If O2 is administered >2L/min for COPD patients does that reduce their respiratory drive? Vader

Physiology of Breathing The upper respiratory system: Mouth Nose Pharynx larynx. The lower respiratory system: Trachea Lungs Bronchi Bronchioles Alveoli Pulmonary capillary network Gas exchange takes place in the alveoli of the lungs. O2 from inspired air diffuses from alveoli to the blood in pulmonary capillaries. CO2 produced during cell metabolism diffuses from the blood to the alveoli and is exhaled.

What happens with COPD Patients: Chronic Bronchitis COPD is Characterized by: Slow progressive obstruction of the airways Periodic exacerbations, often related to respiratory infections Increased symptoms of dyspnea and sputum production Airways narrow Resistance to airflow increases Expiration becomes slow or difficult Emphysema The result is a mismatch between alveolar ventilation and blood flow or perfusion, leading to impaired gas exchange. COPD

Treatment of COPD Patients: Pre-hospital protocols: Asses airway and respiratory status position patient for respiratory ease apply O2: non-rebreather mask 12-15L/min flowing at 80-90% concentration. Hospital protocols: Watch for O2 administration! Hypoxemia becomes the drive to breath; too much O2 will knock out this drive! 1-2L/min

Treatment of COPD Patients: Many patients who have end stage COPD require high flow rates and higher concentration for survival. A safe limit of O2 concentrations has not yet been established Not providing adequate O2 to these patients is much more detrimental

Hypoxic Drive Theory: Hypoxia: Hypoxic Drive Theory: Hypoxia is a condition of insufficient oxygen anywhere in the body, from the inspired gas to the tissues. Hypoxic Drive Theory: Hypoxic Drive Theory is a form of respiratory drive in which the body uses oxygen chemo-receptors instead of carbon dioxide receptors to regulate the respiratory cycle. It is believed when a patient has chronically elevated CO2, that CO2 levels stop being the drive to breath, and that low oxygen levels becomes the main drive to breath.

Hypoxic Drive Theory: COPD patient’s bodies are used to lower O2 and higher CO2 in their blood As time goes on, the COPD patient becomes dependent on the lower O2 in their blood to tell the body to keep breathing. This is why doctors do not want to put a COPD patient on more than 2 to 4 LPM of O2

COPD Clients and Blood Gases: Most COPD patients have normal or near normal blood gas values, therefore maintaining the same ventilatory control as in the healthy individual Other COPD patients have chronically increased PaCO2. State of respiratory acidosis causes the kidneys to retain bicarbonate, slowly stabilizing the pH of CSF, thereby regulating respirations and blood gases into normal ranges.

COPD Patients in Respiratory Crisis: Patients with chronically elevated PaCO2 in a respiratory crisis further indicate retention or inability to blow off CO2 The Haldane Effect Hgb carries both oxygen and carbon dioxide The administration of high flow, high concentration O2 causes the Hgb to dump CO2 into the blood plasma, dramatically increasing the PaCO2 levels. The V/Q Mismatch Alveoli maintain adequate perfusion from surrounding capillaries when equal ventilation occurs. In COPD patients, the alveoli are not adequately ventilated, therein causing a V/Q mismatch. O2 administration leads to vasodilation in previously unperfused alveoli. Sharp increases of PaCO2 (> 70mmHg) leads to CO2 narcosis and patients become lethargic and difficult to arouse.

The Hypoxic Drive is Real If you give a CO2 retainer (COPD patient) too much oxygen, you will knock out his hypoxic drive. BUT, the central chemoreceptors will still work enough to signal the brain to breath . . . . . . which would say the Hypoxic Drive Theory is not true If you increase O2 in 90% of COPD patient’s their CO2 will go up, but the Co2 does not go up because their HYPOXIC DRIVE is knocked out. It goes up due to V/Q mismatching and the Haldane effect.

Conclusion: O2 treatment for a COPD patient must be personalized There is a delicate balance between maintaining the Hypoxic drive and supplying supplemental O2 Emergency personnel frequently give more than 2 liters per minute O2 to COPD patients Hospital personnel typically do not supply more than 2 liters per minute There is currently no established safe levels for O2 administration The Hypoxic Drive Theory is just a theory: More research is needed to substantiate these claims NOT providing O2 to a patient struggling for air seems to undermine ABCs Too much O2 administration causes Hgb to dump CO2 into the bloodstream and cause a rapid increase in CO2 concentration, leading to CO2 narcosis What, then, is the answer?. . .

Conclusion: More research should be done to test what would occur with a slowly increasing flow of O2 from 2 L/min to 15 L/min and how this affects COPD patients If the O2 flow is brought up gradually, will that help the patient expel the built up CO2 in the bloodstream without causing CO2 narcosis?

THE END By: Ashley Fazekas Amanda Feczco Valarie Bach Kristen Puent Shawn Burk