A young man is rescued from a fire and brought to the emergency department (located at sea level). The patient is unconscious, but his vital signs (heart rate, blood pressure, respiratory rate) are stable. Below are arterial blood gas data, from a sample drawn while he is breathing 100% oxygen.
1. What is the relative position of his HbO2 equilibrium curve compared to normal? Is the curve pushed upward or downward? Is it shifted to the left or right? Explain the effect of the changes in his HbO2 equilibrium curve on:
Curve shifted down. Carbon monoxide displaces oxygen from hemoglobin at the pulmonary capillary level. This downward shift of the curve results in a lower SaO2 for a given PaO2. To the extent that SaO2 falls, arterial oxygen content and delivery are reduced. However, the physiologic process of delivering oxygen from the tissue capillariesto the tissue cells is unaffected.
Curve shifted to left. The curve is shifted to the left for two reasons: effect of carbon monoxide (the major reason in this example) and the increased pH (relatively minor). A left shift indicates an increase in the amount of oxygen taken up by hemoglobin in the pulmonary capillaries; this results in a higher SaO2 for a given PaO2 (See Fig. 36-5 and p. 594 in Physiology 3rd ed.) To the extent that SaO2 increases, arterial oxygen content and delivery are increased. However, at the pulmonary capillary level, the leftward shift has much less effect than does the downward shift from carboxyhemoglobin; as a result, SaO2 is always reduced in carbon monoxide poisoning. The leftward shift is actually
tightly (has increased affinity) than normal.
In summary, excess CO adversely affects oxygenation of the patient in two ways:
It lowers SaO2 and O2 content and thereby lowers oxygen delivery to the systemic capillaries.
It impairs transport of oxygenfrom the systemic capillariesto the tissue cells.
Because this patient is breathing 100% oxygen, his PaO2 amounts to about 660 mm Hg (use the alveolar gas equation provided in questions on Chapter 33). The difference between alveolar and arterial PO2 normally widens with increasing FIO2, but even with 100% inspired oxygen the
(PAO2 \u00a8C PaO2) should be no more than about 100 mm Hg. Hence, when the patient breathes 100% oxygen, PaO2 should be at least 500 mm Hg. His PaO2, while seemingly high at 190 mm Hg, is actually much less than expected for his FIO2. This lower-than-expected PaO2 is not caused by an excess of CO per se; CO does not affect the PaO2, only the SaO2 for a given PaO2. The explanation for reduced PaO2 must lie in V/Q imbalance, which in turn must arise from some parenchymal lung problem (e.g., pulmonary edema from smoke inhalation). Thus the physiologic data indicate a parenchymal lung problem from smoke inhalation. In summary, he has:
Excess CO, which impairs oxygen uptake by hemoglobin and oxygen delivery to the tissues, and V/Q imbalance, not directly caused by CO, that impairs oxygen transfer across the alveolarcapillary membranes.
CO has 250 times the affinity for hemoglobin as does oxygen. Fortunately, the binding of CO to hemoglobin is reversible; once the patient is removed from the CO source, this poison will begin to be displaced by oxygen. However, displacement is slow at physiologic PO2 values (80 to 100 mm Hg), where the half-life of COHb is about 6 hours. The higher the PO2, the more quickly O2 will displace CO2
from hemoglobin. Because CO-poisoned patients may die or suffer brain damage if not treated quickly, a high inspired oxygen pressure is mandatory therapy. The following table shows that the higher the PaO2, the quicker HbCO is dissipated.
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