Temperature monitoring and perioperative thermoregulation

Abstract

Most clinically available thermometers accurately report the temperature of whatever tissue is being measured. The difficulty is that no reliably core-temperature-measuring sites are completely noninvasive and easy to use-especially in patients not undergoing general anesthesia. Nonetheless, temperature can be reliably measured in most patients. Body temperature should be measured in patients undergoing general anesthesia exceeding 30 min in duration and in patients undergoing major operations during neuraxial anesthesia. Core body temperature is normally tightly regulated. All general anesthetics produce a profound dose-dependent reduction in the core temperature, triggering cold defenses, including arteriovenous shunt vasoconstriction and shivering. Anesthetic-induced impairment of normal thermoregulatory control, with the resulting core-to-peripheral redistribution of body heat, is the primary cause of hypothermia in most patients. Neuraxial anesthesia also impairs thermoregulatory control, although to a lesser extent than does general anesthesia. Prolonged epidural analgesia is associated with hyperthermia whose cause remains unknown.

Figures

Figure 1

The differences between the tympanic membrane thermocouple (Mon-a-therm) and aural canal temperature measured by a Quickthermo infrared thermometer. The mean difference between core temperature and the infrared monitor was 1.1°C. Three other infrared monitors were evaluated in this study, but none proved sufficiently accurate for clinical use. SD = standard deviation. Reprinted with permission.

Figure 2

Bland and Altman comparison of distal esophageal temperature and “deep sternal” temperatures. The vertical axis is the difference between esophageal and deep sternal temperatures. Mean temperature on the horizontal axis refers to the average between esophageal and deep sternal temperatures at each measurement time. The mean offset was 0.1°C, with a standard deviations of 0.3°C. This accuracy is perfectly adequate for clinical use. Reprinted with permission.

Figure 3

All patients were divided by anesthesiologists’ impression of thermal status. There was no difference in the number of hypothermic (

Figure 4

Tympanic membrane (core) minus forehead skin-surface temperature difference during a thermoneutral control period was 0.1 ± 0.3°C. This difference did not change significantly during vasodilation associated with sweating or vasoconstriction associated with shivering. Results are presented as mean ± SD. Reprinted with permission.

Figure 5

The difference between tympanic membrane (core) and forehead skin-surface temperatures (ΔT) at ambient temperatures (Tambient) between 18 and 26°C. The data were fit to a second-order regression: ΔT = −0.58 + 0.29(Tambient) − 0.01(Tambient)2, r2 = 0.999. Each 1°C change in ambient temperature, starting near 22°C, thus altered skin temperature ≈0.16°C. Results are presented as mean ± SD. Horizontal error bars (variation in ambient temperatures) are not displayed because they were smaller than the size of the markers. Reprinted with permission.

Figure 6

Axillary and esophageal temperatures correlated well during acute malignant hyperthermia in swine, but forehead and neck skin temperatures did not. Rectal temperature also failed to promptly identify onset of malignant hyperthermia. Elapsed time zero indicates an end-tidal PCO2 = 70 mmHg. These data indicate that forehead and neck skin-surface temperatures will not adequately confirm other clinical signs of malignant hyperthermia. Valid core temperature monitoring sites include the distal esophagus, pulmonary artery, nasopharynx, and tympanic membrane. Except during cardiopulmonary bypass, body temperature also can be measured in the mouth, axilla, and bladder. Data presented as means ± SDs. Modified and reprinted with permission.

Figure 7

Linear regression including 913 data pairs from 44 subjects who participated in four heat-balance studies. Mean-body temperature (MBT) was estimated from core (Tcore) and mean-skin (TSkin) temperature and compared to directly measured values. There was a remarkably good relationship between measured and estimated mean-body temperatures: MBTestimated = 0.94 . MBTMeasured + 2.15, r2 = 0.98. Reprinted with permission.

Figure 8

The sweating rate from the unwarmed site in a single typical male volunteer shows the threshold, gain, and maximum intensity during hyperthermia alone (0%) and at 0.8%, and 1.2% end-tidal isoflurane concentration. The thresholds were markedly increased by anesthesia; in contrast, gains and maximum sweating rates were relatively well preserved. Reprinted with permission.

Figure 9

Individual mean-skin and core temperatures at the vasoconstriction (squares) and shivering (circles) thresholds in the eight volunteers. There was a linear relation between mean skin and core temperatures at the vasoconstriction and shivering thresholds in each volunteer (lines): r2 = 0.98 ± 0.02 for vasoconstriction, and 0.96 ± 0.04 for shivering. Relative contributions of skin and core temperatures varied from subject to subject, but on average skin temperature contributed 21 ± 8% to vasoconstriction, and 18 ± 10% to shivering. Reprinted with permission.

Figure 10

The sweating-to-vasoconstriction interthreshold range at each time of day. Data presented as means ± SDs. Values at 3 AM differed significantly from those at other times. Reprinted with permission.

Figure 11

The major autonomic thermoregulatory response thresholds in volunteers given desflurane, alfentanil, dexmedetomidine, or propofol. All the anesthetics slightly increase the sweating threshold (triggering core temperature), while markedly and synchronously decreasing the vasoconstriction and shivering thresholds. Standard deviation bars smaller than the data markers have been deleted. Reprinted with permission, , , .

Figure 12

Finger blood flow without (open circles) and with (filled squares) desflurane administration. Values were computed relative to the thresholds (finger flow = 1.0 ml/min) in each subject. Flows of exactly 1.0 ml/min are not shown because flows in each individual were averaged over 0.1 or 0.05°C increments; each data point thus includes both higher and lower flows. The horizontal standard deviation bars indicate variability in the thresholds among the volunteers; although errors bars are shown only at a flow near 1.0 ml/min, the same temperature variability applies to each data point. The slopes of the flow vs. core temperature relationships (1.0 to ≈0.15 ml/min) were determined using linear regression. These slopes defined the gain of vasoconstriction with and without desflurane anesthesia. Gain was reduced by a factor of three, from 2.4 to 0.8 ml.min-1.°C-1 (P

Figure 13

The core thermoregulatory threshold in 23 healthy children and infants undergoing abdominal surgery with halothane anesthesia. Differences among the groups are not statistically significant. Results are presented as means ± SDs. Reprinted with permission.

Figure 14

The vasoconstriction threshold during light sevoflrurane anesthesia was significantly less in elderly (35.8 ± 0.3°C, n = 10) than in younger patients (35.0 ± 0.5°C, n = 10) (P < 0.01). Open circles indicate the vasoconstriction threshold in each patient; filled squares the show the mean and standard deviations in each group. Reprinted with permission.

Figure 15

Spinal anesthesia increased the sweating threshold but reduced the thresholds for vasoconstriction and shivering. Consequently, the interthreshold range increased substantially. The vasoconstriction-to-shivering range, however, remained normal during spinal anesthesia. Results are presented as means ± SDs. Reprinted with permission.

Figure 16

The number of dermatomes blocked (sacral segments = 5; lumbar segments = 5; thoracic segments = 12) versus reduction in the shivering threshold (difference between the control shivering threshold and spinal shivering threshold). The shivering threshold was reduced more by extensive spinal blocks than by less extensive ones (Δ threshold = 0.74 − 0.06(dermatomes blocked); r2 = 0.58, P < 0.006). The curved lines indicate the 95% confidence intervals for the slope. Reprinted with permission.

Figure 17

Systemic oxygen consumption without (circles) and with (squares) epidural anesthesia. The horizontal standard deviation bars indicate variability in the thresholds among the volunteers; although errors bars are shown only once in each series, the same temperature variability applies to each data point. The slopes of the oxygen consumption versus core temperature relationships (solid lines) were determined using linear regression. These slopes defined the gain of shivering with and without epidural anesthesia. Gain was reduced 3.7-fold, from −412 ml·min-1·°C−1 (r2 = 0.99) to −112 ml·min-1·°C-1 (r2 = 0.96). Reprinted with permission.

Figure 18

Fifteen patients aged

Figure 19

Changes in tympanic membrane temperatures and thermal comfort (mm on a visual analog scale) following epidural lidocaine injections in 6 volunteers in a cool operating room environment. Epidural injections were given after a 15-min control period. Shivering (not shown) started when tympanic temperature decreased about 0.5°C and continued until core temperature returned to within 0.5°C of control. Thermal comfort increased following epidural injections in each volunteer; maximal comfort occurred at the lowest core temperature. Results presented as means ± SDs. Reprinted with permission.