This experimental study puts most common assumptions about hyperventilation in hemorrhagic shock on its head. Common thinking is that trauma pts breathe faster because of shock and metabolic demands not being met. This study suggests trauma pts are breathing faster to elicit a respiratory pump with the negative inspiratory pressures that will enhance cardiac preload.

The Study
To see how this worked, they put 10 healthy individuals in negative pressure pants to get lower body negative pressure (LBNP), that would keep the blood volume in the lower body, and for practical purposes simulate hypovolemia, and without inducing acidemia or lactacidosis that are often seen as drivers of hyperventilation.

The pants successfully reduced BP in the subjects, to get the subjects to near syncope. Lactate and pH stayed normal. CO2 was lower in the late stages, due to hyperventilation. The hyperventilation occurred late in the simulated hypovolemic setting, and was observed differently in different subjects: some had both increases respiratory rate as well as deeper breaths, some only had increased RR, others only deeper breathing.

This experimental study shows us that hyperventilation might well be a compensatory mechanism in hypovolemia to increase cardiac preload, and not to affect ventilation parameters per se. It also shows us we need to be more aware of the heart-lung interactions of the body.

When the bleeding trauma pt breathes faster and/or deeper, they might not be in need of aggressive ventilation with oxygen or ridding themselves of CO2, they might just be in need of better preload and cardiac output.

The study “…supports the notion that this hyper-ventilatory response may be a late protective mechanism designed to restore cardiac filling and perfusion pressures to vital organs in conditions of severe central hypovolemic hypotension“.

If patients are breathing to support the circulation, this might also explain why we can often normoventilate these pts after they are intubated – although positive pressure ventilation can seriously impact their circulation.

This is just an experimental study, but interesting insight into the heart-lung interactions. Faster and deeper breathing in shock might (also) be the body trying to compensate for a circulatory problem.

Hyperventilation in response to progressive reduction in central blood volume to near syncope, Aviat Space Environ Med, 2009.

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  1. Rob Timmings says:

    Given that ventilation rate and depth is driven by pH – particularly stimulated by acidosis, AND all shock patients are acidotic (even marginally), would hyperventilation not simply be a function of shock induced acidaemia or more correctly acidotic CSF detected in the Pons?

    • Thomas D says:

      Well, that’s what we’re usually taught. And low pH is also a driver of increased ventilation, but this study seems to indicate that hypovolemia is an independent driver of increased ventilation, even in the absence of acidaemia.

  2. Fascinating study, thank you for sharing.

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