stokes adams attack

Stokes Adams syndrome

Stokes Adams syndrome also known as Stokes-Adams attack, refers to fainting or syncope that occurs from cardiac arrhythmia. The classical description of a Stokes Adams attack is of
collapse without warning, associated with loss of consciousness lasting a few seconds 1). The affected individual is pale initially, but can become flushed on recovery from the syncopal episode. This flushing does not always occur, and some seizure-like activity can be noted if the Stokes Adams attack is prolonged. Stokes Adams syndrome or Stokes-Adams attack is typically associated with complete heart block (third-degree heart block), but has also been described in other diseases such as tachy-brady syndrome 2).

The term Stokes Adams attack is still commonly used by non-specialist doctors although rarely used by cardiologists and doctors specializing in the management of syncope 3). Heart block still causes syncope but is rare (<3% of cases) 4) and does not often present with classical Stokes Adams attacks. By contrast, various other cardiovascular disorders can present with sudden, transient loss of consciousness. These collapses might previously have been described clinically as Stokes Adams attacks, but improved understanding of cardiovascular physiology and pathology and techniques for investigation, and the development of specific diagnostic classifications have left the term increasingly redundant.

Stokes-Adams attacks are related to paroxysmal or chronic atrioventricular (AV) block (50-60%), sinoatrial (SA) block (30-40%) or paroxysmal tachycardia or fibrillation (0-5%) 5). In between attacks most patients present with sinus rhythm, a large part with widened QRS complex. A minor proportion of patients present with chronic AV block. ECG is very rarely normal.

Many disorders can mimic syncope. Less common causes of cardiovascular syncope include obstructive cardiac lesions (eg, aortic stenosis, atrial myxoma, and hypertrophic cardiomyopathy), cerebrovascular insufficiency, subclavian steal syndrome, psychogenic syncope, hyperventilation, and other situational syncopes such as cough or sneeze syncope, and micturition syncope.

Assessment of patients with collapse begins with a history detailing syncopal episodes, other problems, and potential culprit drugs. Thorough physical examination should be done, including measurement of blood pressure and cardiovascular examination. In addition to a 12–lead electrocardiogram, routine hematological and biochemical investigations will identify potential contributory disorders such as anemia, hyponatremia, and hypothyroidism.

Diagnosis is based on ECG recording during fainting. In patients with sinus rhythm and bundle-branch block or AV block, ECG monitoring should be performed in hospital, since Stokes-Adams syndrome in these patients is a potentially life-threatening disease. In sick sinus syndrome where the suspected arrhythmia is not life-threatening, ambulatory ECG by Holter monitoring can be performed to establish the diagnosis. In cases where ECG monitoring leaves doubt, an electrophysiologic study including His bundle electrography and sinus node recovery time may support the diagnosis, although normal findings do not preclude the diagnosis. Pacemaker implantation should be performed in Stokes-Adams syndrome, as oral drug treatment is ineffective. The dual-chamber pacemaker presents the advantages of both physiological heart rate and AV synchrony, but has troublesome side effects. Most patients with tachycardia/bradycardia syndromes require supplementary anti-arrhythmic treatment, and in some patients additional long-term anticoagulation should be considered.

Adams-Stokes disease

Adams-Stokes disease also called Stokes-Adams disease, refers to a heart block that can slow the heart rate considerably, causing fainting (syncope) or convulsions. It’s caused when the heart’s electrical signals are interrupted as they pass from the upper (atria) to the lower (ventricles) chambers.

Stokes-Adams attack cause

Stokes-Adams attacks are related to paroxysmal or chronic atrioventricular (AV) block (50-60%), sinoatrial (SA) block (30-40%) or paroxysmal tachycardia or fibrillation (0-5%) 6). In between attacks most patients present with sinus rhythm, a large part with widened QRS complex. A minor proportion of patients present with chronic AV block. ECG is very rarely normal.

Many disorders can mimic syncope. Less common causes of cardiovascular syncope include obstructive cardiac lesions (eg, aortic stenosis, atrial myxoma, and hypertrophic cardiomyopathy), cerebrovascular insufficiency, subclavian steal syndrome, psychogenic syncope, hyperventilation, and other situational syncopes such as cough or sneeze syncope, and micturition syncope.

Cardiac arrhythmias

Tachyarrhythmias (eg, ventricular tachycardia) and bradyarrhythmias (eg, sinus arrest and complete heart block) can cause syncope through loss of cardiac output.

Diagnosis

Holter monitoring, external or implantable loop monitoring, and electrophysiological studies.

Treatment

Appropriate antiarrhythmic therapy and insertion of a pacemaker as necessary.

Vasovagal syncope

The commonest cause of the simple faint. Collapse results from hypotension resulting from sudden dilatation of venous capacitance vessels sometimes associated with vagally mediated bradycardia.

Diagnosis

Prolonged head-up tilt test done in controlled surroundings with, if necessary, pharmacological provocation (isoproterenol, glyceryl trinitrate).

Treatment

Advice on avoidance of situations that trigger faints, such as standing for a long time in supermarket queues. If urinary sodium is low, salt supplements can be given to reduce hypovolaemia. There may be a role for -blockers, selective serotonin reuptake inhibitor antidepressants, fludrocortisone, alpha agonists, and, rarely, pacing if there is substantial associated bradycardia.

Orthostatic hypotension

A sudden fall in blood pressure occurring on standing. It can result from hypovolaemia resulting from drugs, dehydration, or from vasodilators and is associated with atherosclerosis, diabetes, and long-lasting confinement to bed.

Diagnosis

An active stand under supervised continuous blood pressure monitoring. A drop of 20 mm Hg systolic or 10 mm Hg diastolic blood pressure within 3 min of standing, with reproduction of symptoms is diagnostic. The value of the cuff sphygmomanometer in assessments is questionable.

Treatment

Volume replacement and modification of drug treatment. Compression hosiery reduces venous pooling in legs. Fludrocortisone increases sodium retention and reduces hypovolaemia. Midodrine, an alpha-receptor agonist, increases blood pressure.

Carotid sinus hypersensitivity (three types)

  1. Cardioinhibitory, resulting in symptomatic asystole of longer than 3 seconds.
  2. Vasodepressor, resulting in systolic blood pressure fall >50 mm Hg.
  3. Mixed, a combination of 1) and 2).

Diagnosis

Carotid sinus massage done by skilled staff in monitored conditions.

Treatment

Advice given to avoid trigger factors such as tight collars. The cardioinhibitory form can be treated with permanent atrioventricular pacing.

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