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Types of breathing

Pathological breathing types are severe disorders of the rhythm and depth of respiratory movements that develop when compensatory mechanisms become depleted. Their appearance serves as a critical vital sign indicating central nervous system depression, the development of coma, or a terminal state.

Kussmaul breathingDeep and noisy breathing characteristic of diabetic ketoacidosis and uremia.
Cheyne-Stokes breathingA wavelike crescendo in the depth of inspirations, alternating with periods of apnea.
Biot's breathingIndicates profound damage to the brainstem structures.
ApneaComplete cessation of breathing lasting up to one minute in periodic forms.
4 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Classification of respiratory disorders

Disruptions in central nervous system regulation lead to the formation of specific respiratory movement patterns. The general classification distinguishes basic frequency disturbances—tachypnea (rapid, shallow breathing) and bradypnea (slow breathing)—as well as cycle delays, such as apneustic breathing (a spasmodic inspiration with a pause).

Against the background of these disorders in severe disease courses, specific periodic pathological types unfold:

Breathing typeKey pattern characteristic
KussmaulRegular cycles: rare, deep, noisy inspiration and forced expiration
Cheyne-StokesWavelike change in depth (from shallow to deep) with apnea pauses
GroccoIncomplete variant of Cheyne-Stokes: wavelike cycles are preserved, but there are no apnea pauses
Biot'sAlternation of regular deep inspirations with prolonged periods of apnea (up to 20–30 sec)
Gasping (gasp)Terminal rare breathing: spasmodic short inspirations and expirations with huge pauses

Kussmaul breathing ("air hunger")

This type is characterized by rare but very deep cycles. It always indicates an extremely severe patient condition and is frequently accompanied by altered consciousness.

Etiologically, Kussmaul breathing is closely linked to severe intoxications and metabolic catastrophes:

  • Diabetic comas. In the ketoacidotic variant, the pattern is combined with a sharp acetone odor on the breath, dry skin, hypotension, and diminished reflexes. In lactic acidosis coma, the acetone odor is absent.
  • Toxic damage. Develops in uremia (combined with encephalopathy and convulsive twitching), as well as in methanol poisoning.
  • Liver failure. The appearance of this rhythm is characteristic of the precoma stage, when toxins critically damage the central nervous system.
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Periodic patterns: Cheyne-Stokes, Grocco, and Biot

These variants develop when adaptation mechanisms fail and brain structures are damaged.

Grocco's breathing serves as a marker of the early stages of comatose states. The pattern appears as a continuous wave: breathing gradually intensifies and then subsides without cessations.

Cheyne-Stokes breathing begins with shallow movements that increase to a noisy maximum by about the 5th to 7th breath, then decrease and transition into apnea (ranging from a few seconds to a minute). The causes include general hypothermia, damage to the respiratory center, and marked pulmonary edema (transition of the rhythm to aperiodic indicates an agonal state). If the pattern is combined with focal neurological symptoms, it is a sure sign of brain herniation.

Biot's breathing reflects organic damage to the brainstem. Rhythmic series of identical inspirations are abruptly cut short by prolonged apnea. The pattern is characteristic of severe hypoxia, shock, and acute cerebrovascular accidents.

Note: In coma caused by traumatic brain injury, breathing is most often described simply as variable, rare, or irregular, without a clear periodic pattern.

Association with hepatic encephalopathy

Pathological breathing (Kussmaul or Cheyne-Stokes) is an important criterion for the progression of hepatocellular failure.

It manifests at stage III (precoma), which is also characterized by:

  • Depression of consciousness to stupor and dysarthria.
  • A sharp increase in neurological markers, particularly the specific "flapping" tremor of the fingers (asterixis).
  • A specific sweetish-aromatic hepatic odor on the breath (Fetor hepaticus).
  • Physical examination: rapid decrease in liver size ("shrinking liver").
  • Increasing jaundice (without pruritus) and hemorrhagic syndrome.

Progression to stage IV (hepatic coma proper) is accompanied by complete loss of consciousness, areflexia, and may end in the complete cessation of breathing (apnea). Laboratory findings confirm the process with hyperbilirubinemia, hypoalbuminemia, and a drop in prothrombin and cholesterol levels.

How to memorize

How to memorize periodic patterns: Grocco — a smooth wave without stops. Cheyne-Stokes — a wave with rest stops (depth change + apnea). Biot — a march with rest stops (identical deep steps-inspirations + apnea).

Class and exam questions

How does Grocco's breathing differ from Cheyne-Stokes breathing?

In Grocco's breathing, there is a wavelike change in the depth of inspirations, but periods of complete cessation of breathing (apnea), which are an obligatory part of the Cheyne-Stokes cycle, are absent. Grocco often precedes more severe disorders.

What does a patient's breath smell like in diabetic coma with Kussmaul breathing?

A sharp acetone odor is typical for ketoacidotic coma. However, in another form—lactic acidosis coma—Kussmaul breathing is present, but there is no acetone odor.

What does the appearance of Biot's breathing indicate?

This is an unfavorable vital sign indicating profound damage to the brainstem structures against the background of organic lesions, severe hypoxia, intoxication, or shock.

At what stage of hepatic encephalopathy do pathological breathing types appear?

Rhythm disturbances (Cheyne-Stokes or Kussmaul) are characteristic of stage III—precoma. They are accompanied by stupor, a "flapping" tremor, dysarthria, and hepatic fetor on the breath.

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What else to study on this topic

  • Spirographic analysis of respiratory patterns
  • Differential diagnosis of coma types (uremic, diabetic)
  • Clinical staging of hepatic encephalopathy
  • Neurological markers of coma (asterixis, areflexia)
  • Mechanisms of gasping respiration and terminal states

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