DESCRIPTION

Tachycardia, or increased heart rate at rest, is defined as follows:

• Adults and adolescents: more than 100 beats/min
• Children 5 to 10 years of age: more than 120 beats/min
• Children 1 to 5 years of age: more than 130 beats/min
• Newborns and infants less than 1 year of age: more than 150 beats/min

PATHOPHYSIOLOGY

• Common toxicologic mechanisms for persistent tachycardia include excessive beta-adrenergic receptor stimulation and anticholinergic effects.
• Physiologic responses to hypotension, hyperthermia, hypoxia, and volume depletion are other possible causes of tachycardia.

Section Outline:

• DESCRIPTION
• PATHOPHYSIOLOGY

DIFFERENTIAL DIAGNOSIS

Toxicologic Causes

• Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.
• Cocaine, amphetamines, and other sympathomimetic agents (ephedrine, phenylpropanolamine, beta-₂-agonist bronchodilators, and many others). Additional clinical and laboratory findings may include hypertension, hyperthermia, agitation, delirium, seizures, track marks, nasal septum erosion or perforation, and rhabdomyolysis.
• Tricyclic antidepressants (TCAs). Additional clinical and laboratory findings might include seizure, hypotension, dysrhythmias, QRS widening, presence of an R wave in ECG lead aVR, and coma.
• Type Ia antiarrhythmic agents (quinidine, procainamide, disopyramide) all cause prolongation of ECG intervals (PR, QRS, QT) and may be associated with ventricular dysrhythmias and torsade de pointes.
• Anticholinergic agents (diphenhydramine, scopolamine, jimsonweed, hydroxyzine, phenothiazines, Dramamine, etc.). Additional clinical and laboratory findings include flushing, dilated and sluggish pupils, diminished bowel sounds, hyperthermia, hallucinations, agitation, delirium, and dry skin.
• Theophylline. Additional clinical and laboratory findings may include tremor, vomiting, seizures, dysrhythmias, hypokalemia, mild metabolic acidosis, or preexisting diagnosis of chronic obstructive pulmonary disease.
• Selective serotonin reuptake inhibitors (SSRI) cause depressed mental status and seizure without dysrhythmia (other than tachycardia) or hypotension.
• Digitalis may produce tachycardia with heart block, vomiting, hyperkalemia (acute), or hypokalemia (chronic intoxication).
• Monoamine oxidase (MAO) inhibitors may cause hyperthermia, hypertension, and altered mental status.
• Carbamazepine is associated with coma, hyponatremia, and nystagmus.
• Marijuana causes dilated pupils and conjunctival injection.
• Cholinergic agents (organophosphate or carbamate pesticides) may cause vomiting, diarrhea, salivation, lacrimation, urination, bronchorrhea, small pupils, and sweating.
• Hallucinogens of any type (LSD, phencyclidine) may cause rhabdomyolysis.
• Mushrooms may produce hallucinogenic or anticholinergic effects.
• Substances that produce methemoglobinemia (e.g., dapsone, nitrates). Methemoglobinemia often causes cyanosis.
• Thyroid hormones may be associated with history of thyroid disease, tremor, and fever.
• Vasodilators (nifedipine, hydralazine, etc.) primarily cause hypotension.
• Withdrawal (from alcohol, opiates, or sedative-hypnotics) is associated with a history of abuse and abstinence, and hypertension.

Nontoxicologic Causes

• All causes of hypotension or hypoxia produce tachycardia, which may be followed by bradycardia as disease worsens.
• Common nontoxic causes of tachycardia include anxiety (a diagnosis of exclusion), anemia, fever, hypoxia, hypotension, pulmonary embolus, renal failure, vasodilation (sepsis, neurogenic shock), volume depletion, and metabolic acidosis.

SIGNS AND SYMPTOMS

Associated physical signs may help to reveal the poison involved when they are associated with tachycardia.

Vital Signs

Hypertension may indicate sympathomimetic toxicity or withdrawal from alcohol, sedative-hypnotics, or MAO inhibitors.

HEENT

• Dilated pupils suggest anticholinergic or sympathomimetic toxicity.
• Conjunctival injection and dilated pupils suggest marijuana.
• Perforated nasal septum may indicate chronic drug abuse.

Dermatologic

• Flushed, dry skin suggests an anticholinergic agent.
• Pale, sweaty skin may be associated with sympathomimetic drugs, cholinergic agents, or hypotension.
• Cyanosis suggests hypoxia or methemoglobinemia.

Cardiovascular

• Tachycardia with no other cardiovascular findings may indicate theophylline toxicity.
• See also SECTION II, Ventricular Dysrhythmias chapter.

Pulmonary

• Mucous membrane irritation and wheezing may result from smoke inhalation or hydrocarbon aspiration.
• Cholinergic agonists may produce bronchorrhea and wheezing.

Gastrointestinal

• Vomiting is commonly associated with iron, salicylate, or theophylline intoxication.
• Diminished bowel sounds suggest an anticholinergic agent.

Renal

Urinary retention suggests an anticholinergic agent.

Fluids and Electrolytes

Hypokalemia suggests a beta-receptor agonist or theophylline.

Musculoskeletal

Rhabdomyolysis often indicates stimulant or hallucinogen abuse.

Neurologic

• Hallucinations and delirium suggest an anticholinergic agent or abuse of stimulants or hallucinogens.
• Anxiety, tremor, and seizures suggest theophylline or withdrawal from alcohol or sedative-hypnotic drugs.
• Coma and seizures suggest tricyclic antidepressant toxicity.
• CNS depression or coma, nystagmus, ataxia, diminished bowel sounds, and hyponatremia suggest carbamazepine.

PROCEDURES AND LABORATORY TESTS

Essential Tests

• ECG should be obtained and continuous cardiac monitoring established.
  • QRS widening, an R wave in ECG lead aVR, and hypotension suggest tricyclic antidepressant poisoning or other type Ia antidysrhythmic agents.
  • Digitalis produces a wide variety of tachydysrhythmias and heart blocks.
• A complete blood count should be obtained to rule out anemia.

Recommended Tests

• Serum electrolytes, BUN, and creatinine should be obtained to assist in assessment of metabolic acidosis and renal insufficiency; acute digitalis toxicity often causes hyperkalemia, and theophylline or beta-agonists produce hypokalemia.
• Arterial blood gases should be performed to assess the contribution of hypoxia to tachycardia.
• Urine toxicology screen should be obtained in patients with persistent tachycardia of unknown cause.
• Metabolic acidosis of unknown etiology with tachycardia should prompt testing of salicylate level, methanol level, ethylene glycol level, serum iron level, lactate level, and carboxyhemoglobin.
• Serum acetaminophen and aspirin levels should be obtained in overdose settings to detect occult overdose.
• CT and LP cultures may be needed to evaluate other causes.
• Orthostatic vital signs should be assessed and central venous pressure monitoring established to evaluate for other possible causes of tachycardia.

Section Outline:

• DIFFERENTIAL DIAGNOSIS
  • Toxicologic Causes
  • Nontoxicologic Causes
• SIGNS AND SYMPTOMS
  • Vital Signs
  • HEENT
  • Dermatologic
  • Cardiovascular
  • Pulmonary
  • Gastrointestinal
  • Renal
  • Fluids and Electrolytes
  • Musculoskeletal
  • Neurologic
• PROCEDURES AND LABORATORY TESTS
  • Essential Tests
  • Recommended Tests

• An intravenous line should be established.
• Treatment of specific effects (e.g., sodium bicarbonate for QRS widening) should be initiated while continuing supportive care.
• The dose and time of exposure should be determined for all substances involved.

DIRECTING PATIENT COURSE

• The need for consultation with a poison center or other specialists should be evaluated.
• A poison center or toxicology consultant should be consulted for patients with metabolic acidosis of unknown etiology with tachycardia, unless the etiology can be determined quickly.

The health-care provider should call the poison control center when:

• cause of persistent tachycardia is unclear.
• coingestant, drug interaction, or underlying disease presents unusual problems.

Admission Considerations

The decision to admit a patient is based on the underlying cause of tachycardia.

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.

ADJUNCTIVE TREATMENT

Control of Heart Rate

• The general approach of Advanced Cardiac Life Support guidelines should be followed.
• Often, agitation is an important contributor to tachycardia; in such cases, a benzodiazepine (diazepam or lorazepam) should be administered in small doses and titrated to effect, and the airway should be monitored closely.
• Tachycardia due to hypoxia, anemia, or electrolyte disorder is corrected by treating the underlying cause.
• beta-receptor blockade may be indicated if other measures are unsuccessful.
  • Esmolol may be administered in an intravenous bolus of 500 µg/kg infused over 1 minute, followed by an infusion of 50 µg/kg/min for 4 minutes.
  • If response to initial esmolol therapy is inadequate, the loading dose should be repeated and 100 µg/kg/min infused for 4 minutes; this titration may be repeated as needed until heart rate is controlled or toxicity (hypotension) develops.
  • Unopposed alpha-receptor stimulation is a theoretical concern during beta- blockade; if heart rate or blood pressure increase dangerously during esmolol infusion, alpha-receptor stimulation may be the cause.

Hypotension

• The health-care provider should administer 10 to 20 ml/kg of 0.9% saline and place the patient in the Trendelenburg position.
  • Further fluid therapy should be guided by central monitoring or right heart catheter to avoid volume overload.
  • If hypotension is unresponsive to saline, a vasopressor should be administered.

Hypertension

If hypertension is not responsive to benzodiazepines, or if end organ damage (aortic dissection, CNS bleed, myocardial infarction) develops, a short-acting, titratable agent may be administered (see SECTION II, Nitroprusside chapter).

Section Outline:

• DIRECTING PATIENT COURSE
  • Admission Considerations
• DECONTAMINATION
• ADJUNCTIVE TREATMENT
  • Control of Heart Rate
  • Hypotension
  • Hypertension

Respiratory and cardiac function should be monitored continuously.

DISCHARGE CRITERIA/INSTRUCTIONS

The asymptomatic patient may be discharged after the tachycardia resolves, the underlying cause is corrected, decontamination is complete, and a psychiatric evaluation, if needed, has been performed.

Symptoms involving the cardiovascular system: tachycardia, unspecified.

See Also: SECTION II, Hypotension, Pulmonary Edema, Ventricular Dysrhythmias, Cholinergic Syndrome, Withdrawal, Methemoglobinemia, and Anion Gap Metabolic Acidosis chapters; SECTION III, Nitroprusside chapter; and SECTION IV, Anticholinergic Compounds chapter.

RECOMMENDED READING

Goldfrank LR, Flomenbaum NE, Weisman RS, et al. 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