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

Our experimental studies since 1972 show that the heart is preserved best during cardiopulmonary bypass when it is in the beating, nonworking state. Results after mitral valve replacement (MVR) from 1968 to 1974 using various techniques of cardiac preservation were compared. In group I were 47 patients (1968 to 1972) in which either profound, topical hypothermia with prolonged ischemic arrest (19) or ventricular fibrillation with continuous coronary perfusion (28) was used. In group II there were 22 patients (1972 to 1974) in whom the heart was in a beating, nonworking state between brief periods of ischemic arrest. In group I 55% (25/47) required inotropic support postoperatively, and 17% (8/47) died. In group II 5% (1/22) required inotropic support postoperatively, and this patient died (5% mortality). Extended periods of ischemic arrest were necessary because of intraoperative complications in this patient. These data show that depressed postoperative myocardial performance occurs rarely when the heart is preserved in the beating, nonworking state during MVR and ventricular fibrillation and prolonged topical hypothermic anoxic arrest are avoided.
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PMID:Depressed cardiac performance after mitral valve replacement. A problem of myocardial preservation during operation. 115 30

Depressed postoperative myocardial performance (low output syndrome) requiring inotropic drugs or balloon counterpulsation is due to subendocardial ischemic damage. Before July, 1972, we needed inotropic drugs in 30 to 52 per cent of 189 patients undergoing coronary revascularization or aortic or mitral valve replacement in whom we used ischemic arrest, profound topical hypothermia, and ventricular fibrillation. The mortality rate ranged from 10 to 17 per cent. Our experimental studies show that morbidity and death in such cases are caused by ischemic injury to the heart resulting from inadequate myocardial protection during bypass. Based on these experimental studies, we have, since July, 1972, employed the following principles clinically: (1) Maintain beating empty heart whenever possible; (2) maintain adequate coronary perfusion pressure (less than 80 mm. Hg); (3) avoid extreme hemodilution; (4) avoid ventricular fibrillation; (5) avoid prolonged hypothermic arrest, limiting ischemic periods to less than 15 minutes; (6) repay myocardial ischemic oxygen debt with total (vented) bypass; and (7) optimize DPTI/TTI (supply/demand ratio) pre- and postoperatively. These principles were followed in 189 consecutive operations, and postoperative inotropic drugs were needed in only 12. The principles were violated in 4 of the 12 patients (6 per cent), and 5 others had identifiable causes of myocardial depression; low output syndrome was unexplained in only 3 patients (1.7 per cent).
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PMID:Depressed postoperative cardiac performance. Prevention by adequate myocardial protection during cardiopulmonary bypass. 118 89

It is recognized that postoperative mortality, infarction and the need for inotropic support are increased following myocardial revascularization in highrisk patients. Operations were carried out in 57 such patients in whom one or more of the following factors were present: ventricular dysfunction-ejection fraction less than 0.4 (17), unstable (8) or preinfarction angina (29), evolving infarction (8), recent infarction (less than two weeks before) (5) and refractory ventricular tachyarrhythmia (4). Combined risk factors were present in nine patients. The following principles were utilized to minimize ischemic injury: (1) avoidance of prebypass hypertension and hypotension, (2) avoidance of extreme hemodilution, (3) avoidance of ventricular fibrillation, (4) maintenance of beating empty heart, when possible, (5) the limiting of ischemic periods to less than 12 minutes (hypothermia 32 degrees C) and (6) repaying myocardial oxygen debt with total (vented) bypass, when necessary. The following results were obtained: inotropic support was required in five patients (9 percent), "new" postoperative infarction occurred in five patients (9 percent) and one patient died (2 percent). These results are comparable to those reported in good-risk patients, and indicate that optimal myocardial protection will allow safe revascularization in a high-risk patient.
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PMID:Myocardial revascularization in high-risk coronary patients. 126 12

It is recognized that some people die from hypothermia even though they are alive and uninjured when rescued. The traditional explanation is that this is due to ventricular fibrillation resulting from the afterdrop of core temperature. This hypothesis was based on inadequate measurement and failure to consider the physiology of cold. It should now be discarded. Most deaths after rescue occur through an imbalance between the active vascular capacity and the circulating fluid volume i.e. relative hypovolaemia or fluid overload. The actual mechanism in any individual case depends both on the history of the cooling and the method of rewarming used. Some deaths will however occur due to continued cooling of the body or to ventricular fibrillation precipitated by rough handling.
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PMID:The cause of death after rescue. 148 74

A postoperative cardiac surgical patient developed ventricular fibrillation immediately after accidental pericardial injection of bupivacaine at room temperature. The possible causes, which include systemic toxicity, local vasoconstriction with myocardial ischaemia, local toxic effect of bupivacaine or local hypothermia, are discussed.
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PMID:Ventricular fibrillation after accidental injection of bupivacaine into the pericardium. 148 30

We studied the effects of cardiac hypothermia on myocardial oxygen consumption of a fibrillating ventricle and evaluated whether myocardial oxygen consumption of a fibrillating ventricle in hypothermia can be accounted for by new mechanical indexes: equivalent pressure-volume area and equivalent heart rate in the isolated cross-circulated canine heart preparation. Equivalent pressure-volume area is the area that is surrounded by a horizontal pressure-volume line at the pressure of a fibrillating ventricle and the end-systolic and end-diastolic pressure-volume relations in the beating state in the pressure-volume diagram. Equivalent pressure-volume area is an analog of the pressure-volume area of a beating heart and has been proposed to be a measure of the total mechanical energy of a fibrillating ventricle. Equivalent heart rate was calculated from myocardial oxygen consumption per minute in both beating and fibrillating states under unloaded conditions as an estimate of the frequency of contractions of individual myocytes on the assumption that individual myocytes during ventricular fibrillation have the same contractility as that in the beating state. We estimated myocardial oxygen consumption per minute of the fibrillating ventricle at various ventricular volumes as a function of both equivalent pressure-volume area and equivalent heart rate. The myocardial oxygen consumption-equivalent pressure-volume area relation during ventricular fibrillation in hypothermia was highly linear, with a correlation coefficient of 0.90 (mean). The relation between estimated and directly measured myocardial oxygen consumption values of a fibrillating ventricle in hypothermia was highly linear (r = 0.98), and the regression line (y = 0.80x + 0.48) was close to the identity line in the working range. Therefore we conclude that equivalent pressure-volume area is the primary determinant of myocardial oxygen consumption during ventricular fibrillation in hypothermia, and myocardial oxygen consumption of a fibrillating ventricle in hypothermia can be accounted for by the combination of equivalent pressure-volume area and equivalent heart rate as in normothermia.
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PMID:Myocardial oxygen consumption of fibrillating ventricle in hypothermia. Successful account by new mechanical indexes--equivalent pressure-volume area and equivalent heart rate. 149 98

We have proposed a new mechanical index, equivalent pressure-volume area (ePVA), as a measure of the total mechanical energy of a fibrillating ventricle. ePVA is an analogue of the pressure-volume area (PVA) of a contracting ventricle and the specific area surrounded by the horizontal pressure-volume line at the pressure of ventricular fibrillation (VF) and the end-systolic and end-diastolic pressure-volume relations in the beating state in the pressure-volume diagram. In the isolated, cross-circulated heart preparation, we obtained myocardial oxygen consumption (VO2) during VF and ePVA at various left ventricular volumes in the control, epinephrine, propranolol and hypothermia runs. ePVA was highly linearly correlated with VO2 in all runs (r = 0.95, 0.98, 0.96 and 0.90, respectively). We also determined equivalent heart rate (eHR) as an estimate of the contraction frequency of individual myocytes in a fibrillating ventricle from mechanically unloaded VO2 in beating and fibrillating states. Using both ePVA and eHR, VO2 during VF was estimated and correlated with directly measured VO2. Estimated VO2 almost agreed with measured VO2 in all runs. We conclude that ePVA is a primary determinant of VO2 during VF, and that VO2 of a fibrillating ventricle can be reasonably accounted for by the combination of ePVA and eHR. This paper is a review of our previous studies on the energetics of a fibrillating ventricle.
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PMID:Energetics of the fibrillating ventricle. 151 Aug 88

Difficulties persist in providing optimum myocardial protection to neonatal hearts undergoing congenital cardiac repair. Controversy on actual ischemic sensitivity of neonatal hearts compared to adult hearts may depend on species, age selected, and conditions of the experimental protocol. In 1985, our laboratory began to investigate this area using the time to ischemic contracture (TIC) model popularized by Hearse and Wechsler and reported that neonates developed TIC in a significantly shorter time than adult hearts. The neonatal heart had rapid lactate accumulation and early rapid decline in glycogen that was not sustained. This led to ATP decline and triggered TIC. The adult heart had a more gradual lactate accumulation with complete glycogen utilization. As a result ATP stores were maintained longer, which prolonged TIC. Neonatal hearts demonstrated sensitivity to alterations in extracellular calcium and only minimal additional detrimental effects of ventricular fibrillation (VF) on TIC. More complete glycogen utilization and a greater tolerance to ischemia was noted in the neonates when constant washout was provided by removing tissue metabolites (Lactate). In neonates moderate hypothermia (25 degrees C) and deep hypothermia of varying levels (19 degrees C, 12 degrees C) demonstrated that lactate accumulation was significantly less than normothermia and ATP decline was slowed. A subgroup of hearts had 40%-50% lower ATP stores before ischemia and significantly shorter TIC. These "at risk" hearts do not have the same safe time for surgical repair. Further developments will result in improved outcomes for this young patient population.
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PMID:Age-related differences in myocardial metabolism affects response to ischemia. Age in heart tolerance to ischemia. 152

Ventricular fibrillation is the mechanism of death in a number of catastrophic events related to the environment. In particular, electrical shock, organophosphate poisoning, and hypothermia are known to give rise to ventricular fibrillation either directly or by causing unstable situations in which fibrillation may be readily provoked. This article reviews these mechanisms of ventricular fibrillation and aspects of treatment unique to environmental hazards.
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PMID:Ventricular dysrhythmia secondary to select environmental hazards. 155 66

We report the case of a 59-year-old woman suffering from profound accidental hypothermia promoted by intoxication with codeine, sedatives, and a beta-blocking agent ingested in a suicidal attempt. Treatment was further complicated by ventricular fibrillation and asystole that was refractory to therapeutic interventions. The comatose patient (Glasgow score 3) was found outdoors in rainy weather--environmental temperature approximately 10 degrees C (50 degrees F)--by children. The skin was rosy when the emergency team arrived. The respiratory rate was low and the ECG showed sinus rhythm with a heart rate of 28/min. No arterial pulsations were detectable, even at the carotid and femoral sites. Because catecholamine therapy failed to increase the heart rate, the patient was suspected to be profoundly hypothermic. After confirming core hypothermia with a rectal temperature of 25 degrees C (77 degrees F) at the initial receiving hospital, transfer to an institution with cardiac surgery facilities was initiated. During this transport and after arrival, ventricular fibrillation occurred at decreasing intervals followed by asystole, which was refractory to large doses of epinephrine. The patient was transferred to the operating room under continuous resuscitation maneuvers and cardiopulmonary bypass was instituted via the femoral vessels. After 110 min of extracorporeal circulation (ECC, flow 4.5 l/min) normothermia was achieved and the asystole reverted spontaneously to sinus rhythm. The patient's course was subsequently complicated by worsening pulmonary gas exchange with signs of pulmonary edema on X-ray films and cardiac failure, which was treated successfully with epinephrine and dopamine. No neurological deficits were detectable after consciousness had returned.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Successful therapy of a cardiac arrest during accidental hypothermia using extracorporeal circulation]. 156 99


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