CARDIORESPIRATORY ARREST

    DEFINITION

    Cardiorespiratory arrest is cessation of cardiac and respiratory
    function.  In practice, the term is also applied to acute severe
    cardiorespiratory dysfunction. 

    Severe dysfunction of either the cardiac or respiratory system, if not
    rapidly corrected, will result in failure of the other.

    TOXIC CAUSES

    Numerous toxic agents may result in cardiorespiratory arrest.  This
    complication is more likely to occur in poisoning of subjects with
    underlying cardirespiratoy disease.  Important examples, classified
    according to underlying mechanism, include: 

          Depression of central respiratory drive
         Barbiturates
         Benzodiazepines and other sedative-hypnotic agents
         Ethanol
         Opioids
         Phenothiazines 
         Propoxyphene
         Tricyclic antidepressants

          Weakness of respiratory muscles
         Botulism
         Certain fish and shellfish poisoning (tetrodotoxin, saxitoxin)
         Cholinesterase inhibitors (organophosphates/carbamates & nerve
           agents) 
         Curare-like neuromuscular blockers
         Snakebite
         Strychnine
         Tetanus

          Non-cardiac pulmonary oedema or pneumonitis
         Chlorine and other irritant gases and vapors
         Cholinesterase inhibitors (organophosphates/carbamates & nerve
           agents)
         Paraquat
         Phosgene
         Pulmonary aspiration of gastric contents or petroleum distillates
         Salicylates

          Decreased cardiac contractility
         Barbiturates
         Beta adrenergic blockers
         Calcium channel blockers
         Ergotamines
         Type Ia or Ic antiarrhythmics
         Tricyclic antidepressants

          Hypotension from volume loss
         Amanitin-containing mushrooms
         Arsenic
         Colchicine
         Copper sulfate
         Iron

          Bradycardia or AV block
         Beta-adrenergic blockers
         Calcium antagonists
         Cholinesterase inhibitors (organophosphates/carbamates & nerve
           agents)
         Digitalis and other cardiac glycosides
         Tricyclic antidepressants

          Ventricular tachycardia or fibrillation
         Amphetamines and related stimulants
         Antihistamines (terfenadine and astemizole)
         Aromatic and halogenated petroleum distillates
         Caffeine
         Chloral hydrate
         Chloroquine and hydroxychloroquine
         Cocaine
         Digitalis and other cardiac glycosides
         Fluoride
         Phenothiazines (especially thioridazine)
         Quinidine and other Type Ia antiarrhythmic agents
         Theophylline

          Cellular Hypoxia
         Carbon Monoxide
         Cyanide
         Hydrogen Sulfide

    NON-TOXIC CAUSES

    Anaphylaxis
    Cardiac arrhythmias
    Cardiac tamponade 
    Electrolyte disturbances
    Hypothermia
    Hypovolaemia
    Myocardial infarction
    Pulmonary Embolus
    Sepsis

    CLINICAL FEATURES

    The patient with cardiopulmonary arrest is usually unresponsive, with
    absent or agonal respirations, and absent or barely detectable pulses.
    The cardiac monitor may show any rhythm, but most often asystole,
    ventricular fibrillation or extreme bradycardia.

    DIFFERENTIAL DIAGNOSIS

    Hypothermia
    Vasovagal syncope

    RELEVANT INVESTIGATIONS

    Treatment takes precedence over investigation in the initial
    management of cardiorespiratory arrest.

    A cardiac monitor is essential to determine the electrical activity of
    the heart and should be applied immediately and followed continuously.

    The following investigations may be useful as resuscitation
    progresses:

         Arterial blood gases
         Chest x-ray 
         ECG
         Serum electrolytes including calcium and magnesium
         Echocardiography

    TREATMENT

    The patient must be treated immediately.  The priorities in management
    are as follows:

         a)   Establish a secure airway, initially by positioning and
              suctioning, then with definitive measures such as
              endotracheal intubation.

         b)   Support breathing by assisting ventilation with a bag-valve
              mask device followed by mechanical ventilation. Administer
              supplemental oxygen.

         c)   Obtain intravenous access by the most rapid means possible
              and commence continuous cardiac monitoring.  Assist the
              circulation with closed chest compressions until a
              spontaneous cardiac output is re-established.  Direct
              current cardioversion of toxic ventricular dysrhythmias is
              almost never successful and should not take precedence over
              correction of hypoxia, external cardiac compression and
              administration of specific antidotes.  External or
              transvenous cardiac pacing may be useful in severe
              bradycardias.

         d)   Drugs:  Atropine and  adrenalin should be administered
              according to standard cardiopulmonary resuscitation
              guidelines.

    Where the causative toxin is known or suspected, the following
    specific antidotes are indicated:

         Beta blockers                 Glucagon 
         Calcium channel blockers      Calcium, Glucagon 
         Cardiac Glycosides            Digoxin-specific Fab fragments
         Chloral Hydrate               Beta-blockers
         Caffeine, Theophylline        Beta-blockers
         Hydrofluoric Acid             Calcium
         Organophosphorus agents       Atropine, Oximes
         Tricyclic antidepressants     Sodium Bicarbonate
         Type 1a/1c antiarrhythmics    Sodium Bicarbonate

    CLINICAL COURSE AND MONITORING

    Not all patients who develop cardiorespiratory arrest will survive the
    acute resuscitation.  However, the prognosis for cardiorespiratory
    arrest of toxic origin is, especially in young otherwise healthy
    subjects, often more favourable than that of arrest from other causes.
    A good outcome is possible even after very prolonged resuscitation. 
    The clinical course is dependent on the underlying agent.  Intensive
    monitoring and support of cardiorespiratory function is necessary
    until toxicity resolves.

    LONG TERM COMPLICATIONS

    Hypoxic brain injury
    Myocardial infarction

    AUTHOR(S)/REVIEWERS

    Author:        Kent R. Olson, MD, University of California,
                   San Francisco.

    Peer Review:   London 3/98:  Drs T. Meredith, L. Murray, A. Nantel,
                   T. della Puppa, J. Pronczuk.
                   Geneva 8/98: D. Jacobsen, L. Murray, J. Pronczuk.