DYNAMICS OF INDICES OF OXYGEN TRANSPORT FUNCTION IN THE BLOOD IN PATIENTS WITH TRAUMATIC SHOCK
Emergency Aid Station,
Kabanov City Clinical Hospital No.1,
Omsk State Medical Academy,
Omsk, Russia
Patients with traumatic shock demonstrate some disorders of systemic hemodynamics which cause development of mixed hypoxia that determines appearance of organ and systemic dysfunctions favoring development of negative clinical outcomes [1]. The objective was to study the dynamics of values of oxygen transport function in patients with traumatic shock of degree 3.
MATERIALS AND METHODS
The work presents the results of a simple blind prospective clinical cohort randomized (the method of envelopes) study with 50 patients (the mean age of 28.3 ± 2.4) with traumatic shock of degree 3. The patients were distributed into 2 groups according to the type of prehospital and hospital infusion therapy. All cases of traumatic shock were caused by road traffic accidents. Acute blood loss was caused by closed and opened fractures of the femoral and/or fibular and tibial bones in combination with fractures of pelvic bones and closed abdominal injury with internal organ injuries: 1) the age of the patients was 18-40; 2) acute period of the disease; 3) absent narcotic and alcohol intoxication; 4) admission to a medical prophylactic facility within an hour after onset of the disease. The exclusion criteria were 1) concurrent sub- and decompensated chronic pathology of kidneys, the heart, the liver and the lungs; 2) previous oncologic pathology; 3) previous hormonal therapy and chemical therapy; 4) diabetes mellitus of types 1 and 2; 5) terminal state; 6) participation in another study; 7) allergic responses to colloid solutions of hemodynamic action on the basis of 4 % modified gelatin (MG). Traumatic shock was diagnosed at the prehospital stage (before infusion therapy) in presence of the fact of an injury or the following signs: consciousness level (GCS ≤ 9), paleness and coldness of the skin, mean arterial pressure (< 35 mm Hg) and shock index (≥ 2.9). Before hospital admission all patients received multimodal analgesia (narcotic and non-narcotic analgetics), infusion therapy with the catheter in the central (subclavian or jugular) vein, inotropic and vascular support with dopamine (5 µg/kg/min), because system hemodynamics was not corrected with infusion therapy. After tracheal intubation all patients received artificial lung ventilation with Chirolog Paravent PAT (Chirana, Slovakia). The group 1 (25 patients) received infusion therapy with non-balanced crystalloid solution of 0.9 % sodium chloride and colloid solution of 4 % MG, the second group (25 patients) – balanced crystalloid solution of isotonic sterofundin and 4 % MG.
The volume of prehospital and hospital blood loss was determined on the basis of shock index, clinical symptoms and estimation of external blood loss [1]. The volume of blood loss and infusion-transfusion therapy (ITT) was almost the same and without significant differences in the patients of the groups 1 and 2 within 24 hours (the table 1). Within the first 24 hours all patients received replacement therapy for anemia and consumption coagulopathy according to the common criteria with transfusion of single-group fresh frozen plasma and packed red blood cells [2].
| Table 1 | |||||||||||
| Volume of blood loss and infusion-transfusion therapy (ITT) in the patients of the groups 1 and 2 within 24 hours (М ± m) | |||||||||||
| Note: the table shows the statistically insignificant intergroup differences, p > 0.1 (Student's test for independent samples). The data is presented as mean (M) ± error in mean (m). |
During the following 2 days the strategy and tactics of infusion therapy depended on time trends of hemostasis, hemoglobin and hematocrit. Infusion therapy depended on the values of central hemodynamics.
The time from initiation of anti-shock measures to hospital admission was 56.9 ± 0.4 min in the group 1 and 56.7 ± 0.538 ± 0.3 in the group 2. At the prehospital stage all patients were directly delivered to the surgery room for emergency surgical treatment. Here anti-shock therapy (initiated at the prehospital stage) and diagnostic examinations were conducted (plain X-ray imaging of the chest, abdominal organs, cranial bones, pelvic bones and injured extremities, ultrasonic examination of abdominal organs, laparoscopy, biochemical data, parameters of hemostasis, clinical blood and urine analysis, estimation of blood group and Rh). Surgical treatment was realized with total intravenous (fentanyl + ketamine + sibazon) anesthesia with muscle relaxants in conditions of ALV with air-oxygen mixture. Surgical treatment was conducted for all patients (n = 50, 100 %). Its volume depended on location and severity of injuries. Surgical treatment was initiated after 8.6 ± 1.1 min in the group 1, 8.8 ± 1.3 min in the group 2. Thereafter the patients were admitted to the intensive care unit for infusion, antibacterial, respiratory and symptomatic therapy. Inotropic and vascular support with dopamine lasted for 48.1 ± 2.4 hours in the group 1 and 47.3 ± 2.1 hours in the group 2.
The values of central hemodynamics were evaluated with impedansometry and non-invasive tetrapolar rheography with Diamant-R complex (Russia) upon admission to the ICU, 12, 24, 48 and 72 hours after admission. The examination included heart rate (HR, min-1), stroke volume (SV, ml), cardiac output (CO, l), cardiac index (CI, l/min/m2), total peripheral vascular resistance (TPVR, dyn×cm×s-5) and circulating blood volume (CBV, l). The automatic hematological analyzer Hemolux 19 (Mindray, China) was used for estimation of hematocrit, amount of red blood cells and hemoglobin. The biochemical analyzer Huma Laser 2000 (Human, Germany) was used for estimation of the level of lactate in the serum of venous blood. The femoral artery was punctured for estimation of arterial blood. Venous blood was estimated with the catheter in the central vein which was used for blood sampling 24, 48 and 72 hours after admission to the ICU. The gas analyzer MEDICA Easy Blood Gas (MEDICA, USA) was used for estimation of oxygen partial pressure (pO2) in arterial (a) and venous (v) blood, as well as for oxygen saturation (S). The following values of oxygen transport function of the blood were estimated: 1) oxygen transport capacity of the blood (ml/l); 2) oxygen level in arterial blood (CaO2, ml/l); 3) oxygen level in venous blood (ÑvO2, ml/l); 4) arteriovenous oxygen difference (ml/l); 5) oxygen transport (OT, ml/min/m2); 6) oxygen consumption (OC, ml/min/m2); 7) oxygen extraction ratio (OER, %). SOFA was used for estimation of intensity of multiple organ dysfunction syndrome.
Statistica 6 (StatSoft, USA, 1999) was used for the systemic statistical analysis. The statistical hypotheses were tested with Wilcoxon test (comparison of two dependent samples), Mann-Whitney test (comparison of two independent samples), Friedman ANOVA (comparison of more than two dependent samples). The relationship between the variables was estimated with Spearman test. The null hypothesis was rejected in case of p < 0.05 [3].
The study was conducted after approval from the bioethical committee of Kabanov City Clinical Hospital No.1 and corresponded to WMA Declaration of Helsinki – Ethical Principles for Medical Research Involving Human Subjects 2000 and the Rules for Clinical Practice in Russian Federation confirmed by the order of Health Ministry of the Russian Federation, June 19, 2003 No.266.
RESULTS
Severity of general condition of the patients in the groups 1 and 2 (at the moment of admission to ICU) was conditioned by traumatic shock of degree 3. It was testified by the values of central hemodynamics and volemic status which did not have any statistically significant differences (the table 2). All patients showed the hypodynamic type of blood circulation that was confirmed by the low values of CO and CI (the table 2). Decrease in cardiac output was accompanied by compensatory increase in TPVR and significant disorders of peripheral circulation that was confirmed by high level of lactate in venous blood (the table 2). Although anti-shock therapy exerted positive influence on the parameters of hemocirculation in the groups 1 and 2 already after 12 hours (the table 2), the patients still showed the hemodynamic type of circulation, which persisted up to the beginning of the second day (the table 3). That’s why the patients of the groups 1 and 2 demonstrated the evident disorders of oxygen consumption in tissues within the first 24 hours (the table 3). Actually, even at the background of inotropic and vascular support, the patients of the groups 1 and 2 did not have any reserves for increasing cardiac efficiency, which is one of the most important and efficient ways for hypoxia compensation, [1] and, as result, for increasing oxygen transport. It is naturally that the above mentioned features of oxygen delivery did not allow achieving elimination of oxygen debt in the period of shock. It was also confirmed by the normal values of arteriovenous difference in oxygen at the background of high values of TPVR and lactate in venous blood (the table 3). Actually, low desaturation of arterial blood should not be considered as manifestation of evident disorders of peripheral blood flow in traumatic shock [4]. The main mechanism of elimination of oxygen debt was desaturation of arterial blood that was testified by oxygen extraction ratio (the table 3). At the same time, the patients of the groups 1 and 2 demonstrated low oxygen transport capacity, which was determined by persistent anemia at the background of transfusion therapy [2] (the table 3).
| Table 2 | |||||||||||||||
| The results of the comparative analysis of the values of central hemodynamics, lactate and hemoglobin in the patients of the groups 1 and 2, Me (Ql; Qh) | |||||||||||||||
| Note: * - statistically significant differences, p < 0.05 (Wilcoxon test for dependent samples); # - statistically significant changes within 3 days of treatment, p < 0.05 (Freedman ANOVA for multiple comparison of dependent samples); statistically insignificant intergroup differences according to terms of treatment (mann-Whitney test for independent samples). The data is presented as median, lower and upper quartiles. |
| Table 3 | |||||||||||||||
| The results of the comparative analysis of central hemodynamics and oxygen transport function of the blood in the patients of the groups I and II, Me (Ql; Qh) | |||||||||||||||
| Note: * - statistically significant differences in comparison with previous treatment, p < 0.05 (Wilcoxon test for dependent samples); # - changes in values within 3 days of treatment are statistically significant, p < 0.05 (Freedman ANOVA for multiple comparison of dependent samples); statistically insignificant intergroup differences according to terms of treatment (Mann-Whitney test for independent samples). The data is presented as median, lower and upper quartiles. |
The shift from the hemodynamic type of circulation to the normodynamic one was registered in the end of the second day that favored the statistically significant increase in oxygen transport and consumption (the table 3). Within this period inotropic and vascular support was discontinued as result of shock development in the patients of the groups 1 and 2. Unfortunately, such type of blood circulation could not completely satisfy high metabolic requirements of the body because of impossible increase in cardiac efficiency [6], which was associated with low SV (the table 3). Compensation of oxygen debt happened by means of increasing desaturation of arterial blood that was confirmed by arteriovenous difference in oxygen and oxygen extraction ratio (the table 3). Moreover, the patients of the groups 1 and 2 demonstrated low oxygen transport capacity because of persistent anemia (the table 3) at the background of transfusion therapy [3].
Shift from normodynamic type of blood circulation to hyperdynamic one was noted on the third day. It determined initiation of hemodynamic compensation of oxygen debt in the groups 1 and 2 (the table 3). It became possible because of significant increase in CO and SV as result of normalizing CBV at the background of ITT (the table 3). Elimination of oxygen debt in the groups 1 and 2 was realized by means of hemodynamic compensation and increasing desaturation of arterial blood (the table 3).
Efficient correction of hemodynamic disorders and initiation of efficient correction of oxygen debt determined improvement in microcirculatory circulation and metabolism, as well as favored decreasing ischemic and hypoxic damage of the organs and systems [6] that was testified by regression of organ and systemic disorders (the table 3). However the available strategy and tactics of transfusion therapy [2] did not allow increasing level of hemoglobin > 90 g/l in the groups 1 and 2 within 3 days. It determined persistence of low oxygen transport capacity (the table 3).
DISCUSSION
The type of blood circulation at the moment of admission allowed maximal objective estimation of severity of condition of the patients and intensity of manifestations of organ and systemic disorders. At that time the patients demonstrated two-phase development of cardiac insufficiency as result of myocardial inadequacy and deficiency of venous return which was determined by absolute and relative hypovolemia [1]. Hypovolemia and decreasing pumping ability of the heart determined increase in total peripheral vascular resistance that conditioned decreasing volumetric blood flow through the capillaries and oxygen delivery to tissues with subsequent development of circulatory and tissue hypoxia resulting in organ and systemic disorders [4]. It is really that generalized disorders of microcirculation and decreasing pumping ability determined development of tissue hypoxia, which became especially dangerous in the catabolic type of metabolic processes (typical of shock) [6]. It resulted in decreasing oxygen transport function that caused decreasing delivery of oxygen to tissues [5]. Hypovolemia, anemia, cardiac and respiratory insufficiency as result of massive blood loss played the leading role in disarrangement of oxygen transport [1]. Therefore, the hemodynamic type of circulation could not satisfy the high metabolic requirements of the body. The main mechanism of elimination of oxygen debt was the increase in desaturation of arterial blood. It is naturally that such compensatory mechanism could not provide adequate demand for oxygen at the background of increasing metabolism [6]. Low oxygen consumption and transport indicated an inability of the hypodynamic type of circulation to provide hemodynamic type of hypoxia compensation [5]. Moreover, non-corrected disorders of microcirculation caused further depression of tissue breathing because of decreasing time of delivery, restoration and consumption of oxygen in tissues [1]. As result of hypoxia the patient’s body initiates anaerobic type of substrate oxidation that favors accumulation of incompletely oxidized metabolic products and development of metabolic acidosis [4]. Development of acidosis is significantly determined by inconsistency between increasing need for oxygen and a possibility of oxygen delivery as result of disordered peripheral perfusion [6].
In its turn, increasing cardiac output leads to increasing oxygen transport and consumption by the beginning of the third day. At that time oxygen debt was eliminated by means of two mechanisms: hemodynamic compensation and desaturation of arterial blood.
The hyperdynamic type of blood circulation supported oxygen transport at relatively high levels (despite of decreasing oxygen transport capacity) that provided increasing oxygen consumption by tissues. However despite of increasing transport and consumption, the patients demonstrated significant oxygen debt that was confirmed by increasing values of arteriovenous difference in oxygen and oxygen extraction ratio. Beginning of effective elimination of ischemic and hypoxic injury to the organs and systems determined the decreasing intensity of multiple organ dysfunction syndrome [1, 6].
CONCLUSION
1. For the patients with traumatic shock of degree 3 it is appropriate to perform 3 day monitoring of the parameters of central hemodynamics (HR, SV, CO, CI, TPVR, CBV, CPV, volume of circulating red blood cells) and oxygen transport and consumption for targeted and pathogenetically determined correction, which favors regression of multiple organ dysfunction syndrome.
2. With persistent events of shock, the patients demonstrate some significant disorders of oxygen transport function of the blood which are expressed in decrease in oxygen transport and consumption by tissues.
3. At this time interval, correction of oxygen debt is realized only by means of increasing desaturation of arterial blood.
4. After correction of disorders of systemic hemodynamics oxygen debt is realized only by means of increasing desaturation of arterial blood, as well as by means of hemodynamic compensation.
5. Within 3 days the patients with traumatic shock demonstrate low oxygen transport capacity, which is not corrected with replacement therapy.