Effects of mode of inhalation of carbon monoxide and of normobaric oxygen administration on carbon monoxide elimination from the blood

Abstract

<jats:p> 1 The half-life of carbon monoxide (CO) in blood was studied retrospectively in 26 fire victims and in 19 cases of CO poisoning. Normobaric oxygen therapy was administered via mechanical ventilation in 19 fire victims, and by facial mask to the rest of the casualties. </jats:p><jats:p> 2 Arterial pH was significantly lower (P &lt; 0.05) and PaO<jats:sub>2</jats:sub> significantly greater (P&lt;0.01) in the mechanically ventilated fire victims compared to the spontaneously breathing fire victims. </jats:p><jats:p> 3 The blood CO half-lives were 91 ± 38 min for the 26 fire victims and 87±40 min for the 19 pure CO intoxica tions. </jats:p><jats:p> 4 The blood CO half-lives were 92 ± 40 min for the 19 mechanically ventilated fire victims and 87 ± 37 min for the 26 spontaneously breathing subjects. </jats:p><jats:p> 5 We conclude that the elimination of CO from blood was a slow process with no significant effects on the blood CO half-life of either the cause of the CO poisoning or the mode of normobaric oxygen therapy. These data suggest that enhancement of the elimination of carbon monoxide by normobaric oxygen in both pure CO poisoning and fire victims is more difficult to achieve and more complex than has previously been reported. </jats:p>

Memory one month after acute carbon monoxide intoxication: a prospective study

“…The initial concentration at the end of exposure to the toxic atmosphere was calculated from CO kinetics, according to the treatment applied before sampling: CO half life was 240 minutes without oxygen treatment and 55 minutes with normobaric oxygen (personal data) which is similar to that reported previously. 13 Treatment was either normobaric or hyperbaric oxygen therapy, according to normalised criteria, 11 in addition to supportive therapy as needed. All the included patients were contacted by phone during the week before the examination, to reduce the loss to follow up, and to ascertain the cause, if any.…”

Corbon monoxide intoxication epidemiology, pathophsiology, clinical evaluation and treatment during childhood, in newborn and fetus

“…If ST elevation is seen, thrombolytic treatment is not suitable, since cause of cardiac ischemia is not thrombotic occlusion of coronary arteries, but instead, related to myocardial injury caused by direct effect of CO. Although arrhythmias that affect hemodynamic status are rarely seen, dysrhythmias, including ventricular extrasystoles and ventricular fibrillation can be detected [27, 28]. …”

“…Therefore, when compared with other cases of CO poisoning, HBO treatment is initiated at lower maternal CO level in pregnant women, and is more aggressive and longer lasting in order to protect the fetus. No correlation has been determined between fetal death and maternal COHb level [27]. Nonetheless, CO exposure may have teratogenic effects of physical deformity, psychomotor disability, or miscarriage.…”

“…If present, complications should be treated [12]. Rapid intervention and delivery of appropriate dose of oxygen constitutes basis of treatment since there is competition with oxygen to bind with hemoglobin, and because binding of CO to hemoglobin is reversible [27]. Half-life of CO is approximately 5 hours in room air, and 1½ hours in 100% oxygen environment, and 25 minutes during HBO treatment under 3 bar pressure.…”

“…If the patient is unconscious or rescued from a fire, endotracheal intubation or mechanical ventilation may be required. Need for HBO should be evaluated [12, 27, 40]. Since lactic acidosis facilitates penetration of oxygen through tissues, it should not be corrected unless pH drops below 7.15 [7, 8].…”