ABG Correction for Hypothermia ============================== >This is an issue that frequently arises in hypothermic patients. The short answer is that the current recommendations are that pH and pCO2 should NOT be corrected for temperature but that pO2 SHOULD. > >Taking once again the case of a hypothermic patient, blood will be warmed to 37 C when analyzed. Since O2 and CO2 will be less soluble at higher temperatures the *measured* values of pCO2 and pO2 will be higher than what really obtains in vivo. The former will result in a lower measured pH than what is actually present. The analysis is complicated by the fact that *ideal* pH and pCO2 is also a function of temperature. I.e., as blood is cooled in vivo, physiologic pH should be *alkaline* for optimal cellular performance. For example at a temperature of 25 C ideal pH is about 7.60 (1). If the physiologic pH is thus 7.60 then the measured pH will be approximately 7.40. Thus no correction is necesarry to interpret the ABG. Similarly because of several variables which tend to alter the 'normal' pCO2 in hypothermia (such as reduced CO2 production which decreses and alveolor hypoventilation which increases it) on balance CO2 is more soluable and thus pCO2 should be lower. Thus, if at a given temperature pCO2 is normally, say 25, the warming of blood prior to analysis will raise the pCO2 to 40. Once again, interpreting the *uncorrected* ABG gives one the correct impression that physiologic pCO2 obtains in vivo. In summary the changes that occur physiologically in hypothermia parallel the changes that occur when blood is warmed for analysis and thus correction of pH and pCO2 is unecessary. >Physiological observation confirm the soundness of this recommendation (1,2,3,4). > >As far as pO2 is concerned, it is felt that uncoreccted values (which are higher than what obtains in vivo) tend to overestimate true O2 content. Thus correction (reduction) of 7.2% for each degree below 37 C is recommended. Granted that oxygen consumption may not be as great in hypothermia as it is at normal body temperatures, nevertheless, the recommedation is to err on the side of overestimating rather than underestimating O2 requirements. > > > >H. Louzon MD > > >(1) > >The effect of pH on the hypothermic ventricular fibrillation threshold. >Swain JA, White FN, Peters RM >J Thorac Cardiovasc Surg, 87: 3, 1984 Mar, 445-51 > >During cardiac operations using hypothermia, the pH measured at 37 degrees C (and corrected to the patient's body temperature) is generally kept at 7.40. However, ectotherms (cold-blooded animals) regulate pH alkaline of 7.40 as temperature falls, e.g., pH 7.58 at 25 degrees C. Hypothermia and acidosis increase the propensity for ventricular fibrillation (VF). This study was undertaken to determine which scheme of pH regulation during hypothermia provided the highest level of cardiac electrical stability. Eleven dogs underwent median sternotomy and implantation of right ventricular and limb electrodes, aortic and central venous pressure catheters, and a probe to measure pulmonary artery blood temperature. To determine the VF threshold, a programmable stimulator was used to find the minimum current needed to produce VF by sweeping the vulnerable period of the cardiac cycle. The animals were divided into two groups for pH management: eight in the clinical scheme (pH 7.4) and seven in the ectothermic scheme, where pH varied with temperature. Control values were recorded prior to cooling and then repeated when core cooling had lowered the temperature to 25 degrees C. In the clinical group, the VF threshold decreased from 23.1 +/- 4.1 mA at 37 degrees C to 17.0 +/- 3.4 mA at 25 degrees C (p = 0.002); in the ectothermic group, the VF threshold was unchanged by hypothermia (23.7 +/- 3.2 to 22.8 +/- 2.8 mA). Heart rate and arterial and central venous pressures were not different between the groups at either temperature. Corrected arterial pH and PCO2 were unchanged from control in the clinical group at 25 degrees C (pH 7.40 +/- 0.01, arterial PCO2 34 +/- 2 torr), whereas arterial PCO2 was maintained at 20 +/- 1 torr to achieve pH 7.59 +/- 0.01 in the ectothermic group. Five of the eight dogs in the clinical group had spontaneous VF while cooling, as compared to one of the seven dogs in the ectothermic group. These studies demonstrate that allowing the corrected pH to rise with hypothermia and remain alkalotic relative to pH 7.4 improves the electrical stability of the heart during hypothermia, as evidenced by the VF threshold at 25 degrees C. Since the ectothermic scheme increases the electrical stability of the heart, it could decrease the incidence of VF during hypothermia and decrease the temperature at which VF occurs during hypothermic cardiopulmonary bypass. > > >(2) > > >Control of acid-base status during hypothermia in man. >Blayo MC, Lecompte Y, Pocidalo JJ >Respir Physiol, 42: 3, 1980 Dec, 287-98 > >Rahn's concepts of acid-base balance during hypothermia were tested in humans by studying eleven men who required extra-corporeal cooling for surgery. Hypothermia was moderate (27-28 degrees C) and maintained for 60-70 min. Extracorporeal blood perfusion (ECBP) was performed with a bubble-oxygenator which allowed changes in blood flow and gas concentrations. Arterial pH (pHa) at the person's body temperature was controlled by varying CO2 flow to the oxygenator in order to maintain in vitro pH measured at 37 degrees C in the normal range. During hypothermia and after rewarming to 37 degrees C, bicarbonate concentration and total CO2 content of arterial and mixed venous blood remained constant. A physiologic solution was introduced into the peritoneal cavity which was used as a tonometer; the values of equilibrated CO2 content in peritoneal fluid were constant. Neither metabolic acidosis nor hypercapnia developed. Blood acid-base balance in vivo during hypothermia was therefore identical to the behavior of blood in vitro. In addition, the interpretation of the results of acid-base studies, in humans with abnormal central temperature is facilitated when measurements are performed at 37 degrees C. > > >(3) > >Ectothermic philosophy of acid-base balance to prevent fibrillation during hypothermia. >Kroncke GM, Nichols RD, Mendenhall JT, Myerowitz PD, Starling JR >Arch Surg, 121: 3, 1986 Mar, 303-4 > >In the ectotherms, or cold-blooded animals, carbon dioxide pressure decreases (PCO2) and pH increases as body temperature falls. This tends to increase coronary blood flow and prevent fibrillation. This concept was investigated in 181 consecutive patients undergoing open heart surgery of all types. In 121 cases, endothermic (warm-blooded) temperature-corrected normal values of pH, PCO2, and oxygen pressure were maintained during extracorporeal circulation as the perfusate temperature was lowered to 24 degrees C prior to aortic cross-clamping and administration of blood cardioplegia solution. In 49 patients (40%), ventricular fibrillation occurred prior to cross-clamping. In the other 60 consecutive cases, in which the ectothermic principle of cooling was applied, the PCO2 was allowed to decrease from 50 to 40 mm Hg and the non-temperature-corrected pH rose from 7.28 to 7.42. Fibrillation occurred in only 12 (20%) of these 60 patients. > > >(4) > >Acid-base control during hypothermia. Acid-base control in children during hypothermia without temperature correction of pH and PCO2. > >Matthews AJ, Stead AL, Abbott TR >Anaesthesia, 39: 7, 1984 Jul, 649-54 > >In 28 children undergoing cardiopulmonary bypass with deep hypothermia for open heart surgery, an attempt was made to maintain pH at 7.4 not corrected for temperature by varying the CO2 concentration supplied to the oxygenator so that the PaCO2 was 5.33 kPa, not corrected for temperature. One to two percent CO2 gave satisfactory results. Five percent CO2 had previously been given. No adverse clinical side effects were noted, and the acid-base status remained stable for 24 hours in 16 patients. There are strong theoretical reasons for maintaining a pH of 7.4, uncorrected for temperature, during hypothermia and a clinical impression was gained of better myocardial function and improved systemic and cerebral perfusion. >