DESCRIPTION

Bradypnea, or decreased rate of respiration at rest, is defined as follows:

• Adults and adolescents: fewer than 12 respirations/min
• Children 6 to 12 years of age: fewer than 12 respirations/min
• Children 1 to 6 years of age: fewer than 20 respirations/min
• Infants 1 month to 1 year of age: fewer than 24 respirations/min

Hundreds of agents can cause depressed respiration; this discussion will focus on major agents that produce depressed respiration directly.

PATHOPHYSIOLOGY

• Bradypnea may be caused directly by depression of the medullary respiration center.
• Bradypnea may be caused indirectly by insensitivity of carotid body CO₂ detection.
• Muscular dysfunction may make an adequate respiratory rate unachievable.
• Neonatal patients or patients with underlying cardiovascular disease do not tolerate hypoxia well.

EPIDEMIOLOGY

Poisoning is common, usually as a therapeutic misadventure.

Section Outline:

• DESCRIPTION
• PATHOPHYSIOLOGY
• EPIDEMIOLOGY

The diagnosis of bradypnea is based on decreased respiratory rate.

DIFFERENTIAL DIAGNOSIS

Associated findings assist in determining the cause of bradypnea.

Common Toxicologic Causes

Further information on each poison is available in SECTION IV, CHEMICAL AND BIOLOGICAL AGENTS.

• Opioids often are associated with miosis, decreased bowel sounds, and depressed mental status.
• Cholinergic agonist drugs such as pilocarpine, bethanechol, and the organophosphate insecticides are associated with salivation, lacrimation, urination, defecation, and muscle weakness.
• Benzodiazepines, barbiturates, ethanol, or hypnotic agents (e.g., chloral hydrate, gamma hydroxybutyrate [GHB], or rohypnol ["roofies"]) are usually associated with midposition pupils and depressed mental status.
• Ethanol intoxication is associated with history and odor of intoxication.
• Nicotine poisoning may be associated with small pupils, nausea, vomiting, and tremors and fasciculations.
• alpha-₂-receptor agonists (clonidine, tetrahydrozoline) produce depression of respiratory drive associated with small pupils and depressed mental status.
• Tricyclic antidepressant toxicity is usually associated with cardiac dysrhythmia in serious cases; anticholinergic effects are often absent.

Uncommon Toxicologic Causes

• Nearly any toxic agent may cause bradypnea as a preterminal event.
• Lomotil (diphenoxylate/atropine) may produce depressed respiration.
• Paralytic agents and diseases (succinylcholine, curare, strychnine, botulism, Guillain-Barré syndrome, polio, rabies, etc.) may produce depressed respiration.

Nontoxicologic Causes

• Altered mental status with localizing neurologic deficits indicates the probable presence of an intracranial lesion.
• Altered mental status without localizing findings may indicate the presence of hypoglycemia, or another metabolic abnormality.
• Any cause of hypotension or hypoxia may lead to bradypnea; for example, asthma, diabetic ketoacidosis, and pneumonia may all produce tachypnea that is followed by bradypnea as the patient tires.
• Many causes of muscle weakness also can cause bradypnea; however, these are generally also preceded by transient tachypnea with falling tidal volume (due to respiratory muscle weakness).
• Many nontoxicologic causes of mental status depression, such as severe electrolyte abnormalities or intracranial events, produce bradypnea when severe.

SIGNS AND SYMPTOMS

• Often the patient is unaware of bradypnea due to concurrent depression of mental status.
• Onset and duration of bradypnea may be extremely rapid or slow, depending on the toxic agent.

Vital Signs

Bradypnea often is associated with initial tachycardia that is followed by bradycardia as the patient's condition worsens.

HEENT

• Pinpoint pupils indicate an opioid as a probable cause; mid-position or dilated pupils may be present in an opioid overdose, however, if a concomitant substance that antagonizes the effect of the opioid has been ingested.
• Dilated pupils may indicate concurrent hypoxia, sympathomimetic effects, or anticholinergic effects.

Dermatologic

Peripheral and central cyanosis may be apparent if the patient is hypoxic.

Cardiovascular

• Tachycardia is a typical initial response to hypoxia; if hypoxia persists, tachycardia is followed by bradycardia.
• Hypotension, cyanosis, and cardiac ischemia or dysrhythmia may develop in severe cases.

Pulmonary

The chest is usually clear on examination unless aspiration has occurred.

Gastrointestinal

• Increased bowel sounds may be present with cholinergic stimulants.
• Decreased bowel sounds are consistent with opioids and sedative and hypnotic agents.

Fluids and Electrolytes

No abnormalities are expected, unless a coingestant complicates the course of bradypnea.

Musculoskeletal

Muscle weakness may contribute to bradypnea in conditions such as botulism and cholinergic poisoning.

Neurologic

Rapid onset of depressed mental status is common but reversible if detected and treated promptly.

PROCEDURES AND LABORATORY TESTS

Essential Tests

Oxygenation (pulse oximetry or arterial blood gas) should be assessed; hypoxia indicates clinically significant disease, and hypercarbia indicates hypoventilation.

Recommended Tests

• If bradypnea persists after initial measures, ventilation should be assessed with an arterial blood gas.
  • Hypoxia indicates clinically significant disease.
  • Elevated pCO₂ indicates hypoventilation.
• ECG should be obtained to detect the presence of tricyclic antidepressants or cardiac complications of hypoxia.
• Negative inspiratory force or other pulmonary function test findings assist in determining the need for endotracheal intubation and in establishing the source of hypoventilation.
• Serum levels of acetaminophen, salicylates, opioids, or other drugs should be obtained as needed to detect coingestions and help guide treatment if they are present.
• Blood, urine, and spinal fluid cultures, urine toxicology screen, and serum levels of specific drugs should be obtained as needed to determine other nontoxicologic causes of bradypnea.
• Chest radiograph should be obtained to assess potential intrathoracic causes of hypoxia and bradypnea.
• Head CT may be needed to evaluate the possibility of an intracranial event.

Section Outline:

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

• Supportive care with oxygen and appropriate airway management is vital, with specific treatment initiated as supportive care continues.
• The dose and time of exposure should be determined for all substances that could be involved.

DIRECTING PATIENT COURSE

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

• cause of bradypnea is unknown.
• coingestant, drug interaction, or underlying disease presents unusual problems.

DECONTAMINATION

• Emesis should not be induced because of the likelihood of depressed mentation.
• Gastric lavage is recommended for all critically ill patients with possible toxic ingestion who are unresponsive to naloxone.
• 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

Naloxone

• Indications. Any patient with depressed mental status.
• Contraindications. None.
• Method of administration. A 2.0-mg intravenous push, which may be repeated for refractory cases or recurrence of adverse effects.
• Potential adverse effects
  • Naloxone may induce withdrawal syndrome.
  • Reversal of opioid effects may unmask a coexistent toxicity, such as cocaine.

Dextrose

• Indications. Treatment of altered mental status.
• Contraindications. None.
• Method of administration
  • Adult dose, D₅₀, 50 ml (25 g), in an intravenous push.
  • Pediatric dose, D₂₅, 2 to 4 ml/kg (0.5-1.0 g/kg), in an intravenous push.

ADJUNCTIVE TREATMENT

• If serious respiratory depression or difficulty protecting the airway is present, the patient should be intubated endotracheally until the cause can be determined and treated.
• Intravenous access and cardiac monitor should be established, and naloxone should be administered.

Section Outline:

• DIRECTING PATIENT COURSE
• DECONTAMINATION
• ANTIDOTES
  • Naloxone
  • Dextrose
• ADJUNCTIVE TREATMENT

• The duration of the illness depends on the cause of bradypnea.
• Complications may develop rapidly; a few minutes of severe hypoxia may produce permanent cardiac or CNS injury or allow aspiration to occur.
• Most patients become bradypneic as the preterminal event.
• Death usually occurs only if the airway is not adequately managed.

• The airway should be managed aggressively; if clinically significant bradypnea develops, the patient should be intubated immediately.
• If vomiting is present, the health-care professional must ensure that aspiration has not occurred.

ICD-9-CM 786.09

Author: Richard C. Dart

Reviewer: Katherine M. Hurlbut