the patient faints it is considered pathognomic for vasovagal syncope. The test may be repeated after the injection of a drug that mimics the action of adrenaline, such as isoproterenol. The NASA site has a good photograph of the test in progress.

When vasovagal syncope is brought about by particular circumstances, as in the case of our hapless maiden earlier, it is termed situational syncope . The triggers which may cause fainting are very diverse, ranging from embarrassment to coughing, swallowing cold liquids to urinating. One specific example of situational syncope is carotid sinus syndrome , when fainting may be induced by looking up, turning the head, or even just wearing a tight collar. The explanation is that the carotid sinus, a dilatation of the carotid artery, has pressure detectors which feed information to the vasomotor centre in the brain stem that controls blood pressure and heart rate. If the carotid sinus becomes hypersensitive, mechanical stimulation may cause a pause in the heart beat - see the trace here - or a drop in blood pressure.

The gravitational stress of rising quickly to a standing position causes blood to pool in the legs and trunk, leading to a decrease in venous return and cardiac output, and a fall in blood pressure. In healthy individuals, autonomic reflexes are activated and rapidly normalise the blood pressure by increasing the heart rate. Where this response is impaired, however, cerebral perfusion may be reduced and lead to syncope. The condition is called postural or orthostatic hypotension, and is defined as a decrease of at least 20 mm Hg in systolic blood pressure when moving from a supine to a standing position. The most frequent cause is hypovolaemia, often induced by the excessive use of diuretics. Many other drugs can have a similar effect, as can various neurological disorders, systemic arterial hypertension and decreased receptor responsiveness as a result of ageing. A wealth of clinical information about this disorder is available from the American Academy of Family Physicians .

Syncope may also be caused by an abnormally slow heartbeat, or bradycardia (<60 beats/min). This can occur when the electrical impulses that regulate the heartbeat are disrupted as a result of ageing, cardiac disease or conditions such as hypothyroidism which impair electrical conduction, or by various medications. Electrical events in the heart during bradycardia are covered in detail in this .pdf file from the New England Journal of Medicine - some of the accompanying ECG traces look positively frightening, with pauses in atrial activity of more than 3 seconds! Treatment depends upon the symptoms experienced and underlying cause, but an artificial pacemaker may be required to increase the heart rate.

Paradoxically, the heart beating too quickly (>100 beats/min) may also lead to syncope, because the ventricles have insufficient time to fill with blood and cannot pump effectively, reducing the supply of oxygen to the brain. This is termed tachycardia and its seriousness primarily depends upon the origin of the rapid beat. In ventricular tachycardia the heartbeat is usually regular at between 150 and 200 beats per minute, with a dissociation between atrial and ventricular activity. The condition is dangerous because it may cause shock or cardiorespiratory arrest, and lead to ventricular fibrillation - the number one cause of sudden cardiac death - which is characterised by rapid, irregular and chaotic heartbeats.

Generally less serious is supraventricular tachycardia (SVT), when the increase in heart rate, typically to between 160 and 200 beats per minute, is caused by abnormal activity in the atrium. SVT is frequently seen in people who are physically fatigued, consume large amounts of coffee, use alcohol or smoke heavily. This type of arrhythmia tends to begin and end suddenly. Specific examples include atrial flutter, caused by an aberrant circuit in the right atrium, and atrial fibrillation, the commonest form of rapid heart rhythm found in hospitalised patients, in which the cardiac impulse originates from several abnormal pacemakers in the atria. A brief summary of the mechanisms involved can be found here , but it does require prior knowledge of the electrical conduction system of the heart.

One type of SVT - sinus arrhythmia - is often seen in teenagers and young adults and rarely needs treatment, giving rise to an interesting speculation. Could the delicate sensibilities of the demure Victorian female be explained by a widespread incidence of this condition - or is a more likely explanation the tightly-laced corsets that were de rigeur at the time?

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A Tour around Syncope

A Tour around Syncope