Hypoxic Drive...No!!!

CriticalCarePractitioner


Hypoxic Drive? No!!!

It was with interest that I just listened to the SMACC presentation on Dogmalysis given by Cliff Reid. One of the many areas he discussed was the often expressed view that you cannot put a patient with chronic respiratory disease on high flow oxygen as you will suppress their hypoxic drive. This is a brief post just to understand the issues involved.

The thought process here is that oxygen administration in patients with chronic lung disease induces hypercapnia through the hypoxic drive and can therefore be dangerous.
This often results in patients who are hypoxic not being given sufficient oxygen in order to compensate.

Central and Peripheral Chemoreceptors

The central chemo receptors monitor carbon dioxide levels in the body. When those carbon dioxide levels are high a signal is sent to speed up the drive to breathe to blow off the excess carbon dioxide. So the levels of carbon dioxide dictate how fast we will breathe.


The peripheral chemo receptors are sensitive to the levels of oxygen in the body. They will send a signal to breathe when the partial pressure of oxygen begins to fall. This is referred to as the hypoxic drive but this drive has a much more minor role in breathing.

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So increased oxygen slows down respiration right?……

COPD patients tend to have chronically elevated levels of carbon dioxide due to the nature of their illness. The theory goes then that because of this chronically elevated level of carbon dioxide in the chemo receptors become tolerant of these high levels and therefore the carbon dioxide ceases to be that person’s drive to breathe. What therefore drives them to breathe is the hypoxic drive, or the lower levels of oxygen.


The hypoxic drive theory then goes on to say that if you give these patients too much oxygen you blunt their hypoxic drive. As their chemo receptors are already tolerant of high levels of carbon dioxide, and therefore they have also lost that drive, their respirations will begin to slow causing a further rise in carbon dioxide levels, and a consequent acidosis.


Aubier and colleagues demonstrated that reduction in respiratory drive is not a major contributor to oxygen induced hypercapnia in patients with acute exacerbation of COPD.

….NO…its more likely the Haldane effect…..

The Haldane effect describes the property of haemoglobin in the blood whereby the deoxygenation of the blood will increase its ability to carry carbon dioxide. Conversely oxygenated blood has a reduced capacity for carbon dioxide.


So if you increase oxygen in the blood by giving them supplemental oxygen then via the Haldane effect carbon dioxide molecules will be displaced in favour of the oxygen.


This then causes an increase of carbon dioxide in the blood or a rising PaCO2. This rise in carbon dioxide is normally excreted through increased minute ventilation however those with chronic COPD cannot increase their minute ventilation.


In the Aubier study above the Haldane effect accounted for 25% of the increase in PaCO2

...and V/Q mismatching...

When oxygen tension within the alveoli is reduced there is vasoconstriction of pulmonary capillaries supporting alveoli. This is known as hypoxic pulmonary vasoconstriction.


A high level of oxygen will increase oxygen tension therefore which will reduce hypoxic pulmonary vasoconstriction. This has the result of a blood supply passing an alveoli with relatively impaired ventilation consequently increasing dead space.


This dead space will then cause the carbon dioxide levels to continue to rise.

So what do we do?

I hope Wilson and Leo( Oxygen induced hypercapnia in COPD: Myths and facts. Crit Care 2012) wont mind me pinching their conclusion to summarise:


“In patients with COPD, hypoxic pulmonary vasoconstriction is the most efficient way to alter the Va/Q ratios to improve gas exchange. This physiological mechanism is counteracted by oxygen therapy and accounts for the largest increase of oxygen-induced hypercapnia. A titrated oxygen therapy to achieve saturations of 88% to 92% is recommended in patients with an acute exacerbation of COPD to avoid hypoxemia and reduce the risk of oxygen-induced hypercapnia.”


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