Rosen & Barkin's 5-Minute Emergency Medicine Consult (766 page)

• Primary cardiac arrest and VT are rare in children.
  
• Usually secondary to hypoxia and acidosis
  
• VT is tolerated for longer periods in children than adults and is less likely to degenerate to VF.
  
• Infants in VT most commonly present with CHF.
  
• VT in children results from:
  
  • Cardiomyopathy
    
  • Congenital structural heart disease
    
  • Congenital prolonged QT syndromes
    
  • Coronary artery disease secondary to vasculitis
    
  • Toxins, poisons, drugs
    
  • Severe electrolyte imbalances, especially of potassium
    

• Procainamide: 3–6 mg/kg over 5 min, may repeat every 5–10 min to max. total dose of 15 mg/kg. Do not exceed 100 mg/dose or 500 mg in 30 min (peds: 15 mg/kg IV/IO over 30–60 min).
  
• Amiodarone: 150 mg IV bolus over 10 min, may repeat; arrest dose is 300 mg IV/IO max. cumulative dose 2.2 g IV/24 h; followed by 1 mg/min for 6 hr, then 0.5 mg/min for 18 hr. (peds: 5 mg/kg IV or IO over 20–60 min, max. 15 mg/kg/d)
  
• MgSO
  ₄
  : 2 g in D
  ₅
  W over 5–10 min followed by infusion of 0.5–1 g/h IV, titrate to control torsades (peds: 25–50 mg/kg IV/IO over 10 min, max. dose 2 g)
  

• Lidocaine: 1–1.5 mg/kg bolus IV push 1st dose, 0.5–0.75 mg/kg 2nd dose, and q5–10min for a max. of 3 mg/kg; tracheal administration 2–4 mg/kg; maintenance infusion 1–4 mg/min if converted. Not recommended for ACS induced VT(peds: 1 mg/kg bolus with infusion 20–50 μg/kg/min)
  
• Adenosine: 6 mg IV push followed by 12 mg IV push if needed in 1–2 min (peds: 1 mg/kg, max. 6 mg). Note: Does not convert VT, do not use if unstable or irregular WCT.
  
• Isoproterenol: 2–10 μg/min, titrate to heart rate (peds: 0.1 μg/kg/min). Note: Do not give with epinephrine, may precipitate VT/VF (no longer part of ACLS protocol), do not give if prolonged QT.
  
• Sotalol: 100 mg IV over 5 min. (peds: Use not recommended for initial management). Note: Do not give if prolonged QT.
  

FOLLOW-UP

• Admit sustained VT to a critical care setting.
  
• Admit nonsustained VT and a history of MI or dilated cardiomyopathy for electrophysiologic studies.
  

• Rare patients with nonsustained VT and a previous evaluation that revealed no structural heart disease can be discharged:
  
  • At low risk for SCD
    
• Patients with automatic internal cardiac defibrillators that are well functioning can also be discharged.
  

All patients discharged with VT should be followed by a cardiologist within 48 hr.

Patients should follow-up with a cardiologist.

• Search for contributing factors such as toxins, metabolic abnormalities, trauma, hypothermia, thrombosis.
  
• Unstable VT requires early cardioversion.
  
• Administer postresuscitation maintenance medications to prevent recurrence.
  
• Watch for bradycardia and GI toxicity after amiodarone administration.
  
• Discontinue any proarrhythmic drugs
  
• Consider b2-blockade for ischemia-induced VT and polymorphic VT.
  

• Connolly SJ, Dorian P, Roberts RS, et al. Comparison of beta-blocker, amiodarone plus beta-blockers, or sotalol for prevention of shocks from implantable cardioverter defibrillators: The OPTIC Study: A randomized trial.
  JAMA
  . 2006;295:165–171.
  
• Pellegrini CN, Scheinman MM. Clinical management of ventricular tachycardia.
  Curr Probl Cardiol.
  2010;35(9):453–504.
  
• Zipes DP, Camm AJ, Borggrefe M, et al. ACC/AHA ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death—executive summary.
  J Am Coll Cardiol
  . 2006;48:1064--1108.
  

Thank you to the prior authors of this chapter, Jennifer Audi and Shannon Straszewski

See Also (Topic, Algorithm, Electronic Media Element)

2010 AHA Guidelines for CPR and ECC

CODES

427.1 Paroxysmal ventricular tachycardia

BASICS

• Vertebrobasilar (VB) vascular system feeds the posterior region of the brain, which includes the brainstem, cerebellum, and inner ear
  
• 2 vertebral arteries (VA) derive from subclavian arteries and give rise to the anterior spinal artery and then join to form the basilar artery
  
• Arteries supplying the brainstem and cerebellum originate from the VB system before it branches into the 2 posterior cerebral arteries (PCA), such that a wide variety of focal neurological deficits arise from VB circulatory dysfunction
  
• Vertebrobasilar insufficiency (VBI) results in inadequate perfusion of VB arterial circulation from thrombotic, embolic, or low-flow states
  

• Mechanism:
  
  • Thrombosis:
    
    • VB ischemia due to underlying VB atherosclerosis and clot formation
      
  • Embolus:
    
    • VB ischemia due to embolization of clot from proximal location
      
  • Low-flow states:
    
    • Hypoperfusion of VB system from systemic (e.g., cardiogenic shock) or localized (e.g., subclavian steal) reduction in blood flow
      
  • Less common etiologies:
    
    • Fibromuscular dysplasia
      
    • Hypercoagulable states
      
• Ischemic mechanisms causing VB insufficiency can herald and lead to VB territory infarcts
  
• Severe episodes of VB hypoperfusion or loss of circulation can lead to:
  
  • “Locked-in” syndrome:
    
    • Quadriplegia (eyelid or eye movement only) with intact consciousness
      
  • “Top-of-basilar” syndrome:
    
    • Pontine and cerebellar dysfunction with diminished level of consciousness
      

DIAGNOSIS

All history and physical exam items may present intermittently

• Dizziness/vertigo (“mild,” “nonviolent”; may be isolated finding)
  
• Onset usually abrupt and spontaneous rather than position induced
  
• May have a flurry of spells within a few weeks time
  
• “Drop attack”
  
• Headache
  
• Nausea/vomiting
  
• Paresis/paresthesia
  
• Seizure
  
• Syncope
  
• Neurologic symptoms localizing to the posterior circulation:
  
  • Visual changes (double vision, blurry vision, blindness)
    
  • Numbness of the face or extremities
    
  • Weakness in arms or legs
    
  • Clumsiness in arms or legs
    
  • Confusion or loss of consciousness
    
  • Difficulty with speech
    
  • Difficulty swallowing
    
  • Pain in neck or shoulder
    

• Brainstem:
  
  • “Crossed” findings (i.e., ipsilateral facial and contralateral body deficits)
    
  • Altered mental status or responsiveness
    
  • Decreased respiratory drive
    
  • Horner's syndrome (enophthalmos, ptosis, miosis, anhidrosis)
    
  • Internuclear ophthalmoplegia
    
  • Nystagmus (especially nonfatigable, vertical/rotatory)
    
  • Paresis/paresthesias
    
• Cranial nerves:
  
  • Extraocular muscle paresis (e.g., diplopia)
    
  • Pupillary abnormalities
    
  • Facial paresthesia
    
  • Facial muscle paresis
    
  • Hearing abnormalities
    
  • Dysphagia
    
  • Dysarthria
    
• Cerebral cortex (PCA circulation):
  
  • Visual disturbances (e.g., homonymous hemianopsia)
    
• Cerebellar:
  
  • Ataxia
    
  • Dysmetria
    
  • Gait abnormality
    
• Cardiovascular:
  
  • Carotid/VA bruit
    
  • Irregular/asymmetric/weak pulses