Biomedical subjects
W R Keatinge
Publications and source records attributed to W R Keatinge.
Hypothermia: dead or alive?
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Factors associated with hypothermia in patients admitted to a group of inner city hospitals.
In a case-control study of factors contributing to hypothermia all fourteen patients (mean age 80 years) admitted to hospital with hypothermia after being found ill indoors also had some other serious illness. They were more likely than control patients to have been alone when taken ill (93 vs 39% of controls), to live alone (86 vs 43%), and to have been found on the floor (79 vs 14%). They were less likely to have been wearing more than indoor clothing (0 vs 50%), or to have had heating on when found (50 vs 89%), but 93% of patients in both groups had heating available. Healthy young adult volunteers who lay immobile on the ground in air at 5 degrees C lightly clothed cooled progressively by 0.57 degrees C (SD 0.32) (rectal T degrees) in 90 min despite doubling of metabolic rate. With better insulation in bed, core temperature stabilised within 90 min, and when they were in an armchair it fell slowly, with no increase in metabolic rate in either case. The findings suggest that hypothermia indoors resulted largely from collapse due to illness when the patient was alone lightly clothed and not in bed. Eight hypothermic patients found outside (in December and January) were younger (mean age 60 years) than the fourteen found indoors; six of these were chronic alcoholics or acutely intoxicated, and six lacked, or had wandered from, a fixed home.
Changes in seasonal mortalities with improvement in home heating in England and Wales from 1964 to 1984.
Changes in summer (July-September) and winter (January-March) mortalities of people aged 70-74 in England and Wales from 1964 to 1984 were compared with possible causal factors. Summer mortalities were little affected by annual temperature or influenza epidemics and fell from 1972-1975 for all causes, coronary and respiratory causes, while cerebrovascular mortality fell more rapidly from that time. Cigarette consumption also fell from 1972-1975; falling consumptions of total fat from 1970 and saturated fat from 1972-1975 probably also contributed to the fall in arterial deaths, and likewise falls in prescription rates for tranquillisers and sedatives from 1976-1978 to the fall in respiratory deaths. From 1964 to 1984 use of central heating increased from 13% to 69% of households, domestic fuel consumption increased, and excess mortality in winter from respiratory disease declined by 69%, even relative to summer mortality and when adjusted for varying coldness of winters. The improvement was partly explained by a decline in influenza epidemics. By contrast, excess mortalities in winter from coronary and cerebrovascular disease, although rising in some early influenza epidemics, did not fall significantly as home heating improved. These thrombotic deaths together accounted for 56% of the total excess winter mortality by 1984. The findings support other indications that most of the excess mortality from arterial thrombosis in winter in England and Wales is due to brief excursions outdoors rather than to low indoor temperatures.
Effects of carbon dioxide on mental performance.
Although elevated levels of inspired CO2 have been recorded in work situations, little is known about effects of concentrations greater than 6% on mental performance. We have measured the effects of inhaling 0, 4.5, 5.5, 6.5, or 7.5% CO2 for 20 min on normal young adults unhabituated to CO2. Performance of reasoning tasks, such as AB logic problems, was significantly slowed at the higher levels of CO2, with a threshold at end-tidal PCO2 close to 51 Torr. Accuracy of reasoning and short-term memory were not significantly affected. More prolonged studies with inhalation of 6.5% CO2 showed that after the first 10 min ventilation tended to increase, end-tidal PCO2 to fall, and slowing of reasoning to recover, but substantial decrement in performance continued for 80 min, by which time performance virtually stabilized. On return to air breathing, preexposure performance was resumed within 10 min. Also caused by 6.5% CO2 was a significant rise in subjectively assessed irritability and discomfort, with no significant change in alertness or in either registration or recall of long-term memory.
Seasonal mortality among elderly people with unrestricted home heating.
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Exceptional case of survival in cold water.
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Increased platelet and red cell counts, blood viscosity, and plasma cholesterol levels during heat stress, and mortality from coronary and cerebral thrombosis.
Recorded deaths from coronary and cerebral thrombosis rise markedly in heat waves. In a British heat wave with little or no distortion due to air-conditioning, outside temperatures of 34.6 degrees C (maximum) and 20.8 degrees C (minimum) were followed by peak mortalities from coronary and cerebral thrombosis one to two days later. Experimental exposure of volunteers to moving air at 41 degrees C for six hours caused core temperature to rise 0.84 degree C, weight to fall 1.83 kg with sweating despite access to water, heart rate to increase 32 beats per minute, and arterial pressure to fall, particularly on standing. The red blood cell count increased 9 percent, and blood viscosity increased 24 percent, mostly after the first hour. The platelet count rose 18 percent, and the platelet volume fell, mostly in the first hour. The plasma cholesterol level increased 14 percent without a change in distribution among lipoprotein fractions. The changes seem able to explain the increased mortality from arterial thrombosis in hot weather.
Effects of fluctuating skin temperature on thermoregulatory responses in man.
Fluctuations in the skin temperature of volunteers in water, of up to +/- 1.5 degrees C, were induced by circulating water through a tube suit at a fluctuating temperature for 80 min. Fluctuations with a cycle length of 2.5, 5.0 or 10.0 min all slowed the fall in core temperature that otherwise occurred in water at 29 degrees C, and reduced thermal comfort. Metabolic rate increased. Symmetrical fluctuations, or ramp fluctuations with either slow cooling and rapid warming phases or slow warming and rapid cooling phases, were all effective. Similar but less clear effects on core temperature were usually produced by fluctuating skin temperature in water at 25 and 33 degrees C; metabolic rate tended to increase during fluctuation in the 25 degrees C experiments, but not in the 33 degrees C experiments. Stability of the temperature of cutaneous receptors appears to be factor in insidious hypothermia produced by immersion in mildly cool water.
Heat exchanges in wet suits.
Flow of water under foam neoprene wet suits could halve insulation that the suits provided, even at rest in cold water. On the trunk conductance of this flow was approximately 6.6 at rest and 11.4 W . m-2 . C-1 exercising; on the limbs, it was only 3.4 at rest and 5.8 W . m-2 . degrees C-1 exercising; but during vasoconstriction in the cold, skin temperatures on distal parts of limbs were lower than were those of the trunk, allowing adequate metabolic responses. In warm water, minor postural changes and movement made flow under suits much higher, approximately 60 on trunk and 30 W . m-2 . degrees C-1 on limbs, both at rest and at work. These changes in flow allowed for a wide range of water temperatures at which people could stabilize body temperature in any given suit, neither overheating when exercising nor cooling below 35 degrees C when still. Even thin people with 4- or 7- mm suits covering the whole body could stabilize their body temperatures in water near 10 degrees C in spite of cold vasodilatation. Equations to predict limits of water temperature for stability with various suits and fat thicknesses are given.
Effects of raised body temperature on reasoning, memory, and mood.
Volunteers' body core temperatures were raised to 38.80-39.05 degrees C within a few minutes by immersion in water at 41 degrees C. Tests were then made with the subjects insulated and cooling slowly. Control immersions were made in water at 37 degrees C when core temperatures remained at 36.60-37.40 degrees C. Neither memory registration nor recall of memories registered an hour earlier, nor immediate ability to recall digit spans forward or backward was affected by the increase in core temperature. The increase in temperature did not have any significant effect on accuracy of performance of verbal logic problems or of two-digit subtractions. However, the increase in core temperature was associated with a significant increase in the speed of performance of the tests, by 11 and 10%, respectively. The warm immersions also induced a significant decrease in alertness and an increase in irritability as assessed subjectively by the volunteers; control immersions had no such effects.
Action of vasodilator agents on inner and outer muscle of bovine coronary arteries.
Noradrenaline and adrenaline (via beta-receptors), adenosine, and prostacyclin all relaxed inner more than outer muscle in coronary arteries contracted by histamine. In submaximal concentrations, noradrenaline, and usually the other dilator hormones, produced proportionately even greater relaxation of inner than outer muscle. Inner and outer strips contracted by 5-hydroxytryptamine showed similar but smaller differences in response to noradrenaline. Outer strips contracted by methacholine were little affected by noradrenaline, though inorganic nitrite relaxed them.
Progressive symptomless hypothermia in water: possible cause of diving accidents.
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Calcium dependence of potassium efflux induced by noradrenaline in sheep carotid arteries [proceedings].
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Immersion hypothermia--preventable deaths.
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Mechanism of slow discharges of sheep carotid artery.
1. Single and double sucrose-gap methods were used to follow changes in membrane potential and conductance of smooth muscle of sheep carotid arteries. 2. K depolarization induced discharges lasting several seconds in various solutions containing Mn, or Mg, or Ca and procaine, sometimes with no other added cations and with only sulphate or ethanesulphonate as anions. 3. Membrane conductance usually rose substantially above resting level in the early part of these discharges, but fell towards resting level during the later part. 4. Large depolarizing currents caused porportionately less voltage displacement than small currents, and reduced voltage displacements induced by superimposed current pulses, even in Cl and HCO3 free solutions, indicating activation of K conductance by depolarization. 5. When procaine was added, or Ca replaced by Mn or Mg, conductance was lower both at rest and on depolarization, and the increase on depolarization often underwent slow inactivation which it never did in simple Ca containing solutions. 6. The results indicate that a slowly inactivated inward current dependent on Ca, Mn or Mg was largely responsible for the slow discharges, and that procaine, Mn or Mg assisted the discharges by reducing the normal rapid outward-rectifying K conductance and allowing it to inactivate on prolonged depolarization.