Patterns Of Breathing

Overview

At rest, a healthy person takes around 12-18 breaths per minute at a tidal volume of about 500 ml. Increased depth or rate of breathing is driven primarily by hypercapnia (increased PaCO₂). Breathing may also increase in metabolic acidosis (Kussmaul breathing) as the body attempts to blow off volatile acids.

You might want to brush up on:

• Hyperventilation and hypoventilation.
• Arterial blood gases.
• Causes of metabolic acidosis and alkalosis.
• Neural control of breathing.

Normal breathing

At rest, a healthy person has a respiratory rate of about 15 breaths/min with a tidal volume of around 0.5 litre. When not at rest, the body produces more CO₂ and so ventilation will increase to accommodate the increased demand need “blow off” CO₂; this is hyperpnoea, not hyperventilation.

Kussmaul breathing

Kussmaul breathing is deep breathing at rest. It is often seen in diabetic ketoacidosis, a metabolic acidosis in which the lungs compensate by eliminating excess CO₂ to offset the acid produced by the body. Because PaCO₂ is reduced, Kussmaul breathing is hyperventilation, by definition, but it is an appropriate response in metabolic acidosis. Kussmaul breathing is sometimes seen in other settings where metabolic acidosis occurs such as sepsis or hypovolaemia.

Is this hyperpnoea? Yes, because we use this term (and tachypnoea) independently of blood CO₂ levels:

• Hyperpnoea – breathing more deeply than normal
• Tachypnoea – breathing faster than normal. Often confused with hyperventilation.

Remember, tachypnoea may or may not be hyperventilation. It depends on whether arterial CO₂ is reduced or not. Kussmaul breathing is generally hyperpnoea not tachypnoea, and it is also hyperventilation because it reduces PaCO₂ to compensate for metabolic acidosis.

Cheynes-Stokes

Cheynes-Stokes breathing is characteristic cycles of apnoea and hyperpnoea. It represents opposing driving drives (hypercapnic and hypoxic) fighting for control of lung ventilation. The apnoea is central - not obstructive - and is triggered by hyperventilation (reduced PaCO₂). Phases of hyperpnoea occur between apnoeic events as the more sluggish hypoxic drive triggers breathing. Each burst of hyperpnoea results in hyperventilation leading to the next phase of apnoea. In healthy people, it can be observed most clearly at high altitude (where hyperventilation is required to maintain normoxia) in subjects who are asleep (when cortical control of breathing is less dominant). In disease, this pattern of breathing is seen in some heart failure patients (probably due to reduced blood flow to the brain) and after strokes that damage the respiratory centres of the brain.