Chapter 18. Faintness and Syncope

Faintness and Syncope: Introduction

The term syncope (Greek: synkope) literally means a “cessation,” a “cutting short,” or “pause.” Medically, it refers to an episodic loss of consciousness and postural tone and an inability to stand because of a diminished flow of blood to the brain. It is synonymous in everyday language with fainting. Feeling faint and a feeling of faintness are also commonly used terms to describe the loss of strength and other symptoms that characterize the impending or incomplete fainting spell. This latter state is referred to as presyncope. Relatively abrupt onset, brief duration, and spontaneous and complete recovery not requiring specific resuscitative measures are other typical features.

Faintness and syncope are among the most common of all medical problems. Practically every adult has experienced some presyncopal symptoms, if not a fully developed syncopal attack, or has observed such attacks in others. Description of these symptoms, as with other predominantly subjective states, is often ambiguous. The patient may refer to the experience as light-headedness, dizziness, a “drunk feeling,” a weak spell, or, if consciousness was lost, a “blackout.” Careful questioning may be necessary to ascertain the exact meaning the patient has given to these words. In many instances the nature of the symptoms is clarified by the fact that they include a sensation of faintness and then a momentary loss of consciousness, which is easily recognized as a faint, or syncope. This sequence also informs us that under certain conditions any difference between faintness and syncope is only one of degree. These symptoms must be clearly set apart from certain types of epilepsy, the other major cause of episodic unconsciousness, and from disorders such as cataplexy, transient ischemic attacks (TIAs), “drop attacks,” and vertigo, which are also characterized by episodic attacks of generalized weakness or inability to stand upright, but not by a loss of consciousness.

Causes of Episodic Faintness and Syncope

From a clinical perspective, syncope is essentially of three main types, all ultimately causing hypotension and each of which may lead to a temporary reduction in the flow of blood to the brain. The first, reflex withdrawal of vascular sympathetic tone (vasodepressor effect), triggered by centrally mediated inhibition of the normal tonic sympathetic influences, is often associated with excessive vagal effect and bradycardia (vagal effect). The type associated with bradycardia is called vasovagal syncope, a special form of neurogenic, or neurocardiogenic syncope, by which is meant the withdrawal of sympathetic tone through a reflex neural mechanism. Neurocardiogenic syncope usually signifies that the inciting stimulus originates in neural receptors within the heart. Each may cause the common faint, the clinical details of which are described later.

The second is a failure of sympathetic innervation of blood vessels and of autonomically activated compensatory responses (reflex tachycardia and vasoconstriction), which occurs with assumption of the upright body position and leads to pooling of blood in the lower parts of the body—causing orthostatic hypotension and syncope. Typically, in individuals with these first two forms of syncope, there is no evidence of underlying cardiac disease.

Syncope of a third type is caused by a primary diminished cardiac output because of disease of the heart itself as in the Stokes-Adams bradyarrhythmia attack, severe aortic or subaortic stenosis, or ischemic heart disease. Greatly reduced blood volume from dehydration or blood loss usually causes only near syncope, but complete loss of consciousness may certainly occur in severe circumstances.

As a rough guide to the relative frequency of the various causes of syncope, the large amount of information from the Framingham Heart Study accumulated by Soteriades and colleagues can be taken as representative: the leading cause was vasovagal, a cardiac cause was established in about 10 percent; and orthostatic hypotension in another 10 percent. Also, 7 percent of cases were attributed to medications, mainly those that interfered with sympathetic tone, and remaining 40 percent could not be categorized.

The three main types of syncope as well as several others that cannot readily be classified within these categories can be further subdivided by their pathophysiologic mechanism, as follows:

I. Neurogenic vasodepressor reactions
II. Failure of sympathetic nervous system innervation (postural–orthostatic hypotension)
III. Reduced cardiac output or inadequate intravascular volume (hypovolemia)
IV. Other causes of episodic faintness and syncope

This list of conditions causing faintness and syncope is deceptively long and involved, but the usual types are reducible to a few well-established mechanisms. So as not to obscure these mechanisms by too many details, only the varieties of fainting commonly encountered in clinical practice and those of particular neurologic interest are discussed below.

Clinical Features of Syncope

The Common Faint (Vasodepressor Syncope)

This is the common faint, seen mainly in young individuals. A familial predisposition is well known (Mathias et al). The evocative factors are usually strong emotion, physical injury—particularly to viscera (testicles, gut)—or other factors (see below). As described earlier, the vasodilatation of adrenergically innervated “resistance vessels” is postulated to lead to a reduction in peripheral vascular resistance, but cardiac output fails to exhibit the compensatory rise that normally occurs in hypotension. Some physiologic studies suggest that the dilatation of intramuscular vessels, innervated by beta-adrenergic fibers, may be more important than dilatation of the splanchnic ones.

Skin vessels, in contrast, are constricted. Vagal stimulation may be superimposed either as a primary or a reactive phenomenon (hence the term vasovagal) causing bradycardia and leading possibly to a slight further drop in blood pressure. Other vagal effects are perspiration, increased peristaltic activity, nausea, and salivation. However, bradycardia probably contributes little to the hypotension and syncope. The term vasovagal was used originally by Thomas Lewis. As Lewis himself pointed out, atropine, “while raising the pulse rate up to and beyond normal levels during the attack, leaves the blood pressure below normal and the patient still pale and not fully conscious.”

The vasodepressor faint occurs (1) in normal health under the influence of strong emotion, particularly in some susceptible individuals (sight of blood or an accident) or in conditions that favor peripheral vasodilatation, e.g., hot, crowded rooms (“heat syncope”), especially if the person is hungry or tired or has had alcoholic drinks; (2) during a painful illness or after bodily injury (especially of the abdomen or genitalia), as a consequence of fright, pain, and other factors (where pain is involved, the vagal element tends to be more prominent in the genesis of the faint); and (3) during exercise in some sensitive persons (see further on).

The clinical manifestations of fainting attacks vary to some extent, depending on their mechanisms and the settings in which they occur. The most common types of faint—namely, vasodepressor and vasovagal syncope, conform more or less to the following pattern. In these types, which are taken in this section as one characteristic manifestation, the patient is usually in the upright position at the beginning of the attack, either sitting or standing. Certain subjective symptoms, the prodrome, mark the onset of the faint. The person feels queasy, is assailed by a sense of giddiness and apprehension, may sway, and sometimes develops a headache. What is most noticeable at the beginning of the attack is pallor or an ashen-gray color of the face; often the face and body become bathed in cool perspiration. Salivation, epigastric distress, nausea, and sometimes vomiting may accompany these symptoms, and the patient tries to suppress them by yawning, sighing, or breathing deeply. Vision may dim or close in concentrically, the ears may ring, and it may be impossible to think clearly (“grayout”). This serves to introduce the common faint that is known to all physicians and most laypersons.

The duration of the prodromal symptoms is variable from a few minutes to only a few seconds. If, during the prodromal period, the person is able to lie down promptly, the attack may be averted before complete loss of consciousness occurs; otherwise, consciousness is lost and the patient falls to the ground. The more or less deliberate onset of this type of syncope enables patients to lie down or at least to protect themselves as they slump. A hurtful fall is exceptional in the young, although an elderly person may be injured.

The depth and duration of unconsciousness vary. Sometimes the person is not completely oblivious to his surroundings; he may still hear voices or see the blurred outlines of people. More often there is a complete lack of awareness and responsiveness. The patient lies motionless, with skeletal muscles fully relaxed. Sphincteric control is maintained in nearly all cases. The pupils are dilated. The pulse is thin and slow or cannot be felt; or they may be tachycardic, the systolic blood pressure is reduced (to 60 mm Hg or less as a rule), and breathing may be almost imperceptible. It is the brief period of hypotension and cerebral hypoperfusion that is the unifying feature of the various forms of syncope. The depressed vital functions, striking facial pallor, and unconsciousness almost simulate death.

Once the patient is horizontal, the flow of blood to the brain is restored. The strength of the pulse soon improves and color begins to return to the face. Breathing becomes quicker and deeper. Then the eyelids flutter and consciousness is quickly regained. However, should unconsciousness persist for 15 to 20 s, convulsive movements may occur. The term convulsive syncope has been used to describe this phenomenon, but it has also been used for an authentic seizure caused by a prolonged period of brain hypoxia. These movements, which are often mistaken for a seizure, usually take the form of brief, mild, clonic jerks of the limbs and trunk and twitchings of the face or a tonic extension of the trunk and clenching of the jaw. Occasionally, the extensor rigidity and jerking flexor movements are more severe, but very rarely is there urinary incontinence or biting of the tongue, features that characterize a generalized tonic-clonic convulsion.

Gastaut and Fischer-Williams used the oculocardiac inhibitory reflex to study the pattern of electroencephalographic (EEG) changes in syncope. They found that the heightened vagal discharge produced by compression of the eyeballs (oculovagal reflex, a cause of syncope in acute glaucoma) could produce brief periods of cardiac arrest and syncope. This effect was produced in 20 of 100 patients who had a history of syncopal attacks. These investigators found that after a 7- to 13-s period of cardiac arrest, there was a loss of consciousness, pallor, and muscle relaxation and changes in EEG activity. Toward the end of this period, runs of bilaterally synchronous theta and delta waves appeared in the EEG, predominantly in the frontal lobes; in some patients there were one or more myoclonic jerks, synchronous with the slow waves. If the hypotension persisted beyond 14 or 15 s, the EEG became flat. This period of electrical silence lasted for 10 to 20 s and was sometimes accompanied by a generalized tonic spasm with incontinence. Following the spasm, heartbeats and large-amplitude delta waves reappeared, and after another 20 to 30 s, the EEG reverted to normal. It is noteworthy that rhythmic clonic seizures or epileptiform EEG activity was not observed at any time during the periods of cardiac arrest, syncope, and tonic spasm.

From the moment that consciousness is regained, there is a correct perception of the environment. Confusion, headache, and drowsiness, the common sequelae of a convulsive seizure, do not follow a syncopal attack. Nevertheless, the patient often feels weak and groggy after a vasodepressor faint and, by arising too soon, may precipitate another faint.

The clinical features of cardiac and carotid sinus syncope are in some ways the same as those described above except that the onset may be absolutely abrupt, without any warning symptoms, and is independent of the patient being in an upright posture. The clinical particulars of these and other forms of syncope are described further on.

Neurogenic Syncope

This term refers to all forms of syncope that result directly from the vascular effects of neural signals coming from the central nervous system. In essence, all the types of syncope in this category are “vasovagal,” meaning a combination of vasodepressor and vagal effects in varying proportions; the only differences are in the stimuli that elicit the reflex response.

A number of stimuli, mostly from the viscera but some of psychologic or emotional origin, are capable of eliciting this response, which consists of a reduction or loss of sympathetic vascular tone coupled with a heightened vagal activity. The nucleus of the tractus solitarius (NTS) in the medulla integrates these afferent stimuli and normal baroreceptor signals with the efferent sympathetic mechanisms that maintain vascular tone (see further on and Chap. 26).

Several lines of study suggest that there are disturbances of both sympathetic control of vascular tone and also of the responsiveness of baroreceptors in neurogenic syncope, but the precise mechanisms are unclear. By the use of microneurography, Wallin and Sundlof have demonstrated an increase in sympathetic outflow in peripheral nerves just prior to syncope, as would be expected; however, this activity then ceases at the onset of fainting. Unmyelinated (postganglionic sympathetic) fibers cease firing during vasovagal fainting at a point when the blood pressure falls below 80/40 mm Hg and the pulse, below 60. This would signify that there is an initial attempt to compensate for the falling blood pressure, following which there is a centrally mediated withdrawal of sympathetic activity. Which one of these mechanisms (perhaps both) is responsible for syncope is not clear. More recently, Bechir and colleagues showed that muscle sympathetic activity as assessed using microneurography is increased in the resting state in patients with orthostatic hypotension and, importantly, does not increase further with venous pooling (induced by lower-body negative pressure). Moreover, in the same patients, the response of the cardiac baroreceptors to pooling was significantly diminished. These data are only partially in agreement with those of Wallin and Sundlof, and they are not in accord with an initial increase in sympathetic activity prior to syncope.

There is agreement that peripheral vascular resistance is greatly reduced just prior to and at the onset of fainting. This drop in resistance has been attributed to an initial adrenergic discharge that, at high levels, causes a vasodilatation (rather than constriction) in intramuscular blood vessels. High levels of epinephrine and the vasodilating effects of nitric oxide acting on vascular endothelium, as well as greatly augmented levels of circulating acetylcholine during syncope, also have been invoked as additional or intermediary factors, but all remain speculative. In the current view, the drop in blood pressure is the result of a transient but excessive activity of sympathetic nerves that paradoxically leads to vascular dilatation in muscle and viscera from an imbalance between beta-adrenergic and alpha-adrenergic activity peripherally.

It has been further suggested, on the basis of reasonable but inconclusive physiologic evidence, that the early sympathotonic attempt to maintain blood pressure leads to overly vigorous contractions of the cardiac chambers and that this, in turn, acts as the afferent stimulus for withdrawal of sympathetic tone in common fainting (see “Neurocardiogenic Syncope,” later).

Also of interest are abnormalities in the response to hypocarbia of patients who are prone to syncope. Norcliffe-Kaufmann and colleagues recorded a greater-than-normal reduction in cerebral blood flow velocity (gauged by transcranial Doppler) and an excessively reduced vascular resistance in the forearm in response to hypocarbia, and the opposite reactions to hypercarbia. They relate the degree of these changes to variations in orthostatic tolerance among patients and suggest that the two aforementioned changes relate to decreased cerebral blood flow that may engender syncope.

Neurocardiogenic Syncope

This entity, a component or perhaps a subtype of vasodepressor syncope, has received attention as a cause of otherwise unexplained fainting in healthy and athletic children and young adults. As mentioned earlier, it may be the final precipitant in the common vasodepressor faint, and the term is used synonymously with vasovagal or vasodepressor syncope by some authors.

Oberg and Thoren were the first to observe that the left ventricle itself can be the source of neurally mediated syncope in much the same way as the carotid sinus when stimulated, produces vasodilatation and bradycardia. During acute blood loss in cats, they noted a paradoxical bradycardia that was preceded by increased afferent activity in autonomic fibers arising from the ventricles of the heart, a reaction that could be eliminated by sectioning these nerves. This concept of the heart as the afferent source of vasodepressor reflexes had been suggested earlier by Bezold, as well as by Jarisch and Zoterman, and came to be known as the Bezold-Jarisch reflex. The inferoposterior wall of the left ventricle is the site of most of the subendocardial mechanoreceptors that are responsible for the afferent impulses to the nucleus tractus solitarius.

For this mechanism to become active, very vigorous cardiac contractions must occur in the presence of deficient filling of the cardiac chambers (hence “neurocardiogenic”). In the simple faint, an initial burst of sympathetic activity is thought to precipitate physiologic circumstances of excessive cardiac contraction. Echocardiographic findings of a diminished ventricular chamber size and vigorous contractions just prior to syncope support this notion (the “empty-heart syndrome”). The remaining baroreceptors in the aorta may be responsible for the increased afferent activity.

According to Kaufmann, a proclivity to primary neurocardiogenic syncope can be identified by the finding of delayed fainting when the patient is placed at a 60-degree upright position on a tilt table. After approximately 10 min of upright posture, the blood pressure drops below 100 mm Hg; soon thereafter, the patient complains of dizziness and sweating and subsequently faints. In contrast, patients with primary sympathetic failure will faint soon after upward tilting. Half of patients with unexplained syncope display a delayed tilt-table reaction, but it is also seen in 5 percent of controls (see “Tilt-Table Testing” further on). The value of isoproterenol as a cardiac stimulant and peripheral vasodilator to enhance the effect of upright posture and expose neurocardiogenic syncope during the tilt-table test is controversial.

Exercise-Induced Syncope

Aerobic exercise, particularly running, is known to induce fainting in some persons, a trait that may become apparent in late childhood or later and may be familial. There is nausea as well as other presyncopal symptoms; the faint can be avoided by discontinuing exercise or not exceeding a threshold of effort set by the patient himself. Such persons do not seem unduly sensitive to nonaerobic exercise and have no recognizable electrocardiographic or structural heart problems. They have a predilection to faint with prolonged tilt-table testing and with isoproterenol infusion, suggesting that this represents a form of neurocardiogenic syncope. For this reason, these patients may benefit from beta-adrenergic-blocking drugs if given under careful supervision. As discussed further on, exercise can also precipitate syncope in patients with a number of underlying cardiac conditions (myocardial ischemia, long QT syndrome, aortic outflow obstruction, cardiomyopathy, structural chamber anomalies, exercise-induced ventricular tachycardia, and, less often, supraventricular tachycardias).

Athletes who faint unpredictably during exercise pose a particularly difficult problem. Obviously those found to have serious heart disease should give up competitive sports, but the majority has no demonstrable cardiac abnormality. Subjecting these patients to intense exercise and other testing sometimes fails to elicit the faints, but many have varying degrees of hypotension when subjected to prolonged head-up tilt, again suggesting that the cause of fainting is essentially neurocardiogenic (see above). Implanted cardiac pacemakers are not curative in these vasodepressor faints, as the main deficiency is in vascular resistance. Unless the results of tilt-table testing are unequivocal and reproducible, it is best to consider the more serious causes of exercise-induced syncope and to treat the patient appropriately.

Carotid Sinus Syncope

The carotid sinus is normally sensitive to stretch and gives rise to sensory impulses carried via the nerve of Hering, a tributary of the glossopharyngeal nerve, to the medulla. Massage of one of the carotid sinuses or of both alternately, particularly in elderly persons, causes (1) a reflex cardiac slowing (sinus bradycardia, sinus arrest, or even atrioventricular block)—the vagal type of response, or (2) a fall of arterial pressure without cardiac slowing—the vasodepressor type of response. Another (“central”) type of carotid sinus syncope was in the past ascribed to cerebral arteriolar constriction, but such an entity has never been validated.

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