What cause fainting?

Causes of fainting

fainting is a sudden, brief loss of consciousness with loss of postural tone followed by spontaneous revival. The patient is motionless and limp and usually has cool extremities, a weak pulse, and shallow breathing. Sometimes brief involuntary muscle jerks occur, resembling a seizure.

(see also causes of stroke)

Near-syncope is light-headedness and a sense of an impending faint without loss of consciousness. It is usually classified and discussed with syncope because the causes are the same.

 

Seizures can cause sudden loss of consciousness but are not considered syncope/fainting. However, seizures must be considered in patients presenting for apparent syncope/fainting because history may be unclear or unavailable, and some seizures do not cause tonic-clonic convulsions. Furthermore, a brief (< 5 second) seizure sometimes occurs with true syncope.

 

Fainingt can be diagnosis depends on the following;

Diagnosis depends on a careful history, eyewitness accounts, or fortuitous examination during the event.

 

Pathophysiology of Fainting

Most syncope results from insufficient cerebral blood flow. Some cases involve adequate flow but with insufficient cerebral substrate (oxygen, glucose, or both).

 

Insufficient cerebral blood flow

Most deficiencies in cerebral blood flow result from decreased cardiac output (CO).

Decreased cardiac output (CO) can be caused by

·         Cardiac disorders that obstruct outflow

·         Cardiac disorders of systolic dysfunction

·         Cardiac disorders of diastolic dysfunction

·         Arrhythmias (too fast or too slow)

·         Conditions that decrease venous return

Decreased cardiac output (CO).can be exacerbated by exercise, vasodilation, and hypovolemia (especially in aortic stenosis and hypertrophic cardiomyopathy), which may precipitate syncope.

 

Arrhythmias cause syncope when the heart rate is too fast to allow adequate ventricular filling (eg > 150 to 180 beats/minute) or too slow to provide adequate output (eg, < 30 to 35 beats/minute).

(see also causes of stroke)

Venous return can be decreased by hemorrhage, increased intrathoracic pressure, increased vagal tone (which can also decrease heart rate), and loss of sympathetic tone (eg, from drugs, carotid sinus pressure, autonomic dysfunction). Syncope involving these mechanisms (except for hemorrhage) is often termed vasovagal or neurocardiogenic and is common and benign.

 

Orthostatic hypotension, a common benign cause of fainting, results from failure of normal mechanisms of the body (eg, sinus tachycardia, vasoconstriction, or both) to compensate for the temporary decrease in venous return that occurs with standing.

 

Cerebrovascular disorders may include (eg, strokes, transient ischemic attacks) rarely cause syncope/fainting because most of them do not involve the centrencephalic structures that must be affected to cause loss of consciousness. However, basilar artery ischemia, due to transient ischemic attack, stroke, or migraine, may cause fainting. Rarely, patients with severe cervical arthritis or spondylosis develop vertebrobasilar insufficiency with syncope when the head is moved in certain positions.

 

Insufficient cerebral substrate

The central nervous system (CNS) requires oxygen and glucose to function. Even with normal cerebral blood flow, a significant deficit of either will cause loss of consciousness . In practice, hypoglycemia is the primary cause because hypoxia rarely develops in a manner causing abrupt loss of consciousness (other than in flying or diving incidents). Loss of consciousness due to hypoglycemia is seldom as abrupt as in syncope/fainting or seizures because warning symptoms occur (except in patients taking beta-blockers); however, the onset may be unclear to the examiner unless the event was witnessed.

 

What are the main causes of fainting?

Causes are usually classified by the mechanism

The most common causes are:

·         Vasovagal (neurocardiogenic)

·         Idiopathic

Many cases of syncope never have a firm diagnosis but lead to no apparent harm. A smaller number of cases have a serious cause, usually cardiac.

 

Evaluation should be done as soon as possible after the event. The more remote the syncopal event, the more difficult the diagnosis. Information from witnesses is quite helpful and best obtained as soon as possible.

 

History

History of present illness should ascertain events leading up to the syncope, including the patient’s activity (eg, exercising, arguing, in a potentially emotional situation), position (eg, lying or standing), and, if standing, for how long. Important associated symptoms immediately before or after the event include whether there was a sense of impending loss of consciousness, nausea, sweating, blurred or tunnel vision, tingling of lips or fingertips, chest pain, or palpitations. Length of time recovering should also be ascertained. Witnesses, if any, should be sought and asked to describe events, particularly the presence and duration of any seizure activity.

 

Review of systems should ask about any areas of pain or injury, episodes of dizziness or near-syncope upon arising, and episodes of palpitations or chest pain with exertion. Patients should be asked about symptoms suggesting possible causes, including bloody or tarry stools, heavy menses (anemia); vomiting, diarrhea, or excess urination (dehydration or electrolyte abnormalities); and risk factors for pulmonary embolism (recent surgery or immobilization, known cancer, previous clots or hypercoagulable state).

 

Past medical history should ask about previous syncopal events, known cardiovascular disease, and known seizure disorders. Drugs used should be identified (particularly antihypertensives, diuretics, vasodilators, and antiarrhythmics—see table Some Drug Causes of Syncope). Family history should note presence at a young age of heart disease or sudden death in any family member.

 

Physical examination

Vital signs are essential. Heart rate and blood pressure are measured with the patient supine and after 3 minutes of standing. Pulse is palpated for irregularity.

General examination notes patient’s mental status, including any confusion or hesitancy suggesting a postictal state and any signs of injury (eg, bruising, swelling, tenderness, tongue bite).

The heart is auscultated for murmurs; if present, any change in the murmur with a Valsalva maneuver, standing, or squatting is noted.

 

 

 

 

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Unexplained recurrent syncope

Ischemic cardiomyopathy, non-ischemic cardiomyopathy, and adult congenital disease, or unexplained syncope that does not otherwise meet criteria for an ICD used for primary prevention

A negative response defines a low-risk subgroup with a high rate of remission of syncope. The use of electrophysiologic testing is controversial in other patients.

 

EEG is warranted if a seizure disorder is suspected.

 

CT and MRI of the head and brain are indicated only if signs and symptoms suggest a focal CNS disorder.

 

Treatment of Syncope/fainting

In witnessed syncope, pulses are checked immediately. If the patient is pulseless, CPR is begun. If pulses are present, severe bradycardia is treated with atropine or external transthoracic pacing. Isoproterenol can be used to maintain adequate heart rate while a temporary pacemaker is placed.

 

Tachyarrhythmias are treated; a direct-current synchronized shock is quicker and safer than drugs for unstable patients. Inadequate venous return is treated by keeping the patient supine, raising the legs, and giving IV normal saline. Tamponade is relieved by pericardiocentesis. Tension pneumothorax requires insertion of a pleural cannula and drainage. Anaphylaxis is treated with parenteral epinephrine.

 

Placing the patient in a horizontal position with legs elevated typically ends the syncopal episode if life-threatening disorders are ruled out. If the patient sits upright too rapidly, syncope may recur; propping the patient upright or transporting the patient in an upright position may prolong cerebral hypoperfusion and prevent recovery.

 

Specific treatment depends on the cause and its pathophysiology. Driving and use of machinery should be prohibited until the cause is determined and treated.

 

Geriatrics Essentials: Syncope

The most common cause of syncope in older adults is postural hypotension due to a combination of factors. Factors include rigid, noncompliant arteries, reduced skeletal muscle pumping of venous return due to physical inactivity, and degeneration of the sinoatrial node and conduction system due to progressive structural heart disease.

 

In older adults, syncope often has more than one cause. For example, the combination of taking several heart and blood pressure drugs and standing in a hot church during a long or emotional service may lead to syncope even though no single factor might cause syncope.

 

what we can say about fainting in a few words

·         Syncope results from global central nervous system dysfunction, usually resulting from insufficient cerebral blood flow.

·         Most syncope results from benign causes.

·         Some less common causes involve cardiac arrhythmia or outflow obstruction and are serious or potentially fatal.

·         Vasovagal syncope usually has an apparent trigger, warning symptoms, and a few minutes or longer of postrecovery symptoms.

·         Syncope due to cardiac arrhythmias typically occurs abruptly and with quick recovery.

·         If a benign etiology is not clear, driving and use of machinery should be prohibited until the cause is determined and treated—the next manifestation of an unrecognized cardiac cause may be fatal.

·         Treatment is directed at the underlying disorder.