Respiratory arrest and cardiac arrest are distinct, but inevitably if untreated, one leads to the other. (See also Respiratory Failure, Dyspnea, and Hypoxia.)
Interruption of pulmonary gas exchange for > 5 minutes may irreversibly damage vital organs, especially the brain. Cardiac arrest almost always follows unless respiratory function is rapidly 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 of Respiratory Arrest
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
Upper airway obstruction may occur in infants < 3 months, who 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
Foreign body
Spasm of the vocal cords
Edema of the vocal cords
Pharyngolaryngeal or tracheal inflammation (eg, epiglottitis, croup)
Tumor
Trauma
Patients with congenital developmental disorders (eg, Down syndrome, laryngeal disorders, congenital jaw abnormalities) 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)
Decreased respiratory effort
Decreased respiratory effort reflects central nervous system (CNS) impairment due to one of the following:
Central nervous system disorder
Adverse medication or illicit drug effect
Metabolic disorder
Central nervous system 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). Combinations of these drugs further increase the risk of respiratory depression (1). 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, older patients, deconditioned patients, patients with chronic respiratory insufficiency or obstructive sleep apnea). Respiratory arrest due to illicit drug use especially use of opioids2). OIRD can lead to catastrophic outcomes such as severe brain damage or death (3).
sedatives), older patients, or patients who have underlying respiratory impairment such as patients with chronic obstructive pulmonary disease (COPD).
Metabolic disorders that cause CNS depression due to severe hypoglycemia or hypotension ultimately compromise respiratory effort.
Respiratory muscle weakness
Weakness may be caused by
Respiratory muscle fatigue
Neuromuscular disorders
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).
Neuromuscular causes include spinal cord injury, neuromuscular diseases (eg, myasthenia gravis, botulism, poliomyelitis, Guillain-Barré syndrome
Etiology references
1. Izrailtyan I, Qiu J, Overdyk FJ, et al: Risk factors for cardiopulmonary and respiratory arrest in medical and surgical hospital patients on opioid analgesics and sedatives. PLoS One 13(3):e019455, 2018. doi: 10.1371/journal.pone.0194553
2. Khanna AK, Bergese SD, Jungquist CR, et al: Prediction of opioid-induced respiratory depression on inpatient wards using continuous capnography and oximetry: An international prospective, observational trial. Anesth Analg 131(4):1012-1024, 2020. doi:10.1213/ANE.0000000000004788
3. Lee LA, Caplan RA, Stephens LS, et al: Postoperative opioid-induced respiratory depression: A closed claims analysis. Anesthesiology 122: 659–665, 2015. doi: 10.1097/ALN.0000000000000564
Symptoms and Signs of Respiratory Arrest
With respiratory arrest, patients are unconscious or about to become so.
Patients with hypoxemia may be cyanotic, but cyanosis can be masked by anemia, carbon monoxide poisoning, or cyanide toxicity. Because anemia lowers hemoglobin, reducing the total amount of deoxygenated hemoglobin when a patient is hypoxemic, cyanosis is not as apparent. Carboxyhemoglobin sometimes makes the skin appear red. In cyanide toxicity, patients may not appear cyanotic despite being functionally hypoxic because cyanide impairs cellular respiration.
Patients being treated with high-flow oxygen 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 carbon dioxide can alert practitioners to impending respiratory arrest in decompensating patients.
Infants, especially if < 3 months, may develop acute apnea without warning, secondary to overwhelming infection, metabolic disorders, or respiratory fatigue.
Patients with asthma or 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 of Respiratory Arrest
Clinical evaluation
Respiratory arrest is 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 (for removal, see Clearing and Opening the Upper Airway).
Treatment of Respiratory Arrest
Clearing the airway
Mechanical ventilation
Treatment is clearing the airway, establishing an alternate airway, and providing mechanical ventilation as needed.
