Hypothermia retards cardiac contraction and prolongs the subphases of the cardiac cycle in varying degrees. Six anaesthetized beagle dogs were catheterized and cooled between ice bags until the aortic blood temperature was 25 degrees C and then rewarmed to normothermia. The speed of relaxation decreased to a half from its value in normothermia as indicated by the time constant of exponential isovolumic ventricular pressure fall and by the change in the negative dp/dt. It is suggested that retardation of relaxation is connected with temperature dependent changes in calcium kinetics. Decrease of cardiac output was mediated mainly by decreased stroke volume indicating sympathetic tone in spite of cold narcosis.
Intravenous administration of warm fluids is used clinically as first aid either alone or as a contributing method, to rewarm hypothermic patients back to normal body temperature. The aim of this study was to determine the effects of an acute volume load in hypothermic conditions on the canine circulatory system. Cardiac catheterization was performed on 18 anaesthetized beagle dogs. Eleven of them were cooled and at a body temperature of 25 degrees C they received 40 ml.kg-1 dextran administered intravenously. The control group received dextran at normal body temperature. During cooling the body from 37 degrees C down to 25 degrees C most of the volume load escaped from the circulation due to extravazation. During rewarming, the opposite effect could be seen and the volume load persisted up to 29 degrees C and signs of cardiac decompensation were observed. According to these results, the intravenous administration of warm fluids to rewarm hypothermic patients should not be used routinely when hypovolaemia is the only result of hypothermia.
Mice enter bouts of daily torpor, drastically reducing metabolic rate, core body temperature (T b), and heart rate (HR), in response to reduced caloric intake. Because central adenosine activation has been shown to induce a torpor-like state in the arctic ground squirrel, and blocking the adenosine-1 (A1) receptor prevents daily torpor, we hypothesized that central activation of the A1 adenosine receptors would induce a bout of natural torpor in mice. To test the hypothesis, mice were subjected to four different hypothermia bouts: natural torpor, forced hypothermia (FH), isoflurane-anesthesia, and an intracerebroventricular injection of the selective A1 receptor agonist N6-cyclohexyladenosine (CHA). All conditions induced profound hypothermia. T b fell more rapidly in the FH, isoflurane-anesthesia, and CHA conditions compared to torpor, while mice treated with CHA recovered at half the rate of torpid mice. FH, isoflurane-anesthesia, and CHA-treated mice exhibited a diminished drop in HR during entry into hypothermia as compared to torpor. Mice in all conditions except CHA shivered while recovering from hypothermia, and only FH mice shivered substantially while entering hypothermia. Circulating lactate during the hypothermic bouts was not significantly different between the CHA and torpor conditions, both of which had lower than baseline lactate levels. Arrhythmias were largely absent in the FH and isoflurane-anesthesia conditions, while skipped beats were observed in natural torpor and periodic extended (>1 s) HR pauses in the CHA condition. Lastly, the hypothermic bouts showed distinct patterns of gene expression, with torpor characterized by elevated hepatic and cardiac Txnip expression and all other hypothermic states characterized by elevated c-Fos and Egr-1 expression. We conclude that CHA-induced hypothermia and natural torpor are largely different physiological states.
Short- and long-term exposures to cold increase blood pressure and may explain the higher wintertime cardiovascular morbidity and mortality. Hypertensive subjects may be more susceptible to adverse cold-related cardiovascular health effects. The aim of our study was to assess the effect of short-term cold exposure on central aortic blood pressure among untreated hypertensive men.
We conducted a population-based recruitment of 41 hypertensive men and a control group of 20 men without hypertension (aged 55-65 years) who underwent whole-body cold exposure (15-minute exposure to temperature -10 °C, wind 3 m/s, winter clothes). Central aortic blood pressure, augmentation index, and subendocardial viability ratio were measured by radial artery applanation tonometry.
Short-term cold exposure increased the central aortic blood pressure similarly both in both hypertensive men, from 130/93 to 162/107 mm Hg (P
Two types of cold exposures were carried out in humans. A. Fourteen subjects were exposed 4-7 times within 2 weeks to the following conditions: ambient temperature was decreased from 28 degrees C to between plus and minus 5 degrees C; the subjects wore a bathing suit and remained in a resting position during the exposure which lasted for 1h. B. Nine conscripts were studied before and after a 10-day exercise, during which they were exposed to moderately cold conditions during day and night. The exercise did not require increased physical activity. In two thirds of the subjects A, metabolic reactions and shivering threshold were shifted to a lower weighted mean body temperature as well as a lower esophageal temperature ("hypothermic" type of adaptation). This modification in the thermoregulatory system was linked with a reduction in thermal discomfort and cold sensation. No change was found in the resting metabolic rate nor was there any indication of the development of non-shivering thermogenesis. Similar modifications were found in 4 of the 9 soldiers (study B). These 4, however, had particularly high shivering thresholds before the 10-day exercise and the values found thereafter were no lower than those found in the remaining five and in the subjects of group A before the cold-exposure regimen.
The effect of water temperature on the outcome of nearly drowned children was studied retrospectively. All patients under 16 years of age, who required admission to the paediatric intensive care unit (PICU) or who died despite life support measures between January 1, 1985 and December 31, 1994 in Southern Finland, were included in the study. The authors created a Near Drowning Severity Index (NDSI) and an age-adjusted NDSIage as tools to evaluate the effect of submersion duration and water temperature on the outcome of nearly drowned children. The predictive performance of the NDSI and the NDSIage were compared with the duration of submersion to predict the outcome. Of the 48 patients 11 were female and 37 were male. Their ages ranged from 0.8 to 15 years and the median was 3.7 years. The submersion time ranged from 0.5 to 90 min and the median time was 6.3 min. The median temperature of water was 16 degrees C (range 0-37 degrees C). The NDSI had a sensitivity of 93.9% and specificity of 90.6% in predicting the outcome after submersion incidents. The inclusion of age (NDSIage) in the formula did not increase predictive performance of the NDSI. With a cut-off value of 10 min, the duration of submersion alone had a sensitivity of 96.6% and specificity of 89.5% in predicting the outcome. In conclusion the effect of a potentially beneficial rapid development of hypothermia by cold water on the outcome of nearly drowned children could not be proved.
The effects of repeated exposure to cold temperature on cognitive performance were examined in 10 male subjects who were exposed to control (25 degrees C) and cold (10 degrees C) conditions on 10 successive days. A cognitive test battery (ANAM-ICE) was administered each day to assess complex and simple cognitive functioning accuracy, efficiency and response time. Rectal (T(rect)) and skin temperatures, thermal sensations, metabolic rate (M) and cardiovascular reactivity were also recorded. With the used cold exposure, inducing cold sensations and discomfort, superficial skin cooling (6-7 degrees C) and a slightly lowered T(rect) (0.4 degrees C) we observed three distinct patterns of cognitive performance: 1) negative, reflected in increased response times and decreased accuracy and efficiency; 2) positive, reflected in decreased response time and increased efficiency; and 3) mixed, reflected in a pattern of increases in both accuracy and response time and decreases in efficiency, and a pattern of decreases in both accuracy and response time. T(rect), thermal sensations, diastolic blood pressure (DBP) and heart rate (HR) were independent predictors of decreased accuracy, but also decreased response time. Cognitive performance efficiency was significantly improved and response times shorter over the 10-d period both under control and cold exposures suggesting a learning effect. However, the changes in cognitive performance over the 10-d period did not differ markedly between control and cold, indicating that the changes in the thermal responses did not improve performance. The results suggest that cold affects cognitive performance negatively through the mechanisms of distraction and both positively and negatively through the mechanism of arousal.