Apneustic and periodic breathing
Apneustic breathing is characterized by a prolonged, shallow inspiration followed by a quick expiration and another prolonged inspiration. The underlying pathology is the desynchronization of inspiratory neurons and hyperactivity of the post-inspiratory pool against the background of a general decrease in the impulse activity of respiratory cells.
Periodic breathing is manifested by wave-like alternation of pauses and respiratory movements of varying intensity:
- Cheyne-Stokes respiration: characterized by a gradual increase in breathing amplitude, its subsequent decline, and the onset of a prolonged period without breathing (apnea), after which the cycle resumes.
- Biot's respiration: differs by the occurrence of long apnea pauses (up to 25–30 seconds) alternating with respiratory cycles of normal depth and rhythm.
- Gasping (gasping): represents rare, convulsive, and deep inspirations-expirations with long intervals. This is a terminal form that occurs in severe hypoxia and in an agonal state, when neurons stop responding to carbon dioxide and pain stimuli.
Pathogenesis of periodic forms
The key difference of periodic breathing is the preservation of high synchrony in the work of inspiratory neurons with a general drop in signal amplitude in the respiratory center.
The formation of a pathological rhythm relies on three links:
- Energy deficit: the next generation of the inspiratory impulse is possible only after replenishing ATP stores in neurons.
- Electrolyte disturbances: failures in ion distribution across damaged membranes lead to fluctuations in membrane potential and action potential.
- Fluctuation of excitability: cyclical changes in the excitability threshold of respiratory center neurons determine the periodic change in the frequency and depth of inspirations.
Disorders of afferent regulation
Changes in the functioning of the respiratory center are often associated with the distortion of afferent signals reaching it:
- Deficiency of excitatory stimuli: occurs with ethanol or narcotic poisoning, a drop in chemoreceptor sensitivity (in premature infants), and depression of the reticular formation (overdose of barbiturates, benzodiazepines, neuroleptics). It manifests as rare shallow breathing (bradypnea), hypoxemia, hypercapnia, and acidosis.
- Excess of excitatory stimuli: provoked by stress, encephalitis, strokes in the medulla oblongata region, psychogenic neuroses, and trauma (chest, abdomen, burns). Clinically expressed as frequent shallow breathing (tachypnea), hypoxia, and acidosis.
- Excess of inhibitory stimuli: develops with intense chest pain (pleurisy, trauma) or irritation of the airways by irritants (ammonia), hot or cold air, as well as in acute bronchitis.
Disorders of efferent regulation
Associated with damage to nerve pathways transmitting signals from the brain to the muscles:
| Level of lesion | Causes | Clinical and pathophysiological picture |
|---|---|---|
| Pathways from the center to the diaphragm | Spinal cord ischemia/trauma, multiple sclerosis, poliomyelitis | Loss of automatism. Breathing is regulated only by consciousness. During sleep, breathing stops (Ondine's curse syndrome). |
| Corticospinal pathways | Tumors, ischemia, syringomyelia, trauma | Loss of voluntary control. Breathing becomes strictly automatic ("machine-like"), without the ability to change its depth by willpower. |
| Spinal pathways, motor neurons, synapses | Poliomyelitis, botulism, neuritis, myasthenia gravis, muscle relaxants | Decrease in the amplitude of respiratory movements, appearance of periodic episodes of apnea. |
Briefly: answers to topical questions
What is characteristic of Kussmaul breathing and in what conditions does it occur?
Kussmaul breathing ("air hunger") is characterized by regular cycles: rare, but deep and noisy inspiration followed by an enhanced expiration. It is usually observed against the background of impaired consciousness and indicates an extremely serious condition of the patient.
Conditions/causes:
- Diabetic comas: ketoacidotic and lactic acidosis.
- Diabetic ketoacidosis as a state of acute acidosis, in which deep, noisy Kussmaul breathing appears.
- Renal failure / uremia, including the terminal stage of chronic kidney disease with uremic coma; noisy acidotic breathing against the background of metabolic acidosis.
- Liver failure.
- Methanol poisoning.
Which types of breathing are classified as terminal?
Terminal types include gasping respiration, a synonym for which is terminal rare breathing.
- Gasping (Gasp) — deep convulsive short inspirations-expirations with long intervals between them.
This type of pathological breathing occurs in conditions of deep hypoxia and in an agonal state, serving as a direct precursor to clinical death. With its development, neurons of the respiratory center cease to respond to any afferent influences, including pain stimuli and hypercapnia.
To memorize efferent pathway disorders: "Ondine sleeps — automatism is silent" (when pathways to the diaphragm are damaged, breathing depends on consciousness and stops during sleep); "Corticospinal block — automatism's doom" (voluntary control is lost, breathing becomes machine-like).
Class and exam questions
What is the main difference between Biot breathing and Cheyne-Stokes respiration?
In Cheyne-Stokes respiration, the amplitude of inspirations wave-like increases and decreases before the onset of a pause. In Biot's respiration, apnea pauses lasting up to 25–30 seconds occur suddenly between periods of regular breathing of normal rhythm.
What is gasping respiration and when does it occur?
Gasping (gasping) is rare convulsive inspirations and expirations with long pauses, which are a precursor to clinical death. It occurs in deep hypoxia and in an agonal state, when neurons lose sensitivity to hypercapnia and pain.
What is the mechanism underlying Ondine's curse syndrome?
The syndrome develops when pathways running from the respiratory center to the diaphragm are damaged. A person loses the automatic rhythm of breathing and can breathe only consciously, therefore, when falling asleep and losing consciousness, respiratory movements cease.
What else to study on this topic
- Mechanisms of ion imbalance formation in neurons during hypoxia
- Pathophysiology of respiratory acidosis in bradypnea and tachypnea
- Toxic depression of the reticular formation by barbiturates and benzodiazepines
- Features of neuromuscular transmission impairment in botulism and myasthenia gravis
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