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DIFFERENTIAL DIAGNOSIS
Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.
Toxicologic Causes
- beta-receptor blocker drugs may produce hypotension, hyperglycemia, atrioventricular (AV) block, ventricular dysrhythmia, CNS depression, and seizures.
- Calcium channel blockers may produce hypotension, CNS depression, sinus bradycardia, AV block, asystole, and ventricular dysrhythmia.
- Clonidine or imidazoline drugs (tetrahydrozoline) may produce miosis, CNS depression, apnea, hypotonia, and initial hypertension followed by hypotension.
- Digitalis glycosides frequently cause nausea and vomiting, visual distortion and halos, atrial and ventricular dysrhythmia, and AV block.
- Cholinergic agents (organophosphate and carbamate pesticides, bromocriptine, acetylcholine, physostigmine, pyridostigmine) cause vomiting, diarrhea, salivation, lacrimation, urination, bronchorrhea, small pupils, and sweating. Nicotinic effects such as fasciculation and muscle weakness suggest organophosphate or carbamate pesticide exposure.
- Opioids may cause miosis and respiratory depression and may be associated with track marks.
- Sympathomimetics (cocaine, amphetamines) may cause early hypertension, tachycardia, tachydysrhythmia, hyperthermia, agitation, seizures, and rhabdomyolysis.
- Iron often causes nausea, vomiting, diarrhea, gastrointestinal bleeding, CNS depression, anion gap metabolic acidosis, leukocytosis, hyperglycemia, and radiopacities on abdominal films.
- Tricyclic antidepressants often cause tachycardia, CNS depression, coma, seizures, QRS widening, and R wave in lead aVR.
- Theophylline may cause nausea, vomiting, tachydysrhythmia, hypokalemia, mild metabolic acidosis, and seizures.
- Sedative agents may cause CNS depression, coma, and hypothermia.
- Vasodilators usually cause tachycardia.
Nontoxicologic Causes
- All causes of dysrhythmia or hypoxia other than poisoning.
- Hypothermia, hypoxia, sepsis, spinal cord injury, myocardial infarction, blood loss, and severe fluid loss from any cause.
SIGNS AND SYMPTOMS
Physical signs may help reveal the poison involved when they occur in the setting of hypotension.
Vital Signs
- Severe bradycardia or atrioventricular block suggests beta-adrenergic blocker, calcium channel blocker, cardiac glycoside, cholinergic agent, or alpha-1- or alpha-2-adrenergic agonists.
- Tachydysrhythmia suggests sympathomimetic or anticholinergic drugs, theophylline, tricyclic antidepressants, or phenothiazine.
- Hypothermia may produce bradycardia.
- Marked hyperthermia suggests severe sympathomimetic poisoning, neuroleptic malignant syndrome, monoamine oxidase (MAO) inhibitor overdose, or serotonin syndrome.
HEENT
- Dilated pupils suggest hypoxia.
- Pinpoint pupils suggest opioid, clonidine, or imidazoline drugs.
- Blurred or yellow vision or halos may indicate digitalis toxicity.
- Salivation, lacrimation, and small pupils suggest cholinergic agents or nicotine.
Dermatologic
- Cyanosis indicates hypoxia or methemoglobinemia.
- Diaphoresis may be caused by a cholinergic agent.
- Dry, flushed skin suggests an anticholinergic agent.
Cardiovascular
- QRS prolongation suggests tricyclic antidepressants, phenothiazine, antihistamine, procainamide, quinidine, or propoxyphene.
- Bradycardia or atrioventricular block suggests beta-adrenergic blocker, calcium channel blocker, cardiac glycoside, alpha-1- or alpha-2-adrenergic agonists, or cholinergic agents.
Pulmonary
- Bronchorrhea may be caused by a cholinergic agent (carbamate or organophosphate insecticide).
- Respiratory depression can occur with opioids, sedatives, clonidine, or imidazoline drugs.
Gastrointestinal
- Vomiting is common with digitalis, iron, and cholinergic agents.
- Iron also may cause hematemesis or hematochezia.
- Decreased bowel sounds suggest anticholinergics, opioids, or beta-receptor blockers.
Renal
- Recurrent urination may be caused by cholinergic agents.
- Urinary retention may develop with anticholinergic agents.
Fluids and Electrolytes
- Hyperkalemia suggests digitalis poisoning.
- Hyperglycemia may be caused by beta-receptor blockers.
- Increased anion gap acidosis may be due to lactic acidemia induced by hypoperfusion or by iron toxicity.
Neurologic
- Mental status depression or seizures may be caused by beta-receptor blocker, cholinergic agent, opioid, sedative-hypnotic, clonidine, and numerous other medications.
- Hypotonia may indicate clonidine or imidazoline drug.
PROCEDURES AND LABORATORY TESTS
Essential Tests
- ECG and continuous cardiac monitoring
- Pulse oximetry or arterial blood gas is used to evaluate other possible causes of hypotension.
- Serum electrolytes are measured to evaluate for metabolic acidosis, hypoglycemia, hypokalemia, and renal function.
Recommended Tests
- Serum cholinesterase assesses organophosphate or carbamate poisoning.
- Serum acetaminophen and aspirin levels in an overdose setting are measured to detect occult overdose with analgesic medications.
- Urine toxicology screen may be useful in patients with persistent hypotension of unknown cause.
- Creatine kinase is used to detect muscle injury when seizures, agitation, or prolonged hypotension may have occurred.
- Chest radiography is used if hypoxia is present.
- Abdominal radiography is used to evaluate for radiopaque pills, suggesting iron overdose.
- Swan-Ganz catheterization may be useful in assessing hemodynamic function and volume status.
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- Intravenous access should be established; if hypotension is unresponsive to treatment or is worsening, the patient should be intubated endotracheally until the cause can be determined and treated.
- Dose and time of exposure should be determined for all substances involved.
- Specific treatment (e.g., naloxone for mental status depression) should be initiated while supportive care continues.
DECONTAMINATION
- Induction of emesis is not recommended.
- Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult (36-42 French) patients for large ingestion presenting within 1 hour of ingestion or if serious effects are present.
- One dose of activated charcoal (1-2 g/kg) should be administered without a cathartic if a substantial ingestion has occurred within the previous few hours.
ANTIDOTES
- Calcium chloride has been used for bradycardia or hypotension secondary to calcium channel blocker overdose; optimal dose is unknown.
- Glucagon is used for bradycardia and hypotension secondary to beta-blocker or calcium channel blocker overdose.
- Sodium bicarbonate has been used to treat QRS widening and ventricular dysrhythmia secondary to myocardial sodium channel blocking agents (tricyclic antidepressant, quinidine, propoxyphene): 1 to 2 mEq/kg intravenous bolus, repeated as needed without exceeding an arterial pH of 7.55.
ADJUNCTIVE TREATMENT
Hypoxia and electrolytes should be corrected as clinically indicated.
Hypotension
- Intravenous fluid
- Patients with no evidence of volume overload can receive 10 to 20 ml/kg 0.9% saline.
- If pressure is unresponsive to initial bolus, further fluid therapy should be guided with central pressure measurement.
- Volume overload should be avoided because many agents that cause hypotension are also myocardial depressants.
- Dopamine. The initial dosage is 2 to 5 µg/kg/min by intravenous infusion, titrated to effect; dosages above 20 µg/kg/min are unlikely to have further effect.
- Norepinephrine. If hypotension is unresponsive to dopamine, 0.1 to 0.2 µg/kg/min continuous infusion, titrated to effect, can be administered.
- Hypotension due to alpha- blockade may, in theory, be more receptive to reversal by alpha- agonists; phenylephrine (0.25 mg/ml in NaCl 0.9%) can be administered at 40 µg/min, titrated to effect.
Bradycardia
- Atropine. Adult dose is 0.5 to 1 mg intravenously, repeated in 5 minutes if necessary to a maximum of 2 mg; pediatric dose is 0.02 mg/kg intravenously, repeated every 5 minutes as needed to a maximum dose of 1 mg in children, 2 mg in adolescents.
- Isoproterenol. If bradycardia and hypotension are unresponsive to atropine, isoproterenol should be considered; adult dose, 5 µg/min infusion, titrated to effect; pediatric, 0.1 µg/kg/min, titrated to effect.
- Cardiac pacing may be needed in bradycardic patients unresponsive to the above measures.
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PATIENT MONITORING
- Cardiac and respiratory function should be monitored continuously.
- Arterial pressure monitoring (A line) may be helpful in management of persistent hypotension.
EXPECTED COURSE AND PROGNOSIS
- Duration of hypotension is related to the underlying cause.
- Drugs with prolonged absorption or half-life may produce prolonged hypotension.
- Hypotension secondary to intravascular volume loss or dysrhythmias generally resolves when these are effectively treated.
Section Outline:
If clinical evidence of hypoperfusion is not present, blood pressure may be appropriate for patient.
ICD-9-CM 972Poisoning by agents primarily affecting the cardiovascular system.
See Also: SECTION II, Bradycardia chapter; SECTION III, Calcium Gluconate, Chloride, and Sodium Bicarbonate chapters; and SECTION IV, Amphetamines, Antidepressants—Tricyclic, Calcium Channel Blocking Drugs, Clonidine, Cocaine, Digoxin, Glucagon, Iron, MAO Inhibitors, Organophosphate Insecticide, and Phenothiazine chapters.
RECOMMENDED READING
Hessler R. Cardiovascular principles. In: Goldfrank LR, et al., eds. Goldfrank's toxicologic emergencies, 6th ed. Norwalk, CT: Appleton & Lange, 1998.
Author: Katherine M. Hurlbut
Reviewer: Richard C. Dart