Rosen & Barkin's 5-Minute Emergency Medicine Consult (649 page)

• 831.00 Closed dislocation of shoulder, unspecified
  
• 831.01 Closed anterior dislocation of humerus
  
• 831.02 Closed posterior dislocation of humerus
  

BASICS

• Collective term used to describe dysfunction in the sinus node’s 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
  

• 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:
    
    • β-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

Symptoms represent CNS hypoperfusion from bradydysrhythmia or traditional cardiovascular presentations

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

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

• Ascertaining etiology
  
• 12-lead EKG
  
• CXR
  

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

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
  

Most electrophysiologic studies are no longer recommended due to poor sensitivity and specificity.

• 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: β-blockers, calcium channel blockers, clonidine, digoxin
  
• Excessive vagal tone
  

TREATMENT

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

• 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
  

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: O
    ₂
    , warming, glucose
    

• 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 μg/min IV, titrate to goal heart rate/BP, max. 10 μg/min (peds: 0.1 μg/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
  

1st-line definitive therapy is a permanent demand pacemaker to provide a “floor” to bradydysrhythmia:

• Patients with additional tachydysrhythmias will require additional nodal agents.
  

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

FOLLOW-UP

• 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.
  

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

• Need for formal cardiac electrophysiology evaluation
  
• Need for permanent pacemaker placement
  

• 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.
  

• 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.
  

• Adán 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.