Pathological breathing patterns represent a group of respiratory disorders characterized by altered rhythm, depth, and sequence of inspiration and expiration. They arise due to damage to the respiratory center, impaired afferent drive, or injury to efferent motor pathways. Major forms include apneustic, periodic, and terminal respiration.
LocalizationLesions of respiratory center neurons in the brainstem
Apnea in Biot RespirationDuration of respiratory pauses reaches 25–30 seconds
PathophysiologyATP deficiency, ionic imbalance, and neuronal excitability fluctuations
Ondine's CurseLoss of automatic respiratory control leading to apnea during sleep
Apneustic and Periodic Respiration
Apneustic respiration is characterized by a prolonged, shallow inspiration followed by a rapid expiration and another prolonged inspiration. It is caused by desynchronization of inspiratory neurons and hyperfunction of the post-inspiratory pool against a background of reduced overall respiratory neuronal firing.
Periodic respiration is manifested by wave-like alternating pauses and respiratory efforts of varying intensity:
Cheyne–Stokes respiration: characterized by a gradual waxing and waning of respiratory amplitude followed by a prolonged period of no breathing (apnea), after which the cycle repeats.
Biot respiration: distinguished by sudden long periods of apnea (up to 25–30 seconds) alternating with regular, normal-depth breathing cycles.
Gasping (gasping): represents infrequent, convulsive, deep breaths separated by long intervals. It is a terminal respiratory pattern occurring during severe hypoxia and agonal states, when respiratory neurons no longer respond to hypercapnia or pain stimuli.
Pathophysiology of Periodic Patterns
The key feature of periodic respiration is preserved high synchrony among inspiratory neurons despite a general reduction in signal amplitude within the respiratory center.
Pathological rhythm generation relies on three main components:
Energy deficit: generation of subsequent inspiratory bursts is possible only after replenishing neuronal ATP stores.
Electrolyte disturbances: impaired ion transport across damaged membranes leads to fluctuations in membrane potential and action potentials.
Excitability fluctuations: cyclical shifts in the activation threshold of respiratory center neurons determine periodic changes in respiratory rate and depth.
Impairments in Afferent Regulation
Altered respiratory center function is frequently linked to abnormal afferent input:
Deficiency of excitatory drives: occurs in ethanol or opioid toxicity, decreased chemoreceptor sensitivity (in premature infants), and reticular formation depression (overdose of barbiturates, benzodiazepines, or neuroleptics). Clinically manifests as slow, shallow breathing (bradypnea), hypoxemia, hypercapnia, and acidosis.
Excess of excitatory drives: triggered by severe stress, encephalitis, brainstem strokes (medullary infarction), psychogenic neuroses, and traumatic injuries (chest, abdomen, burns). Clinically manifests as rapid, shallow breathing (tachypnea), hypoxia, and acidosis.
Excess of inhibitory drives: develops during intense chest pain (pleuritis, trauma) or irritation of the airway mucosa by irritants (ammonia fumes), hot or cold air, and acute bronchitis.
Impairments in Efferent Regulation
These are caused by damage to efferent nerve pathways transmitting impulses from the brain to respiratory muscles:
Reduced amplitude of chest wall movements and appearance of periodic apneic episodes
Mnemonic
To remember efferent pathway lesions: "Ondine sleeps — automatic control stops" (diaphragmatic pathway lesion causes reliance on voluntary breathing, leading to apnea during sleep); "Corticospinal block — automatic machine takes over" (voluntary control is lost, breathing becomes strictly mechanical).
Frequently asked questions
What are the characteristics and causes of Kussmaul breathing?
Kussmaul breathing ("hyperpnea") is characterized by deep, rapid, labored, and noisy respirations with a regular rhythm. It typically occurs in patients with altered mental status and indicates severe underlying metabolic derangement.
Key causes/conditions:
Diabetic comas: ketoacidotic and hyperosmolar/lactic acidosis states.
Diabetic ketoacidosis (DKA) as an acute metabolic acidosis driving respiratory compensation.
Renal failure / Uremia, including end-stage renal disease (ESRD) with uremic coma leading to deep acidotic breathing.
Hepatic failure.
Methanol toxicity.
Which breathing patterns are classified as terminal?
Terminal breathing patterns primarily include gasping respiration (also known as agonal breathing or agonal gasps).
Gasping (Gasp): brief, deep, convulsive inspiratory efforts separated by prolonged periods of apnea.
This pattern occurs during severe tissue hypoxia and agonal states as a direct precursor to clinical death. When gasping develops, respiratory center neurons no longer respond to afferent signaling, including hypercapnia and pain.
What is the main difference between Biot respiration and Cheyne–Stokes respiration?
In Cheyne–Stokes respiration, tidal volume gradually waxes and wanes before an apneic pause. In Biot respiration, apneic pauses lasting up to 25–30 seconds occur abruptly between periods of regular, normal-depth breathing.
What is gasping respiration and when is it observed?
Gasping (gasping) consists of infrequent, convulsive inspirations and expirations separated by prolonged pauses. It is a harbinger of clinical death, occurring during profound hypoxia and agonal states when respiratory center neurons cease responding to hypercapnia and noxious stimuli.
What is the mechanism underlying Ondine's curse?
Ondine's curse arises from damage to autonomic pathways descending from the brainstem to the diaphragm. Patients lose automatic respiratory rhythmicity and rely entirely on conscious voluntary effort to breathe; consequently, breathing ceases when voluntary control is lost during sleep.
Go deeper
Mechanisms of neuronal ionic imbalance during hypoxia
Pathophysiology of respiratory acidosis in bradypnea vs. tachypnea
Toxic depression of the reticular activating system by barbiturates and benzodiazepines
Impairment of neuromuscular transmission in botulism and myasthenia gravis