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

Our recent clinical studies suggest that the U wave represents Purkinje repolarization. To test this hypothesis, transmembrane potentials of Purkinje fibers (P) and the ventricular muscle (V) were simultaneously recorded from canine P-V preparations perfused in a tissue bath, and effects of various factors causing prominent U waves were studied. These include low stimulating frequency (bracycardia), low potassium (K) concentration, hypothermia, and quinidine. Bracycardia increased the difference between action potential duration of P and V, and decreased the rate of repolarization in P. Similarly, the difference of P and V action potential duration was increased markedly by low K and hypothermia, and slightly by quinidine, while the slope of phase 3 was significantly decreased by all these factors. In several intact animals either hypokalemia or hypothermia was produced using hemodialysis or extracorporeal circulation, and recorded electrocardiograms were compared with the P and V action potentials obtained under similar perfusing conditions in subsequent tissue bath study. Such comparison revealed a good temporal correlation between phase 3 repolarization in P and the electrocardiographic U wave. These results, although indirect, appear to support the theory that P repolarization caused the genesis of the U wave.
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PMID:Purkinje repolarization as a possible cause of the U wave in the electrocardiogram. 113 93

To determine the reasons for clinical failure of Melrose solution, potassium arrest was studied in isolated working rat hearts. Eight control hearts were stable for 2-1/2 hours. After 1/2 hour of work, 42 experimental hearts were subjected to 1 hour of ischemis by aortic cross-clamping with unmodified ischemia in eight hearts and ischemia with simultaneous intracoronary injection of 5 ml. of 4 degrees C. (1)Krebs-Henseleit buffer in seven hearts (2)potassium chloride buffer in six hearts, (3)potassium citrate buffer in eight hearts (both 26 mEq. per liter of K, approximately 300 mOsm. per liter), (4)Melrose solution in seven hearts (greater than 200 mEq. per liter of K, greater than 400 mOsm. per liter), (5)hypertonic potassium citrate buffer in six hearts (26 mEq. per liter of K, greater than 400 mOsm. per liter). The pH of all solutions was 7.8 plus or minus 0.1. After recovery isotonic potassium citrate- and potassium chloride-arrested hearts and time-matched control hearts showed no significant differences in cardiac output, coronary flow, systolic pressure, or heart rate. Hypertonic potassium citrate decreased the recovery of cardiac function after arrest and Melrose arrest was not significantly different from unmodified ischemia. Intracoronary cold isotonic Krebs-Henseleit buffer was better than Melrose arrest but inferior to 26 mEq. er liter of potassium arrest. Arrest with 26 mEq. per liter of potassium augments perfusion hypothermia and prevents significant functional and histologic myocardial damage during 1 hour of ischemis. Previous authors assumed that hypertonicity and citrate were responsible for poor results with Melrose solution, but high potassium concentration is the major deleterious factor with hypertonicity playing a contributory role.
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PMID:The mechanism of myocardial damage following potassium citrate (Melrose) cardioplegia. 113 99

The risk of open heart surgery can be lowered by combination of different methods of myocardial protection. 1. Cardioplegia with a potassium free Mg-1-aspartate and Procaine-solution (Cardioplegin). 2. Coronary perfusion after ischemia longer than 35-40 minutes in case of excessive left ventricular hypertrophy or failure. 3. Hypothermia. Surface cooling gives an additional safety if coronary perfusion is not ideal possible in case of multiple coronary stenoses. For patients with this dispositions a continuous coronary perfusion with cardioplegic solution might be advisable, as it was presented by Gercken in his paper. This method was used three times already in human, but is still in an experimental stage.
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PMID:Induced ischemic cardiac arrest. Clinical and experimental results with magnesium-aspartate-procaine solution (Cardioplegin). 119 31

Isolated perfused working rat hearts were subjected to elective cardiac arrest for 20 or 30 min. Various methods of arrest were studied, either singly or in combination and with or without coronary perfusion. The functional recovery of the heart following the termination of arrest was found to be related to the concentration of ATP and creatine phosphate in the myocardium at the end of the period of arrest. In turn, these concentrations were dependent upon the method used to induce arrest. Normothermic ischemic arrest led to a marked reduction in high energy phosphates and a poor functional recovery. In contrast, coronary perfusion with hypothermic solutions or solutions containing high concentrations of potassium, induced arrest without depleting ATP or creatine phosphate. These procedures conferred considerable protection on the myocardium and thus permitted good recoveries. The energy status and recovery associated with ischemic arrest could be improved by combining the ischemia with hypothermia or potassium arrest. The latter, while increasing recovery significantly, still failed to afford complete protection to the myocardium. Potassium chloride gave greater protection than potassium citrate. When topical hypothermia was combined with ischemia, a time and temperature relationship was demonstrated but effective protection could only be obtained with severe topical hypothermia over a relatively short time period. The results stress the importance of maintaining high energy phosphates during arrest, and this requires the provision of a continuous supply of oxygen and nutrient, which may perhaps be best achieved by ensuring continuous and adequate coronary perfusion.
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PMID:Ischemic damage and metabolism during elective cardiac arrest. 120 80

Because use of the bubble oxygenator during open-heart surgery is associated with complications such as hemolysis, pulmonary insufficiency and oliguria, a membrane oxygenator was used in conjunction with hypothermia in 37 infants. The main features of the oxygenator are gravitational blood flow, oxygenation into an airless, collapsible blood reservoir, low-flow roller pump flow back to the patient, accurate determination of flows and careful use of a heat exchanger. Gas flow (98% oxygen, 2% carbon dioxide) for the unit of 2 m2 is maintained at 3 to 4 1/min. Specific precautions are taken to ensure absence of bubbles. Three prime solutions are used, the final one having an osmolality of 381 mOsmol and containing 129.9 meq of sodium, 3.8 of potassium and 94.0 of chloride and 2001 mg/dl of glucose. Six patients died, but none of the deaths could be directly related to the use of the oxygenator. Respiratory complications were minimal, as were other complications. The technique is reliable in oxygenating blood in an tracorporeal circulation, but further familiarity with the membrane oxygenator for use in open-heart surgery in infants is desirable before firm conclusions can be drawn as to its value.
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PMID:Use of a membrane oxygenator for open-heart surgery in infants. 126 May 50

Brain death is associated with loss of hypothalamic, pituitary and brain stem function resulting in apnea, bradycardia and hypotension, poikilothermia, and diabetes insipidus. In order to preserve body functions mechanical ventilation is continued with the aim to maintain an arterial partial pressure of oxygen of more than 100 mmHg. Previous fluid restrictions and the application of diuretics during the treatment of high intracranial pressure frequently result in dehydration. Progressive vasodilation may induce severe hypotension and fluid replacement with cristalloids and if necessary colloids may be called for until the central venous pressure reaches 10 cm H2O. Continuous substitution of potassium and the use of hypotonic solutions such as glucose 5% may avoid hypokalaemia and hypernatraemia, respectively. Inotropic support with dopamine (5-10 micrograms/kg.min) or adrenaline (0.01-0.1 micrograms/kg.min) may be needed to maintain normal mean arterial blood pressure (65 mmHg). Polyuria (5000 ml/24 h) can be treated by continuous intravenous infusion of antidiuretic hormone (0.5-2-10 U/h). Hypothermia must be prevented by warming all fluids (37 degrees C) and covering the patient with heat saving blankets.
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PMID:[Management of the organ donor]. 128 68

The effects of plain ischemia (34 degrees C) and the protective role of hypothermia (20 degrees C) alone or in combination with cardioplegia (St Thomas' Hospital [STH] or glucose-potassium-nifedipine [GPN]) on the intracellular kinetics of the activator calcium of cardiac muscle were quantified and compared from the interval-force behaviour (mechanical restitution) of right and left ventricles of the perfused rat heart. Plain ischemia caused a major depression in the restitution of force of contraction of both ventricles, deranged the mixed linear-exponential functions by significantly increasing the time constants of the fitted mechanical restitution curves (MRC) and altered the control right/left ventricle interval-force relationship. The right ventricle was found to be more susceptible to ischemic damage than the left ventricle, and its inotropic reserve was virtually abolished by 1 h of plain ischemia. Hypothermic preservation during ischemia improved the mechanical restitution, salvaged the inotropic reserve and optimized right/left ventricle interval-force relationship, but the time constants of the fitted MRCs were still prolonged. However, both the cardioplegic formulations were equally effective in normalizing the time constants of the fitted curves. In general, right ventricle functions were better preserved by STH cardioplegia and left ventricle functions were better preserved by GPN cardioplegia. Cardioplegic interventions did not further improve the ventricular inotropic reserve compared with hypothermic preservation. Additional beneficial effects of cardioplegic formulations were directed towards stabilizing the linear-exponential functions and hence restitution of force of contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intracellular kinetics of the activator calcium of rat heart after ischemic arrest and cardioplegia: quantitative comparison of right and left ventricles. 137 92

Canine hearts were arrested with crystalloid cardioplegic solution (45 minutes at 7 degrees C) to determine whether either cardioplegia or hypothermia impairs the production of endothelium-derived relaxing factor or damages the vascular smooth muscle of epicardial coronary arteries. In addition, isolated coronary artery segments were exposed to either cold (7 degrees C) or warm (37 degrees C) crystalloid cardioplegic solution and physiologic salt solution in vitro for 45 minutes. After cardiac arrest or incubation with the solutions, segments of epicardial coronary artery were prepared and studied in organ chambers. Cardioplegic arrest of the heart or exposure to cardioplegic solution in vitro (7 degrees or 37 degrees C) did not alter endothelium-dependent relaxation of epicardial coronary artery segments in response to adenosine diphosphate or acetylcholine (10(-9) to 10(-4) mol/L). Cardioplegic arrest did not alter G protein-mediated, endothelium-dependent relaxation in response to sodium fluoride. In addition, smooth muscle contraction in response to potassium ions (voltage-dependent) or prostaglandin F2 alpha (receptor-dependent) and relaxation in response to isoproterenol (cyclic adenosine monophosphate-mediated) or sodium nitroprusside (cyclic guanosine monophosphate-mediated) was unaltered after exposure to cardioplegic solution or hypothermia. These experiments demonstrate that hyperkalemic crystalloid cardioplegia does not irreversibly alter function of epicardial coronary arteries. We hypothesize that coronary artery endothelial cell dysfunction identified in previous studies of cardioplegia may have been due to the effects of barotrauma or shear stress on the vasculature and not the effect of cardioplegia per se.
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PMID:Crystalloid cardioplegia and hypothermia do not impair endothelium-dependent relaxation or damage vascular smooth muscle of epicardial coronary arteries. 143 18

Patients having cardiac surgery experience a myriad of fluid and electrolyte disorders. Cardiopulmonary bypass (CPB) can cause multiple physiologic alterations, including electrolyte disturbances, acid-base imbalances, atelectasis, diminished pulmonary compliance, hemolysis, and thromboembolism. Cardioplegic solutions and induced hypothermia impose alterations in potassium metabolism and pH. The stress of surgery increases catecholamine circulation and augments antidiuretic hormone release, both of which affect fluid and electrolyte equilibrium. Dilution of the circulating blood volume from pump perfusate and volume resuscitation with crystalloid and colloid solutions produce fluid, electrolyte, and hemostatic disorders. Nonpulsatile flow produced by CPB can alter renal function. This article describes the metabolic alterations that are iatrogenically produced by cardiac surgery and the nursing and medical therapies aimed at correcting such alterations.
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PMID:Fluid and electrolyte imbalances after cardiac surgery. 152 37

Even during adequate general anesthesia, hypertension is a common phenomenon in patients undergoing aortocoronary bypass grafting (CABG). In such cases application of vasodilators is recommended in order to decrease myocardial oxygen consumption. This study was performed to compare two commonly used substances, i.e., nitrates and nifedipine, with regard to their influence on hemodynamics, renal blood flow, kidney function, and the requirement for homologous blood transfusions. METHODS. Forty-four patients gave their informed consent to the study. They were randomly divided into 2 groups: group 1 received nitroglycerin (3.0 micrograms/kg.min), group 2 nifedipine (Adalat, 0.5 microgram/kg.min) in order to prevent hypertension in the phase before onset of cardiopulmonary bypass (CPB). Anesthesia was induced by etomidate and succinylcholine and maintained as a modified neuroleptanalgesia with fentanyl (up to 50 micrograms/kg), midazolam (0.3 mg/kg.h), and pancuronium (0.1 mg/kg). Systolic blood pressure was kept within the range of 120-160 mm Hg; in case of higher values boluses of either 0.25 mg nitroglycerin or 0.5 mg nifedipine were administered. Cardiac index, stroke volume index, rate-pressure product, intrapulmonary shunt, and pulmonary and total peripheral resistances were evaluated at five predefined points: (1) after induction of anesthesia; (2) before incision; (3) before cannulating the aorta; (4) after decannulating the aorta; and (5) at the end of operation. Creatinine and free-water clearances as well as sodium and potassium excretion were calculated for three phases of the operation: (A) induction of anesthesia--onset of CPB; (B) during CPB; and (C) end of CPB--end of operation. CPB was performed using a membrane oxygenator (Sorin 51) and a nonpulsatile blood flow of 2.5 1/min.m2, which was reduced during mild hypothermia of 30-32 degrees C to 1.7 l/min.m2. Mean arterial pressure in both groups was kept at approximately 70 mm Hg. In case of lower pressures norepinephrine (50-100 micrograms/bolus) was administered; higher pressures were treated as described above. Volume substitution was performed initially by 500 ml hydroxyethyl starch and continued, if necessary, by homologous blood or 5% human albumin in order to keep the hematocrit greater than 30 in the phases before and after CPB. RESULTS. Group 2 showed significantly higher values of cardiac index and stroke volume index at point 3 while the rate-pressure product was clearly lower, indicating better myocardial performance and lower oxygen consumption than in group 1. Creatinine and free-water clearances in all three phases did not differ. However, sodium excretion during CPB was significantly higher in the nifedipine group while potassium excretion showed no differences. The average requirement for blood and blood substitutes was lower in group 2, but the difference could not be confirmed statistically because of the large dispersion of values. Nevertheless, 4 patients in the nifedipine group but no patient in group 1 did not need homologous blood transfusion. CONCLUSION. In comparison to nitrates, nifedipine showed some advantages in the treatment of hypertension during CABG: (1) it provided better myocardial performance; (2) it had a more reliable but not too long-lasting effect on elevated total peripherial resistance, leading to better hemodynamic stability; and (3) by not affecting the capacitance vessels it may necessitate fewer homologous blood transfusions.
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PMID:[Nifedipine versus nitroglycerin in aortocoronary bypass surgery. The effect on hemodynamics, kidney function and homologous blood requirement]. 153 39


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