The previous article explored the foundations of the respiratory drive along with its physiologic determinants. Breathing is a primarily central-mediated process with a high degree of automaticity at baseline physiological states. Rhythm and frequency are determined by respiratory centers located in the pons and medulla of the brain stem that integrate sensory information regarding the body’s internal and external environments from chemoreceptors and mechanoreceptors and use it to modulate the body’s ventilatory patterns.
Metabolic Acidosis and the Respiratory Drive
Barring the presence of severe neurological impairment, acute metabolic acidosis is a potent stimulator of the respiratory drive. Both central and peripheral chemoreceptors are sensitive to changes in pH.
When extracellular H+ concentration rises, the drop in arterial pH is detected by peripheral chemoreceptors located in the carotid bodies. This, in turn, directly stimulates the inspiratory centers in the dorsal respiratory group (DRG) located in the medulla to increase the minute ventilation.
Metabolic Acidosis and Endotracheal Intubation
As previously mentioned, metabolic acidosis stimulates the respiratory drive to compensate by increasing alveolar ventilation. In patients with severe metabolic acidosis, the degree of alveolar hyperventilation is often much higher that can be provided through invasive ventilation. For this reason, the general recommendation is to avoid invasive ventilation whenever possible and to support work of breathing with a trial of non-invasive ventilation (NIV) instead. When intubation cannot be avoided, it is important to recognize severe metabolic acidosis as a physiologically challenging airway with potentially devastating consequences if ignored.
Take home message: Brief periods of apnea in a maximally compensated patient may be catastrophic. Sudden loss of alveolar ventilation leads to a sudden elevation of arterial CO2 which may decrease the pH past the threshold of tolerance for an individual patient. If intubation cannot be avoided, then priority should be placed on the maintenance of spontaneous ventilation and avoidance of apnea throughout the entire process. This means that rapid sequence intubation (RSI) should be avoided in favor of awake intubation (Video Laryngoscope, Fiberoptic etc..).
There is no great evidence to suggest the use of bicarbonate therapy as a potential intervention to facilitate intubation in severe metabolic acidosis. This is because bicarbonate eventually generates CO2 which can worsen the pH in a maximally compensated patient with no further capacity for ventilatory compensation.
With severe metabolic acidosis, it is not uncommon to encounter patients with minute ventilations that are likely well over 40 L/min (ex. 1-1.5L tidal volume at RR of 40/min), whereas safe invasive ventilation may be difficult to achieve as the minute ventilation approaches approximately 30 L/min. This gross mismatch will inevitably lead to dyssynchronous patient-ventilator interactions. In these scenarios, the optimal approach may be to set the ventilator to modes that support the work of breathing while allowing the patient to set their own respiratory rate i.e.: Pressure Control or Pressure Support.
- Metabolic acidosis stimulates the peripheral chemoreceptors, sending feedback signals to the respiratory centers to drastically increase alveolar ventilation.
- Avoid invasive ventilation in these patients if possible, a trial of NIV should be attempted first.
- Bicarbonate therapy may be detrimental and yield the opposite effect if used to facilitate intubation.
- If invasive ventilation cannot be avoided, maintaining spontaneous respiration throughout the process is key.
- Improve patient-ventilator interaction post-intubation by utilizing pressure modes where the patient can set their own respiratory rate.
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