Blood carboxyhemoglobin monitoring for evaluation of severity of traumatic shock and reperfusion injuries (analytical review with results of our own observations)

S.V. Kursov, O.V. Beletskiy, K.I. Lyzogub, M.V. Lyzogub

Abstract


Carbon monoxide (CO) is the native product of organism metabolism. In biology, carbon monoxide is naturally produced by the action of heme oxygenase 1 and 2 on the heme from hemoglobin breakdown. This process produces a certain amount of carboxyhemoglobin in healthy persons, even if they do not breathe any carbon monoxide. CO functions as an endogenous signaling molecule modulates functions of the cardiovascular system, suppresses, reverses, and repairs the damage caused by inflammatory responses and may play the role of potential therapeutic agent. On the other hand, CO combines with hemoglobin to produce carboxyhemoglobin, which occupies the space in hemoglobin that normally carries oxygen, but it is ineffective for delivering oxygen to bodily tissues. Furthermore, CO also binds to other molecules, such as myoglobin and mitochondrial cytochrome oxidase. Exposures to carbon monoxide may cause significant damage to the heart and central nervous system. Thus, excessive endogenous CO production and excessive carboxyhemoglobin generation may play a significant role in tissue damage and multiorgan dysfunction formation. Apart from hemoglobin breakdown, heme compounds of cell membrane and mitochondrial enzymes may become the source of endogenous CO and carboxyhemoglobin production. Cell damage in traumatic shock and ischemia/reperfusion circumstances, tissue blood loss, blood transfusions and intensive reactive oxygen species generation can lead to foregoing events. Currently, many investigators consider an endogenous CO and carboxyhemoglobin production in critical states as a compensatory mechanism that promotes cytoprotection and contributes to patients’ survivability. We have studied the results of these investigations by means of the evaluation of CO production activity and the estimation of carboxyhemoglobin content in patient blood and СO in expiratory air. We have compared these results with the outcomes of our observation. Carboxyhemoglobin blood concentration no more than 4 % was presented in the majority of foreign investigations in patients in critical states. In our study, there have been examined patients with polytrauma with the symptoms of a wound shock at an early hospital stage. The indices of central hemodynamics and the saturation of capillary blood with oxygen, the perfusion index value have been determined according to the Masimo company techniques. All the patients were delivered to emergency department with normal carboxyhemoglobin blood concentration. Pathological carboxyhemoglobin was detected after reperfusion emergence. Fast fluid resuscitation, hypertonic solution use, epinephrine administration were associated with increase of the blood pressure, perfusion index (PI) and carboxyhemoglobin blood concentration. PI value is equal to 0.6–1.5 % in compensatory shock (I–II state severity) and associated with elevation of carboxyhemoglobin blood concentration in level 4–10 %. PI value is equal to 0.1–0.5 % in decompensatory shock (III–IV state severity) and associated with elevation of carboxyhemoglobin blood concentration in level 12–20 %. In the most severe cases, carboxyhemoglobin blood concentration increased up to 26 %. Blood reinfusion was associated with the increase of blood carboxyhemoglobin up to 10–14 %. So, endogenous CO production and carboxyhemoglobin generation in trauma with shock is strongly associated with shock state severity. The most active CO production in shock occurred in reinfusion period after capillary blood flow increased. The carboxyhemoglobin blood concentration in traumatic shock may be very increased. CO level and carboxyhemoglobin blood content in shock and reperfusion can play a significant role in hypoxia and mitochondrial dysfunction formation.


Keywords


carbon monoxide; carboxyhemoglobin; ischemia/reperfusion; traumatic shock; mitochondrial dysfunction; review

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DOI: https://doi.org/10.22141/2224-0586.1.80.2017.94449

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