respirator mask for copd patients - Page 2Register Today!
- Oct 5, '05 by elnskiA COPD pt, would normally thrive w/ low pO2 anyway.. It 'swhat we call the hypoxic drive.unlyk us normal peeps. Chronically evidenced w/ and elevated HCO3 and BE most of the tym to compensate their pH. I wouldnt worry if they have a pO2 of 8, cuz a lot of them have been hypoxic all their lives anyway. More accurate delivery of FiO2 is without a doubt via a venturi, cuz when theyr acutely exacerbated and when distressed they become mouth breathers in an attempt to blow off CO2.. A good SpO2 doesnt all the tym indicate the pts ventilation is well..they may have sats of >95%, but guess what? the CO2 is already on the ceiling..thus they become drowsy and unresponsive.. due to acidosis..
the more O2 we deliver, the more they will retain CO2..when CO2 reacts w/ water it will form carbonic acid, thus the ph goes down.. acidosis occurs...
Tho there are COPD who are not chronic retainers.. as much as possible keep pt from receiving too much O2 ..just enough to perfuse and maintain their respi drive active..
too much 02 is toxic as we all know, careful Px of it shld be monitored.. we give Hi FiO2 if only if it is a lyf threatening situation...
- Jan 15, '11 by firemedicdeeHow long will it take for the high flow O2 to shut a COPDer down to vent status?
- Mar 10, '11 by dmc_rrtIf 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.
- Mar 12, '11 by GreyGullQuote from dmc_rrtAnd 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.If the Hypoxic Drive to Breath theory is correct,
Quote from firemedicdeeThere is no magic recipe to determine this and it may or may not apply to other types of patients besides COPDers.How long will it take for the high flow O2 to shut a COPDer down to vent status?
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.