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Communications to the Editor |

Half-life of Blood Carboxyhemoglobin Half-life of Blood Carboxyhemoglobin FREE TO VIEW

Takeshi Shimazu, MD
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Affiliations: Osaka University Graduate School of Medicine Osaka, Japan,  LDS Hospital Salt Lake City, UT

Correspondence to: Takeshi Shimazu, MD, Department of Traumatology and Acute Critical Medicine (D-8), Osaka University Graduate School of Medicine, 2–15 Yamadaoka, Suita-shi, Osaka, 565-0871 Japan; e-mail: shimazu@hp-emerg.med.osaka-u.ac.jp



Chest. 2001;119(2):661-663. doi:10.1378/chest.119.2.661
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To the Editor:

I read with interest the article by Weaver et al (March 2000)1on the half-life of blood carboxyhemoglobin (COHb) in carbon monoxide poisoning patients because we also have analyzed the elimination process of carbon monoxide in clinical and experimental settings.2 They retrospectively analyzed 93 patients with carbon monoxide poisoning and calculated the half-life of COHb based on single exponential decrease which is described as Ct = C0* e(− kt), where C0 and Ct are COHb concentrations at time 0 and at any time, respectively, and k is the decay constant. They also hypothesized that the COHb half-life of carbon monoxide-poisoned patients will be longer than that of human volunteers breathing carbon monoxide under experimental protocol partly because of greater carbon monoxide burden in patients with carbon monoxide accumulation in tissue as well as onto hemoglobin. However, I am afraid there were a couple of misunderstandings and confusion regarding the physiologic nature of the carbon monoxide absorption and elimination process, which can be described precisely using physiologic models.

First, the carbon monoxide elimination process exhibits biphasic decreases of COHb concentration compatible with a two-compartment model: an initial rapid decrease (distribution phase), followed by a slower phase (elimination phase).2 In other words, COHb elimination should be described by the sum of two exponentials rather than a commonly accepted single exponential decrease. Such biphasic shape is more prominent when the duration of exposure to carbon monoxide is short because of distribution of carbon monoxide from hemoglobin (COHb) to tissues as well as elimination from the lung. However, as the half-life of the initial phase is short, it might not always be clearly noticeable if the peak COHb is low and/or if the blood samples were not taken early enough. The authors commented that there were no differences in the COHb half-life calculated using all COHb measurements compared to the half-life calculated by using either the first and second or the first and last COHb measurements in the same patients. The biphasic decrease can still be observed in carbon monoxide-poisoned patients if measurement of COHb is made more closely from earlier time (Fig 1 ).

Secondly, the authors did not consider the fact that the half-life of COHb is affected significantly by the duration of exposure to carbon monoxide, which determines what they call carbon monoxide burden in tissues and hemoglobin. It is only after approximately 5 to 6 h that the blood COHb concentration reaches a plateau after exposure to carbon monoxide (Fig 2 ). So if the exposure time is less than several hours, carbon monoxide distribution in the body does not reach equilibrium and the elimination process would not follow the single exponential decay. The apparent discrepancy between reported COHb half-lives could be explained by considering the duration of exposure. For example, Peterson and Stewart3exposed their subjects to 500 parts per million of carbon monoxide for 2.3 h, yielding the peak COHb of 25%, while Pace et al4 studied the half-life after the volunteers rebreathed a mixture of 250 mL of carbon monoxide and 2 L of air (approximately 11% carbon monoxide) from a rubber bag for 30 s, causing peak COHb of 4%. So it is a matter of course that the half-life obtained by Pace et al4 is much shorter than that by Peterson and Stewart.3

The half-life of COHb is affected indeed by various factors, such as duration of carbon monoxide exposure, time for transport, fraction of inspired oxygen during transport, minute ventilation, Pao2, etc, but there is no mystery that would cause unexplainable differences of COHb half-life between and within experimental and clinical studies.

Figure Jump LinkFigure 1. Serial blood COHb concentrations in a 44-year-old man who was exposed to carbon monoxide for about 30 min during a fire. He suffered from mild smoke inhalation injury, minor burns, and carbon monoxide poisoning. Transfer from the scene to the hospital took 20 min, during which time he was given oxygen with a face mask. The first blood sample was taken soon after admission (point A). The patient was then intubated and received mechanical ventilation with 100% oxygen for 5 h. The ordinate depicts blood COHb concentration (percent) on a logarithmic scale, and the abscissa is time after admission in minutes. The elimination curve clearly demonstrates biphasic decreases of COHb; an initial rapid decrease (A to D) was followed by a slower phase. The curve is closely simulated as y = 57.7*exp(− 0.0283t) + 14.3*exp(− 0.00632t), where y is COHb at time t (minutes after admission); exp = exponent. The half-lives for the initial and second phases are 24.5 min and 110 min, respectively.Grahic Jump Location

Figure Jump LinkFigure 2. Blood COHb concentrations during long-term exposure to carbon monoxide and elimination process in a sheep model. The animal was exposed to 500 parts per million of carbon monoxide in the air by mechanical ventilation for 10 h with intubation and general anesthesia, and then received ventilation with room air for 3 h.2Grahic Jump Location
Weaver, LK, Howe, S, Hopkins, R, et al (2000) Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure.Chest117,801-808. [CrossRef] [PubMed]
 
Shimazu, T, Ikeuchi, H, Sugimoto, H, et al Half-life of blood carboxyhemoglobin after short-term and long-term exposure to carbon monoxide.J Trauma2000;49,126-131. [CrossRef] [PubMed]
 
Peterson, JE, Stewart, RD Absorption and elimination of carbon monoxide by inactive young man.Arch Environ Health1970;11,165-171
 
Pace, N, Strajman, E, Walker, EL Acceleration of carbon monoxide elimination in man by high pressure oxygen.Science1950;111,652-654. [CrossRef] [PubMed]
 

Half-life of Blood Carboxyhemoglobin

To the Editor:

We appreciate Dr. Shimazu’s comments regarding our observations of carboxyhemoglobin half-life (COHb t½) in a series of patients that were poisoned with carbon monoxide.1Dr. Shimazu points out that carbon monoxide elimination exhibits a biphasic decrease of carboxyhemoglobin (COHb) concentration compatible with a two-compartment model, where there is an initial rapid decrease (distribution phase) followed by a slower phase (elimination phase). Dr. Shimazu refers to his own work,2 in which he and his colleagues measured absorption and elimination of carbon monoxide in four sheep (short-duration carbon monoxide exposure) in an experimental protocol. However, the authors provided no information to support the finding that carbon monoxide absorption and elimination by sheep is identical to that in humans. Information regarding similarities or differences between humans and sheep is important in order to draw inferences and compare it to that of a retrospective study,1 in which data from 93 carbon monoxide-poisoned patients treated with oxygen were analyzed. As stated in our article,1 we inspected the COHb t½ calculated using all COHb measurements compared to the COHb t½ calculated by using either the first and second, or the first and last COHb measurements in the same patients and found no difference in the COHb t½.

Alternatively, it is possible that Dr. Shimazu’s observations from sheep experiments do extrapolate to humans. In the few patients in which we had multiple COHb measurements, if the initial COHb measurement occurred relatively late in the course of COHb elimination, it is possible that an early rapid fall in COHb may have been missed.

The data from the patient with carbon monoxide poisoning provided by Dr. Shimazu in Figure 1 may suggest a biphasic COHb t½, but other explanations of the biphasic appearance of this curve are possible. The explanations include changes in the patient’s alveolar ventilation, alterations in gas exchange efficiency, or variability in cardiac output during the time of the COHb measurements. All of these factors influence COHb t½, as we noted in our article.1 Only if all of the above-mentioned factors are controlled during the time of the COHb measurements, could one conclude that the COHb t½ of this patient was biphasic.

The second point of Dr. Shimazu is that we did not consider that carbon monoxide elimination may be affected by the duration of exposure to carbon monoxide. As we stated in our article,1 our study was retrospective and in many of the carbon monoxide-poisoned patients it was impossible to determine the duration of their carbon monoxide exposure. We accept that the COHb t½ may be affected by the duration and dose of carbon monoxide exposure. However, in clinical carbon monoxide poisoning, it is unknown if the duration or dose of carbon monoxide exposure affects the COHb t½.

Dr. Shimazu appears to have missed the major contribution of our article.1 Dr. Shimazu states, “ . . . there is no mystery that would cause unexplainable differences of COHb half-life between and within experimental and clinical studies.” One of the main findings of our study is that the COHb t½ of clinically carbon monoxide-poisoned patients is different than the COHb t½ measured in humans under controlled experimental conditions. A second finding of our study is to show that age, gender, smoking, smoke inhalation, loss of consciousness, initial COHb, or a metabolic acidosis did not affect the COHb t½.

We appreciate Dr. Shimazu’s interest in our work and his comments and observations, which are important to further understanding of carbon monoxide absorption and elimination.

References
Weaver, LK, Howe, S, Hopkins, R, et al Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure.Chest2000;117,801-808. [CrossRef] [PubMed]
 
Shimazu, T, Ikeuchi, H, Sugimoto, H, et al Half-life of blood carboxyhemoglobin after short-term and long-term exposure to carbon monoxide.J Trauma2000;49,126-131. [CrossRef] [PubMed]
 

Figures

Figure Jump LinkFigure 1. Serial blood COHb concentrations in a 44-year-old man who was exposed to carbon monoxide for about 30 min during a fire. He suffered from mild smoke inhalation injury, minor burns, and carbon monoxide poisoning. Transfer from the scene to the hospital took 20 min, during which time he was given oxygen with a face mask. The first blood sample was taken soon after admission (point A). The patient was then intubated and received mechanical ventilation with 100% oxygen for 5 h. The ordinate depicts blood COHb concentration (percent) on a logarithmic scale, and the abscissa is time after admission in minutes. The elimination curve clearly demonstrates biphasic decreases of COHb; an initial rapid decrease (A to D) was followed by a slower phase. The curve is closely simulated as y = 57.7*exp(− 0.0283t) + 14.3*exp(− 0.00632t), where y is COHb at time t (minutes after admission); exp = exponent. The half-lives for the initial and second phases are 24.5 min and 110 min, respectively.Grahic Jump Location
Figure Jump LinkFigure 2. Blood COHb concentrations during long-term exposure to carbon monoxide and elimination process in a sheep model. The animal was exposed to 500 parts per million of carbon monoxide in the air by mechanical ventilation for 10 h with intubation and general anesthesia, and then received ventilation with room air for 3 h.2Grahic Jump Location

Tables

References

Weaver, LK, Howe, S, Hopkins, R, et al (2000) Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure.Chest117,801-808. [CrossRef] [PubMed]
 
Shimazu, T, Ikeuchi, H, Sugimoto, H, et al Half-life of blood carboxyhemoglobin after short-term and long-term exposure to carbon monoxide.J Trauma2000;49,126-131. [CrossRef] [PubMed]
 
Peterson, JE, Stewart, RD Absorption and elimination of carbon monoxide by inactive young man.Arch Environ Health1970;11,165-171
 
Pace, N, Strajman, E, Walker, EL Acceleration of carbon monoxide elimination in man by high pressure oxygen.Science1950;111,652-654. [CrossRef] [PubMed]
 
Weaver, LK, Howe, S, Hopkins, R, et al Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure.Chest2000;117,801-808. [CrossRef] [PubMed]
 
Shimazu, T, Ikeuchi, H, Sugimoto, H, et al Half-life of blood carboxyhemoglobin after short-term and long-term exposure to carbon monoxide.J Trauma2000;49,126-131. [CrossRef] [PubMed]
 
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