Rosen & Barkin's 5-Minute Emergency Medicine Consult (83 page)

• Unresponsive patient
  
• Pulseless
  
• Agonal or absence of spontaneous respirations
  

• Confirm asystole in 2 limb leads to exclude VF.
  
• Confirm lead and cable connections.
  
• Confirm monitor power is on.
  
• Confirm monitor gain is up.
  
• Identify reversible causes (see above)
  

Arterial blood gas (potassium and hemoglobin)

Cardiac US to exclude pericardial tamponade

“Fine” VF (which may be mistaken for asystole)

TREATMENT

• No intervention should be made for a patient with a valid Do Not Resuscitate document.
  
• No intervention if patient can be verified as dead:
  
  • Rigor mortis
    
  • Dependent livedo
    
  • Injury incompatible with life (e.g., decapitation)
    

• Initiate CPR, with emphasis on minimally interrupted, high-quality chest compressions
  
• Confirm asystole with cardiac monitor
  
• Place airway device (ETT preferred, but BVM acceptable), confirm placement, and provide 100% inspired oxygen and a slow ventilation rate (6–12 breaths/minute). Minimize interruption in chest compressions during airway placement
  
• Establish IV or IO access.
  
• Apply continuous waveform capnography to optimize quality of chest compressions (PETCO
  ₂
  correlates with cardiac output and myocardial blood flow during CPR)
  
• Epinephrine every 3–5 min.
  
• Consider and treat potentially reversible causes (see above)
  
• Sodium bicarbonate if hyperkalemia or drug overdose suspected
  
• No proven benefit to an empiric single countershock
  
• No proven benefit to electrical pacing
  
• Provide defibrillation without delay, IF the patient develops VF or VT
  

• Initiate induced hypothermia in comatose patients with return of spontaneous circulation
  
• Consider termination of resuscitation efforts if the following conditions are met:
  
  • High-quality chest compressions performed for a period of time
    
  • Tracheal intubation to ensure normal oxygenation
    
  • Fine VF excluded
    
  • Reversible causes corrected or excluded
    
  • Bedside US without pericardial effusion
    
  • No tension pneumothorax clinically
    

• Epinephrine: 1 mg (peds: 0.01 mg/kg) IV q3–5min
  
• Sodium bicarbonate: 1 mEq/kg IV only if:
  
  • Pre-existing acidosis
    
  • Hyperkalemia
    
  • Tricyclic antidepressant overdose is suspected.
    

FOLLOW-UP

All patients with return of spontaneous circulation

None—all patients with return of spontaneous circulation need admission to an ICU for post-arrest care

A permanent pacemaker may be considered only if asystole is found to be due to primary heart block

ICU for cardiac monitoring and induced hypothermia as appropriate

• Emphasis on high-quality, minimally uninterrupted chest compressions while considering reversible causes of asystole
  
• Resuscitation is likely to be successful only if reversible causes are found and corrected immediately
  

• Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation.
  Circulation.
  2004;109:1960–1965.
  
• Bernard SA, Gray TW, Buist MD, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia.
  N Engl J Med
  . 2002;346(8):557–563.
  
• Levine RL, Wayne MA, Miller CC. End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.
  N Engl J Med
  . 1993;337;301–306.
  
• Neumar RW, Otto CW, Link MS, et al. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.
  Circulation
  . 2010;122:S729–S767.
  
• Silvestri S, Ralls GA, Krauss B, et al. The effectiveness of out-of-hospital use of continuous end-tidal carbon dioxide monitoring on the rate of unrecognized misplaced intubation within a regional emergency medical services system.
  Ann Emerg Med.
  2005;45:497–503.
  

CODES

427.5 Cardiac arrest

BASICS

• Inability to perform coordinated movements
  
• Caused by a disorder of the cerebellum or its connections:
  
  • Ipsilateral signs with lateral cerebellar lesions
    
  • Truncal ataxia with midline lesions
    

Usually cerebellar in origin, but may occur with sensory, motor, or vestibular dysfunction:

• Trauma
  
• Mass lesions
  
• Vascular disorders
  
• Infections or postinfectious processes
  
• Toxins/drugs
  
• Metabolic/endocrine derangements
  
• Demyelinating diseases
  
• Congenital malformations
  
• Hereditary disorders:
  
  • Inborn errors of metabolism
    
  • Progressive degenerative ataxias
    
• Nutritional deficiencies
  

DIAGNOSIS

• Gait disturbance:
  
  • Ataxia often presents with unsteady gait
    
  • Initial sense of insecurity while walking
    
  • Problems with special skills (bicycling, skiing, climbing)
    
  • Sense of imbalance
    
  • Wide base stance and staggering gait
    
  • Test tandem gait to identify subtle ataxia
    
• Limb ataxia:
  
  • Incoordination
    
  • Intention tremors
    
  • Clumsiness with writing, picking up objects, buttoning
    
  • Dysmetria: Under- or overshooting on finger-to-nose and heel-to-shin testing
    
  • Dysdiadochokinesis: Difficulty with rapid alternating movements
    
• Truncal ataxia:
  
  • Head tremors
    
  • Truncal instability
    
  • Titubation: Swaying of the head/trunk while at rest
    
• Dysarthria and bulbar symptoms:
  
  • Slurred speech
    
  • Staccato, scanning speech
    
  • Choking from incoordination of swallowing
    
• Visual abnormalities:
  
  • Blurry vision
    
  • Vertigo:
    
    • Distinguish central from peripheral vertigo
      
    • Peripheral vertigo is often severe, triggered by movement, and may be accompanied by ear pain, hearing loss, or tinnitus
      
  • Nystagmus:
    
    • Gaze-evoked nystagmus: Repetitive drifts to the midline followed by fast phase to the eccentric side
      
    • Rebound nystagmus
      
• Abnormalities of muscle tone and strength:
  
  • Isometrataxia: Difficulty sustaining constant force during hand use:
    
    • Ask patient to hold slight, steady pinching pressure against examiner’s finger (examiner will feel irregular pressure)
      
  • True muscle weakness or hypotonia uncommon in cerebellar disease
    
• Sensory ataxia:
  
  • Paresthesias
    
  • Numbness
    
  • Cautious, steppage gait
    
  • Marked worsening of coordination with eyes closed:
    
    • A positive Romberg sign is the classic finding in sensory ataxia
      
  • Loss of position/vibration sense
    
  • Difficulty with fine motor skills