Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEART ARREST”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 55 records · Page 3Linked to original sources

Extracellular amino acids as markers of myocardial ischemia during cardioplegic heart arrest.

Extracellular levels of amino acids in the myocardial interstitium are sensitive indicators of myocyte function. Lowered ATP leads to a rapid extracellular appearance of amino acids with a high intra- to extracellular concentration ratio, such as taurine and glutamate. Nitrogen fluxes are reflected by glutamine, while alanine, glycine, serine and leucine are markers of proteolysis. In addition, degradation of membrane phospholipids is reflected by other primary amines, such as phosphoethanolamine. The time course of these changes was determined before, during and after cardioplegic heart arrest. Two regions of the heart were monitored in 20 patients by means of microdialysis sampling. After only 20 min of heart arrest, extracellular taurine, glutamate and phosphoethanolamine increased transiently up to 25 times the basal level. Ten-20 min later, glutamine increased by 6 times. A doubling of alanine, glycine, serine and leucine levels took place 30 min after release of the aortic cross-clamp. After 2 h, all were at levels similar to those recorded 15-30 h later. Levels of taurine and glutamate in the anterior wall of the heart correlated significantly with those of its lateral wall. The response to surgery and heart arrest was studied in a group of patients with ischemic heart disease as well as in another group of patients, who underwent heart surgery for nonischemic reasons. The response of taurine and glutamine was significantly higher for the patients with ischemic heart disease, in spite of a shorter mean time of heart arrest. No sex differences were recorded. High levels of amino acids coincided frequently with clinical events, which were suggestive of ischemia, but were also recorded in a few patients without diagnosed events. We conclude that monitoring of extracellular amino acids is valuable for evaluation and development of cardioprotective strategies.

Adult↗

Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. I. The adequately perfused beating, fibrillating, and arrested heart.

The effects of hypothermia (32 degrees, 28 degrees, and 22 degrees C.) on left ventricular flow distribution (microspheres) and oxygen uptake in adequately perfused, beating, empty, fibrillating, and arrested hearts were studied. Minute left ventricular oxygen uptake fell progressively as myocardial temperature was reduced under all conditions. In beating hearts, however, left ventricular oxygen uptake per beat increased significantly due to the inotropic effect of hypothermia and diastolic compliance fell. Cold fibrillating hearts consumed slightly less oxygen per minute than beating hearts at comparable temperatures as fibrillation became less forceful with hypothermia. Myocardial wall tension, however, was always higher in fibrillating than beating hearts at each level of hypothermia. The lowest myocardial oxygen requirements were always found in arrested hearts (70 to 80 per cent less than either beating empty or fibrillating hearts) at any myocardial temperature. Left ventricular coronary flow remained distributed evenly across the beating heart at all myocardial temperatures and in fibrillating hearts at 28 degrees, and 22 degrees C. Left ventricular flow became redistributed toward the subendocardium in fibrillating hearts at 37 degreegs and 32 degrees C. and in arrested hearts at all myocardial temperatures.

Animals↗

[Heart arrest].

Explore the source record for details and available documents.

Heart Arrest↗

[Metabolic and ultrastructural changes in the myocardium during heart arrest in patients undergoing surgery for ischemic heart disease].

The authors give an account of metabolic changes in the ultrastructure of the myocardium which develop during cardioplegic arrest of the heart muscle by cold during aortocoronary reconstruction operations. Using the technique of arteriovenous differences before myocardial ischemia and after its termination, the assessed differences in arterial blood and blood from the sinus coronarius as regards the blood sugar level, lactate, pyruvate, potassium, phosphorus, unsaturated fatty acids and triglycerides. The results revealed a marked disorder of the carbohydrate and ion metabolism and severe impairment of the ultrastructure of the heart muscle during cardiac arrest.

Adult↗

Duration of preoperative electrocardiographic QRS complex and the incidence of heart arrest after aorto coronary bypass surgery.

Sudden heart arrest (HA) in the early phase after aorto coronary bypass surgery represents a serious event necessitating resuscitation, and for those who survive usually also an extra stay in the coronary care unit. Since such episodes of heart standstill may be related to conduction defects, a study was conducted to determine whether the duration of the QRS complex on the preoperative ECG is a marker for this morbid event. A cohort of 1011 consecutive patients operated on between 1982 and 1986 and followed to January 1st, 1993 were included in the study. Incidence of lethal or non-lethal HA during the first 4 weeks after surgery was considered as the primary endpoint and total mortality as the secondary endpoint. The incidence of HA was 40/1011 = 4%, with the majority of events (60%) being lethal. Independent risk factors of HA using the multivariate logistic model were previous coronary artery bypass surgery, presence of mitral regurgitation, left ventricular ejection fraction and the intraoperative cross-clamp time of aorta. Adjusting for the effect of confounder variables showed that the gradient effect of QRS complex duration on the endpoint HA was still present (p = 0.012). The duration of the QRS complex taken from the preoperative ECG had a gradient effect on the incidence of HA. With a baseline level of QRS <70 ms, the following odds ratios (OR) for HA were found: OR = 1.38 (95% CI 0.60-3.31) for QRS 70-80 ms; OR = 2.27 (95% CI 0.87-5.90) for QRS >90-120 ms; and OR = 3.38 (95% CI 1.06-11.50) for QRS > 120 ms, when adjusting for the risk factors. Cumulative survival at 5 years after surgery was 28+/-7.1% for patients experiencing HA versus 87+/-1.2% for patients free from this event. Our results underline the importance of the QRS complex duration as a preoperative marker for HA after aorta coronary bypass surgery, when adjusting for other risk factors. Although the one-year survival is poor for patients experiencing HA, there is no increase in mortality during the late follow-up.

Coronary Artery Bypass↗

Spectral analysis of small-amplitude electrical activity in the cold potassium-arrested heart.

Recent reports have suggested that small-amplitude electrical activity may persist following the administration of potassium cardioplegia. This report confirms the presence of small-amplitude electrical activity in the potassium-arrested heart and describes a canine model that may be used to measure microvolt plunge-electrode potentials during ischemic arrest. Thirty-one adult mongrel dogs were placed on cardiopulmonary bypass and underwent 90 minutes of ischemic arrest. The heart was arrested with 10 ml per kilogram of body weight of crystalloid cardioplegia (20 mEq of KCl/L) at 4 degrees C. Core temperature was maintained at 26 degrees C and myocardial temperature, within a range of 8 degrees to 10 degrees C with topical ice-slush saline solution. Cardioplegic solution, 10 ml/kg, was reinfused every 30 minutes during the 90 minutes of ischemia. Electrical activity and transmural temperature were continuously monitored over the anterior surface of the left ventricle with specially designed plunge electrodes. Visual electrical and mechanical activity ceased in each animal after the infusion of cardioplegic solution, and was associated with an isoelectric electrocardiogram. However, microvolt (10(-6)V) small-amplitude electrical activity was recorded at a myocardial temperature of 10 degrees C in each animal during ischemic arrest, and the activity from 6 animals was stored on magnetic tape. Spectral analysis of electrical activity during cardioplegic arrest indicated that the fundamental frequency of small-amplitude electrical activity was in the range of 3.25 Hz. These data confirm the presence of small-amplitude electrical activity in the cardioplegia-arrested heart at 10 degrees C.

Animals↗

Effect of small-amplitude electrical activity on myocardial preservation in the cold potassium-arrested heart.

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.

Adenosine Triphosphate↗

Comparison of the distribution of intramyocardial pressure across the canine left ventricular wall in the beating heart during diastole and in the arrested heart. Evidence of epicardial muscle tone during diastole.

Computations of compliance of the left ventricle (LV) during diastole assume passive tissue characteristics. To evaluate this assumption, we measured diastolic LV intramyocardial pressure simultaneously in the subepicardium and subendocardium in 18 open-chest dogs, using 1-mm in diameter micromanometers. Subepicardial pressure, 26 +/- 1 mm Hg (mean +/- SEM) exceeded subendocardial pressure, 14 +/- 1 mm Hg (P less than 0.001), and it exceeded left ventricular end-diastolic pressure (LVEDP) (9 +/- 1 mm Hg) (P less than 0.001). After an infusion of dextran-40 (10 dogs), subepicardial diastolic pressure increased to 42 +/- 4 mm Hg which was higher than diastolic subendocardial pressure, 26 +/- 2 mm Hg (P less than 0.001) and LVEDP, 24 +/- 2 mm Hg (P less than 0.001). Following cardiac arrest (12 dogs) with the intramyocardial probes unchanged in position, LV intracavitary pressure, 9 +/- 1 mm Hg, and subendocardial pressure, 13 +/- 3 mm Hg, did not differ significantly from the pressures in the beating heart. Subepicardial pressure, 9 +/- 1 mm Hg, was lower than in the beating heart (P less than 0.001). Following distention of the arrested LV (12 dogs), subepicardial pressure, 31 +/- 7 mm Hg, was lower than both subendocardial pressure, 58 +/- 12 mm Hg (P less than 0.001) and LV intracavitary pressure, 54 +/- 11 mm Hg (P less than 0.001). These observations indicate that tone is maintained by the subepicardium during diastole. Furthermore, the LV wall does not appear to behave as a passive shell during ventricular filling.

Animals↗