Effect of the 30 degree lateral recumbent position on pulmonary artery and pulmonary artery wedge pressures in critically ill adult cardiac surgery patients.

BACKGROUND: Despite demonstrated benefits of lateral positioning, critically ill patients may require prolonged supine positioning to obtain reproducible hemodynamic measurements. OBJECTIVES: TO determine the effect of 30 degree right and left lateral positions on pulmonary artery and pulmonary artery wedge pressures after cardiac surgery in critically ill adult patients. METHODS: An experimental repeated-measures design was used to study 35 patients with stable hemodynamics after cardiac surgery. Subjects were randomly assigned to 1 of 2 position sequences. Pulmonary artery and pulmonary artery wedge pressures were measured in each position. RESULTS: Measurements obtained from patients in the 30 degree left lateral position differed significantly (all Ps < .05) from measurements obtained from patients in the supine position for pulmonary artery systolic, end-diastolic, and mean pressures. Pulmonary artery wedge pressures did not differ significantly; however, data were available from only 17 subjects. The largest mean difference in pressures between the 2 positions was 2.0 +/- 2.1 mm Hg for pulmonary artery systolic pressures, whereas maximum differences for end-diastolic and pulmonary artery wedge pressures were 1.4 +/- 2.7 mm Hg and 1.6 +/- 2.4 mm Hg, respectively. Clinically significant position-related changes in pressure occurred in 12 (2.1%) of 581 pressure pairs. Clinically significant changes occurred in end-diastolic pressure in 2 subjects and in pulmonary artery wedge pressure in 1 subject. CONCLUSIONS: In patients with stable hemodynamics during the first 12 to 24 hours after cardiac surgery, measurements of pulmonary artery and pulmonary artery wedge pressures obtained in the 30 degree lateral and supine positions are clinically interchangeable.

Epidural anesthesia and the thermoregulatory responses to hyperthermia--preliminary observations in volunteer subjects.

BACKGROUND: Clinical reports associate the use of epidural anesthesia with an increase in core temperature in women in labor. We tested the hypothesis that epidural anesthesia alters thermoregulatory responses to hyperthermia in human volunteers. METHODS: Each of four volunteers were studied on two days: Control and Anesthesia. On the Control day, the subject was warmed via the skin, and the core (esophageal) temperature threshold for sweating (detected on the forehead) was determined. The subject was then cooled until sweating stopped. The subject was warmed again, and a second sweating threshold was determined. The difference between the first and second sweating thresholds was noted. On the Anesthesia day, two sequential sweating threshold measurements were obtained in a similar fashion; however, a mid-thoracic level of epidural anesthesia was established before the second sweating threshold measurement. The first and second sweating threshold differences were compared between the two study days. The presence or absence of sweating on the thigh was noted during all four warming periods. RESULTS: Average skin temperatures were similar (about 37 degrees C) during all four sweating threshold measurements. On the Control day, the second sweating threshold value was always slightly less than the first (average difference (mean+/-SD): -0.18+/-0.14 degrees C). In contrast, on the Anesthesia day, the second sweating threshold value (determined with an epidural block) was always greater than the first (average difference: +0.37+/-0.16 degrees C). Epidural anesthesia, therefore, increased the sweating threshold by 0.55+/-0.27 degrees C. Epidural anesthesia blocked sweating in the thigh in two of the subjects. CONCLUSIONS: An epidural block alters the thermoregulatory responses to warming by increasing the threshold for thermoregulatory sweating and, in some cases, preventing leg sweating.

Sleep deprivation alters body temperature dynamics to mild cooling and heating not sweating threshold in women.

Sleep deprivation alters thermoregulatory responses. We used control of skin temperature to produce mild thermal challenge, both cool (32 degrees C) and warm (38 degrees C), and recorded esophageal and rectal temperatures, sweat rate and forearm blood flow in six healthy young women at rest. We discovered that after one night of sleep deprivation (1) both mean esophageal and rectal temperatures were reduced, (2) the mean threshold for sweating was not altered, and (3) there was no direct indication that skin blood flow was set at different levels with skin temperature neutral or cool. Peripheral vasodilation was attenuated when skin temperature was held at 38 degrees C. Following this period of mild hyperthermia, esophageal and rectal temperatures decreased much more rapidly in sleep-deprived subjects when skin temperature was cooled and held constant at 32 degrees C. We conclude that sleep-deprived women lose heat rapidly in response to a mild cooling stimulus. Sleep-deprived humans may be more vulnerable to heat loss with reduced ability to warm even at temperatures thought to be associated with thermal comfort.

Circadian temperature and cortisol rhythms during a constant routine are phase-delayed in hypersomnic winter depression.

Circadian temperature, cortisol, and thyroid-stimulating hormone (TSH) rhythms during a constant routine were assessed in 6 female controls and 6 female patients with hypersomnic winter depression (seasonal affective disorder, SAD) before and after morning bright light treatment. After sleep was standardized for 6 days, the subjects were sleep-deprived and at bed rest for 27 hours while rectal temperature, cortisol, and TSH levels were assessed. The minimum of the fitted rectal temperature rhythm was phase-delayed in the SAD group compared to the controls 5:42 AM vs. 3:16 AM (p < .005); with bright light treatment, the minimum advanced from 5:42 AM to 3:36 AM (p = .06). The minimum of the cortisol rhythm was phase-delayed in the SAD group compared to the control group, 12:11 AM vs. 10:03 PM (P < .05); with bright light treatment, the minimum advanced from 12:11 AM to 10:38 PM (P = .06) [corrected]. The acrophase of the TSH rhythm was not significantly phase-delayed in SAD subjects compared to control, though the trend appeared to be toward a phase-delay (p = .07). After bright light therapy, the TSH acrophase was not significantly different in the SAD subjects; the trend was a phase-advance (p = .09). Overall, the data suggest that circadian rhythms are phase-delayed relative to sleep in SAD patients and that morning bright light phase-advances those rhythms.

Effect of facial cooling on tympanic temperature.

BACKGROUND: In clinical practice, tympanic temperature is used as an estimate of body temperature. Theoretically, temperature recorded directly from the tympanum reflects the temperature of arterial blood circulating to the brain. However, some studies do not support this connection. Ear-based thermometers in clinical use, commonly called tympanic thermometers, detect heat emission from the aural canal and tympanum. Dissociation of core body temperature and tympanic temperature would suggest that factors other than arterial blood perfusion affect tympanic temperature. METHODS: In a controlled laboratory experiment with four adult volunteers, esophageal and tympanic temperatures were recorded repeatedly at 2-minute intervals during whole-body heating and cooling. Facial cooling, produced by a small electrical fan, was used in three subjects. RESULTS: The gradient between tympanic and esophageal temperature was inconsistent across subjects, with tympanic temperature both higher and lower than esophageal temperature. Correlations between esophageal and tympanic temperature varied widely across subjects. Fanning the face produced a decrease in tympanic temperature without an accompanying decline in esophageal temperature. CONCLUSIONS: Facial cooling in the form of fanning altered the relationship between tympanic and esophageal temperature. This result suggests the possible lowering of tympanic temperature by cooled facial venous blood flow. Use of tympanic temperature in circumstances in which facial temperature may be different from that of other regions of the body deserves further study.

Control of skin blood flow in the neutral zone of human body temperature regulation.

In humans, matching of heat loss and heat production in the "neutral" zone, defined operationally in terms of a range of skin temperatures (Tsk), is accomplished by regulation of skin blood flow (SkBF). Our studies were designed to reveal the characteristics of control of SkBF [from measurements of forearm blood flow (FBF)] in this zone. We controlled the temperature of water sprayed on most of the body of supine men and women at 33 or 35 degrees C in a square-wave pattern (15 min at each temperature) or a step pattern (60 min at 33 degrees C separated by short periods at 35 degrees C). FBF followed Tsk (0.5 ml.min-1.degrees C-1). Esophageal temperature changed approximately 0.11 degrees C with each 2 degrees C change in Tsk, falling with Tsk increase and vice versa. Little influence on FBF, < 0.1 ml.min-1.100 ml-1. degrees C-1, was observed when only the forearm was sprayed with 33 and 35 degrees C water. We conclude that SkBF control in the 33-35 degree C range of Tsk is dominated by the feedforward reflex influence of Tsk on SkBF. The reflex response overcompensates for the effect of Tsk on thermal balance in the neutral zone, so that equilibrium core temperature has an inverse relationship to Tsk.

Reproducibility of core temperature threshold for sweating onset in humans.

The control of sweating in humans has been described quantitatively in terms of skin and core temperatures (Tsk and Tcore, respectively). However, the precision with which features of the relationship between sweat rate and Tcore at a given Tsk can be reproduced in the short term is not known. We focused on the threshold Tcore. We held Tsk at 38 degrees C until sweating began for two periods separated by a period of cooling with Tsk at 32 degrees C in six men and three women. The esophageal temperature (Tes) at which sweating began was invariably lower in the second period of heating (average difference 0.09 degree C; maximum 0.17 degree C). Also, the rate of rise in Tes was invariably higher (average 148%) during the second period of heating. Thus, although a threshold cannot be reproduced within the error of Tes measurement, the consistency and small magnitude of the downward shift recommend our protocol as a practical method for evaluating other influences on thermoregulation, provided that the effects are big enough to be seen against a background of an expected small decrease. From the fundamental point of view, the consistency of the downward displacement has provocative implications, e.g., the rate of change in Tcore influences sweating or thermosensitive units in slow-responding thermal compartments contribute to the Tcore input signal.

Shivering following cardiac surgery: predictive factors, consequences, and characteristics.

BACKGROUND: Shivering is common after cardiac surgery and may evoke harmful hemodynamic changes. Neither those changes nor factors increasing probability of shivering are well defined. OBJECTIVES: (1) To identify factors linked with risk of shivering by comparing age, weight, body surface area, gender, intraoperative details, anesthetics, postoperative temperatures, hemodynamics, and therapeutics in shivering vs nonshivering patients. (2) To describe temperatures, hemodynamics, therapeutics, myocardial oxygen consumption correlates (rate-pressure product, heart rate, systemic vascular resistance) in shivering and nonshivering groups, and shivering and nonshivering periods. (3) To characterize the electromyogram to determine whether the tremor is cold-induced. METHODS: A descriptive design with a time series component was used to study a convenience sample of 10 shivering and 10 nonshivering adults for 4 hours during early recovery from cardiac surgery. Pulmonary artery and skin (facial, calf, trunk) temperature were measured every 60 seconds; heart rate and arterial pressure, every 15 minutes; cardiac output, 3 times. Electromyogram was recorded intermittently. Medications and treatments were noted. RESULTS: Lower skin temperature was significantly related to shivering risk. Heart rate was significantly higher initially in shiverers and remained higher by 13.6 beats per minute. Significantly more nitroprusside was used to control arterial pressure before than after shivering. No significant differences were noted between groups in core temperature, age, weight, body surface area, anesthesia type, intraoperative temperature; or surgery, circulatory bypass, or cardiac cross-clamp duration. The electromyogram pattern during shivering was typical of that produced by cold. CONCLUSIONS: These results suggest that true shivering occurs after cardiac surgery. Skin, but not core, temperature and elevated heart rate predict shivering. Shivering may be more likely in hemodynamically unstable patients.

Maximal skin blood flow is decreased in elderly men.

When subjected to total body heating and exercise, skin blood flow does not increase as much in elderly as in young subjects. It is not known whether this age-related decline is due to the autonomic dysfunction that develops in the elderly or to changes at the level of the blood vessels of the skin. We used local heating of the forearm to quantify the intrinsic ability of the cutaneous vasculature to dilate in seven young men (avg age 31 yr) and seven elderly men (avg age 71 yr). A water spray was used to maintain a neutral skin temperature of 32-35 degrees C for > 10 min, followed by 60 min of a 42 degrees C skin temperature to induce maximal skin blood flow. Forearm blood flow was measured by venous occlusion plethysmography with a mercury-in-Silastic circumference gauge. At the neutral skin temperature, forearm blood flows in the elderly subjects were comparable to those in the young subjects: 3.0 +/- 0.5 vs. 2.8 +/- 1.0 ml.min-1 x 100 ml-1. During the last 10 min of heating, however, blood flows were much lower in the elderly than in the young subjects: 11.1 +/- 2.7 vs. 19.9 +/- 5.2 ml.min-1 x 100 ml-1 (P = 0.002). We conclude that aging results in a reduction of the maximal conductance of the cutaneous vasculature.

Reproducibility of the vascular response to heating in human skin.

Blood flow in human skin increases enormously in response to direct heating. If local skin temperature is held above 42 degrees C, blood flow eventually stabilizes at a level beyond which other influences, barring change in blood pressure, can produce no further increase. If this maximal level is a reproducible characteristic of an individual's cutaneous vasculature, it could be useful in comparing individuals; for example, in their response to hyperthermia. Our experiments were carried out to discover whether the maximal response of the vasculature of the skin of the forearm can be reproduced within reasonable limits and, also, to clarify the time course of the response. We used water sprayed over the surface of the forearms of 10 subjects to hold skin temperature above 42 degrees C for 60 min. During the last 10 min of heating, forearm blood flow (via venous occlusion plethysmography) was stable, at a level ranging from 16 to 38 ml.min-1.100 ml-1. This level, normalized to a blood pressure of 100 mmHg, was reproduced in a given individual on four or five occasions, with an average coefficient of variation of 10%. The response was 77 +/- 11% (SD) complete after 20 min of heating. Elapsed time at 90% of the final value was 35 +/- 9 (SD) min. We conclude that the maximal forearm blood flow response to local heating is a reproducible characteristic of the cutaneous vasculature with potential utility in the scaling of responses between and within individuals.

Specialized brain cooling in humans?

Humans, compared to other species, have exceptional capability for dissipation of heat from the entire skin surface. We can secrete more than two liters per hour of sweat, indefinitely. The corresponding potential for evaporative cooling is near a thousand watts, sufficient to compensate for the extreme high levels of heat production during exercise. Also, the blood vessels of our skin have exceptional capability to dilate and deliver heat to the body surface. These are our special adaptations for thermal stress. They allow prolonged heavy exercise with modest elevations in the temperature of the fluid that cools all the internal organs, not just the brain-arterial blood. The vascular architecture of the human head is radically different from that of animals that exhibit SBC. These species have special adaptations that reflect their dependence on respiratory evaporation, particularly the limitation imposed on capability to dispose of heat produced during exercise. The increase in blood temperature in an intense sprint would heat the well-perfused brain rapidly. But the heat exchange over the large surface area of contact between a venous plexus cooled by respiratory evaporation and the meshwork of arterial vessels in the carotid rete precools blood bound for the brain. Specialized cooling of the brain (SBC) has not been demonstrated by direct measurements in humans. Changes in tympanic temperature (Tty) are taken as evidence for SBC. This continues an unfortunate tradition of exaggeration of the significance of Tty. In the only direct measurements available, brain temperature was unaffected by fanning the face although Tty did fall. What may appear to be a remnant of the carotid rete heat exchanger in humans is the intimate association between a short segment of the internal carotid artery and the plexus of veins in the cavernous sinus. Fortunately, the brain need not rely for its cooling on countercurrent heat exchange across this small surface area of contact. In humans, SBC stands for skin: the body cooler--we use our entire skin surface for heat dissipation.

Effects of dehydration on thermoregulatory responses of horses during low-intensity exercise.

Effects of dehydration on thermoregulatory and metabolic responses were studied in six horses during 40 min of exercise eliciting approximately 40% of maximal O2 consumption and for 30 min after exercise. Horses were exercised while euhydrated (C), 4 h after administration of furosemide (FDH; 1.0 mg/kg i.v.) to induce isotonic dehydration, and after 30 h without water (DDH) to induce hypertonic dehydration. Cardiac output was significantly lower in FDH (144.1 +/- 8.0 l/min) and in DDH (156.6 +/- 6.9 l/min) than in C (173.1 +/- 6.2 l/min) after 30 min of exercise. When DDH, FDH, and C values were compared, dehydration resulted in higher temperatures in the middle gluteal muscle (41.9 +/- 0.3, 41.1 +/- 0.2, and 40.6 +/- 0.2 degrees C, respectively) and pulmonary artery (40.8 +/- 0.3, 40.1 +/- 0.2, and 39.7 +/- 0.2 degrees C, respectively). Temperatures in the superficial thoracic vein and subcutaneous sites on the neck and back and peak sweating rates on the neck and back were not significantly different in DDH and C. In view of higher core temperatures during exercise after dehydration and decrease in cardiac output without concomitant increases in peripheral temperatures or reduced sweating rates, we conclude that the impairment of thermoregulation was primarily due to decreased transfer of heat from core to periphery.

Dim light melatonin onset and circadian temperature during a constant routine in hypersomnic winter depression.

The onset of melatonin secretion under dim light conditions (DLMO) and the circadian temperature rhythm during a constant routine were assessed in 6 female controls and 6 female patients with winter depression (seasonal affective disorder, SAD) before and after bright light treatment. After sleep was standardized for 6 days, the subjects were sleep-deprived and at bedrest for 27 h while core temperature and evening melatonin levels were determined. The DLMO of the SAD patients was phase-delayed compared with controls (2310 vs 2138); with bright light treatment, the DLMO advanced (2310 to 2135). The minimum of the fitted rectal temperature rhythm was phase-delayed in the SAD group compared with the controls (0542 vs 0316); with bright light treatment, the minimum advanced (0542 vs 0336).