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

Hemodynamic parameters were compared in 28 patients with ischemic heart disease subject to cardiopulmonary bypass surgery with non-pulsatile (group 1) and pulsatile flow (group 2). Systolic, diastolic and mean blood pressure (MBP) was assessed, total peripheral vascular resistance (TPVR) was calculated, esophageal, rectal and skin temperature was measured. Volumetric perfusion rate was the same in both groups. Pulse pressure was maintained at the level of 35 mmHg. MBP at the stage of hypothermia plateau and during warming decreased in both groups. It was significantly lower in group 1 at the beginning of warming and during clamp relief from the aorta. At the end of cooling period TPVR was lower with the use of pulsatile than non-pulsatile flow. It increased drastically towards the end of hypothermia plateau in group 1. During clamp relief from the aorta TPVR values did not significantly differ from baseline in group 2 and remained high in group 1. The warming rate happened to be greater in pulsatile than in non-pulsatile flow.
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PMID:[Changes in hemodynamic indices during perfusion with pulsatile and steady currents in aortocoronary bypass surgery]. 262 47

During the mitral valve replacement on a 48-year-old male with mitral valve stenosis, ST-T changes (ST elevation and T inversion) suddenly appeared just before the start of cardiopulmonary bypass. Myocardial ischemia was suspected before we noticed the cardioplegic solution (about 10 degrees C) had been dripping on the surface of the right ventricle by mistake for about five minutes. After pouring warm saline over the myocardial surface, the EKG returned to normal within ten minutes. In this case, there appeared the elevation of the J point which is characteristic of profound hypothermia and is easily mistaken as myocardial ischemia because of ST segment elevation. It is very important to observe even a trivial intraoperative action which is not directly related with the operative procedure.
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PMID:[Intraoperative ST-T changes resembling myocardial ischemia due to accidental myocardial cooling]. 272 25

We evaluated the plasma elimination of recombinant human superoxide dismutase (rHSOD) when given before reperfusion in an experimental canine model of global hypothermic myocardial ischemia. Adult mongrel dogs were placed on cardiopulmonary bypass, and core temperature was reduced to 25 degrees C. Hypothermic global myocardial ischemia was maintained for 90 minutes with intermittent crystalloid cardioplegic solution. Five minutes before reperfusion, rHSOD was administered via the pump oxygenator as a bolus injection. Plasma rHSOD levels were measured at 0, 3, 5, 10, 20, 30, 60, and 120 minutes after injection. Animals were rewarmed and weaned from bypass. Three experimental groups received either 4, 8, or 16 mg/kg rHSOD. Based on previously reported dose-response data, we conclude that desirable peak serum concentrations are achieved with 16 mg/kg rHSOD. In the setting of hypothermic cardiopulmonary bypass and global myocardial ischemia, single bolus administration of rHSOD before reperfusion is an effective method due to the prolonged serum half-life.
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PMID:Pharmacokinetics of superoxide dismutase during hypothermic cardiopulmonary bypass. 280 4

Many patients undergoing cardiac surgery have some degree of myocardial hypertrophy. To assess the response of hypertrophied myocardium to simulated cardiac surgery, left ventricular hypertrophy was induced in rats by aortic banding, and ventricular function was measured by means of the isolated, isovolumic heart perfusion technique. The hypertrophied hearts had a greater susceptibility to ischemic injury than nonhypertrophied control hearts, as manifested by a greater degree of diastolic contracture during the recovery period after 30 minutes of ischemic arrest at 37 degrees C. Hypothermia without cardioplegia during a 2-hour arrest did not completely preserve diastolic function in the hypertrophied hearts, but cardioplegia combined with hypothermia completely protected the hypertrophied hearts against 2 hours of ischemia. The results suggest a need for both hypothermic and cardioplegic preservation techniques in patients with myocardial hypertrophy who have cardiac surgical procedures requiring a significant period of myocardial ischemia.
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PMID:Increased injury of hypertrophied myocardium with ischemic arrest: preservation with hypothermia and cardioplegia. 293 42

This study assesses the ability of the free-radical scavenger peroxidase to enhance cardioplegic protection when given during or before myocardial ischemia. Forty-four isolated isovolumetric buffer-perfused rat hearts were studied. In a first series of experiments that consisted of three groups, hearts were subjected to 90 min of normothermic global ischemia followed by 45 min of reperfusion. One group received a crystalloid cardioplegic solution given as a single dose at the onset of arrest. A second group received cardioplegic solution supplemented with superoxide dismutase (200,000 U/liter), and a third group received cardioplegic solution supplemented with peroxidase (6000 U/liter). Based on comparisons of postreperfusion coronary flow, left ventricular developed pressure, maximum dP/dt, and diastolic pressure, we found that the best protection was provided by peroxidase-enriched cardioplegia. A second series of experiments was then undertaken to assess the effects of the latter enzyme given as a pretreatment. Hearts were subjected to 3 hr of global ischemia, during which myocardial protection was provided by hypothermia (15 degrees C) along with multidose cardioplegia. The treatment group was given peroxidase (10,000 U/liter) added to the perfusate fluid for 15 min before the onset of cardioplegic arrest without further enzyme supplementation during ischemia or reperfusion. Hearts perfused with standard buffer for an equal period of time served as controls. While the two groups demonstrated the same degree of postischemic increase in myocardial stiffness, peroxidase-pretreated hearts had a significantly better recovery of contractile indexes at 30 and 45 min of reflow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of cardioplegic protection with the free-radical scavenger peroxidase. 302 57

Anesthesia and surgery have a wide range of effects on the cardiovascular system. Even in healthy patients having minor operations, anesthetic agents can cause significant cardiac depression and hemodynamic instability. Virtually all anesthetic agents have intrinsic myocardial depressant properties, although some may mask this with sympathetic stimulation. The vasodilatory effects of the volatile agents can result in serious hypotension when combined with this negative inotropy. In the patient with pre-existing cardiac disease, these cardiovascular anesthetic effects become much more serious. These patients will not tolerate wide swings of hemodynamic variables, and the cardiodepressant effects of anesthetics are more pronounced in them. The stress of anesthesia and surgery frequently unmasks previously undiagnosed heart disease. Surgery itself provides many insults to the cardiovascular system, and these may be additive with the effects of anesthesia. These include loss of blood and other volume shifts, release of various substances into the circulation, hypothermia, sudden changes in cardiac preload and afterload, myocardial ischemia, and effects of drugs or blood products given for surgical reasons. The signs and symptoms of these surgical stresses to the cardiovascular system are often masked by anesthesia.
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PMID:Cardiovascular effects of anesthesia and operation. 333 99

Effects of moderate spontaneous hypothermia on left ventricular systolic and diastolic function during acute myocardial infarction were documented in 17 anesthetized dogs with micromanometric pressure and ventriculographic dimension recordings acquired at baseline and at 1 and 3 h after coronary occlusion. In Group 1 (n = 5), core temperature was allowed to decline spontaneously. In Groups 2 (n = 6) and 3 (n = 6), core temperature was maintained at normothermic levels. Hypothermia impaired isovolumic relaxation markedly despite its lack of effect on ventricular volumes or ejection fraction. At 32.3 degrees C, tau 1/2, defined as the time needed for the left ventricular pressure at the time of peak negative rate of change of left ventricular pressure (dP/dt) to fall by 50%, was increased by 129% 3 h after occlusion. In addition, at this temperature significant changes were found in heart rate, cardiac output, minute work, peak positive and peak negative dP/dt, systolic ejection time, mean velocity of circumferential fiber shortening, mean aortic pressure and end-diastolic pressure. Thus, hypothermia evolving under conditions of general anesthesia profoundly alters left ventricular function in the setting of acute myocardial infarction, a phenomenon that requires consideration and control in studies of myocardial ischemia and left ventricular function in experimental animals.
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PMID:Sensitivity of isovolumic relaxation to hypothermia during myocardial infarction. 333 99

This study examined anatomic differences between the adult and the newborn heart as they relate to myocardial preservation and compared standard techniques of myocardial preservation used in operations for congenital heart disease. The biventricular endocardial surface area/ventricular mass ratios were calculated in 10 neonatal (2.5 +/- 0.2:1) and 10 adult (0.6 +/- 0.1:1) pigs (p less than 0.001). Three groups of neonatal pigs underwent 1 hour of global myocardial ischemia while being supported by cardiopulmonary bypass. Myocardial protection was by deep systemic hypothermia (group 1), moderate systemic hypothermia and cardioplegia (group 2), or by deep systemic hypothermia and cardioplegia (group 3). Left ventricular end-systolic pressure-dimension and end-diastolic pressure-dimension relationships were measured before and after cardiopulmonary bypass. Septal temperatures remained below 20 degrees C in groups 1 and 3 but rose above 20 degrees C in group 2. Groups 1 and 2 had moderate and mild ventricular stiffening, respectively, whereas group 3 showed no diastolic dysfunction. Ventricular contractility was increased (p less than 0.05) in group 3. Techniques for myocardial preservation used during operations for congenital heart disease must consider the large endocardial surface area/mass ratio and the rewarming effects of systemic blood. The combination of deep systemic hypothermia and cardioplegia provided superior myocardial protection compared with the other techniques tested.
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PMID:Myocardial preservation in the neonate. Beneficial effects of cardioplegia and systemic hypothermia on piglets undergoing cardiopulmonary bypass and myocardial ischemia. 341 86

The value of verapamil hydrochloride as a myocardial preservative when administered prior to or during periods of myocardial ischemia was studied in patients with normal preoperative cardiac function during elective coronary artery bypass grafting. Myocardial protection included systemic hypothermia (28 degrees C) and hypothermic hyperkalemic cardioplegia. Patients were randomly divided into four groups. Group 1 received intravenous administration of verapamil prior to aortic cross-clamping. Group 2 received intravenous verapamil plus verapamil in the cardioplegic solution. Group 3 received verapamil in the cardioplegic solution only. Group 4 was given no verapamil. Oxygen extraction during the reperfusion period was greatest in Group 4. However, the incidence of pacing was 50 to 78% in Groups 2 and 3, who were given verapamil in the cardioplegic solution. These groups also had a greater need for inotropic agents for discontinuation of cardiopulmonary bypass (CPB). This study indicates that verapamil may be a useful pretreatment prior to CPB and ischemia, but is not effective and may even be detrimental when administered during ischemic periods to patients with good myocardial function.
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PMID:Verapamil and myocardial preservation in patients undergoing coronary artery bypass surgery. 348 96

Presently myocardial protection can be obtained in three main ways: 1) energy conservation through chemical induction of rapid and complete diastolic arrest, 2) slowing of the metabolic rate and degradative process through the use of hypothermia, and 3) prevention or reversal of unfavourable ischemic-induced changes with various protective agents. These methods of myocardial protection and their effectiveness, the calcium metabolism during myocardial ischemia, and the effects of calcium channel blockers are briefly reviewed and discussed. It is stressed that myocardial protection during ischemic arrest is a complex entity, and that new modes of myocardial protection are needed in the future.
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PMID:Cardioplegia and myocardial ischemia during cardiopulmonary bypass. 352 Nov 95


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