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

The effects of left ventricular venting and distention on myocardial protection during heterogenous distribution of cardioplegic solution remain undefined. This study was undertaken to determine if left ventricular venting enhances and distention impairs myocardial cooling and recovery of global and regional left ventricular function. Twenty-one pigs were placed on cardiopulmonary bypass and subjected to 80 minutes of ischemic arrest with the mid-left anterior descending artery occluded. Hearts were protected with multidose potassium (25 mEq/L) crystalloid cardioplegic solution supplemented with topical (4 degrees C) and systemic (28 degrees C) hypothermia. During arrest, the left ventricle was vented in seven pigs, seven pigs were not vented, and seven others had systemic pump blood infused into the left ventricle to maintain an end-diastolic pressure of 15 mm Hg. Parameters measured included left ventricular temperature, stroke work index, compliance (end-diastolic pressure-end-diastolic volume curves) and wall motion scores (two-dimensional echocardiography). Distended hearts had the lowest mean left ventricular temperature beyond the left anterior descending arterial occlusion (10.1 degrees +/- 1.8 degrees C distended [p less than 0.025 from vented and nonvented groups] versus 14.2 degrees +/- 0.7 degrees C vented versus 15.5 degrees +/- 1.2 degrees C nonvented), the highest postischemic stroke work index (0.78 +/- 0.09 gm-m/kg distended versus 0.62 +/- 0.07 gm-m/kg vented versus 0.66 +/- 0.07 gm-m/kg nonvented at end-diastolic pressure = 10 mm Hg), and the best wall motion scores (0.7 +/- 0.04 distended [p less than 0.025 from vented and nonvented groups] versus 5.5 +/- 1.80 vented versus 4.8 +/- 1.20 nonvented). Postischemic end-diastolic pressure-end-diastolic volume curves were unchanged from preischemic values in each group. We conclude that during heterogenous cardioplegic arrest, left ventricular venting offers no additional myocardial protection and may negate the beneficial effects of moderate (end-diastolic pressure = 15 mm Hg) left ventricular distention.
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PMID:Effects of left ventricular venting and distention during heterogenous distribution of cardioplegic solution. 334 57

Recent experimental studies have shown that pressure-controlled intermittent coronary sinus occlusion effectively reduces both infarct size and myocardium at risk after coronary artery occlusion. This study was undertaken to determine whether this modality was equally effective in altering reperfusion damage after a period of ischemic arrest. Fourteen pigs were placed on cardiopulmonary bypass and subjected to 2 hours of ischemic arrest with multidose potassium crystalloid cardioplegia supplemented with topical and systemic hypothermia (28 degrees C). During arrest, the mid-left anterior descending artery was occluded with a snare, which was released immediately after aortic unclamping. In seven pigs, a 7F balloon-tipped catheter was positioned in the coronary sinus and pressure-controlled intermittent coronary sinus occlusion was performed for 60 minutes after aortic unclamping. Seven other pigs served as controls. Parameters measured included stroke work index, ejection fraction, and myocardial pH in the distribution of the distal left anterior descending artery. Pigs treated with pressure-controlled intermittent coronary sinus occlusion had a significantly higher myocardial pH (6.99 +/- 0.06 versus 6.67 +/- 0.05, p less than 0.01), ejection fraction (50% +/- 2% versus 33% +/- 6%, p less than 0.01), and stroke work index (0.87 +/- 0.07 versus 0.61 +/- 0.05 gm-m/kg, p less than 0.01) after 60 minutes of reperfusion compared with those of the group not treated in this way. We conclude that pressure-controlled intermittent coronary sinus occlusion effectively reverses reperfusion damage after periods of ischemic arrest.
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PMID:Reversal of reperfusion injury after ischemic arrest with pressure-controlled intermittent coronary sinus occlusion. 335 98

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

Since hypothermia is commonly used to lower local and general metabolism during cardiopulmonary bypass, we attempted to identify its specific effects on glucose-insulin interactions. A group of nondiabetic patients undergoing hypothermic (28 degrees C) cardiopulmonary bypass with ischemic (cold) cardiac arrest was compared to a similar group operated on under normothermic conditions with potassium cardioplegia. In the absence of exogenous dextrose administration, hypothermia blocked insulin secretion for the duration of the operation. It also inhibited insulin secretion in response to an exogenous dextrose load (e.g., the priming fluid of the cardiopulmonary bypass circuit) or a glucagon injection, but this inhibition was lifted by rewarming. Blood glucose levels, which during normothermia were mildly elevated even in the absence of dextrose administration, remained normal during the hypothermic phase of cardiopulmonary bypass. By the end of the rewarming period, however, blood glucose levels had reached the same level as observed under normothermic bypass, a fact suggesting that the cold inhibition of hepatic glucose production had been only temporary. Cold inhibition of hepatic glucose production also explains why glucose clearance after a sudden dextrose load was initially faster at low body temperature than at normal temperature. Glucose-clamp studies indicated that insulin resistance was initiated by anesthesia and surgical trauma, and further accentuated by cardiopulmonary bypass, in association with elevated levels of hormones indicative of surgical stress. Regardless of body temperature changes, the assimilation of glucose by nondiabetic subjects during and immediately after bypass called for the infusion of large doses of insulin. A comparison with diabetic subjects showed that insulin-dependent patients (type I diabetes) required no more insulin during cardiopulmonary bypass than normal subjects, whereas patients with type II diabetes exhibited a marked insulin resistance during the operation and in the immediate postoperative period.
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PMID:Glucose-insulin interactions during cardiopulmonary bypass. Hypothermia versus normothermia. 351 20

The effect of two different myocardial preservation techniques on perioperative myocardial necrosis during coronary artery bypass surgery was assessed by serial myocardial creatine kinase determinations in 100 consecutive patients operated on by the same surgeon. Topical hypothermia with cold potassium cardioplegia was used randomly in 50 patients (group 1), and topical hypothermia with local interruption of the coronary circulation was used in the other 50 patients (group 2). Myocardial creatine kinase was measured by column chromatography every 6 hours for 36 hours after surgery. There was no significant difference between the two groups in terms of age, sex, functional class, extent of coronary artery disease, number of bypassed arteries, ejection fraction, or cardiopulmonary bypass time. Myocardial creatine kinase release (mean +/- standard error of the mean) was 193 +/- 33 IU/L X hours in group 1 patients operated on with cardioplegia and 210 +/- 31 IU/L X hours in group 2 patients operated on with topical hypothermia (p greater than 0.5). Myocardial creatine kinase peaks were 9.2 +/- 1.9 IU/L and 10.0 +/- 1.6 IU/L, respectively (p greater than 0.5). Perioperative myocardial infarction, as defined by serum enzyme activity and electrocardiographic criteria, occurred in 4 patients in group 1 and 3 patients in group 2. Thus, the addition of cardioplegia to topical hypothermia, although perhaps offering technical advantages, does not appear to improve myocardial protection over topical hypothermia with local interruption of the coronary circulation during coronary artery bypass surgery.
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PMID:Cold potassium cardioplegia versus topical hypothermia and intermittent aortic occlusion for myocardial protection during coronary artery surgery: a randomized clinical study. 351 46

Two solutions, our cardioplegic solution and Collins' solution, were tested with regard to preservation of the heart under deep hypothermia before transplantation. The setup used was the isolated perfused working rat heart model and 4 hours of preservation at 0 degree C. The following three groups were prepared: Group 1: the heart was arrested with the cardioplegic solution (potassium: 20 mmol/L, sodium: 87 mmol/L) and then flushed with and stored in Collins' solution (potassium: 117 mmol/L, sodium: 10 mmol/L); Group 2: the heart was arrested with and stored in Collins' solution; and Group 3: the heart was arrested with and stored in the cardioplegic solution. The recovery of cardiac function was more satisfactory in Group 1 than in Groups 2 and 3. The increase in lactate was greater, and adenosine triphosphate and total adenine nucleotide were more depleted during storage in Group 2 than in Groups 1 and 3. In Group 3 myocardial sodium accumulation and potassium depletion during storage were greater than in Groups 1 and 2, and myocardial sodium and calcium overload after reperfusion were greater than in Group 1. Myocardial calcium overload after reperfusion in Group 2 was also greater than that in Group 1. These findings plus coronary vascular resistance analysis revealed that Collins' solution damages the heart during arrest procedures and that the cardioplegic solution is less effective for storage of the arrested heart under deep hypothermia. Therefore the heart should be first arrested with the cardioplegic solution and then flushed with and kept in Collins' solution for simple cold storage.
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PMID:Cold storage of the rat heart for transplantation. Two types of solution required for optimal preservation. 354 Apr 58

Factors influencing total coronary vascular resistance (CVR) during hypothermia were studied in 30 mongrel dogs. Complete isolation of the heart in situ was achieved by transection of all cardiac neural and vascular connections in 15 dogs (denervated, Group I). Cardiac innervation was maintained in the other 15 dogs using systemic normothermic cardiopulmonary bypass (innervated, Group II). The aortic root was perfused with heparinized oxygenated blood at a constant flow rate at variable myocardial temperatures. Electromechanical arrest was achieved using potassium chloride (KCl) (25 meq/liter) added to the coronary perfusate. In each group, 5 dogs were maintained at a flow rate of 10 cc/kg/min without KCl and allowed to beat spontaneously, another 5 at a flow rate of 10 cc/kg/min and arrested with KCl, and the remaining 5 at a flow rate of 5 cc/kg/min with KCl. Total coronary vascular resistance was calculated from aortic root pressure, right atrial pressure, and flow rate and expressed in units per 100 grams of cardiac tissue. At 37 degrees C, resistance was lower in the denervated arrested (1.3 +/- 0.2) than in the innervated arrested hearts (2.1 +/- 0.2) (P less than 0.001). Preservation of spontaneous electromechanical activity in the innervated hearts resulted in a lower resistance (0.4 +/- 0.1) (P less than 0.001). A progressive decrease in myocardial temperature to 15 degrees C resulted in a corresponding decrease in coronary vascular resistance to a plateau value (0.5 to 0.7 U) in all arrested groups. The data suggest that at normothermia, innervation increases vascular tone in the coronary vascular bed, while electromechanical activity decreases it.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Factors influencing coronary vascular resistance during hypothermia. 357 65

A multicenter survey evaluated the clinical presentation, treatment, and outcome of accidental hypothermia. Data were collected from 13 emergency departments, with 401 of the 428 cases presenting during a two-year study period. Core temperatures ranged from 35 C to 15.6 C (mean, 30.57 C +/- 3.53) with 272 cases (63.6%) less than or equal to 32.2 C. There were no significant differences by age in presenting temperature, rewarming strategies, or mortality. The first hour rewarming rate was significantly (P less than .05) faster in the population less than or equal to 59 years (1.08 +/- 1.39 C/hr) than in those greater than or equal to 60 years (0.75 +/- 1.16 C/hr). Male core temperatures averaged 30.27 +/- 3.44 C versus female temperatures of 31.1 +/- 3.61 C. There were no clinically significant differences in male (N = 296) versus female (N = 132) profiles. High ethanol levels (315 to 800 mg%) did not affect outcome. Nine of 27 (33%) patients who received CPR initiated in the field survived, versus six of 14 (43%) with CPR begun in the ED. The profile of the CPR versus non-CPR population differed significantly (P less than .05) in location (outdoors), initial temperature (24.8 +/- 3.77 C vs 30.94 +/- 3.12 C), third-hour rewarming rate (2.28 +/- 1.53 C vs 1.17 +/- 1.18 C/hr), and numerous laboratory parameters. Tracheal intubation was performed without incident in 117 cases, of which 97 were less than or equal to 32.2 C. There were 73 fatalities (17.1%). Of these, 84.9% (N = 62) were less than or equal to 32.2 C. Predisposing conditions in this group included "serious" illness (30), systemic infection (28), trauma (15), immersion (ten), frostbite (seven), and overdose (two). The initial pulse, hemoglobin, and first-hour rewarming rate was lower in the deceased population, while the potassium, urea nitrogen, creatinine, and phosphorus were elevated. Excluding treatment combinations, outcome with exclusive use of a single rewarming strategy was passive external rewarming, 14 deaths below 32.2 C, 13 above; active external rewarming, six deaths below 32.2 C, two above; active core rewarming, 38 deaths below 32.2 C, none above. Refinements of the American Heart Association's CPR standards in hypothermia and a Hypothermia Survival Index are proposed.
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PMID:Multicenter hypothermia survey. 363 69

Recent reports indicate that small-amplitude electrical activity may be present in the cold potassium-arrested heart. Twenty-four mongrel dogs were placed on cardiopulmonary bypass and cooled to a rectal temperature of 26 degrees C. Myocardial preservation was provided with a combination of systemic hypothermia 26 degrees C. potassium (20 mEq/L) crystalloid cardioplegic solution (10 ml/kg) infused initially and every 30 minutes during 90 minutes of ischemic arrest, and topical hypothermia. Myocardial temperature was maintained between 8 degrees and 10 degrees C. Electrical activity and transmural myocardial temperature were monitored with specially designed plunge electrodes. Left ventricular stroke work index, cardiac index, and maximum rate of rise of left ventricular pressure were measured before bypass and 45 minutes after ischemic arrest. Biopsy specimens were taken before bypass and at 15 and 45 minutes after ischemic arrest. The specimens were used to measure adenosine triphosphate and to analyze electron microscopic ultrastructure. Small-amplitude electrical activity was present in 16 of 24 animals during cardioplegic arrest. Cardiac index decreased 18 ml/min/kg (not significant), left ventricular stroke work index fell by 0.28 +/- 0.1 gm-m/beat/kg (p less than 0.007), and maximum rate of rise of left ventricular pressure decreased 409 mm Hg/sec (p less than 0.01) in the eight animals without small-amplitude electrical activity. Adenosine triphosphate concentration was unchanged and electron microscopic ultrastructure was well preserved. In contrast, small-amplitude electrical activity (16 animals) resulted in a decrease in cardiac index of 67 ml/min/kg (p less than 0.001), a decrease in left ventricular stroke work index of 0.79 +/- 0.8 gm-m/beat/kg (p less than 0.001), and a fall in maximum rate of rise of left ventricular pressure of 775 mm Hg/sec (p less than 0.001). Adenosine triphosphate concentration decreased from 25 to 21 mumol/gm (p less than 0.04) and electron microscopic ultrastructure was poorly preserved (p less than 0.001). This study demonstrates that small-amplitude electrical activity in the cardioplegia-arrested heart at 10 degrees C impairs myocardial preservation.
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PMID:Effect of small-amplitude electrical activity on myocardial preservation in the cold potassium-arrested heart. 370 77

The effect of blood transfusions on the electrolyte, metabolic and hemodynamic status of 31 patients undergoing major laparotomies was studied. Two groups were compared: Group I, 11 patients receiving continuous intraoperative blood transfusions exceeding 5 units at a rate over 0.3 ml/kg/min, and Group II, 20 patients receiving transfusions of 1-5 units at a rate below the limit. Transiently increased potassium values (5.2 +/- 0.3 mmol/l) were found in Group I during the rapid transfusion phase. The difference was statistically significant (P less than 0.05) when compared to Group II (4.3 +/- 0.2 mmol/l). There was also a significant correlation (r = 0.64; P less than 0.05) between the increase in serum potassium concentrations and the respective potassium load caused by the blood transfused. Most of the hyperpotassemic patients had surgery of the abdominal aorta. During the rapid transfusion, the patients in Group I had significantly lower concentrations of serum ionized calcium (P less than 0.05) and higher central venous pressures (P less than 0.05), but more periods of hypotension when compared to Group II. After the transfusion the massively transfused patients had slight metabolic alcalosis, the BE and pH differing significantly (P less than 0.05) from the values of Group II. It is concluded that hyperpotassemia may occur during rapid transfusions (over 0.4 ml/kg/min) of stored blood, especially in patients undergoing surgery of the abdominal aorta, even without simultaneous shock, acidosis or hypothermia. Calcium administration may be of benefit especially in situations where combined hyperpotassemia and hypocalcemia reduce the myocardial performance.
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PMID:Electrolyte and acid-base disturbances caused by blood transfusions. 370


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