COPD References
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Hanson CW 3rd, Marshall BE, Frasch HF, Marshall C.
Causes of hypercarbia with oxygen therapy in patients with chronic
obstructive pulmonary disease.
Crit Care Med 1996 Jan;24(1):23-8.

OBJECTIVES: To compare data derived from a computer model of the pulmonary
circulation with data from a case series of patients with chronic
obstructive pulmonary disease (COPD). To evaluate the specific factors
contributing to CO2 retention due to oxygen therapy in patients with acute
exacerbations of COPD. DESIGN: Data from a computer model of the pulmonary
circulation were compared with a previous case series. PATIENTS: Patient
data were derived from previous case series. INTERVENTIONS: Simulated
application of oxygen therapy. MEASUREMENTS AND MAIN RESULTS: The computer
model of the pulmonary circulation generates data comparable with those data
from a series of patients with COPD treated with supplemental oxygen and
permits identification of the causes for hypercarbia. Therapy with
supplemental oxygen alters hypoxic pulmonary vasoconstriction and modulates
the Haldane effect, resulting in changes in physiologic deadspace.
CONCLUSION: Changes in physiologic deadspace are sufficient to account for
the hypercarbia developed by patients with acute exacerbations of COPD
when treated with supplemental oxygen.

Tinits P
Oxygen therapy and oxygen toxicity.
Ann Emerg Med 1983 May;12(5):321-8

When oxygen therapy is warranted, the minimum effective dose generally
should be given. Hypoxemic patients who have normal baseline ABG may be
treated initially with an intermediate to high FiO2 in the range of 35% to
100%, depending on the severity of the respiratory distress. The majority of
patients with exacerbations of COPD who are not in extremis may be given an
initial FiO2 of 28%, especially if their previous response to oxygen is
known. When treating patients who have chronic severe hypercapnia (eg, those
requiring chronic home oxygen), the initial FiO2 should be 24% even though
renal compensation of the respiratory acidosis has occurred. Further mild
elevation of the PaCO2, due mainly to the V/Q mismatch that oxygen therapy
induces, may be sufficient to precipitate unacceptable hypercapnia. Patients
with exacerbations of COPD who are obviously in extremis, with severe
hypoxemia and acidosis, should start with an FiO2 of 24% unless they are
being mechanically ventilated. The severity of the hypoxemia and acidosis is
more predictive for the development of CO2 narcosis and respiratory failure
than is the degree of hypercapnia in these patients. The FiO2 can be
increased to 28% and incrementally higher if low FiO2 is tolerated. The use
of a high FiO2 is subject to the following guidelines for prevention of
clinically significant oxygen toxicity: 100% oxygen at atmospheric pressure
is safe if given for less than six hours; 70% oxygen is probably safe for 24
hours; and after this time, 45% should be the approximate upper limit to
the FiO2.(ABSTRACT TRUNCATED AT 250 WORDS)