BRADYCARDIA AND ATRIOVENTRICULAR BLOCK

    DEFINITION

    Bradycardia is a heart rate of less than 60 beats/minute (in adults). 

    Atrioventricular (AV) block is a disturbance of electrical conduction
    through the atrioventricular node. AV block may be classified as first
    degree (prolonged PR interval); second degree (Type I or II
    intermittent P-QRS dissociation), or third degree (complete AV block).

    TOXIC CAUSES

    The more important causes include:

         Beta-adrenergic blockers
         Calcium antagonists
         Cholinesterase inhibitors (organophosphates, carbamates & nerve
         agents)
         Clonidine and other centrally-acting alpha-2 adrenergic agonists
         Digitalis and other cardiac glycosides
         Opioids 
         Phenylpropanolamine, phenylephrine (hypertension with reflex
         bradycardia)

    NON-TOXIC CAUSES

    Coronary artery ischaemia or myocardial infarction 
    Hyperkalaemia 
    Hypoxaemia (severe)
    Hypothermia 
    Hypothyroidism 
    Intrinsic conduction system disease 
    Raised intracranial pressure 
    Vaso-vagal syncope

    CLINICAL FEATURES

    Patients with bradycardia or AV block may be asymptomatic, or may
    present with dizziness or syncope. 

    The other clinical features that are observed depend on the causative
    agent.  Patients with severe hypertension secondary to a potent
    vasoconstrictor (e.g., phenylpropanolamine) may have bradycardia or AV
    block as a reflex baroreceptor response. Poisoning by beta blockers
    and calcium channel blockers is usually accompanied by hypotension.
    Cholinesterase inhibitors usually cause excessive sweating, abdominal
    cramps and diarrhoea.  Digitalis glycosides often cause vomiting and,
    with acute overdose, the serum potassium level is often elevated.
    Opioids and clonidine usually cause depressed mental status and
    miosis. 

    RELEVANT INVESTIGATIONS

    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
         Serum digoxin or digitoxin (if cardiac glycoside poisoning
         suspected)
         Serum and red blood cell cholinesterase activity (if
         organophosphorus poisoning suspected) 

    TREATMENT

    In the patient with no evidence of end-organ hypoperfusion, simple
    observation, establishment of intravenous access, administration of
    supplemental oxygen and cardiac rhythm monitoring may be all that is
    required.

    In the patient with evidence of end-organ hypoperfusion, the following
    additional measures should be undertaken:

         a)   Administer  atropine. The initial dose is 0.5 mg
              intravenously (children: 0.01 mg/kg).  This dose may be
              repeated to a maximal total of 3 mg (children: 0.05 mg/kg).

              Do NOT administer atropine to patients with hypertension and
              reflex bradycardia, as this may aggravate the hypertension.
              In cholinesterase inhibitor poisoning, much larger doses of
              atropine may be needed to effectively treat the cholinergic
              syndrome. 

         b)   Administer specific antidotes if indicated (see below).

         c)   Consider continuous intravenous infusion of  isoprenaline 
              1 to 10 mcg/min and/or insertion of a transvenous or
              transcutaneous pacemaker.

    In the unconscious patient, management should proceed as for
    cardiorespiratory arrest.

    Where the causative toxin is known or suspected, the following
    specific antidotes are indicated if either the patients has evidence
    of end-organ hypoperfusion or there is a reasonable likelihood of
    clinical deterioration.

         Beta-adrenergic blocker       Glucagon
         Calcium channel blockers      Calcium, glucagon
         Digitalis glycosides          Digoxin-specific Fab fragments
         Opioids                       Naloxone
         Organophosphorus compounds    Atropine, oximes

    CLINICAL COURSE AND MONITORING

    The clinical course is dependent on the underlying agent.  Intensive
    monitoring and support of cardiorespiratory function and serum
    electrolytes is necessary until toxicity resolves.

    LONG-TERM COMPLICATIONS

    Hypoxic brain damage
    Myocardial infarction

    AUTHOR(S)/REVIEWERS

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

    Reviewers:     London 3/98: Drs T Meredith, L Murray, A Nantel,
                   T della Puppa, J Pronczuk.