Serum-Enzymes in Relation to Electrocardiographic Changes in Accidental Hypothermia

Serum Enzyme Levels During Experimental Hypothermia in Man

“…It has been found that factors such as the degree of respiratory depression, hypotension and acidosis are the best predictors of enzyme levels, rather than the duration and depth of hypothermia [Maclean et al, 1968]. Some of these factors would lead directly to a lack of myocardial glucose and oxygen.…”

“…This response is also seen in human patients in hypothermia artificially induced for surgical procedures [Rehn, Kohnlein and Brintzinger, 1961;Atanasov, 1965;Kingsley, 1966] and in accidental hypothermia [Duguid, Simpson and Stowers, 1961;Prescott, Peard and Wallace, 1962;Maclean, Griffiths and Emslie-Smith, 1968;Maclean, Murison and Griffiths, 1974]. The enzyme elevations probably indicate skeletal-and cardiac-muscle damage [Maclean et al, 1968] and attempts have been made to correlate them with electrocardiogram [ECG] changes occurring in hypothermia [Maclean et al, 1968]. Anaesthetized and paralysed patients, who do not shiver, respornd to hypothermia with cardiac slowing, an increase in PR, QT and QTc [QT/RR] intervals, the appearance of a J wave, manifest in some leads as 'ledging' of the base of the QRS complex, and flattening or inversion of the T wave [Biorck and Johansson, 1955;Emslie-Smith, 1956;1958; Emslie-Smith, Sladden and Stirling, 1959;Hockaday, 1972].…”

“…Alterations of rhythm also occur; particularly ventricular extrasystoles [Keatinge and Evans, 1961;Keatinge, 1969], atrial fibrillation [Keatinge 1969] and ventricular fibrillation [Golden, 1973]. The terminal event in hypothermia is almost certainly cardiac but enzyme elevations are poor predictors of mortality [Maclean et al, 1968] and, in those patients coming to autopsy, a characteristic pathology cannot be demonstrated [Duguid et al, 1961;Prescott et al, 1962;Maclean et al, 1968;Mant, 1964]. It is therefore likely that ultrastructural damage is involved and it has been suggested that enzyme release may be due to Marcus and Edwards increased membrane permeability [Blair et al, 1961] or to mitochondrial disruption [Kingsley, 1966].…”

Creatine Kinase and the Diagnosis of Myocardial Infarction

“…Whatever the cause, most patients with hypothermia have a raised serum CK [69]. The presence of a normal serum CK-MB should exclude coincident myocardial infarction, but CK-MB has been reported to increase in such patients [70]; so the interpretation of a raised value may not always be easy.…”

Serum Enolase and Pyruvate Kinase Activities in the Diagnosis of Myocardial Infarction

“…This group comprised a random series of patients admitted to the Royal Hospital of Sheffield, excluding patients with possible MI. The total number of patients was 108 and they were divided into the following disease categories: gastrointes tinal (19); neurological (10); haematological (5); endocrine (12); renal (18); liver (18), and other diseases (26). This group had serum enolase determinations performed on a similar basis to the CCU patients, with the object of assessing the specificity of enolase for IHD; this was prompted by results obtained in the latter group.…”