Respiratory and cardiac arrest are distinct, but inevitably if untreated, one leads to the other. (See also respiratory failure on p. see Respiratory Failure and Mechanical Ventilation, dyspnea on p. see Symptoms of Pulmonary Disorders: Dyspnea, and hypoxia on p. see Approach to the Critically Ill Patient: Oxygen Desaturation.)

Interruption of pulmonary gas exchange for > 5 min may irreversibly damage vital organs, especially the brain. Cardiac arrest almost always follows unless respiratory function is immediately restored. However, aggressive ventilation may also have negative hemodynamic consequences, particularly in the periarrest period and in other circumstances when cardiac output is low. In most cases, the ultimate goal is to restore adequate ventilation and oxygenation without further compromising a tentative cardiovascular situation.

Etiology

Respiratory arrest (and impaired respiration that can progress to respiratory arrest) can be caused by

• Airway obstruction
• Decreased respiratory effort
• Respiratory muscle weakness

Airway obstruction: Obstruction may involve the

• Upper airway
• Lower airway

Infants < 3 mo are usually nose breathers and thus may have upper airway obstruction secondary to nasal blockage. At all ages, loss of muscular tone with decreased consciousness may cause upper airway obstruction as the posterior portion of the tongue displaces into the oropharynx. Other causes of upper airway obstruction include blood, mucus, vomitus, or foreign body; spasm or edema of the vocal cords; and pharyngolaryngeal tracheal inflammation (eg, epiglottitis, croup), tumor, or trauma. Patients with congenital developmental disorders often have abnormal upper airways that are more easily obstructed.

Lower airway obstruction may result from aspiration, bronchospasm, airspace filling disorders (eg, pneumonia, pulmonary edema, pulmonary hemorrhage), or drowning.

Decreased respiratory effort: Decreased respiratory effort reflects CNS impairment due to one of the following:

• CNS disorder
• Adverse drug effect
• Metabolic disorder

CNS disorders that affect the brain stem (eg, stroke, infection, tumor) can cause hypoventilation. Disorders that increase intracranial pressure usually cause hyperventilation initially, but hypoventilation may develop if the brain stem is compressed.

Drugs that decrease respiratory effort include opioids and sedative-hypnotics (eg, barbiturates, alcohol; less commonly, benzodiazepines). Usually, an overdose (iatrogenic, intentional, or unintentional) is involved, although a lower dose may decrease effort in patients who are more sensitive to the effects of these drugs (eg, the elderly, those with chronic respiratory insufficiency).

CNS depression due to severe hypoglycemia or hypotension ultimately compromises respiratory effort.

Respiratory muscle weakness: Weakness may be caused by

• Neuromuscular disorders
• Fatigue

Neuromuscular causes include spinal cord injury, neuromuscular diseases (eg, myasthenia gravis, botulism, poliomyelitis, Guillain-Barré syndrome), and neuromuscular blocking drugs.

Respiratory muscle fatigue can occur if patients breathe for extended periods at a minute ventilation exceeding about 70% of their maximum voluntary ventilation (eg, because of severe metabolic acidosis or hypoxemia).

Symptoms and Signs

With respiratory arrest, patients are unconscious or about to become so.

Patients with hypoxemia may be cyanotic, but cyanosis can be masked by anemia or by carbon monoxide or cyanide intoxication. Patients being treated with high-flow O₂ may not be hypoxemic and therefore may not exhibit cyanosis or desaturation until after respiration ceases for several minutes. Conversely, patients with chronic lung disease and polycythemia may exhibit cyanosis without respiratory arrest. If respiratory arrest remains uncorrected, cardiac arrest follows within minutes of onset of hypoxemia, hypercarbia, or both.

Impending respiratory arrest: Before complete respiratory arrest, patients with intact neurologic function may be agitated, confused, and struggling to breathe. Tachycardia and diaphoresis are present; there may be intercostal or sternoclavicular retractions. Patients with CNS impairment or respiratory muscle weakness have feeble, gasping, or irregular respirations and paradoxical breathing movements. Patients with a foreign body in the airway may choke and point to their necks, exhibit inspiratory stridor, or neither. Monitoring end-tidal CO₂ can alert practitioners to impending respiratory arrest in decompensating patients.

Infants, especially if < 3 mo, may develop acute apnea without warning, secondary to overwhelming infection, metabolic disorders, or respiratory fatigue. Asthmatics or patients with other chronic lung diseases may become hypercarbic and fatigued after prolonged periods of respiratory distress and suddenly become obtunded and apneic with little warning, despite adequate oxygen saturation.

Diagnosis

• Clinical evaluation

Respiratory arrest is usually clinically obvious; treatment begins simultaneously with diagnosis. The first consideration is to exclude a foreign body obstructing the airway; if a foreign body is present, resistance to ventilation is marked during mouth-to-mask or bag-valve-mask ventilation. Foreign material may be discovered during laryngoscopy for endotracheal intubation (see Respiratory Arrest: Clearing and Opening the Upper Airway for removal).

Treatment

Treatment is clearing the airway, establishing an alternate airway, and providing mechanical ventilation (see Respiratory Failure and Mechanical Ventilation: Overview of Mechanical Ventilation).

Last full review/revision January 2010 by Charles D. Bortle, EdD; Richard Levitan, MD

Content last modified February 2012