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Stokes-Adams Attacks

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Stokes-Adams Attacks

ETIOLOGY AND PATHOPHYSIOLOGY

para>Rare during pregnancy

Initial Tests (lab, imaging)

Syncope requires frequent and close follow-up.

Admission Criteria/Initial Stabilization

Syncope in the setting of known AV node conduction abnormality or of an unknown cause. See first-line treatments to be used when intracardiac pacing is not available. External pacing may be life-saving.

Institution of proper treatment with resolution of symptoms

After the diagnosis has been made and a pacemaker has been implanted (if required), instruct patient regarding pacemaker guidelines.

Excellent with proper institution of exogenous pacing; further symptoms are not expected.

11 Kojic EM, Hardarson T, Sigfusson N, et al. The prevalence and prognosis of third-degree atrioventricular conduction block: the Reykjavik study. J Intern Med. 1999;246(1):81 " 86.22 Vukomanovic V, Stajevic M, Kosutic J, et al. Age-related role of ambulatory electrocardiographic monitoring in risk stratification of patients with complete congenital atrioventricular block. Europace. 2007;9(2):88 " 93.33 D az-Castro O, Orizaola P, V ‘zquez S, et al. Images in cardiovascular medicine. "Stokes-Adams epilepsy " : sometimes we need the electroencephalogram. Circulation. 2005;112(8):e101 " e102.44 Sigurd B, Sand Έe E. Management of Stokes-Adams syndrome. Cardiology. 1990;77(3):195 " 208.55 Tomassoni AJ, Sanders S, Marcolini EG. Emergency department treatment of beta blocker and calcium-channel blocker poisoning. EM Critical Care. 2014:4:1 " 16.66 Epstein AE, Dimarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary. Heart Rhythm. 2008;5(6):934 " 955.http://www.heart.org/HEARTORG/CPRAndECC/Science/Guidelines/2010-AHA-Guidelines-for-CPR-ECCUCM317311_SubHomePage.jsp. Accessed 2014.77 Dretzke J, Toff WD, Lip GY, et al. Dual chamber versus single chamber ventricular pacemakers for sick sinus syndrome and atrioventricular block. Cochrane Database Syst Rev. 2004;(2):CD003710.88 Epstein AE, DiMarco JP, Ellenbogen KA, et al. 2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. Circulation. 2013;127(3):e283 " e352.

I45.9 Conduction disorder, unspecified

  • MedicationsDigoxin (common)Calcium channel blockers Ž ²-Blockers (e.g., sotalol)ClonidinePropafenone (Rythmol), a class IC antiarrhythmicIsoproterenol
  • Other causes:Myocardial ischemia involving the AV nodeDegenerative (fibrosing) and infiltrative diseases involving the heart and its conduction system (e.g., Len ƒ ¨gre disease, systemic sclerosis, valvular disease, infective endocarditis, sarcoidosis)Degeneration of the AV node secondary to agingNeuromuscular diseases (e.g., myotonic muscular dystrophy or Kearns-Sayre syndrome)Postoperative cardiac damage
  • The abrupt development of complete AV block, especially at His bundle level, may result in a prolonged period of asystole because of a slow and delayed response of the quiescent subsidiary (escape) ventricular pacemaker.
  • Marked bradycardia secondary to AV conduction abnormality may lead to prolonged QT interval and paroxysmal torsades de pointes.
  • Abrupt termination of tachyarrhythmia leading to precipitous decrease in heart rate.
  • Degree of cerebral dysfunction related to duration of cardiac block and effect on cerebral circulation.
  • Digoxin (common)
  • Calcium channel blockers
  • Ž ²-Blockers (e.g., sotalol)
  • Clonidine
  • Propafenone (Rythmol), a class IC antiarrhythmic
  • Isoproterenol
  • Myocardial ischemia involving the AV node
  • Degenerative (fibrosing) and infiltrative diseases involving the heart and its conduction system (e.g., Len ƒ ¨gre disease, systemic sclerosis, valvular disease, infective endocarditis, sarcoidosis)
  • Degeneration of the AV node secondary to aging
  • Neuromuscular diseases (e.g., myotonic muscular dystrophy or Kearns-Sayre syndrome)
  • Postoperative cardiac damage
  • May be associated with complete congenital atrioventricular block (CCAVB)
  • Of children with CCAVB, 40% experience syncopal episodes (2).

RISK FACTORS

  • Use of the medications listed under "Etiology and Pathophysiology " 
  • Coronary artery disease
  • Endocarditis and myocarditis
  • Mitral/aortic valve disease
  • History of previous AV nodal dysfunction/cardiac surgery
  • Bundle-branch and/or fascicular block
  • Acute myocardial infarction (MI) (especially acute right coronary artery occlusion)
  • Amyloidosis
  • Chagas disease
  • Lyme disease
  • Connective tissue diseases involving the heart (e.g., systemic lupus erythematosus, rheumatoid arthritis, sarcoidosis)
  • Hyperkalemia
  • Acidosis
  • Rheumatic fever

GENERAL PREVENTION

  • Avoid negative chronotropic drugs (e.g., Ž ²-blockers, calcium channel blockers, digoxin, clonidine) in at-risk patients.
  • Prevention of cardiovascular disease through diet/exercise

COMMONLY ASSOCIATED CONDITIONS

  • Myocardial ischemia/acute MI
  • High-degree AV conduction abnormality
  • Atrial standstill
  • Right bundle-branch block (RBBB)
  • CCAVB
  • Systemic manifestations of connective tissue disease
  • Sick sinus syndrome
  • Neuromuscular disease
  • Sudden death
  • Heart failure

DIAGNOSIS

HISTORY

  • History of predisposing factor/related conditions
  • Angina
  • Fatigue/exercise intolerance
  • Dyspnea
  • Altered sensorium/loss of consciousness unrelated to position/exertion
  • Acute onset of syncopal/near-syncopal symptoms ( ‚ ± palpitations)

PHYSICAL EXAM

  • Acute bradycardia
  • Hypotension
  • Pallor
  • Reactive hyperemia with recovery
  • Convulsions or seizure-like activity without postictal state
  • Pulse <50 bpm

DIFFERENTIAL DIAGNOSIS

  • Seizure
  • Vertigo
  • Transient ischemic attack
  • Orthostatic hypotension
  • Vasovagal syncope
  • Hypoglycemia
  • Neurocardiogenic syncope
  • Cardiac arrhythmiasVentricular tachycardiaSupraventricular tachycardiaReentrant tachycardiaWolff-Parkinson-White syndromeSinus arrestSinus exit blockSick sinus syndromeTransition from normal sinus rhythm to atrial fibrillation or vice versa
  • Brugada syndrome
  • Carotid sinus hypersensitivity
  • Ventricular tachycardia
  • Supraventricular tachycardia
  • Reentrant tachycardia
  • Wolff-Parkinson-White syndrome
  • Sinus arrest
  • Sinus exit block
  • Sick sinus syndrome
  • Transition from normal sinus rhythm to atrial fibrillation or vice versa

DIAGNOSTIC TESTS & INTERPRETATION

  • Cardiac enzymes (i.e., troponin-I)
  • EEG with cardiac monitoring (to differentiate between syncope and seizure disorder) (3)
  • ECG: partial/complete heart block at onset of symptoms with slow or no ventricular escapeBradycardiaAV block 50 " “60%Sinoatrial block 30 " “40%Widened QRS, possibly of RBBB type, QTc >45 msec 4%Ventricular fibrillation/tachycardia <1%Marked ventricular slowing during sleepWolf-Parkinson-White delta waves (infrequent)
  • Serum digoxin level (other medication levels if appropriate)
  • Thyroid-stimulating hormone level
  • Hematocrit/hemoglobin
  • Blood electrolyte levels (especially potassium)
  • Transthoracic echocardiogram if cardiomyopathy/valvular disease is suspected
  • Bradycardia
  • AV block 50 " “60%
  • Sinoatrial block 30 " “40%
  • Widened QRS, possibly of RBBB type, QTc >45 msec 4%
  • Ventricular fibrillation/tachycardia <1%
  • Marked ventricular slowing during sleep
  • Wolf-Parkinson-White delta waves (infrequent)
  • ECG, event monitor, or 24-hour Holter monitor
  • Renal failure may lead to falsely elevated creatinine kinase.
  • Coronary catheterization to rule out coronary ischemia if suspected
  • Electrophysiologic testing to assess cardiac conduction system if ECG testing is ambiguous
  • Tilt-table test to evaluate neurogenic etiology
  • Myocardial biopsy if infiltrative disease suspected
  • Myocardial ischemia
  • Evidence of degenerative/infiltrative disease involving the AV node/His bundle

TREATMENT

GENERAL MEASURES

  • Inpatient assessment in a monitored setting
  • Continued treatment for prevention of future episodes in an ambulatory setting
  • Cessation of precipitating medications
  • Pacemaker implantation should be performed; oral medications are inferior therapy (4).
  • Avoid: isoproterenol, digoxin, fosphenytoin, phenytoin
  • Treat calcium channel blocker toxicity with calcium gluconate 60 mg/kg/dose over 5 minutes (max: 3,000 to 6,000 mg/dose) every 10 to 20 minutes; can repeat for 3 to 4 additional doses
  • Treat Ž ²-blockers toxicity with glucagon IV bolus 3 to 10 mg, then infuse at a rate of 2 to 5 mg/hr.
  • For moderate Ž ²-blocker or calcium channel blocker toxicity, consider high-dose insulin (with glucose) or vasopressor therapy (5).
  • Symptomatic Ž ²-blocker and calcium channel blocker toxicity should be admitted to the ICU for support and continuous cardiac monitoring (5).
  • Blood pressure support for shock resulting from combined Ž ²-blocker and calcium channel blocker toxicity with methylene blue bolus 1 mg/kg over 10 minutes, then infuse at 1 mg/kg/hr for 10 hours (5)
  • Treat mixed or multidrug toxicity with lipid resuscitation therapy (Intralipid) or molecular absorbent recirculating system (5).

MEDICATION

  • No medication currently is recommended for long-term treatment of symptomatic arrhythmias (6)[A].
  • For symptomatic bradyarrhythmias (7)[C]Atropine 0.5 mg IV push to be given during the complete heart block with hypotension; may be repeated q3 " “5min with a maximum total dose of 3 mg; less likely to be effective if atrial rate is already adequate or in patients who have undergone cardiac transplantationPrecautions: Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate.Contraindications: narrow-angle glaucoma, reflux esophagitis, obstructive GI disease, unstable cardiovascular status in acute hemorrhage or thyrotoxicosis, myasthenia gravis
  • Correction of precipitating conditions (e.g., hypokalemia, acidosis)
  • Atropine 0.5 mg IV push to be given during the complete heart block with hypotension; may be repeated q3 " “5min with a maximum total dose of 3 mg; less likely to be effective if atrial rate is already adequate or in patients who have undergone cardiac transplantationPrecautions: Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate.Contraindications: narrow-angle glaucoma, reflux esophagitis, obstructive GI disease, unstable cardiovascular status in acute hemorrhage or thyrotoxicosis, myasthenia gravis
  • Precautions: Doses of atropine sulfate of <0.5 mg may paradoxically result in further slowing of the heart rate.
  • Contraindications: narrow-angle glaucoma, reflux esophagitis, obstructive GI disease, unstable cardiovascular status in acute hemorrhage or thyrotoxicosis, myasthenia gravis
  • For arrhythmias and heart blockEphedrine 5 to 25 mg IV push, titrate to patient response; repeat in 5 to 10 minutes if necessary; 25 to 50 mg IM or SC, range from 10 to 50 mgPrecautions: hypertension and tachycardia; risk of serious adverse effects; caution in patients with cardiovascular disease, pregnancy, limited use in pediatric patientsContraindications: angle-closure glaucoma; should not be used if vasopressor drugs are contraindicated; known hypersensitivity to ephedrinePossible interactions: Concurrent use of certain monoamine oxidase inhibitors and catecholamines may result in increased hypertensive effects/hypertensive crisis; concurrent use of dopamine and epinephrine with cyclopropane/halogenated hydrocarbon anesthetic may sensitize the heart to the arrhythmic action of sympathomimetic drugs.
  • Ephedrine 5 to 25 mg IV push, titrate to patient response; repeat in 5 to 10 minutes if necessary; 25 to 50 mg IM or SC, range from 10 to 50 mgPrecautions: hypertension and tachycardia; risk of serious adverse effects; caution in patients with cardiovascular disease, pregnancy, limited use in pediatric patientsContraindications: angle-closure glaucoma; should not be used if vasopressor drugs are contraindicated; known hypersensitivity to ephedrine
  • Possible interactions: Concurrent use of certain monoamine oxidase inhibitors and catecholamines may result in increased hypertensive effects/hypertensive crisis; concurrent use of dopamine and epinephrine with cyclopropane/halogenated hydrocarbon anesthetic may sensitize the heart to the arrhythmic action of sympathomimetic drugs.
  • Precautions: hypertension and tachycardia; risk of serious adverse effects; caution in patients with cardiovascular disease, pregnancy, limited use in pediatric patients
  • Contraindications: angle-closure glaucoma; should not be used if vasopressor drugs are contraindicated; known hypersensitivity to ephedrine

ISSUES FOR REFERRAL

SURGERY/OTHER PROCEDURES

  • Transthoracic pacing should be attempted as a temporizing device if a patient is bradycardic and hemodynamically unstable.
  • Intracardiac pacing is the treatment of choice for patients with complete heart block and Stokes-Adams syncope (6)[A].
  • Dual chamber may be more effective than single chamber pacing in AV block (8)[B].
  • Transvenous pacing as interim measure to stabilize
  • See 2012 American College of Cardiology/American Heart Association/Heart Rhythm Society focused update incorporated into the 2008 guidelines for device-based therapy of cardiac rhythm abnormalities for suggested intervention based on precipitating cause (9).
  • Emergency insertion of a ventricular pacemaker is required when ventricular fibrillation/tachycardia is present.

INPATIENT CONSIDERATIONS

  • Telemetry
  • Out of bed with assist if patient has history of falls due to syncope

ONGOING CARE

FOLLOW-UP RECOMMENDATIONS

  • Routine pacemaker check if permanent pacemaker has been implanted
  • Follow-up Holter and/or event monitoring for 2 weeks after causal medication has been discontinued
  • Discontinuation of driving, heavy machinery operation; caution about fall risks

DIET

PATIENT EDUCATION

PROGNOSIS

COMPLICATIONS

  • Sudden death (uncommon)
  • Cerebral hypoxic damage and other end-organ damage with protracted bradycardia with hypotension

REFERENCES

ADDITIONAL READING

  • Bedford Laboratories. Ephedrine Sulfate Injection. USP (50 mg/mL) Prescribing Information. Bedford, OH: Bedford Laboratories; 1998.
  • Elizari ‚ MV, Acunzo ‚ RS, Ferreiro ‚ M. Hemiblocks revisited. Circulation. 2007;115(9):1154 " “1163.
  • Hood ‚ R. Syncope in the elderly. Clin Geriatr Med. 2007;23(2):351 " “361.
  • Jensen ‚ G, Sigurd ‚ B, Sandoe ‚ E. Adams-Stokes seizures due to ventricular tachydysrhythmias in patients with heart block: prevalence and problems of management. Chest. 1975;67(1):43 " “48.
  • McEvoy ‚ GK, ed. Ephedrine. In: AHFS Drug Information 2003. Bethesda, MD: American Society of Health " “System Pharmacists; 2003:1235 " “1241.
  • Vanden Hoek ‚ TL, Morrison ‚ LJ, Shuster ‚ M, et al. Part 12: cardiac arrest in special situations: 2010 American Heart Association Guidelines for cardioresuscitation and emergency cardiovascular care. Circulation. 2010;122(18)(Suppl 3):S829 " “S861.
  • You ‚ C, Chong ‚ C, Wang ‚ T, et al. Unrecognized paroxysmal ventricular standstill masquerading as epilepsy: a Stokes-Adams attack. Epileptic Disord. 2007;9(2):179 " “181.

CODES

ICD10

ICD9

SNOMED

  • Stokes-Adams attack (disorder)
  • Stokes-Adams syndrome (disorder)

CLINICAL PEARLS

  • Syncope due to Stokes-Adams attacks frequently can be confused for epilepsy.
  • Stokes-Adams attacks usually require insertion of a pacemaker for definitive treatment unless due to a reversible condition, such as medication toxicity.
  • External pacing may serve as a bridge until more definitive management can be accomplished.