Book pp. 958–960 · asked 5 times in NTRUHS papers

In one breath

Periodic breathing is a repeating cycle of apnea and over-breathing, produced when the CO₂ feedback loop overshoots; in healthy people it follows a few minutes of voluntary hyperventilation, and when the same pattern appears in disease it is called Cheyne-Stokes respiration (heart failure, renal failure, brain disease, high altitude, premature infants). Kussmaul breathing is the deep rapid air hunger of diabetic ketoacidosis, and Biot’s respiration is three or four normal cycles cut off by abrupt apnea, which points at the medulla. Sleep apnea syndrome, sudden infant death syndrome, hysteric hyperpnea and Ondine’s curse complete the list of named patterns.

Builds on: Chemical control of breathing · Asphyxia, hypercapnia and hypocapnia · Leads to: Acclimatization to high altitude · Artificial respiration

Periodic breathing

Definition: cyclical repetition of apnea alternating with over-breathing (hyperpnea) in a normal individual.

  • It is typically seen after voluntary hyperventilation kept up for 2–3 minutes.
  • The apnea–hyperpnea cycles then continue on their own for some time.

Why the cycles happen

  1. Hyperventilation has removed CO₂, so the CO₂ drive on ventilation is gone and apnea follows.
  2. During the apnea, PCO₂ builds up and PO₂ falls, which stimulates ventilation through the chemoreceptors.
  3. Breathing restarts, and PO₂ returns to normal.
  4. Losing that hypoxic drive stops breathing again — another apnea — and PCO₂ starts accumulating once more, producing the next burst of hyperventilation.
  5. The cycles continue until PCO₂ climbs gradually back to normal.

Why a normal person does not do this all the time: the respiratory center adjusts the depth of each breath so that arterial PCO₂ never drops below its critical value. Once PCO₂ does go below that level, apnea appears.

Worth knowing, though not in your pages: on a real trace the breaths do not switch on and off abruptly — they wax and wane in depth, a crescendo followed by a decrescendo, and then the pause. That waxing-and-waning shape is what you are expected to draw.

Cheyne-Stokes respiration

Periodic breathing occurring in disease is called Cheyne-Stokes respiration. A few healthy people show it while deeply asleep, but its usual settings are congestive cardiac failure, uremia and diseases of the brain.

  1. These patients have increased sensitivity to CO₂, because neural pathways are disrupted.
  2. CO₂ accumulates, producing hyperventilation, which lowers PCO₂.
  3. The low PCO₂ removes the CO₂ drive, so apnea follows — and PCO₂ rises again.
  4. Because the response to PCO₂ is exaggerated, that rise produces another burst of hyperventilation, and the cycle repeats.

Causes

  • Premature infants
  • Unacclimatized people at high altitude
  • Deep sleep in some people
  • Heart failure
  • Renal failure

Worth knowing, though not in your pages: in heart failure the delay in the loop is usually attributed to a prolonged lung-to-brain circulation time — the chemoreceptors are reading stale blood, so the correction always arrives late and overshoots. Your book explains the same overshoot as increased CO₂ sensitivity; both descriptions are of one unstable feedback loop.

Draw it: normal, periodic and Biot's breathing

Three traces, stacked, sharing one time axis, tidal volume up the side. A — normal: even breaths of equal height, evenly spaced. B — periodic (Cheyne-Stokes): breaths that grow taller then shorter (crescendo–decrescendo), followed by a flat stretch labelled “apnea”, then the whole cycle repeats. Under it write “PCO₂ ↓ during hyperpnea → apnea → PCO₂ ↑ → hyperpnea”. C — Biot’s: three or four normal-sized breaths, a deep gasp, then an abrupt flat line labelled “sudden apnea”, and the pattern starts again with no waxing or waning. Label A normal, B periodic, C Biot’s, and in one line say what distinguishes B from C: gradual versus abrupt.

Other abnormal breathings

PatternWhere it is seen
Kussmaul breathingDiabetic ketoacidosis
Biot’s respirationMeningitis, medullary and brainstem damage, raised ICP, morphine poisoning
Sleep apnea syndromeAdults, during REM sleep
Sudden infant death syndromePremature infants, in sleep
Hysteric hyperpneaHysteria
Ondine’s curseBrain injury

Kussmaul breathing

  • The breathing pattern of diabetic ketoacidosis, described by Kussmaul.
  • Metabolic acids accumulate — acetoacetic acid and β-hydroxybutyric acid — producing metabolic acidosis, which stimulates the respiratory centers.
  • The result is rapid and deep respiration, Kussmaul’s “air hunger”.

Kussmaul is not periodic

Kussmaul breathing is continuous deep rapid breathing driven by a metabolic acidosis: there is no apnea in it. Periodic breathing and Cheyne-Stokes respiration alternate hyperpnea with apnea, and are driven by an unstable CO₂ loop. Examiners set these two side by side deliberately.

Biot’s respiration

  • Three to four cycles of normal respiration, then abrupt onset of apnea. Deep gasps usually come just before the apnea.
  • Seen in meningitis, diseases affecting the medulla, raised intracranial pressure, morphine poisoning and brainstem damage.

Sleep apnea syndrome

  • In the adult syndrome there is marked loss of tone of the pharyngeal muscles during REM sleep, so the airway is obstructed during inspiration and apnea results.
  • The person wakes up, breathes normally for a while, falls asleep and has another bout.
  • So apnea recurs repeatedly through the night.
  • Because of those repeated night-time apneas, patients get morning headache and fatigue, and sleeplessness during the day.

Worth knowing, though not in your pages: your book’s phrase for the daytime symptom is “sleeplessness”. The usual clinical picture is the other way round — excessive daytime sleepiness, because the night’s sleep was broken. Write the book’s fragmented night sleep, and add the daytime sleepiness.

Sudden infant death syndrome

  • SIDS is thought to be sleep apnea occurring in a preterm baby.
  • The respiratory center stops firing rhythmically, so the baby goes apneic while asleep and does not survive it.
  • The cause is not known. Most of those affected are preterm, many with arrhythmias on the back of long QT syndrome, and a mother who smokes heavily is a further risk.

Hysteric hyperpnea

  • Sudden, spontaneous hyperpnea in a patient with hysteria.
  • It washes out CO₂, giving alkalosis and then convulsions.
  • Treatment: let the patient breathe into a face mask until recovery.

Applied: why a face mask stops the fit

Breathing into a mask means rebreathing the patient’s own expired air, which is rich in CO₂. PCO₂ climbs back towards normal, the respiratory alkalosis is corrected, and the convulsions settle. Nothing is given to the patient — the cure is simply not letting the CO₂ escape.

Ondine’s curse

  • After brain injury, some patients lose automatic control of breathing but keep voluntary breathing. They need respiratory assistance intermittently, particularly when they are not attending to it.
  • The name is borrowed from a German legend, in which a water nymph’s faithless lover is condemned to stay alive only for as long as he keeps choosing each breath — so he dies the night he finally falls asleep.

Exam-answer skeleton: "What is periodic breathing? Explain its mechanism, and name the conditions in which Cheyne-Stokes respiration occurs" (short note)

  1. Define periodic breathing: cyclical apnea alternating with hyperpnea in a normal person, classically after 2–3 minutes of voluntary hyperventilation.
  2. Draw the trace: crescendo–decrescendo breaths, then apnea, repeating.
  3. Mechanism step 1: hyperventilation washes out CO₂, the CO₂ drive is lost, apnea follows.
  4. Mechanism step 2: during apnea PCO₂ rises and PO₂ falls, the chemoreceptors restart breathing, PO₂ is restored, the hypoxic drive is lost and apnea returns — cycles continue until PCO₂ is back to normal.
  5. Say why it does not normally happen: the respiratory center keeps arterial PCO₂ above its critical level by grading the depth of each breath.
  6. Define Cheyne-Stokes respiration: the same pattern arising in disease, with increased sensitivity to CO₂ from disrupted neural pathways.
  7. List its causes: premature infants, unacclimatized people at high altitude, deep sleep in some normal people, heart failure, renal failure.
  8. If marks remain, contrast it with Biot’s respiration — abrupt apnea after three or four normal breaths, indicating medullary or brainstem damage.

Asked in exams