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COPD Patient


briguy222

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If bradypnoea occurs before arrival at hospital, this is far more likely to be due to exhaustion than hypercapnia. The overall minute volume of the patient may drop, (respirations slow), as the patient's oxygenation needs are met. Ventilation is still a problem for them and thus the bronchodilators are now needed. Also in the home environment now you may start to see patients with O2/Helium mixtures, usually 30/70% which they use for exercise or walking longer distances. This is usually the same mixture used in the ER.

If a respiratory arrest occurs suddenly, then it was probably likely to happen with or without oxygen.

CO2 "narcosis" is what can knock out the ventilatory drive at high levels in combination with the underlying accute illness such as sepsis or PNA. The V/Q mismatch will have to be appreciated and dealt with. If these patients do end up on ventilators, they may be on much higher then 28% O2 and need a creative ventilator strategy to get them to a good baseline for weaning.

Hypoxic and ventilatory drives exist. That is how WE exist. The ventilatory response of "normal" humans to isocapnic hypoxia is triphasic. First, there is a rapid increase in expired minute ventilation known as the acute hypoxic ventilatory response (AHVR), which occurs with a time constant in the order of seconds. Second, there is a fall in expired minute ventilation known variously as hypoxic ventilatory depression (HVD), hypoxic ventilatory decline, or ventilatory "roll-off" with a time constant in the order of minutes. Third, there is a progressive rise in expired minute ventilation with a time constant in the order of hours that appears to be related to ventilatory acclimatization to altitude.

Any disease process can change a person's overall physiologic responses to hypoxia. Obesity, lung disease, pulmonary hypertension, lung and heart transplants, etc all may change the way a person "breathes" as their body changes to tolerate the disease. There are many other disease processes besides COPD that also retain CO2 either for metabolic or ventilatory reasons.

Jeff Whitnack's summation of current studies on the hypoxic drive theory is an excellent read as well as the references he used. You can find this in an earlier post in this thread.

Athletes train in altitudes to develop increased O2 carrying capacity. Hypoxia-induced secondary polycythemia is a major contributor to increased work capacity at altitude. COPD patients that live in a chronic "hypoxic" state may also develop polycythemia. This is the body's way of acclimating to chronic hypoxia. If the patient is polycythemic, then they may tolerate lower SpO2s easier. Not every one can live comfortably at 88% SpO2. Polycythemia creates many other medical problems though that are related to the increased chances of clotting. These patients are usually on supplemental O2 and blood thinners.

If the person is still smoking then you will not be able to determine their "actual" oxygen saturation by SpO2. Carbon Monoxide may contribute 2 - 10% of the SpO2.

However, NOT all COPD patients live at a hypoxic level. Many athmatics are classified as COPD but have normal PaO2. COPD is a broad term.

There have been hundreds of studies done and are being done on all the the different diseases and their reponses to O2 and CO2. Everybody arrives at a slightly different conclusion then someone else. Everyone uses a different group of human specimens and different methodologies. Humans are hard to study because they usually don't have just one pure disease process. It would be hard to make a general "text book" statement for treatment that fits each and every one even with the same "similar" disorders or disease processes. Understanding the diseases processes and human physiology allows the practitioner the opportunity to use clinical judgement and sometimes common sense in treating the patient. And, there are always protocols to guide the medical professionals until a definitive diagnosis or treatment plan is made. ( Or just follow tniuqs suggestions).

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