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DESCRIPTION
Bradycardia, or decreased heart rate at rest, is defined as follows:
- Adults and adolescents: fewer than 60 beats/min
- Children 5 to 10 years of age: fewer than 65 beats/min
- Children 1 to 5 years of age: fewer than 75 beats/min
- Newborns and infants less than 1 year of age: fewer than 110 beats/min
PATHOPHYSIOLOGY
- Common toxicologic mechanisms for persistent bradycardia include beta-adrenergic receptor blockade, blockade of myocardial sodium or calcium channels, cholinergic effect, and increased vagal tone.
- Other mechanisms for bradycardia involve myocardial infarction; electrolyte abnormalities; cerebral edema; and physiologic response to hypoxia, hypothermia, and hypertension are other possible causes.
- Geriatric patients with underlying cardiovascular disease may be less tolerant of bradycardia than other populations.
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DIFFERENTIAL DIAGNOSIS
Toxicologic Causes
Associated findings may help confirm the identity of the poison involved in the patient with bradycardia. Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.
- beta-receptor blocking drugs also produce hypotension, hyperglycemia, atrioventricular (AV) block, ventricular dysrhythmia, CNS depression, and seizures.
- Calcium channel blocking drugs may produce hypotension, CNS depression, AV block, and ventricular dysrhythmia.
- Clonidine or imidazoline drugs (tetrahydrozoline) may produce small pupils, CNS depression, apnea, and hypotonia.
- Opioid drugs also may produce small pupils, CNS depression, and apnea perhaps with evidence of intravenous drug abuse.
- Digitalis glycosides frequently cause nausea and vomiting, visual complaints and halos, atrial and ventricular dysrhythmias, and AV block.
- Cholinergic agents (organophosphate or 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 that are present in addition to the cholinergic effects suggest organophosphate or carbamate pesticide exposure.
- Ergot alkaloids, baclofen, skeletal muscle relaxants, lithium, lidocaine, flecainide, quinidine, amiodarone, bretylium, encainide, methyldopa, bufotoxin, mushrooms (inocybe, clitocybe), tetrodotoxin, and saxitoxin, all may be associated with bradycardia.
Nontoxicologic Causes
- All causes of hypotension or hypoxia may produce bradycardia.
- Hypothermia, electrolyte abnormalities (hyperkalemia, hypermagnesemia), hypoxia, increased intracranial pressure, myocardial infarction, congenital heart disease, and uncal herniation all can cause bradycardia.
SIGNS AND SYMPTOMS
If hypotension is not present, the heart rate may be appropriate for the patient even if it meets the definition for bradycardia.
Vital Signs
- Hypotension is common with severe bradycardia.
- Hypertension may be present if bradycardia is a reflex physiologic response.
- Hypothermia commonly produces bradycardia.
HEENT
- Dilated pupils suggest hypoxia.
- Pinpoint pupils suggest an opioid, clonidine, or imidazoline drug.
- Blurred or yellow vision or halos may indicate digitalis toxicity.
- Lacrimation suggests a cholinergic agent.
Dermatologic
Cyanosis suggests hypoxia or methemoglobinemia.
Pulmonary
- Bronchorrhea suggests a cholinergic agent (carbamate or organophosphate).
- Congestive heart failure may develop as a result of bradycardia from any cause.
Gastrointestinal
- Nausea and vomiting are common with digitalis and cholinergic agents.
- Decreased bowel sounds suggest opioids or beta-receptor blockers.
Renal
- Hyperkalemia suggests digitalis poisoning.
- Hyperglycemia may be caused by beta-receptor blockers
- Recurrent urination may be caused by cholinergic agents.
Neurologic
- Mental status depression or seizures may be caused by beta-receptor blockers, cholinergic agents, and numerous other medications.
PROCEDURES AND LABORATORY TESTS
Essential Tests
- ECG and continuous cardiac monitoring should be obtained in all patients with bradycardia.
- Digitalis may cause any type of dysrhythmia.
- beta-receptor blockers and calcium channel blocking drugs cause sinus bradycardia, AV block, and asystole.
- Myocardial ischemia may cause, or be produced by, bradycardia.
- Pulse oximetry or arterial blood gases should be performed to evaluate other possible causes of bradycardia.
- Serum electrolytes should be obtained to evaluate for hyperkalemia, hypermagnesemia, hypocalcemia, and hypoglycemia.
Recommended Tests
- Serum cholinesterase is used to assess organophosphate or carbamate poisonings.
- Serum acetaminophen and aspirin levels should be obtained in overdose settings to detect occult overdose with analgesic medications.
- Urine toxicology screen should be obtained in patients with persistent bradycardia of unknown cause.
- Arterial pressure monitoring (A line) may be helpful in management of bradycardia associated with hypotension.
- Swan-Ganz catheterization may be helpful to assess hemodynamic function.
- Chest radiograph may be obtained to evaluate hypoxia.
- Head CT may be ordered to evaluate for evidence of intracranial structural lesion or increased intracranial pressure.
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- Intravenous access should be established.
- If hypotension unresponsive to initial intravenous isotonic fluid bolus is present, the patient should be intubated endotracheally until the cause can be determined and treated.
- The 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 continuing supportive care.
DIRECTING PATIENT COURSE
The health-care provider should call the poison control center when:
- cause of bradycardia is unclear.
- coingestant, drug interaction, or underlying disease presents unusual problems.
Admission Considerations
Patients with bradycardia should be admitted unless a reversible, physiologic cause is identified.
DECONTAMINATION
- Induction of emesis is not recommended for patients with bradycardia.
- Gastric lavage should be performed in pediatric (tube size 24-32 French) or adult patients (tube size 36-42 French) in most cases because bradycardia represents a serious toxic effect.
- One dose of activated charcoal (1 to 2 g/kg) should be administered without a cathartic if a substantial ingestion has occurred within the previous few hours.
ANTIDOTES
- Calcium chloride is used primarily for bradycardia or hypotension secondary to calcium channel blocker overdose; the optimal calcium chloride dose is unknown.
- Glucagon is used primarily for bradycardia and hypotension secondary to beta-blocker overdose.
ADJUNCTIVE TREATMENT
- Hypoxia and electrolytes should be corrected as clinically indicated.
- If bradycardia is associated with hypotension, atropine should be administered.
- Adult dose is 0.5 to 1.0 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.
- If bradycardia and hypotension are unresponsive to atropine, isoproterenol should be considered.
- Adult dose is 5 µg/min infusion, titrated to effect.
- Pediatric dose is 0.1 µg/kg/min, titrated to effect.
- Intravenous fluid
- In patients with hypotension and no evidence of volume overload, 10 to 20 ml/kg 0.9% saline may be administered.
- If pressure is unresponsive to the initial bolus, further fluid therapy should be guided by central pressure measurement.
- Volume overload should be avoided because many agents that cause bradycardia are also myocardial depressants.
- Dopamine, 2 to 5 µg/kg/min, may be administered by intravenous infusion and titrated to desired effect; doses above 20 µg/kg/min are unlikely to have any further effect. If the patient is unresponsive to dopamine, 0.1 to 0.2 µg/kg/min of norepinephrine may be administered by continuous infusion and titrated to desired effect.
- Cardiac pacing may be considered if the patient is unresponsive to other attempts at treatment.
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EXPECTED COURSE AND PROGNOSIS
The duration of bradycardia is related to the underlying cause; drugs with prolonged absorption or half-life may produce prolonged bradycardia, whereas bradycardia secondary to increased vagal tone is generally short lived.
DISCHARGE CRITERIA/INSTRUCTIONS
Discharge only asymptomatic patients whose bradycardia was transient and not caused by a poisoning.
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See Also: SECTION III,
Calcium Gluconate and
Chloride, and
Glucagon chapters; and SECTION IV,
beta-Receptor Blocking Drugs,
Calcium Channel Blocking Drugs,
Clonidine,
Digoxin and
Cardiac Glycosides, and
Organophosphate Insecticides chapters.
ICD-9-CM 427.89
Other specified cardiac dysrhythmias.
RECOMMENDED READING
Goldfrank LR, Flomenbaum NE, Weisman RS, Lewin NA. Vital signs and toxic syndromes. 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