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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

CPB has been a key element in the safe and effective practice of cardiac surgery since its inception more than 30 years ago. Refinements in the apparatus, methods of tissue preservation, and innovations in technique have lowered the morbidity and mortality rates from these procedures. Despite these factors, the pump-oxygenator apparatus itself and the processes of hemodilution, hypothermia, and anticoagulation, which are intrinsic to its operation, effect temporary physiologic derangements in organ system functions. Although all of these phenomena resolve spontaneously, some require treatment while others do not. Therefore, appropriate clinical management of this group of patients, must be based on an understanding of CPB techniques and the anticipated physiologic sequelae. Hypertension should mostly be controlled because high systemic vascular resistance exacerbates the tendency for bleeding and stresses fresh anastomoses. Volume, urine flow, and potassium loss must be monitored strictly and treatment initiated promptly. Cardiac dysfunction requires cautious, individualized pharmacologic, and sometimes mechanical support in the perioperative and postoperative periods. Laboratory values should never be treated routinely. CPB is not without intrinsic risk of serious clinical complication, and these must be anticipated after surgery. The potential for complication increases when CPB exceeds 2 hours and rises sharply when pump time is prolonged more than 3 to 4 hours. Excessive pump time exacerbates blood trauma, produces abnormal capillary membrane permeability, and predisposes the patient to tissue anoxia. The potential for embolism and pulmonary complications is increased. Permanent organ system damage can be avoided through strict attention to myocardial and tissue preservation, meticulous filtration, precise technique, and avoidance of prolonged extracorporeal circulation.
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PMID:Physiologic principles and clinical sequelae of cardiopulmonary bypass. 351 Oct 11

Protective action of aprotinin froom ischemic myocardial damage was evaluated in 9 patients compared to non-treated 18 patients, who underwent open heart surgery (22 ACB, 3 AVR and 2 MVR) with respect to the alterations of beta-glucronidase, acid-phosphatase, MB-CPK and m-GOT. Cold cardioplegia with glucose-insulin-potassium solution was used in this investigation. Average arrest time was 78.6 +/- 4.9 minutes associated with hypothermia between 25 and 28 degrees C in rectal temperature. Aprotinin was administered in 9 patients intravenously with 5,000 KIU/Kg 30 minutes prior to CPB and then 5,000 KIU/Kg in the prime solution. Activity of beta-glucronidase was significantly suppressed in the aprotinin-treated group compared to the non-treated group following cardioplegia and in the reperfusion period up to 6 hours, however, acid-phosphatase failed to demonstrate significant difference among two groups. Serum MB-CPK and m-GOT levels in the aprotinin-treated group did not elevate the beginning of reperfusion following cardioplegia. These data suggest that aprotinin add myocardial protection to cold cardioplegia.
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PMID:Additive protection of aprotinin, protease inhibitor to cold cardioplegia from ischemic myocarium. 615 91

The basic physiologic characteristics of acid-base equilibria during hypothermia were briefly reviewed. By graphic analysis, four possible clinical strategies for managing the acid-base status of the patient undergoing H-CPB were documented. The effect of hemodilution on buffer capacity was charted in a manner applicable to common current operative procedures. During hypothermia for cardiac operations as presently conducted, the perfusionist is in control of the temperature of the body and the perfusion preservation of the body and brain; the surgeon must assume responsibility for preservation of the heart. The literature pertinent to the relationship of the acid-base state to the functions and structural preservation of the heart and brain during the conditions of cooling to and rewarming from deep hypothermia associated with cardiopulmonary bypass, aortic cross clamping, cardioplegia and total circulatory arrest have been reviewed. The evidence is overwhelming that myocardial anoxia caused by aortic occlusion or total circulatory arrest at any temperature to 15 degrees C. result in progressive acidosis which, of itself, is myotoxic. In contrast, alkalinity is ionotropic. Myocardial ischemia, in both adults and infants, should be prevented and treated by alkaline perfusion cooling and by frequent coronary perfusion of a cardiopreservative solution which is extremely cold (4 to 8 degrees C.), oxygenated, has a pH of 7.8, slightly hyperosmolar and which has a hematocrit of 20 per cent (imidazole, erythrocytes and plasma protein colloid), a cardioplegic ionic pattern and energy substrates. Reperfusion of the heart should begin at a 37 pH of 7.8. Evidence is strong that the use of CO2 added to any gas mixture is harmful. It increases myocardial acidosis; it does not increase cerebral blood flow during hypothermia. Protection of the unperfused brain of an infant should emphasize prevention of circulatory arrest prolonged to more than 40 minutes. Temporary reperfusion at that time limit should be used. Probably the best general management of the body for H-CPB is alpha-stat, which preserves biologic neutrality. The uncorrected analyzer reads pH 7.4 and Pco2 at any temperature. However, the need for preservation of the hypoxic heart is overwhelming and, thus, the best acid-base management for cardiac hypothermic operations is significant respiratory alkalosis. The most appropriate sites for the collection of blood samples for gas analysis and measuring temperatures were discussed; "body temperature" is the most unreliable parameter measured. The major characteristics of an "ideal" cardiopreservative solution were described.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The importance of acid-base management for cardiac and cerebral preservation during open heart operations. 642 51

Systemic venous oxygen saturation is clinically used as an indicator of a satisfactory oxygen supply demand balance on cardiopulmonary bypass (CBP). Cerebral desaturation has been associated with postoperative cognitive dysfunction and has an incidence of 17% to 23% on bypass. We tested the hypothesis that systemic venous saturation did not correlate with jugular bulb venous saturation. Blood was drawn from the radial artery, jugular bulb catheter, and venous return line for determination of pH, oxygen tension and saturation, and carbon dioxide tension at four times during bypass: warm 1 (following initiation of CPB); cold 1 (stable hypothermia); cold 2 (hypothermia prior to rewarm); and warm 2 (nasopharyngeal temperature 36 degrees C to 37 degrees C). Correlations of jugular bulb and systemic venous saturation at cold 1 were r = 0.29, r2 = 0.08, and p = 0.0005, and at warm 2 were r = 0.22, r2 = 0.05, and p = 0.007. We conclude that systemic saturation is a poor indicator of cerebral saturation. The poor association of jugular and systemic pump venous saturations underscores our inability to evaluate adequacy of cerebral perfusion. Jugular saturation is lower than pump venous return blood, especially at times of lower oxygen delivery, thus either continuous invasive or noninvasive evaluation of cerebral oxygenation is required to evaluate the adequacy of cerebral perfusion.
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PMID:Jugular bulb saturation and mixed venous saturation during cardiopulmonary bypass. 757 50

Metabolic responses during recovery from cardiac operations for various congenital heart defects were studied in 30 mechanically ventilated pediatric patients in two groups: infants 1 year or less (group I) and children more than 1 year old (group II). Oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured using a pediatric metabolic monitor intermittently after induction of anesthesia, after skin closure, 2 to 4 hours postoperatively, and on the first postoperative morning in the pediatric intensive care unit. Energy expenditure and respiratory quotient were determined from respiratory gas measurements. Rectal and skin temperatures and hemodynamic variables were recorded at the same time. VO2 increased during rewarming 2 to 4 hours after the operation by 12 +/- 15% in group I and by 24 +/- 19% in group II, while rectal temperature increased by 2.0 +/- 1.2 degrees C and 1.8 +/- 1.4 degrees C, respectively. No further increase in VO2 occurred until the first postoperative morning. A hypermetabolic response was not seen in all cases despite marked thermal changes. High-dose fentanyl anesthesia partly explains the low responses. On the other hand, low cardiac output may also compromise oxygen supply. Sixty-three percent of infants were treated for cardiac failure before surgery and 75% needed inotropic support immediately after the operation. Low central venous oxyhemoglobin saturation values (ScvO2 < 60%) were observed during rewarming, indicating an increase in oxygen extraction secondary to an increased oxygen demand in the brain during recovery from anesthesia, and a low cardiac output or delayed restoration of cerebral blood flow after CPB and deep hypothermia.
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PMID:Oxygen consumption following pediatric cardiac surgery. 788 Sep 92

Although much has been learned about cerebral physiology during CPB in the past decade, the role of alterations in CBF and CMRO2 during CPB and the unfortunately common occurrence of neuropsychologic injury still is understood incompletely. It is apparent that during CPB temperature, anesthetic depth, CMRO2, and PaCO2 are the major factors that effect CBF. The systemic pressure, pump flow, and flow character (pulsatile versus nonpulsatile) have little influence on CBF within the bounds of usual clinical practice. Although cerebral autoregulation is characteristically preserved during CPB, untreated hypertension, profound hypothermia, pH-stat blood gas management, diabetes, and certain neurologic disorders may impair this important link between cerebral blood flow nutrient supply and metabolic demand (Figure 5). During stable moderate hypothermic CPB with alpha-stat management of arterial blood gases, hypothermia is the most important factor altering cerebral metabolic parameters. Autoregulation is intact and CBF follows cerebral metabolism. Despite wide variations in perfusion flow and systemic arterial pressure, CBF is unchanged. Populations of patients have been identified with altered cerebral autoregulation. To what degree the impairment of cerebral autoregulation contributes to postoperative neuropsychologic dysfunction is unknown. It must be emphasized that not the absolute level of CBF, but the appropriateness of oxygen delivery to demand is paramount. However, the assumption that the control of cerebral oxygen and nutrient supply and demand will prevent neurologic injury during CPB is simplistic. A better understanding of CBF, CMRO2, autoregulation and mechanism(s) of cerebral injury during CPB has lead to a scientific basis for many of the decisions made regarding extracorporeal perfusion.
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PMID:Cerebral blood flow and metabolism during cardiopulmonary bypass. 846 2

Forty patients undergoing CPB for coronary artery surgery, using a standardized technical setting, were randomized to receive either Ringer's acetate, dextran 70 (Macrodex), polygeline (Haemaccel) or albumin 4% for volume replacement during and after surgery. The choice of fluid did not affect early complement activation (C3 activation products). Higher values of the terminal complement complex (TCC) were found only at the end of the operation in patients receiving polygeline. There were no differences between any two of the four groups during the postoperative course. The use of blood transfusion or autotransfusion and the degree of haemodilution and hypothermia did not affect complement activation. We conclude that complement activation in association with open-heart surgery is only marginally affected by the choice of fluid for volume replacement.
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PMID:Complement activation during and after open-heart surgery is only marginally affected by the choice of fluid for volume replacement. 888 61

Microscopic cerebral arterial air emboli (MCAAE) cause neurologic injury during cardiac surgery. We used a mathematical model of gas absorption to gain a preliminary assessment of what physical or physiologic parameters affect MCAAE absorption in the setting of cardiac surgery with its unique set of normal values. Simulated MCAAE of radii 50 and 200 microns have absorption times of 2 and 32 min, respectively. Predicted absorption times depend dramatically on PaN2. MCAAE are predicted to be absorbed twice as quickly at a PaN2 of 0 vs. 380 mmHg (FiO2 approximately equal to 0.50). Moderate hypothermia (27 degrees C) is predicted to cause only small decreases in absorption time. Changes in cerebral blood flow (for example, as affected by hemoglobin concentration, PaCO2, PaO2, collateral circulation, anesthetics, or cerebral metabolism) probably have only small effects on absorption time. Intravascular perfluorocarbons are predicted to cause small-to-moderate decreases in absorption time. In conclusion, there is probably only one important determinant of MCAAE absorption time during normothermic or moderately hypothermic CPB: arterial nitrogen partial pressure.
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PMID:Computer simulation of microscopic cerebral air emboli absorption during cardiac surgery. 956 86

This study aimed to assess whether the use of the physiological shunt equation could (within the first five minutes of initiating CPB) serve as a 'screen' to differentiate normal and dysfunctional oxygenator performance. If dysfunction severe enough to require replacement was necessary, the normothermic patient could be weaned from CPB and replacement would be carried out under safe, controlled conditions. This technique would require postponing the induction of hypothermia (if used), aortic cross-clamping, and arresting the heart until after this screen was completed. This study demonstrates that a strong negative correlation exists between the degree of blood shunting and the membrane's 0 2 transfer performance (r = -0.874). This relation enables us to predict 0 2 transfer performance when only the shunt fraction is known. Of the 41 oxygenators used in this study, 40 demonstrated normal, or below-normal, shunt fractions. Oxygen transfer performance at or above predicted levels would be anticipated for these oxygenators. One of the 41 oxygenators had mildly elevated shunt fractions, which we predicted would be associated with mild 0 2 transfer dysfunction. Based on the performance screen worksheet we created, replacement was not necessary since the oxygenator maintained high levels of 0 2 transfer in reserve despite its marginal performance dysfunction. Assessment of oxygenator performance dysfunction in this earliest phase of CPB would greatly reduce the incidence of emergency oxygenator replacement secondary to actual or perceived oxygenator failure later in the course of the procedure.
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PMID:The proposed use of a 'screening test' to assess oxygenator performance. 1014 66

The ECF operation is designed to improve postoperative outcome by enhancing factors that are critical in optimal functioning of the Fontan circulation, including preservation of ventricular and pulmonary vascular function, avoidance of dysrhythmias, and prevention of stasis and flow turbulence in the Fontan circuit. Preoperative strategies include an early bidirectional Glenn procedure, and avoiding ancillary intracardiac procedures at the time of the Fontan by performing them at the time of the Glenn operation. Operative strategies include minimizing the duration of CPB by performing the conduit to pulmonary artery anastomosis off bypass, using partial instead of full CPB by cannulating the IVC alone, avoiding hypothermia, avoiding cross-clamping of the aorta, avoiding atrial incisions and suture lines, using a tubular conduit to construct the Fontan pathway, making a large conduit to pulmonary artery anastomosis, incorporating the conduit into aggressive pulmonary arterioplasties, and offsetting of the superior and inferior cavopulmonary anastomoses.
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PMID:Extracardiac conduit variation of the Fontan procedure. 1094 50


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