45. Acute and chronic alveolar hyperventilation

Last updated on May 25, 2019 at 10:18

There are some reasons someone might hyperventilate to cover physiological needs, like during exercise. However, these cases are not alveolar hyperventilation. By definition is alveolar hyperventilation the case when alveolar ventilation exceeds the actual need. The definition also requires a decrease of arterial pCO2 below 36 mmHg.

The causes are as follows:

  • Hypoxaemia
    • High altitude
    • Cardiac shunt
  • Pulmonary disorders (early phases)
    • Pneumonia
    • Fibrosis
    • Oedema
    • Pulmonary embolism
    • Bronchial asthma
  • Cardiovascular disorders
    • Congestive heart failure
    • Hypotension
  • Metabolic disorders
    • H+ stimulates the respiratory centre
    • Acidosis (Kussmaul breathing)
      • Diabetic ketoacidosis
      • Renal acidosis
      • Lactic acidosis
    • Liver failure
  • Neurological and physiological disorders
    • CNS lesions
    • Anxiety
    • Fear
    • Pain
  • Drugs
  • Fever
  • Sepsis

Dyspnoea of pulmonary origin and dyspnoea of cardiac origin (cardiac dyspnoea) have different consequences. Cardiac dyspnoea induces alveolar hyperventilation while pulmonary dyspnoea doesn’t.

There’s some data that visiting a physician can evoke hyperventilation (like fear does perhaps?). This hyperventilation can explain some of the symptoms seen in the office.

Consequences of alveolar hyperventilation
  • Hypocapnia → cerebral vasoconstriction → syncope
  • Respiratory alkalosis
    • → relative decrease of ionized Ca2+ in plasma → neuromuscular excitability increases → tetany → laryngospasm → suffocation
    • → Extracellular K+ concentration decreases → risk for arrhythmia increases
    • → The O2-saturation curve of haemoglobin is shifted to the left → Hb binds O2 too strongly → tissue oxygenation is reduced

Reduced pCO2 causes vasoconstriction in the brain. In severe cases can the vasoconstriction be enough to cause hypoperfusion and eventually syncope.

In alveolar hyperventilation the pCO2 level is decreased, causing respiratory alkalosis.

When the blood becomes more alkaline will albumin become more ionized to its negative form. This causes it to bind more Ca2+, which reduces the ratio between ionized (free) Ca2+ and bound calcium in the blood. Only ionized calcium is physiologically active, so the active amount of calcium in the blood is effectively reduced. Calcium blocks sodium channels and inhibits depolarization. When calcium levels are reduced will the threshold for depolarization be lowered. This causes increased neuromuscular excitability, which can cause tetany that might affect the larynx, which can cause suffocation and death.

Alkalosis causes hypokalaemia by moving potassium out of the plasma and interstitial fluids into the urine. This is caused by the effects of intercalated cells in the collecting duct. The kidney wants to conserve H+ ions, but to do so it must excrete K+ ions to maintain electroneutrality. Hypokalaemia is arrhythmogenic through several mechanisms. Hypokalaemia makes the membrane potential more negative, making it harder to reach the threshold for depolarization.

Lastly will the alkalosis cause a left-shift of the oxygen-haemoglobin dissociation curve, meaning that oxygen now binds more strongly to haemoglobin. This causes the amount of oxygen released from haemoglobin into the tissues to be decreased.

Oxygen dissociation – left and right shift
The oxygen-haemoglobin dissociation curve

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44. Alveolar hypoventilation. Causes and consequences.

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46. Ventilation-perfusion mismatch (VQ). Causes and consequences

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