Abstract
The work of breathing is the energy consumed by the respiratory muscles throughout the respiratory cycle.
What is meant by the term ‘work of breathing’?
The work of breathing is the energy consumed by the respiratory muscles throughout the respiratory cycle.
Mathematically, for a single breath:
However, the work of breathing usually refers to the rate of work rather than the work for a single respiratory cycle. It should really be called the power of breathing and measured in watts (J/s).
Quiet tidal breathing is usually very efficient, requiring relatively little work. The energy required for tidal breathing is usually less than 2% of basal metabolic rate (BMR). Lung pathology can increase the work of breathing substantially, in some cases up to 30% of BMR, with the potential for respiratory muscle fatigue and respiratory failure.
What are the two main components that comprise the work of breathing?
The work of breathing is composed of elastic work and resistive work. In normal lungs, elastic work is responsible for most (approximately 65%) of the overall work of breathing:
Elastic work is the work done on inspiration to overcome the elastic forces of the:
– Chest wall (outward);
– Lung parenchyma (inward);
– Alveolar surface tension (inward).
– Obesity, which opposes outward chest wall elastic recoil;
– Pulmonary fibrosis, which reduces the compliance of the lung parenchyma;
– Infant respiratory distress syndrome, in which there is insufficient pulmonary surfactant, leading to increased alveolar surface tension.
Resistive work is the work done against friction – the energy used is ‘wasted’, as it is dissipated as heat (and sound). The resistive work of breathing is the work done to overcome:
– Tissue resistance. As the tissues move against each other during lung inflation and deflation, frictional forces cause an increase in tissue resistance. Tissue resistance usually accounts for around 10% of the total resistive work. Tissue resistive work is increased by any condition that increases the amount of interstitial lung tissue, such as pulmonary fibrosis.
– Airway resistance. Gas molecules are subject to frictional forces when they interact with each other and with the walls of the airways.
What factors affect airway resistance?
The resistance to gas flow is affected by two main factors: turbulence and the airway radius.
Turbulent gas flow results in a much higher airway resistance than laminar gas flow does. During normal tidal breathing, gas flow is usually only turbulent in the trachea, but may become turbulent in the larger bronchi during peak inspiratory flow. If the velocity of gas flow increases (e.g. with increasing respiratory rate, RR), gas flow becomes turbulent in the larger bronchi for a greater portion of the respiratory cycle, increasing airway resistance. The point at which gas flow changes from laminar to turbulent is estimated using the Reynolds number.
Reynolds number=vρdη
where ν is velocity of gas flow, ρ is the density of gas, d is the airway diameter and η is the viscosity of gas.
A Reynolds number of 2000 predicts an 80% chance of turbulent flow. A Reynolds number of 200 predicts an 80% chance of laminar flow.
Airway radius. According to the Hagan–Poiseuille equation, resistance to gas flow is proportional to r4 (r is the radius). Therefore, small reductions in airway radius can have a large impact on the resistance to flow.
where ΔP is the pressure drop along the tube, Q̇ is flow, η is the viscosity of the fluid, l is tube length and r is the radius.
Darcy’s law1 states:
ΔP = Q ̇ RΔP=Q̇RTherefore, if ΔP is pressure difference and Q̇ is flow, then the resistance to flow R = 8ηl/πr4.