SHOCK AND HYPOTENSION

    DEFINITION

    Shock is inadequate perfusion of vital organs.

    Hypotension is a systolic blood pressure less than 90 mm Hg systolic
    or a mean arterial blood pressure less than 65 mm Hg. 

    Although shock and hypotension frequently occur together, this is not
    always the case because tissue perfusion is also determined by
    vascular resistance.

    TOXIC CAUSES

    There are many toxic causes of hypotension and/or shock.  Important
    examples, classified according to mechanism, include: 

         1) Decreased cardiac contractility:
              Barbiturates
              Beta adrenergic blockers
              Calcium channel blockers (especially diltiazem and
              verapamil)
              Carbon monoxide
              Clonidine and other centrally acting alpha-2 adrenergic
              agonists
              Opioids 
              Type Ia or Ic antiarrhythmics (e.g., quinidine,
              procainamide, disopyramide, encainide, flecainide)
              Tricyclic antidepressants

         2)  Loss of peripheral vascular resistance:
              Albuterol and other beta-2 adrenergic stimulants
              Alpha-adrenergic blockers
              Calcium channel blockers (dihydropyridines)
              Carbamazepine
              Hydralazine
              Nitrites
              Phenothiazines
              Sedative-Hypnotics
              Tricyclic antidepressants

         3)  Volume loss:
              Amanitin-containing mushrooms
              Arsenic
              Colchicine
              Corrosives
              Copper sulfate
              Iron
              Salicylates

         4)  Bradycardia or AV block:
              Beta-adrenergic blockers
              Calcium channel blockers (diltiazem and verapamil)
              Cardiac glycosides (digoxin and digitoxin)
              Cholinesterase inhibitors (organophosphorus agents and
              carbamates)

    NON-TOXIC CAUSES

    Anaphylaxis
    Cardiac failure
    Hypothermia
    Hypovolaemia
    Myocardial infarction/ischaemia
    Pulmonary embolus
    Sepsis
    Spinal injury

    CLINICAL FEATURES

    The clinical features of shock result from hypoperfusion of vital
    organs. 
    Reduced cerebral perfusion manifests as altered mental status, most
    frequently anxiety, agitation and combativeness.  Reduced renal
    perfusion manifests as decreased urine output. Reduced coronary
    perfusion manifests as chest pain and evidence of ischaemia or
    infarction on the electrocardiograph.

    The blood pressure is usually low, and the pulse rate may be either
    fast, normal or slow depending on the pharmacologic cause. The skin
    signs may be cool and sweaty (in patients with increased vascular
    resistance), normal or warm and flushed (in patients with decreased
    vascular resistance). Inadequate tissue perfusion may lead to lactic
    acidosis.

    DIFFERENTIAL DIAGNOSIS

    Hypoglycaemia

    RELEVANT INVESTIGATIONS

    Arterial blood gases
    Serum electrolytes
    Chest x-ray
    ECG
    Cardiac monitoring
    Blood Sugar Level
    Lactate
    Drug screening and specific drug levels

    TREATMENT

    The priorities in management are as follows:

    1.   Assess the airway and establish patency if necessary. Assist
         ventilation if necessary.  Administer supplemental  oxygen to
         all patients. 

    2.   Establish intravenous access and give  intravenous fluids  
         (crystalloid or colloid).  Following an initial bolus of from 250
         to 500 mLs (10 mL/kg in children), the clinical response should
         be evaluated.  If the patient is obviously hypovolaemic, continue
         IV fluids.  Insert a urinary catheter and begin measurement.

    3.   Correct hypothermia. Hypothermic patients may have resistant
         hypotension until normal core temperature is achieved.

    4.   If hypotension persists, consider the following measures:

         a)   Administration of specific antidotes (see below)
         b)   Administration of intravenous inotropes, for example:
                    dobutamine 2.5 to 20 mcg/kg/min
                    dopamine 5 to 15 mcg/kg/min
                    norepinephrine (noradrenalin) 4 to 8 mcg/min
                    epinephrine (adrenalin) 1 mcg/min

         Inotrope administration rate should be titrated to blood pressure
         response.  Advanced fluid and inotrope administration may require
         measurement of central or pulmonary artery pressures and/or
         evaluation of right and left ventricular filling by
         echocardiography.

         c)   Transcutaneous or transvenous cardiac pacing where severe
              bradycardia is contributing to hypotension.

    5.   Temporary haemodialysis or haemofiltration may be necessary if
         acute renal failure develops.

         Specific antidotes:

         Albuterol & beta-2 agonists        Beta blockers
         Beta blockers                      Glucagon
         Calcium channel blockers           Calcium, glucagon
         Caffeine, Theophylline             Beta blockers
         Carbon monoxide                    Oxygen
         Cyanide                            Nitrites, thiosulfate,
                                            hydroxocobalamin
         Opioids                            Naloxone
         Quinidine & other Type Ia agents   Sodium bicarbonate
         Tricyclic antidepressants          Sodium bicarbonate

    CLINICAL COURSE AND MONITORING

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

    LONGTERM COMPLICATIONS

    Hypoxic brain injury
    Myocardial infarction

    AUTHOR(S)/REVIEWERS

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

    Reviewers:     London, March 1998:  Drs T Meredith, L Murray,
                   A Nantel, T della Puppa, J Pronczuk.
                   Geneva, August 1998, D. Jacobsen, L. Murray,
                   J. Pronczuk.