[rs] Carbon Monoxide Poisoning

RESPIRATORY SYSTEM

Carbon Monoxide Poisoning

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 HbO 2 equilibrium curve on:

The amount of oxygen delivered from the lungs to the tissue capillaries The amount of oxygen delivered from the tissue capillaries to the individual tissue cells

The patient's HbO2 equilibrium dissociation curve is shifted downward and to the left.

Curve shifted down. Carbon monoxide displaces oxygen from hemoglobin at the pulmonary capillary level. This downward shift of the curve results in a lower SaO 2 for a given PaO2. To the extent that SaO 2 falls, arterial oxygen content and delivery are reduced. However, the physiologic process of delivering oxygen from the tissue capillaries to 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

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detrimental, because it inhibits oxygen unloading in the systemic capillaries. Thus oxygen delivery from the systemic capillaries to the tissue cells is reduced, because hemoglobin holds on to oxygen more 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 oxygen from the systemic capillaries to the tissue cells.

2. Is his PaO2 less than, equal to, or higher than expected under the circumstances (100% inspired oxygen, normal PaCO2)? Explain your answer.

Because this patient is breathing 100% oxygen, his PaO 2 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 FIO 2, but even with 100% inspired oxygen the

(PAO 2

¨C 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.

3. What is the relative affinity of CO and O2 for hemoglobin? Based on this information, how should a victim of CO poisoning be treated?

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 CO

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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.

PO2 (mm Hg)

Half-life COHb

Inspired oxygen

100

6 hours

21% (ambient air)

600

3 hours

100%, at ambient air pressure

1200

2 hours

100%, in hyperbaric chamber

1800

1 hour

100%, in hyperbaric chamber

4. Describe and explain how each of the following conditions would affect this patient's PaO2, SAO2, and arterial oxygen content. Assume that each condition occurs alone (i.e., nothing else is abnormal).

Physiologic problems rarely occur in isolation, but here you are to assume nothing else is abnormal except the indicated condition.

Condition

PaO2 SaO2

O2 content

Anemia

NE

NE

D

Excess CO

NE

D

D

Fever

NE

D*

D

Acidosis

NE

D*

D

I*

I

Alkalosis

NE

Hypoventilation

D

D

D

Hyperventilation

I

I

I

3

V/Q imbalance

D

D

D

High altitude

D

D

D

Abbreviations: NE, no effect; D, decreased; I, increased.

*For a given PaO2, effect is from shift in HbO2 equilibrium curv

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