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Stokes-Adams syndrome

Refer to fainting and convulsions induced by complete heart block with a pulse rate of 40 beats per minute or less.

Refers to a periodic fainting spell in which there is a periodic onset and offset of blockage of heart due to disorder of heart rhythm that may last for seconds, hours, days, or even weeks before the conduction returns.

It is characterised by decrease in cardiac output and loss of consciousness due to a transient arrhythmia.

Typically an attack occurs without warning leading to sudden loss of consciousness.

Prior to an attack, a patient may be pale with hypoperfusion.

Normal periods of unconsciousness last approximately thirty seconds; if abnormal movements are present, they will consist of twitching after 15–20 seconds.

The abnormal movements, occur because of brainstem hypoxia and not due to cortical discharge as evident by EEG findings which show no epileptiform activities.

Breathing continues normally throughout the attack.

On recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.

Fainting does not depend on the patient’s position.

Can occur during sleep, and the presenting symptom may simply be feeling hot and flushed on waking.[5] [6]

May be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic.

The ECG will show asystole, an AV block, or ventricular fibrillation during the attacks.

Caused by any temporary lack of cardiac output.

This in turn could most commonly be caused by cardiac asystole, heart block, or ventricular fibrillation.

Paroxysmal supraventricular tachycardia or atrial fibrillation is the underlying cause in up to 5% of patients, and the resulting lack of blood flow to the brain is responsible for the faint.

Treatment

Initial treatment involve the use of drugs like isoprenal and epinephrine.

Definitive treatment involves the insertion of a pacemaker, after electrocardiography confirms this type of approach.

If undiagnosed or untreated, has a 50% mortality within a year of the first episode, while the prognosis following treatment is very good.

refers to a periodic fainting spell in which there is a periodic onset and offset of blockage of heart due to disorder of heart rhythm that may last for seconds, hours, days, or even weeks before the conduction returns.

It is characterised by decrease in cardiac output and loss of consciousness due to a transient arrhythmia. For example, bradycardia due to complete heart block.

Typically an attack occurs without warning leading to sudden loss of consciousness.

Prior to an attack, a patient may be pale with hypoperfusion.

Normal periods of unconsciousness last approximately thirty seconds; if abnormal movements are present, they will consist of twitching after 15–20 seconds.

The abnormal movements, occur because of brainstem hypoxia and not due to cortical discharge as evident by EEG findings which show no epileptiform activities.

Breathing continues normally throughout the attack.

On recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.

Fainting does not depend on the patient’s position.

Can occur during sleep, and the presenting symptom may simply be feeling hot and flushed on waking.[5] [6]

May be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic.

The ECG will show asystole, an AV block, or ventricular fibrillation during the attacks.

Caused by any temporary lack of cardiac output.

This in turn could most commonly be caused by cardiac asystole, heart block, or ventricular fibrillation.

Paroxysmal supraventricular tachycardia or atrial fibrillation is the underlying cause in up to 5% of patients, and the resulting lack of blood flow to the brain is responsible for the faint.

Treatment

Initial treatment involve the use of drugs like isoprenal and epinephrine.

Definitive treatment involves the insertion of a pacemaker, after electrocardiography confirms this type of approach.

If undiagnosed or untreated, has a 50% mortality within a year of the first episode, while the prognosis following treatment is very good.

refers to a periodic fainting spell in which there is a periodic onset and offset of blockage of heart due to disorder of heart rhythm that may last for seconds, hours, days, or even weeks before the conduction returns.

It is characterised by decrease in cardiac output and loss of consciousness due to a transient arrhythmia. For example, bradycardia due to complete heart block.

Typically an attack occurs without warning leading to sudden loss of consciousness.

Prior to an attack, a patient may be pale with hypoperfusion.

Normal periods of unconsciousness last approximately thirty seconds; if abnormal movements are present, they will consist of twitching after 15–20 seconds.

The abnormal movements, occur because of brainstem hypoxia and not due to cortical discharge as evident by EEG findings which show no epileptiform activities.

Breathing continues normally throughout the attack.

On recovery the patient becomes flushed as the heart rapidly pumps the oxygenated blood from the pulmonary beds into a systemic circulation which has become dilated due to hypoxia.

Fainting does not depend on the patient’s position.

Can occur during sleep, and the presenting symptom may simply be feeling hot and flushed on waking.

May be diagnosed from the history, with paleness prior to the attack and flushing after it particularly characteristic.

The ECG will show asystole, an AV block, or ventricular fibrillation during the attacks.

Caused by any temporary lack of cardiac output.

This in turn could most commonly be caused by cardiac asystole, heart block, or ventricular fibrillation.

Paroxysmal supraventricular tachycardia or atrial fibrillation is the underlying cause in up to 5% of patients, and the resulting lack of blood flow to the brain is responsible for the faint.

Treatment

Initial treatment involve the use of drugs like isoprenal and epinephrine.

Definitive treatment involves the insertion of a pacemaker, after electrocardiography confirms this type of approach.

If undiagnosed or untreated, has a 50% mortality within a year of the first episode, while the prognosis following treatment is very good.

Caracterized by dizziness, dyspnea, and syncope.

Caused by an abnormality of the electrical conduction system that begins with a slow heart rate , and evolves into asystole.

Electrical impulses originating in the atrium or sinus node are blocked at the atrioventricular node (AV node) preventing the impulses from traveling to the ventricles.

Occurs with third-degree atrioventricular block or complete heart block.

With heart stoppage loss of oxygen to the brain results in fainting, and convulsions may occur if the heart stops for longer than 15 seconds.

May result from ischemia caused by a myocardial infarction, drugs, hyperkalemia, congenital heart disease, aging , diseases of the aortic and mitral valves, postoperative complications, acute rheumatic fever, endocarditis, myocarditis, Lyme disease, and almost any other systemic infectious disease, infiltrative and connective tissue diseases such as tumors, sarcoidosis, and amyloidosis.

Age is a risk factor.

Prevalence of third-degree atrioventricular block is 0.02%, and the incidence rate is 5 to 10% for those over age 70 years.

Symptoms include light-headedness, fatigue, dizziness or dyspnea followed by syncope usually in while a lying or standing position.

Physical examination will often be normal.

Laboratory testing should include drug levels and blood electrolytes, cardiac enzymes to assess for a myocardial infarction), a complete blood count for infection, or tests for connective tissue diseases.

Electrocardiogram may confirm the diagnosis of an electrical conduction block.

Holter monitor may be worn to establish abnormal arrhythmia.

Echocardiogram can be used to identify other structural defects that may be associated with conduction abnormalities.

An intracardiac electrophysiology study is helpful to assess the electrical conduction system of the heart.

Implantation of a pacemaker is still the treatment of choice.

Anticholinergics or sympathomimetics may be prescribed temporarily during emergencies while a temporary pacemaker is inserted until a permanent pacemaker can be implanted.

Mental status impairment episodes are usually brief, and most often, patients will recover immediately.

Pacemaker implantation associated with significant improvement in most patients.

After pacemaker implantation, the individual experiencing Stokes-Adams syndrome participates in an exercise program with four progressive phases following the surgical intervention.

Complications include: permanent brain neurological impairment and seizures, trauma from falling during fainting spells, heart failure, and sudden cardiac death.

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