respirator mask for copd patients

Specialties Pulmonary

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dmc_rrt

59 Posts

If the Hypoxic Drive to Breath theory is correct, it should happen immediatly as soon as the PaO2 becomes greater then 60mmhg. When the PaO2 is less than 60mmhg the peripheral O2 recepters kick in. As stated earlier PaO2 60mmhg = Sats of 90% (Approx.). COPDers rely on the PaO2 receptors for their drive to breath, unlike pts with normal lung function that rely on the CO2 receptors.

GreyGull

517 Posts

If the Hypoxic Drive to Breath theory is correct,

And it isn't correct. There are several other explanations for a rise in CO2 which more accurately relates to the patient's condition for both acute and chronic conditions.

How long will it take for the high flow O2 to shut a COPDer down to vent status?

There is no magic recipe to determine this and it may or may not apply to other types of patients besides COPDers.

Your assessment should include how hypoxic the patient is and what is their V/Q mismatch and shunting problems. SpO2 only gives you a general idea about the oxygen saturation and the PaO2 is reflected by the oxyhemoglobin dissociation curve. You can also have an SpO2 of 95% with a PaO2 of 65 mmHg on an FiO2 of 1.0. which gives you an A-a gradient of near 400 mmHg. This is a serious situation and with it you might also have hypoxic pulmonary vasoconstriction. Fortunately these problems are anticipated in the hospital and BiPAP can usually alleviate any immediate rise in PaCO2. (PreHospital CPAP may or may not work and may cause an increased work of breathing in some patients.) It is no longer the "hypoxic drive" boogie man that happens as we now have better explanations for the rise in PaCO2 such as the Haldane Effect or the release of hypoxic pulmonary vasoconstriction. In the small percentage of COPD patients who are actually CO2 retainers, other means of ventilation might be easier than seeing how hypoxic you can make a patient to stimulate their breathing and see which organs survive or if the patient does.

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