Syncope is the cutting off or transient loss of consciousness. Although the term is usually applied to unconsciousness caused by a temporary decrease in cerebral blood flow, in this discussion a broader definition is employed that includes the brief disturbances in consciousness due to changes in the chemical composition of the blood as in hyperventilation or hypoglycemia. Syncope is extremely common; in fact, it has been found to occur in as many as 25 to 30 per cent of young, healthy adult males. It should be carefully differentiated from such disorders as epilepsy, vertigo, cataplexy, and strokes, all of which may produce transient disturbances in consciousness, generalized weakness, or inability to stand erect.
The loss of consciousness in syncope may not be complete, but may consist of varying degrees of impaired sensorium with transient blurring of vision, weakness, and loss of postural tone. Such attacks may be described by the patient as dizziness, faintness, light-headedness, or a “drunk feeling.” These partial manifestations have the rapid onset,, brief duration, and complete recovery characteristic of the fully developed faint.
Syncope is most frequently caused by a reduction in cerebral blood flow below a critical level and is usually associated with a sharp fall in blood pressure. This, in turn, is the result of either a loss of peripheral resistance, as seen in vasodepressor faint and in orthostatic hypotension, or a decrease in cardiac output, as in Adams-Stokes attacks. In many patients, however.. loss of consciousness is not caused by reduction of blood pressure but by a decrease in such essential blood components as glucose, carbon dioxide, or oxygen. In other instances, as in micturition syncope and cough syncope, the faint seems to result from cerebral ischemia caused by extracardiac disturbances.
There are several features common to almost all types of syncope. Electroencephalographic changes usually appear, and consist of high voltage, 2- to 4-cycle per second slow waves that promptly return to normal after consciousness is regained. Convulsive movements, such as tonic or clonic contractions of the arms or turning of the head, can occur in all types of fainting, depending On the degree and duration of the cerebral ischemia. Fully developed seizures with tongue biting and urinary incontinence, however, are unusual. Recovery is usually hastened in the recumbent posture, which helps to restore the normal cerebral circulation.
The critical level of cerebral blood flow necessary to maintain consciousness has been estimated to be about 30 ml. per 100 grams of brain per minute. (Normal value is 50 to 55 ml.) The duration of asystole or the degree of hypotension necessary to produce critical levels of cerebral ischemia varies, depending upon the posture of the patient, the ability of the cerebral vessels to dilate, and other factors. In normal subjects in the erect posture, a mean arterial blood pressure as low as 20 to 30 mm. of mercury or an asystole of four or five seconds’ duration is necessary to produce syncope. In the recumbent position, longer periods of asystole may occur before loss of consciousness develops.
Chronic orthostatic hypotension
Chronic orthostatic hypotension is a disorder of the autonomic nervous system in which syncope occurs when the patient assumes the upright posture. The condition is sometimes seen in diabetic neuropathy and in tabes dorsalis, but in many patients the site or nature of the neurologic lesion is unknown. These people have an abnormality in the baroreceptor reflexes that ordinarily compensates for the pooling of blood in the lower extremities and viscera. When an attempt is made to stand upright, there is an inadequate degree of reflex arteriolar constriction, with a subsequent reduction in venous return.
This is associated with an immediate and sharp fall in arterial blood pressure, followed by syncope. The pulse rate remains unchanged during the episode, and there are none of the usual prodromal symptoms of pallor, sweating, and nausea seen in vasodepressor faint. These patients may have other aspects of autonomic dysfunction, such as impotence, bladder disturbances, and loss of sweating in the lower trunk. There is said to be a reduction in the 24-hour urinary excretion of norepinephrine and possibly of epinephrine as well.
Orthostatic hypotension has also been associated with a rare form of Parkinson-like syndrome in which tremor, rigidity, muscular wasting, iris atrophy, and ocular palsies are prominent manifestations. This condition is sometimes referred to as the Shy-Drager syndrome.
Failure of postural adaptation also appears following extensive sympathectomy for hypertension or during administration of vasodilating agents and ganglionic blocking medications. Patients recovering from chronic wasting illnesses associated with prolonged bed rest may experience syncope when they attempt to assume the upright position.
Vasodepressor Syncope (the Common Faint).
Vasodepressor syncope is by far’ the most frequent cause of transient loss of consciousness. The term vasovagal attack has also been applied to this type of fainting. The condition is characterized by a fall in blood pressure associated with the development of a variety of autonomic manifestations. In the early presyncopal period, there may be pallor, nausea, and sweating; in later stages pupillary dilatation, yawning, hyperpnea, and bradycardia appear. When the mean arterial pressure falls below critical levels, loss of consciousness and characteristic electroencephalographic changes occur. Bradycardia is often severe at the onset of unconsciousness, and pulse rates of 50 to 60 per minute may be observed even after recovery.
The duration of syncope is brief, ranging from a few seconds to several minutes. In the post- syncopal period the patient may complain of headaches, weakness, nervousness, and slight confusion. Vasodepressor faint is most often evoked by sudden emotional stress associated with fear, anxiety, or pain. Hypodermic injections, trauma, minor surgery, and the sight of or withdrawal of blood are common precipitating events. Attacks usually occur in the standing or upright posture, and consciousness returns quickly once the patient is recumbent.
The initial event in this complex vascular and neurogenic reaction is dilatation of the vascular bed throughout the body, particularly in peripheral muscles. Vasodilatation in the limb muscles is a normal response to emotional stimuli, and is thought to represent preparation for “fight or flight.” The absence of immediate muscle activity, however, and the fall in peripheral resistance are not compensated for by an increase in cardiac output, and. as a result there is a reduction in cerebral blood flow.
Being A Medical Student, You Must Know The Types of Syncope And How You Can do Treatment of Fainting
Carotid Sinus Syncope.
In relatively fe patients this is the mechanism of syncope. Mai persons, particularly those more than 80 years i age, show reflex slowing of the heart and fall blood pressure during massage of one or batik carotid sinuses. Such responses are also seen frequently in patients with cardiac disorders,, hypertension, or diseases of the carotid vessel® I such as atherosclerotic thrombosis or stenosis. The I most common response to carotid sinus massage at] either sinus bradycardia or sinoatrial block, bo’Jui of which may be abolished by administration off atropine. Much less frequently, there may be a pure vasodepressor response without slowing off the heart.
In a third but rare type of carotid response, fainting may appear in a few seconds without significant changes in either blood pressure or pulse; such instances probably occur only with vigorous pressure and when the opposite carotid is already thrombosed. Carotid sinus syncope is not accompanied by the prodromal symptoms seen in the common faint nausea, sweating, pallor, etc.). It is more frequent in men. and usually occurs in the erect posture. It sometimes follows sudden head turning or pressure of a tight collar.
Cough syncope usually follows a paroxysm of explosive and vigorous coughing. It is commonly observed in men but rarely in women. In adults, the condition is often associated with chronic lung disease or bronchitis; in children, it may occur during severe pertussis. The syncope is brief, and there are no post syncopal residua. The condition has also been described following hearty laughter. The loss of consciousness has been attributed to an increase in the intrathoracic and intra-abdominal pressure caused by vigorous coughing.
This, in turn, is thought to produce a sudden sharp elevation in cerebrospinal fluid pressure, thereby “squeezing” blood from the intracranial and cerebral vessels. Other theories maintain that the condition is due to a Valsalva effect with reduction in cardiac output or to cerebral “concussive effect” caused by rapid rise in the cerebrospinal fluid pressure. There is clinical evidence to suggest that the pres ence of an intracerebral lesion such as brain tumor or stenosis of a major cerebral artery may produce increased susceptibility to syncope following paroxysms of cough. Such cases may have focal neurologic symptoms such as paresthesias or clonic movements of one limb prior to loss of consciousness.
This trick, often indulged in by school boys, consists of sudden manual compression of the chest of the victim after he has been hyperventilating for about a minute. Loss of consciousness also occurs in a similar prank in which the individual hyperventilates in the squatting position, quickly stands, and then performs the Valsalva maneuver. The increase in intrathoracic pressure in both tricks interferes with the flow of blood in the heart and lungs and further reduces the cerebral blood flow and arterial blood pressure, which have already been impaired by hyperventilation. Voluntary syncope has also been observed in muscular teenage boys who can maintain a prolonged Valsalva maneuver by vigorous stretching of the trunk and back muscles. Such instances of “stretch syncope” are often self-induced to provide a curiously satisfying experience.
Hysterical fainting is seen almost entirely in young women with emotional illness. It differs from the vasodepressor faint and the hyperventilation syndrome in that the patient is relatively free of anxiety and shows little concern regarding the tainting episodes. The attack usually occurs in the presence of others. The patient generally slumps to the floor gracefully, sometimes dramatically, without injury or awkwardness. It thus resembles the mid-Victorian drawing-room swoon. In the present era, hysterical fainting often occurs in groups of young women during mass excitement, particularly that caused by the presence of screen or television idols.
During the attack the patient may be motionless or may show bizarre resisting movements. The attack may last from several minutes to as long as an hour or more, with fluctuations ad responsiveness. There are no abnormalities in pulse, blood pressure, or skin color.
This form of syncope is most often seen during or immediately after micturition in adult men who rise in the middle of the night to void. The loss of consciousness is brief and there is no post syncopal confusion or weakness. Many such people give a history of drinking large quantities of beer before retiring, and considerable bladder deflation may take place during micturition. A similar fainting may be observed following drainage of a distended bladder in urinary retention or after removal of a large quantity of ascitic fluid by abdominal paracentesis. Sharpey-Schafer suggested that the loss of consciousness may be due to a reflex vasodilatation of the peripheral vascular system, a situation thought to be the converse of the paroxysmal hypertension seen in paraplegics during bladder distention. Others have attributed the syncope to a Valsalva maneuver during micturition or to peripheral vasodilation associated with a warm bed and perhaps the recent consumption of alcohol.
The diagnosis of syncope depends almost entirely upon a careful history of the attack and the setting in which it occurs. Differentiation of syncope from an akinetic epileptic seizure, such as a petit mal or psychomotor attack, may be difficult. Careful evaluation of the encephalographic findings, the onset and duration of the attack, and the post syncopal manifestations can usually distinguish these conditions. These factors are also helpful in differentiating the various types of syncope. In vasodepressor fain:. the patient usually has prodromal signs of autonomic hyperactivity such as pallor, sweating, salivation, and bradycardia.
In cardiac arrest, orthostatic hypotension, and carotid sinus syncope, loss of consciousness occurs abruptly, and prodromal symptoms are not usually present. Post Syncopal confusion, headache, and weakness often follow vasodepressor faint and the hyperventilation syndrome. In chronic orthostatic hypotension and Adams-Stokes attacks, recovery of consciousness is rapid and complete without post syncopal symptoms.’ Most types of fainting occur in the erect or upright position, but in cardiac arrest syncope may appear while the patient is recumbent.
The duration of syncope is brief in postural hypotension but prolonged in hyperventilation and hypoglycemia. Most of these differentiating manifestations can be determined by careful history, but special methods of examination may be necessary. These consist of voluntary hyperventilation for approximately two minutes, massage of the carotid sinuses, and observations of pulse and blood pressure during change in posture from recumbent to erect position. Laboratory examinations, such as electrocardiogram or electroencephalogram, and blood sugar studies may also be necessary to arrive at a correct diagnosis.
Therapy in syncope consists primarily of treatment of the underlying disorder. In all types of fainting, recovery is usually aided by maintaining the patient in a recumbent position with elevation of the lower extremities. Application of cold water to the face and head and inhalation of spirits of ammonia or other pungent aromatics are time-honored and certainly do no harm.