Comprehensive Physiology Wiley Online Library

Carbon Monoxide Toxicity

Full Article on Wiley Online Library



Abstract

The sections in this article are:

1 Body CO Stores
1.1 Location
1.2 Carbon Monoxide Exchanges Between Lung and Body Stores and Processes That Determine HbCO and Body CO Stores
1.3 Endogenous CO Production
1.4 Carbon Monoxide Metabolism as a CO Sink
2 Carbon Monoxide Binding to Proteins Found in Mammalian Tissues
2.1 Structure and Reactivity of CO
2.2 Carbon Monoxide and O2 Competition
2.3 Carbon Monoxide Binding to Hb
2.4 Effects of CO Binding to Hb on Oxygenation in Peripheral Tissues
2.5 Extravascular CO‐Binding Proteins
Figure 1. Figure 1.

Carbon monoxide uptake in a normal human subject as a function of inspired [CO]. PB, barometric pressure; , average partial pressure of O2 in lung capillaries; , alveolar ventilation rate; Vb, blood volume; M, equilibrium constant; , diffusing capacity of the lungs; [COHb]0, control value prior to CO exposure; , rate of endogenous CO production. Calculated with the Coburn‐Forster‐Kane (CFK) equation 36.

From Peterson and Stewart 131
Figure 2. Figure 2.

Effects of alveolar ventilation (), CO diffusing capacity of the lungs (), alveolar partial pressure of O2 (), and endogenous CO production (), on uptake of CO. In each case one variable was changed and other variables are the same as in Fig. 1. Data are shown for 8‐h exposures. [CO]i, CO in inspired air.

Calculated using the CFK equation 36
Figure 3. Figure 3.

Schematic representation of processes that determine body CO stores in a normal human subject. Pco, partial pressure of CO; Hgb Catab, hemoglobin catabolism; COHb, carboxyhemoglobin; COMb, carboxymyoglobin; CO‐X, CO not explained by CO bound to Hb or Mb; intravasc., intravascular; extravasc., extravascular.

From Coburn 32
Figure 4. Figure 4.

Diurnal variation in [HbCO]. Data were computed with the CFK equation for a normal subject who was exposed to ambient CO during waking hours and zero inspired [CO] during sleeping hours. Lower tracing, [HbCO] was computed with 20, 75, 6, 0.007. Upper tracing, 10, 50, 6, 0.07. Note CO exposure included a constant raised environmental level and intermittent 5 min increases in , which is similar to exposures seen with cigarette smokers.

From Coburn et al. 34
Figure 5. Figure 5.

Degradation of heme to CO plus bilirubin. C*, methene carbon atom that is precursor of the carbon atom in CO. Me:CH3; V:CHCH2; and P:CH2COOH.

Figure 6. Figure 6.

Observed and calculated effects of HbCO on the HbO2 dissociation curve. Calculated curves were obtained with the method of Roughton and Darling 144. Percent saturation COHb, right to left: 0%, 6.7%, 18.2%, 31%, 40%, and 55.5%.

From Okada et al. 122
Figure 7. Figure 7.

Calculated venous () as a function of [HbCO] at different arteriovenous O2 saturation differences. In determining A‐V[O2Hb], O2Hb percent saturation was computed as percent of total Hb, including Hb bound with CO. Lines calculated with the method of Roughton and Darling 144.

From Collier 45
Figure 8. Figure 8.

Calculated tissue / as a function of blood [HbCO]. Mean tissue is assumed to equal mean capillary , which is calculated with the Haldane equation 70, using mean capillary values () of 40 or 50 mmHg. The Pco/ ratio was derived with a value for tissue of 1 mmHg. Errors in this estimate can arise 1) if CO and O2 are not in chemical equilibrium with Hb in blood traversing capillaries and 2) from assumptions about tissue . The CO/O2 ratios are probably falsely high due to the low value used for tissue .



Figure 1.

Carbon monoxide uptake in a normal human subject as a function of inspired [CO]. PB, barometric pressure; , average partial pressure of O2 in lung capillaries; , alveolar ventilation rate; Vb, blood volume; M, equilibrium constant; , diffusing capacity of the lungs; [COHb]0, control value prior to CO exposure; , rate of endogenous CO production. Calculated with the Coburn‐Forster‐Kane (CFK) equation 36.

From Peterson and Stewart 131


Figure 2.

Effects of alveolar ventilation (), CO diffusing capacity of the lungs (), alveolar partial pressure of O2 (), and endogenous CO production (), on uptake of CO. In each case one variable was changed and other variables are the same as in Fig. 1. Data are shown for 8‐h exposures. [CO]i, CO in inspired air.

Calculated using the CFK equation 36


Figure 3.

Schematic representation of processes that determine body CO stores in a normal human subject. Pco, partial pressure of CO; Hgb Catab, hemoglobin catabolism; COHb, carboxyhemoglobin; COMb, carboxymyoglobin; CO‐X, CO not explained by CO bound to Hb or Mb; intravasc., intravascular; extravasc., extravascular.

From Coburn 32


Figure 4.

Diurnal variation in [HbCO]. Data were computed with the CFK equation for a normal subject who was exposed to ambient CO during waking hours and zero inspired [CO] during sleeping hours. Lower tracing, [HbCO] was computed with 20, 75, 6, 0.007. Upper tracing, 10, 50, 6, 0.07. Note CO exposure included a constant raised environmental level and intermittent 5 min increases in , which is similar to exposures seen with cigarette smokers.

From Coburn et al. 34


Figure 5.

Degradation of heme to CO plus bilirubin. C*, methene carbon atom that is precursor of the carbon atom in CO. Me:CH3; V:CHCH2; and P:CH2COOH.



Figure 6.

Observed and calculated effects of HbCO on the HbO2 dissociation curve. Calculated curves were obtained with the method of Roughton and Darling 144. Percent saturation COHb, right to left: 0%, 6.7%, 18.2%, 31%, 40%, and 55.5%.

From Okada et al. 122


Figure 7.

Calculated venous () as a function of [HbCO] at different arteriovenous O2 saturation differences. In determining A‐V[O2Hb], O2Hb percent saturation was computed as percent of total Hb, including Hb bound with CO. Lines calculated with the method of Roughton and Darling 144.

From Collier 45


Figure 8.

Calculated tissue / as a function of blood [HbCO]. Mean tissue is assumed to equal mean capillary , which is calculated with the Haldane equation 70, using mean capillary values () of 40 or 50 mmHg. The Pco/ ratio was derived with a value for tissue of 1 mmHg. Errors in this estimate can arise 1) if CO and O2 are not in chemical equilibrium with Hb in blood traversing capillaries and 2) from assumptions about tissue . The CO/O2 ratios are probably falsely high due to the low value used for tissue .

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Ronald F. Coburn, Henry Jay Forman. Carbon Monoxide Toxicity. Compr Physiol 2011, Supplement 13: Handbook of Physiology, The Respiratory System, Gas Exchange: 439-456. First published in print 1987. doi: 10.1002/cphy.cp030421