The proper functioning of the human organism depends on the appropriate supply of cells with energy which is necessary for them to maintain their function. The generation of energy which is the product of food conversion occurs in the presence of oxygen taken from air in breathing processes. The oxygen atmospheric pressure equal 160 mmHg is gradually lowered and in the lungs the oxygen is combined with the hemoglobin of the erythrocytes present in the capillaries of the pulmonary vesicles. Further exchange occurs through the walls of the pulmonary vesicles in accordance with the pressure gradient. Oxygen molecules diffuse from the lumen of the vesicles to blood in accordance with the pressure gradient. The oxygen molecules diffuse into blood due to the fact that in the pulmonary vesicles in the vesicle air the oxygen pressure is PO₂ = 100 mmHg and it is higher than the oxygen pressure in the blood reaching the vesicle which is equal PO₂ = 40 mmHg (1). A significant role in oxygen transportation is played by hemoglobin (Hb) which is a protein composed of two polypeptide α chains and two β chains as well as four iron (Fe) subunits. During the blood circulation in the body hemoglobin releases oxygen which diffuses into the cells and the oxygen pressure slowly decreases. Another important role off hemoglobin is the transportation of carbon dioxide CO₂ from tissues to the lungs (2).

One of the reasons for the disruption of the proper process of oxygen transportation to the cells are the toxic effects of carbon monoxide (CO). In 1857 the physiologist Claude Bernard for the first time described the influence of CO on tissue hypoxia which occurred due to the reducing of the capacity of oxygen transportation in blood. Carbon monoxide is able to form stable bonds with metalloproteins, especially hemoglobin, myoglobin, hydroperoxidase, cytochrome oxidase and cytochrome p-450. Carbon monoxide possesses 200-300 times higher binding affinity to hemoglobin than oxygen and it competes with oxygen for the four heme groups of hemoglobin with which it forms carboxyhemoglobin (COHb). The formation of carboxyhemoglobin blocks the possibility of oxygen transportation to tissues and as a result leads to the occurrence of tissue hypoxia (3-5). This process contributes to the shifts of the oxyhemoglobin dissociation curve to the left which causes difficulties in diffusing into cells. The decreased amount of oxygen stimulates the respiratory function thus increasing the minute ventilation and causing further increase of the COHb concentration (5, 6). Besides competing for the bonds to hemoglobin carbon monoxide also possesses 40 times higher affinity to myoglobin which is a hemoprotein present in the skeletal muscles and in the myocardium in which it acts as a temporary oxygen reservoir. The bonding of myoglobin with CO molecules results in the creation of a non-active form – carboxymyoglobin (COMb) which is of particular significance for cardiologically ill patients. The limitation of oxygen consumption in the muscles may in a short time lead to lowering the cardiac output and next to circulatory failure (5, 7, 8). Acute carbon monoxide intoxication equally strongly affects the functioning of the central nervous system as that of the circulatory system. The increasing if the concentration of COHb in the central nervous system (CNS) results in the deceleration of the processes of the a-a3 cytochrome system and next in the lowering of the intracellular ATP level, the effect of which is the occurrence of convulsions in the intoxicated person. The consequence is the degeneration of neurons in particularly sensitive areas of the CNS. The conducted anatomopathological studies have demonstrated a significant level of neuron damage especially in the cerebral cortex and in the medulla oblongata. CO intoxication also causes metabolic disorders resulting in the increasing of the amount of lactates and pyruvates (5, 7). The population which is particularly vulnerable to CO are pregnant women. Fetal hemoglobin has got higher affinity for CO than the mother’s hemoglobin and also the fetal elimination coefficient is slower, due to which even if the mother does not suffer from severe intoxication symptoms, she may experience the consequences of the intoxication after the period of initial latency which lasts from 1 to 6 weeks. The delayed symptoms may include memory disorders, personality changes, euphoria, impaired judgment and impaired abstract thinking, weakening of concentration (5, 8).

The symptoms of carbon monoxide intoxication are differentiated and they depend on the blood level of carboxyhemoglobin. With a COHb concentration of 4% the ability to visually distinguish between small lighting differences becomes deteriorated. A symptom which is also observed is the deterioration of the results of certain psychological tests, e.g. the selection of the appropriate letters, appropriate colors or supplementing missing letters. A carboxyhemoglobin concentration of 8-10% results in much more serious errors in test examinations i.e. arithmetic errors, errors in finding plural words etc. As the COHb concentration in the blood increases, the intoxication symptoms become more serious. A very dangerous symptom is increasing weakness, even paralysis of limb muscles usually occurring when the HbCO concentration reaches 50%. This state is very dangerous because it makes it impossible to seek rescue by escaping from the place of exposure and only external help may save the person who is at risk. The clinical course of carbon monoxide intoxication correlates with the baseline HbCO level and with the time of exposure. The COHb concentration which is considered critical is ca. 60% (8). The level of carbon monoxide intoxication in persons exposed to it depends on the CO concentration in the room in which one is staying, on the time of exposure and on the physical activity affecting minute ventilation (tab. 1). Together with the increasing of the blood concentration of carboxyhemoglobin symptoms typical for particular systems occur. The most common symptoms are CNS disorders which include headache and dizziness, disorders of memory and of attention concentration, visual disturbance, agitation, confusion, fainting, convulsions and coma. Symptoms typical for the disorders of the cardiovascular system are discomfort in the chest during minimal effort and rest pain. Simultaneously the examination may show tachycardia, hypo- or hypertension, supraventricular and ventricular arrhythmias, conduction blocks, pulmonary edema, acute coronary syndrome, sudden cardiac arrest. Symptoms related to the respiratory system include tachypnoe and the feeling of dyspnea. Moreover the present symptoms may be nausea and vomiting – related to the disorders within the digestive system as well as weakening of the muscle strength (9). The intoxicated patient’s skin is usually pale blue or grayish in color. The “Cherry Red” symptom described in literature in which the skin becomes rosy occurs very rarely and it is present on the corpses of intoxicated persons after long exposure to the toxic atmosphere. In patients who are alive it may occur in case of acute intoxication during the first phase with a high concentration of CO in the surrounding air (3, 7).

The non-specific symptoms of carbon monoxide intoxication are very differentiated and may be associated with the symptoms of stroke, hypoglycemia, acute psychosis, alcohol intoxication or influenza, the morbidity peak of which occurs in the autumn-winter period, similarly as in case of carbon monoxide intoxications. Appropriate diagnosing may therefore be difficult, especially when the taken history does not obtain the information about the possible exposure to CO. The possibility of carbon monoxide intoxication should be particularly taken into consideration when similar symptoms have occurred simultaneously in a few persons staying in one room or when the intoxicated person has recently stayed in a room where there was a device which could have been a potential source of carbon monoxide.

In case of carbon monoxide intoxication an issue which is of very high importance is the safety of the persons providing help because even short exposure to the harmful gas may result in the increasing of the number of intoxicated persons. In cases of justified suspicion of carbon monoxide intoxication already at the stage of accepting the report the emergency dispatcher may advise the reporting person to open the doors and windows (in order to allow for better ventilation of the rooms and for the inflow of uncontaminated air) and to leave the place where the intoxication occurred. After the Medical Rescue Team has arrived at the call point the rescue operations should begin from moving the intoxicated patient from the contaminated atmosphere as soon as possible. The Medical Rescue Team should above all assure their own safety and if there is a real threat for their health and life they should leave the evacuation of the intoxicated persons to the Fire Brigade. After the intoxicated person has been moved to a safe location it is necessary to perform the assessment of the vital functions, assessing sequentially: A – the patency of the airways, B – breathing, C – blood circulation, D – consciousness (10).

The basic treatment method for persons intoxicated with carbon monoxide is oxygen therapy. Oxygen in 100% concentration should be administered through a strictly adherent facial mask. In case of diagnosing respiratory failure the patient should be intubated and ventilated with positive end-expiratory pressure. The duration of oxygen therapy depends on the severity of the intoxication. The half-life of carbon monoxide elimination with breathing atmospheric air is ~320 minutes and with breathing 100% oxygen it reduces to 30-90 minutes. Further shortening of this time is possible thanks to applying treatment in a hyperbaric chamber. Simultaneously with applying oxygen therapy it is necessary to introduce symptomatic treatment aimed at the prevention or the treatment of lung edema and brain edema through the administration of Maitol and steroid drugs e.g. hydrocortisone. In case of the occurrence of hypotension caused by the increasing of the size of the venous bed liquid therapy should be introduced and convulsions should be treated by administering anticonvulsants e.g. Relanium (10-12).