Sick Sinus Syndrome, Emergency Medicine

Basics

Description

Collective term used to describe dysfunction in the sinus nodes automaticity and impulse generation
Mechanism:
- Caused by progressive degeneration of the intrinsic functions of the sinoatrial (SA) node
- Characterized by periods of unexplained sinus node dysfunction leading to bradyarrhythmias, often without appropriate atrial or junctional escape rhythms
Syndrome includes:
- Chronic SA nodal dysfunction
- Frequently depressed pacemakers
- Arteriovenous nodal conduction disturbances
- Sluggish return of SA nodal activity after DC cardioversion
Presents in all age groups (mean age >65 yr)
Male/female ratio is 1:1

Etiology

Intrinsic causes:
- Most common cause: Idiopathic degenerative fibrosis of sinus node
- Coronary artery or SA nodal artery disease
- Cardiomyopathy
- Ion channel mutations/familial SSS
- Leukemia and metastatic disease
- Infiltrative cardiac or collagen vascular disease, including amyloidosis
- Surgical trauma
Inflammatory diseases:
- Rheumatic heart disease
- Chagas disease
- Pericarditis and myocarditis
Extrinsic causes (not true SSS but similar presentation):
- Drugs:
  - ²-blockers, calcium channel blockers, clonidine
  - Digoxin, amiodarone
  - Lithium, phenytoin
- Autonomically mediated syndromes (cholinesterase deficiency)
- Hyperkalemia/hypokalemia
- Hypothyroidism
- Hypothermia
- Hypoglycemia
- Sepsis/infection

Associated with congenital abnormalities and subsequent surgical repair, as well as with congenital SA nodal artery deficiency

Diagnosis

Signs and Symptoms

Symptoms represent CNS hypoperfusion from bradydysrhythmia or traditional cardiovascular presentations
History

Asymptomatic
Palpitations/fatigue
Syncope/presyncope/dizziness
Anginal equivalents (chest pain/SOB)
Activity intolerance
Sudden death

Physical Exam

Bradycardia
Alternating bradycardia and atrial tachycardia
Altered mental status
Cyanosis
Transient ischemic attack/stroke

Essential Workup

Ascertaining etiology
12-lead EKG
CXR

Diagnosis Tests & Interpretation

Lab

Serum electrolytes (including magnesium and calcium)
Cardiac markers
Digoxin level, if appropriate
Thyroid function testing

Imaging
EKG:

Most common finding: Chronic, inappropriate sinus bradycardia
Sinus pauses or SA block
Atrial fibrillation with slow ventricular response
Prolonged pauses after cardioversion or carotid massage
Bradyarrhythmias may alternate with supraventricular tachydysrhythmia.
Tachy " brady syndrome: Bursts of atrial tachycardia interspersed with bradycardia

Diagnostic Procedures/Surgery
Most electrophysiologic studies are no longer recommended due to poor sensitivity and specificity.

Differential Diagnosis

Other bradydysrhythmias
Other tachyarrhythmias: In particular, be careful to distinguish SSS from atrial fibrillation, because DC cardioversion or the use of nodal agents in presumed Afib can be harmful if SA node dysfunction coexists.
Electrolyte derangements
Medication toxicity: ²-blockers, calcium channel blockers, clonidine, digoxin
Excessive vagal tone

Treatment

Pre-Hospital

Advanced life support transport
Oxygen supplementation
Cardiac monitoring
Atropine if bradycardic and hemodynamically unstable
Transcutaneous pacing for unstable patients

Initial Stabilization/Therapy

Atropine if a bradydysrhythmia is causing unstable signs/symptoms: Angina, mental confusion, or hypotension
Transcutaneous pacing if atropine unsuccessful
If this fails, emergent transvenous pacing

Ed Treatment/Procedures

Supraventricular tachydysrhythmia alternating with bradycardia:

Unstable:
- Cardiovert
- Anticipate subsequent profound bradycardia
Stable patients:
- Cardiac monitoring
Digoxin, diltiazem, verapamil, or magnesium can be used for tachydysrhythmia
Any medication may cause profound bradycardia
Bradycardia:
- Discontinuation of medications that alter sinus node function
- Correct reversible causes of SA nodal depression: O2, warming, glucose

Rewarming is critical in hypothermia as atropine may cause myocardial instability:

Anticoagulate patients with atrial fibrillation and tachy " brady syndrome.

Medication

Atropine: 0.5 " 1 mg IV/ET:
- Repeat q5min as necessary, max. dose of 0.04 mg/kg (peds: 0.02 mg/kg, min., 0.1 mg)
Diltiazem: 0.25 mg/kg IV over 2 min followed in 15 min by 0.35 mg/kg IV over 2 min
Verapamil: 2.5 " 5 mg IV bolus over 2 min:
- May repeat with 5 " 10 mg q15 " 30min max. 20 mg
- Peds <1 yr: 0.1 " 0.2 mg/kg over 2 min; repeat q30min 1 " 15 yr: 0.1 " 0.3 mg/kg over 2 min, max. dose 5 mg/dose, can repeat once.
Digoxin: 0.5 mg IV initially then 0.25 mg IV q4h until desired effect (max. 1 mg IV)
Isoproterenol: 2 " 3 ¼g/min IV, titrate to goal heart rate/BP, max. 10 ¼g/min (peds: 0.1 ¼g/kg/min) " do not coadminister with epinephrine and only use in unstable patient
Epinephrine: 1 mg IV (peds: 0.01 mg/kg IV): For cardiac arrest
Glucagon: 0.05 " 0.15 mg/kg IV (peds: 0.05 " 0.10 mg/kg)
Heparin: Load 80 U/kg IV; infusion at 18 U/kg/h
Magnesium: 1 " 2 g IV

First Line
1st-line definitive therapy is a permanent demand pacemaker to provide a "floor " to bradydysrhythmia:

Patients with additional tachydysrhythmias will require additional nodal agents.

Second Line
No clear evidence to distinguish between 1st- and 2nd-line treatment.

Follow-Up

Disposition

Admission Criteria

New onset
Symptomatic: CHF, syncope, chest pain, dizziness
Persistent bradyarrhythmia or tachydysrhythmia
Advanced age; >60 yr
Patients should be admitted to a telemetry floor with cardiology consultation.
Most will require permanent pacing.

Discharge Criteria

Asymptomatic, otherwise healthy patients can be evaluated as outpatients.
Holter monitoring

Issues for Referral

Need for formal cardiac electrophysiology evaluation
Need for permanent pacemaker placement

Followup Recommendations

High incidence of CAD is present in patients with sick sinus syndrome, so a complete cardiovascular risk-factor evaluation and prevention is needed.
Patient with atrial fibrillation and tachy " brady syndrome need long-term anticoagulation.
All patients require evaluation by a cardiologist or EP specialist for permanent pacemaker.

Pearls and Pitfalls

Patients who are asymptomatic on ED arrival may have normal EKGs. Consider obtaining a rhythm strip or Holter monitor if clinical suspicion remains high.
Use of any nodal agents (BB, CCB, or digoxin) in patients with SSS-related tachydysrhythmia risks SA block or SA arrest and should only be administered when prepared for transcutaneous pacing.

Additional Reading

Ad ¡n V, Crown LA. Diagnosis and treatment of sick sinus syndrome. Am Fam Physician. 2003;67(8):1725 " 1732.
Anderson JB, Benson DW. Genetics of sick sinus syndrome. Card Electrophysiol Clin. 2010;2(4):499 " 507.
Brady WJ Jr, Harrigan RA. Evaluation and management of bradyarrhythmias in the emergency department. Emerg Med Clin North Am. 1998;16(2):361 " 388.
Dobrzynski H, Boyett MR, Anderson RH. New insights into pacemaker activity: Promoting understanding of sick sinus syndrome. Circulation. 2007;115:1921 " 1932.
Kaushik V, Leon AR, Forrester JS Jr, et al. Bradyarrhythmias, temporary and permanent pacing. Crit Care Med. 2000;28:N121 " N128.
Mangrum JM, DiMarco JP. The evaluation and management of bradycardia. N Engl J Med. 2000;342:703 " 709.
Rubenstein JJ, Schulman CL, Yurchak PM, et al. Clinical spectrum of the sick sinus syndrome. Circulation. 1972;46:5 " 13.
Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricular conduction blocks. Emerg Med Clin North Am. 2006;24:1 " 9.

Codes

ICD9

427.81 Sinoatrial node dysfunction

ICD10

I49.5 Sick sinus syndrome

SNOMED

36083008 Sick sinus syndrome (disorder)
233913007 Familial sick sinus syndrome (disorder)

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