First aid: Syncope

In the fourth part of our series, Samena Chaudhry and Magnus Harrison explain the management of syncope

Many of us will have fainted or seen someone else faint - in medicine, this is called syncope. Syncope is defined as a transient loss of consciousness associated with a decrease in cerebral blood flow.¹ Differentiating true syncope from other "non-syncopal" conditions causing a loss of consciousness is important because the mechanisms of syncope range from nearly normal (physiological) to abnormal and life threatening.

In syncope, bradycardia (a slow heart rate), hypotension, and a weak thready pulse are common. Unconsciousness results in muscular relaxation and may cause the tongue to fall into the oropharynx, obstructing or partially obstructing the airway - this itself is life threatening.² Although many causes of syncope exist, we will briefly focus on the commonest causes seen in the emergency department.

Presyncope

Presyncope is the period of time when inadequate cerebral circulation and the resulting lack of nutrition and oxygen start to take effect. Early manifestations include pale skin colour that may be cool and moist ("a cold sweat"). Some people say they feel bad, or that everything is going dark just before losing consciousness. By recognising presyncope, you can prevent a person from falling.

Causes of syncope

The causes of syncope can be grouped into cardiac and non-cardiac causes (box 1). Cardiac syncope is associated with increased mortality and may lead to sudden death. Syncope affects 30% of adults at some point in their lives and is a common problem in people presenting at emergency departments.¹ One reason postulated for syncope being so common reflects our incomplete evolutionary adaptation to the upright body position as standing upright requires blood pressure regulation to drive blood against gravity up to the head.³

Vasovagal syncope

In young people, neurocardiogenic (vasovagal) syncope is the most common form. The vagus nerve transmits afferent signals from the aortic arch baroreceptors, regulating arterial pressure. Increases in arterial flow stimulate the vagus nerve, inhibiting sympathetic drive and decreasing blood pressure. When someone stands in an upright position, blood pools in the lower limbs and activates the autonomic cycle. The resulting increase in sympathetic nervous activity causes vasoconstriction (narrowing of vessels), increased heart rate, and maintains the blood pressure.

DAVID PARKER/SPL
Tilt test

But in vasovagal syncope, vasodilatation and bradycardia occur rather than the appropriate physiological responses of vasoconstriction and tachycardia (fig 1). Researchers have offered several explanations for this. One is that there is an excessive pooling of blood in the veins in the lower limbs because of abnormalities in them. Another explanation is that a central nervous system abnormality leads to abnormal regulation of venous tone.^{4 5}

Vasovagal syncope may be triggered in certain situations (situational syncope). These include passing urine, coughing, defecation, or swallowing and in circumstances which would often induce fainting, for example, standing, fasting, having an injection, visiting the dentist, and drinking excess alcohol.

It is thought that the triggering event stimulates adrenergic tone, followed by vagal overactivation and then sympathetic withdrawal. In the case of the emotionally induced vasovagal faint, cortical areas of the brain trigger the afferent pathways in the reflex arc, resulting in increased sympathetic nervous system stimulation. This is then followed by the presyncopal phase characterised by epigastric discomfort, dizziness or vertigo, and nausea. These prodromal symptoms are induced by the increased parasympathetic tone. They may last from less than one second to several minutes. These events proceed to syncope unless the person lies down or removes the triggering stimulus.³

Carotid sinus hypersensitivity

One specific example of situational syncope is carotid sinus syndrome or hypersensitivity (CSH) when fainting may be induced by looking up, turning the head, or even just wearing a tight collar. In CSH, mechanical deformation of the carotid sinus (located at the bifurcation of the common carotid artery) leads to an exaggerated response with bradycardia or vasodilatation, resulting in syncope.^{3 4}

There are two types of CSH. In the more common cardioinhibitory type, the heart rate decreases resulting in sinus bradycardia or asystole. In vasodepressor CSH, the contractility of the muscular blood vessel walls (vasomotor tone) decreases without a change in heart rate. This results in a drop in blood pressure because of a change in the balance of parasympathetic and sympathetic effects on peripheral blood vessels.^{4 5}

One way of seeing if CSH is the cause of syncope is by manually massaging the carotid sinus while taking an electrocardiogram, but this should only be done by an experienced doctor in controlled conditions. In the cardioinhibitory CSH, asystole lasting more than three seconds may occur. In vasodepressor CSH, the systolic blood pressure may drop more than 50 mm Hg without a decrease in the heart rate.

You should talk to patients about their condition and advise them not to massage their neck or wear shirts with tight collars or wash the front of the neck vigorously. However, some people with reoccurring attacks may benefit from a pacemaker.⁶

Orthostatic hypotension

Orthostatic hypotension is not a specific disease but is due to abnormal blood pressure regulation triggered by different things. The gravitational stress of rising quickly to a standing position causes blood to pool in the legs and trunk. This in turn leads to a decrease in venous return and cardiac output, and a fall in blood pressure. In healthy people, autonomic reflexes are activated and rapidly normalise the blood pressure by increasing the heart rate. When 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 common cause is hypovolaemia, often induced by the excessive use of diuretics.⁶

Cardiac syncope

Cardiac syncope results from inadequate effective cardiac output and may reflect serious underlying structural heart disease. A cardiac cause for syncope is a major risk of sudden death and mortality.³ There are two major types of cardiac syncope: electrical (arrhythmias) or mechanical (obstructive).

Obstructive cardiac lesions

Several heart disorders can result in an obstruction of blood flow through the heart. The obstruction impedes cardiac output resulting in ineffective blood pressure, which in turn results in cerebral ischaemia. Causes include obstructed heart valves (aortic stenosis and mitral stenosis are the most common examples); obstructed blood vessels (such as a massive pulmonary embolus); and cardiac tumours. Obstruction to blood flow from the left ventricle - for example, aortic stenosis - classically brings about syncope on exertion. If this occurs, the person needs urgent valve replacement.

Cardiac arrhythmias

Rhythm disturbances are among the most common and potentially hazardous causes of syncope and dizziness. Syncope from arrhythmia most commonly results from ventricular tachycardia, which accounts for 11% of all cases of syncope.³

There are two major categories of life threatening, syncope inducing cardiac arrhythmias: bradycardias and tachycardias. In normal supine people, ventricular rates as slow as 35-40 beats/min and fast rates not exceeding 180 beats/min usually do not compromise cerebral blood flow. Pulse rates outside these limits, however, may impair cerebral circulation and function. Tachycardias do this by compromising heart filling time and bradycardias by causing a low cardiac output (cardiac output=heart rate ¥ stroke volume).

Bradyarrhythmia and heart block

Although bradyarrhythmias occur at all ages, they are most common in elderly people and are usually due to ischemia or fibrosis of the conduction system.³ First degree block occasionally occurs in people who have no heart disease, in which case no treatment is necessary. Second degree heart block, such as Mobitz type I (or Wenckebach block), may involve a gradually lengthened delay in conduction through each heart beat. Mobitz type II block is when there is an occasional delay in conduction. This may affect the pulse rate and may cause symptoms of fainting or dizziness.

Complete or third degree heart block due to complete absence of conduction through the atrioventricular node results in a very slow heart rate, between only 25-30 beats a minute. The person may faint or collapse as a result, which may also be referred to as Stoke Adams attack. Digitalis, beta blockers, calcium channel blockers, and other drugs may also cause bradyarrhythmias. These can be treated effectively by inserting a cardiac pacemaker.

Tachycardias

Tachycardias can be divided into ventricular tachycardias (VT) and supraventricular tachycardias (SVTs). SVTs comprise abnormal heart rhythms either originating in the atria or due to an aberrant pathway connecting the atrium and ventricle leading to a short circuit in the heart. With rare exceptions, SVT does not cause syncope nor does it cause sudden death. The most common exception to this rule is in patients with Wolff-Parkinson-White syndrome, in which SVT may rarely degenerate into the much more dangerous ventricular tachycardia.⁵ Wolff-Parkinson-White is a very rare cause of sudden death resulting from an additional electrical connection between the atria and the ventricles. In most people, it does not cause any symptoms and is only detected on a routine electrocardiogram.

Ventricular tachycardia is caused by electrical signals that arise from the ventricles themselves, instead of following the normal pattern of arising in the atria and spreading throughout the heart. Ventricular tachycardias may be sustained or non-sustained, and they may occur in either or both ventricles.

There are several different kinds, and their severity ranges from mostly without symptoms to a life threatening condition that must be treated immediately with a defibrillator to prevent death (fig 2). This arrhythmia is common in people with heart disease and those patients with depressed left ventricular function or myocardial ischaemia are at particular risk.³

When evaluating someone with syncope of unknown cause, you need to decide whether they have underlying heart disease, especially ventricular muscle damage due to coronary artery disease, or a viral infection of the heart muscle.

Drugs

Among the drugs that may precipitate syncope are those commonly prescribed to treat high blood pressure, such as angiotensin converting enzyme inhibitors, calcium channel blockers, beta blockers, and alpha blockers.⁶ Paradoxically, drugs used to treat arrhythmias may provoke arrhythmias and syncope as a side effect. Some drugs prescribed by psychiatrists may both lower arterial pressure or induce arrhythmias, for example, fluoxetine and haloperidol. Recreational drugs, such as amphetamines and cocaine, may also trigger arrhythmias and syncope. Excessive treatment with diuretics can decrease blood volume and lead to syncope.

Diagnosis

History and physical examination are the most specific and sensitive ways to evaluate syncope. People with syncope use a variety of terms to describe their symptoms, and these include dizziness, faintness, light headedness, blackouts, and a sense of falling or flying. Those with vasovagal syncope may describe a feeling of warmth associated with sweating and a sense of "greying out." Most of these episodes occur when people are standing and when an episode occurs they are unresponsive for less than a minute, but may complain of fatigue for hours after.

In people who have Stokes Adams attacks (syncope due to transient heart block) there is often little warning and they collapse suddenly. Witnesses may remark that the person went very pale but afterwards flushed profusely. By contrast, people who have tachyarrhythmias may experience palpitations before the blackout. When taking the history you should ask about the frequency of such episodes, triggering events, and the speed of onset (table). You should also obtain a detailed account of the event from a witnesses.

ECG showing ventricular tachycardia

Physical examination should include measurement of vital signs including both lying and standing blood pressure - in orthostatic syncope the ability to maintain blood pressure is reduced when standing. The heart must be examined for any valvular abnormalities as well as its rate and rhythm. You need to examine the patient for signs of trauma (head injury, cuts, and fractures) that may have occurred when they fainted. The patient should have a detailed neurological examination, including evaluation for carotid bruits and cranial nerve deficits to exclude a stroke. This is because a haemorrhage or a seizure can also present as syncope. Other principal differential diagnoses are epileptic seizures and hypoglycaemia. Drugs taken by patients experiencing syncope should also be reviewed.

Investigations

After a thorough history, physical examination, and electrocardiography, the cause of syncope remains undiagnosed in about 50% of patients.⁶ Screening tests are often useful because disease can present atypically in elderly patients. These tests include a white blood cell count to detect occult infection and a haematocrit to detect anaemia. Electrolyte, blood urea, nitrogen, and creatinine measurements help in assessing hydration status and in ruling out electrolyte disorders. You should order other more specialised tests if indicated by the history and examination. You should take a resting electrocardiogram in all patients, which may reveal ischaemia.

Treatment

Fainting might seem rather innocuous, but if cerebral ischaemia is not corrected, permanent neurological damage or death is possible. If a person experiences presyncope or actually loses consciousness, position him or her in the supine position (on their back) with the legs slightly elevated and loosen any tight clothing. This promotes blood flow to the brain. If someone who is about to faint can lie down right away, he or she may not lose consciousness. But if they must maintain an upright posture, the person should avoid standing still. Walking increases venous return via the pumping action of the leg muscles on the leg veins. Standing and straining at the same time should be avoided whenever possible. If someone must strain to urinate, interruption of straining every few seconds is helpful. Men who experience "bathroom syncope" should sit to urinate. Treatment of the primary problem, such as prostate surgery for urinary obstruction or treatment of bronchitis to eliminate cough may eliminate the trigger for the syncopal episodes. It is helpful to recognise situations where episodes are likely to take place and avoid them - for example, looking away during blood testing and avoiding prolonged standing.

Exceptions to the supine position rule include pregnant women or those with respiratory difficulties or chest pain. A pregnant woman can be placed on her side with the legs slightly elevated to prevent further problems caused by the weight of the fetus on the vena cava. When respiratory difficulties or chest pain are present, the person should be positioned to allow ease of breathing, which is usually in a seated upright position.

In an unconscious patient, the most critical step is following ABC to maintain an open airway and making certain that the person is breathing and has a pulse.⁷ It is important to avoid dehydration and postural hypotension. Many healthy people follow very low sodium diets with the idea that salt restriction is a healthy way of eating. However, some of those people are  chronically dehydrated and suffer syncopal episodes, especially if they do heavy exercise and sweat a lot.

Syncopal spells related to arrhythmias require specific treatment and a detailed explanation is beyond the scope of this article. Supraventricular tachyarrhythmias may be cured by catheter mediated (radiofrequency) ablation or treated with drugs. Bradyarrhythmias may require the implantion of a pacemaker. Ventricular tachyarrhythmias causing syncope are treated with implantable cardioverter defibrillators. These devices can also act as pacemakers and prevent syncope arising from slow heart rates (bradyarrhythmias).⁸

The history, examination, and initial elecrocardiography are the most important steps in the assessment of syncope.

Samena Chaudhry, senior house officer in cardiothoracic surgery,
Email: sxc602@doctors.org.uk

Magnus Harrison, consultant in emergency medicine, University Hospital North Staffordshire, Stoke-On-Trent


studentBMJ 2005;13:177-220 May ISSN 0966-6494

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