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Results for “HEART ARREST”

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At least 271 records · Page 15Linked to original sources
PubMed1977

Studies of the effects of hypothermia on regional myocardial blood flow and metabolism during cardiopulmonary bypass. V. Profound topical hypothermia during ischemia in arrested hearts.

This study compares the effects of 60 minutes of ischemic arrest with profound topical hypothermia (10 dogs) on myocardial (1) blood flow and distribution (microspheres), (2) metabolism (oxygen and lactate), (3) water content (wet to dry weights), (4) compliance (intraventricular balloon), and (5) performance (isovolumetric function curves) with 180 minutes of cardiopulmonary bypass with the heart in the beating empty state (seven dogs). Studies performed before and 30 minutes after 1 hour of ischemic arrest with profound topical hypothermia showed: (1) total left ventricular blood flow increased 50 per cent but became redistributed away from the subendocardium (endocardial/epicardial flow ratio fell from 1.13 to 0.77,(2) left ventricular oxygen consumption fell 30 per cent while left ventricular oxygen extraction fell from 51 to 29 per cent; (3) lactate extraction fell from 15 to 4 per cent (two dogs produced lactate); (4) left ventricular endocardial (papillary muscle) water content rose 2.4 per cent; (5) left ventricular compliance decreased from 1.68 to 1.01 ml. H2O/mm. Hg (at 25 ml.); (6) left ventricular performance was depressed 49 per cent below control values. In contrast, 3 hours of cardiopulmonary bypass in the beating empty heart produced only minimal changes in these variables.

Animals↗
PubMed2001

[Circular hemorrhagic subendocardial necrosis after heart arrest and resuscitation].

A 19 year old boy, previously healthy suffered a cardiac arrest by getting up. Ten minutes afterwards the general practitioner commenced cardiopulmonary resuscitation, 15 minutes later ventricular fibrillation developed and the emergency physician carried out intubation and repeated defibrillation. During the next few hours a stabilization of the circulatory system was achieved. Five days after the cardiac arrest brain death occurred. The postmortem findings on the heart (only a heart section was performed) showed extensive circular hemorrhagic subendocardial necrosis with initial organization of the left ventricular wall and the septum with a well-preserved subendocardial area. In the right ventricular wall only a few small areas of organization were observed. All lesions were consistent with the cardiac arrest suffered 5 days previously. The morphological changes differ from those of a usual hemorrhagic infarction and of the sequences of a cardiopulmonary resuscitation. The circular subendocardial necroses occur after a cardiac arrest which exceeds the resuscitation time of the heart. They do not respect the area of coronary distribution and their hemorrhagic component develops after successful reanimation within the necrotic myocardium.

Adult↗
PubMed1987

Ischemic heart arrest: nitrogenous metabolism in energy-depleted human myocardium.

Seventeen patients undergoing radical correction of Fallot's tetrad or defects of interventricular septum were investigated. Needle biopsies from the left ventricular apex region were obtained at the 1st min after cross-clamping of the aorta and at the end of cardiac arrest to determine adenosine triphosphate (ATP), glutamate, aspartate, alanine and ammonia. The losses of ATP during clamping period were related to decrease in glutamate. The fall in ATP by more than 20% of the initial level was accompanied by a significant decrease in aspartate, an accumulation of alanine and ammonia in cardiac tissue but did not affect glutamine content. The data obtained prove the participation of specific nitrogenous compounds of human heart, and especially glutamate, in response to energy depletion during ischemia.

Adenosine Triphosphate↗