Syncope

Syncope: Excerpt from Professional Guide to Signs & Symptoms (Fifth Edition)

A common neurologic sign, syncope (or fainting) refers to transient loss of consciousness associated with impaired cerebral blood supply or cerebral hypoxia. It usually occurs abruptly and lasts for seconds to minutes. An episode of syncope usually starts as a feeling of light-headedness. A patient can usually prevent an episode of syncope by lying down or sitting with his head between his knees. Typically, the patient lies motionless with his skeletal muscles relaxed but sphincter muscles controlled. However, the depth of unconsciousness varies—some patients can hear voices or see blurred outlines; others are unaware of their surroundings.

In many ways, syncope simulates death: The patient is strikingly pale with a slow, weak pulse, hypotension, and almost imperceptible breathing. If severe hypotension lasts for 20 seconds or longer, the patient may also develop convulsive, tonic-clonic movements.

Syncope may result from cardiac and cerebrovascular disorders, hypoxemia, and postural changes in the presence of autonomic dysfunction. It may also follow vigorous coughing (tussive syncope) and emotional stress, injury, shock, or pain (vasovagal syncope, or common fainting). Hysterical syncope may also follow emotional stress but isn’t accompanied by other vasodepressor effects.

Emergency interventions

History and physical examination

If the patient reports a fainting episode, gather information about the episode from him and his family. Did he feel weak, light-headed, nauseous, or sweaty just before he fainted? Did he get up quickly from a chair or from lying down? During the fainting episode, did he have muscle spasms or incontinence? How long was he unconscious? When he regained consciousness, was he alert or confused? Did he have a headache? Has he fainted before? If so, how often does it occur?

Next, take the patient’s vital signs and examine him for any injuries that may have occurred during his fall.

Medical causes

Aortic arch syndrome

With this syndrome, the patient experiences syncope and may exhibit weak or abruptly absent carotid pulses and unequal or absent radial pulses. Early signs and symptoms include night sweats, pallor, nausea, anorexia, weight loss, arthralgia, and Raynaud’s phenomenon. He may also develop hypotension in the arms; neck, shoulder, and chest pain; paresthesia; intermittent claudication; bruits; vision disturbances; and dizziness.

Aortic stenosis

A cardinal late sign, syncope is accompanied by exertional dyspnea and angina. Related findings include marked fatigue, orthopnea, paroxysmal nocturnal dyspnea, palpitations, and diminished carotid pulses. Typically, auscultation reveals atrial and ventricular gallops as well as a harsh, crescendo-decrescendo systolic ejection murmur that’s loudest at the right sternal border of the second intercostal space.

Cardiac arrhythmias

Any arrhythmia that decreases cardiac output and impairs cerebral circulation may cause syncope. Other effects—such as palpitations, pallor, confusion, diaphoresis, dyspnea, and hypotension—usually develop first. However, with Adams-Stokes syndrome, syncope may occur without warning. During syncope, the patient develops asystole, which may precipitate spasm and myoclonic jerks if prolonged. He also displays an ashen pallor that progresses to cyanosis, incontinence, bilateral Babinski’s reflex, and fixed pupils.

Carotid sinus hypersensitivity

Syncope is triggered by compression of the carotid sinus, which may be caused by turning the head to one side or by wearing a tight collar. The fainting episode is usually of short duration.

Hypoxemia

Regardless of its cause, severe hypoxemia may produce syncope. Common related effects include confusion, tachycardia, restlessness, and incoordination.

Orthostatic hypotension

Syncope occurs when the patient rises quickly from a recumbent position. Look for a drop of 10 to 20 mm Hg or more in systolic or diastolic blood pressure as well as tachycardia, pallor, dizziness, blurred vision, nausea, and diaphoresis.

Transient ischemic attacks

Marked by transient neurologic deficits, these attacks may produce syncope and decreased level of consciousness. Other findings vary with the affected artery but may include vision loss, nystagmus, aphasia, dysarthria, unilateral numbness, hemiparesis or hemiplegia, tinnitus, facial weakness, dysphagia, and staggering or uncoordinated gait.

Vagal glossopharyngeal neuralgia

With this disorder, localized pressure may trigger pain in the base of the tongue, pharynx, larynx, tonsils, and ear, resulting in syncope that lasts for several minutes.

Other causes

Drugs

Quinidine may cause syncope—and possibly sudden death—associated with ventricular fibrillation. Prazosin may cause severe orthostatic hypotension and syncope, usually after the first dose. Occasionally, griseofulvin, levodopa, and indomethacin can produce syncope.

Special considerations

Continue to monitor the patient’s vital signs closely. Prepare the patient for an electrocardiogram, Holter monitor, carotid duplex, carotid Doppler, and electrophysiology studies.

Pediatric pointers

Syncope is much less common in children than in adults. It may result from a cardiac or neurologic disorder, allergies, or emotional stress.

Patient counseling

Advise the patient to pace his activities, to rise slowly from a recumbent position, to avoid standing still for a prolonged time, and to sit or lie down as soon as he feels faint.

Book Source Details

• Book Title: Professional Guide to Signs & Symptoms (Fifth Edition)
• Author(s): Springhouse
• Year of Publication: 2006
• Copyright Details: Professional Guide to Signs & Symptoms (Fifth Edition), Copyright © 2006 Lippincott Williams & Wilkins.

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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.

More About This Book: Title: Professional Guide to Signs & Symptoms (Fifth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2006 ISBN: 1-58255-510-9

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