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*Department of Anesthesiology and Intensive Care Medicine, Donauspital/SMZO; Private practice, Vienna, Austria; Department of Cardiothoracic and Vascular Anesthesia, University of Vienna, Austria; Department of Anesthesiology, University of Louisville, Kentucky; and OUTCOMES RESEARCHTM Institute, Louisville, Kentucky, and ||Ludwig Boltzmann Institute, University of Vienna, Austria
Address correspondence and reprint requests to Daniel I. Sessler, MD, Outcomes Research Institute, 501 E. Broadway Ave., Louisville, KY 40202. Address e-mail to sessler{at}louisville.edu
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Abstract |
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IMPLICATIONS: The threshold for cold-induced vasoconstriction is reduced in the dependent arm, but the gain of vasoconstriction is increased. Consequently, the core temperature triggering intense vasoconstriction was similar in each arm, suggesting that the thermoregulatory system compensates for the hydrostatic effects of the lateral position.
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Introduction |
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An additional factor that may influence thermoregulatory responses is patient position. For example, blood pressure in unanesthetized humans remains unchanged in the lateral position (11) but decreases in the anesthetized individual (12). Furthermore, body temperature is altered by postural shifts in unanesthetized subjects. It is also well established that baroreceptor loading promotes hypothermia by reducing the vasoconstriction threshold (13).
Blood pressure in a dependent arm during anesthesia exceeds that in the upper arm because of hydrostatic forces. It seems likely that increased intraluminal pressure will, at least for a time, maintain vasodilation in the dependent arm even after hypothermia triggers a central thermoregulatory vasoconstrictor response. If so, the threshold and gain of vasoconstriction in the dependent arm would decrease. We therefore tested the hypotheses that the threshold and gain of cold-induced vasoconstriction are reduced in the dependent arm during anesthesia.
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Methods |
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The volunteers fasted 8 h before arriving at the laboratory. To avoid circadian fluctuations, studies were scheduled to start at 9:00 AM. Volunteers were minimally clothed during the protocol; ambient temperature was maintained at 22°C–23°C. An IV catheter was inserted into the left forearm for fluid administration. One liter of lactated Ringer’s solution was given before the induction of anesthesia; during maintenance of anesthesia, fluid was given as necessary to maintain mean arterial blood pressure >60 mm Hg.
General anesthesia was induced by the administration of 3–4 mg/kg propofol and 0.9 mg/kg rocuronium. The trachea was then intubated, and anesthesia was maintained with desflurane, 0.4 minimum alveolar anesthetic concentration in air and oxygen. The lungs were mechanically ventilated to maintain an end-tidal carbon dioxide partial pressure near 35 mm Hg. Additional rocuronium was administered, as necessary, to maintain one or two mechanical twitches in response to supramaximal train-of-four stimulation of the ulnar nerve at the wrist.
After the induction of anesthesia, the volunteers were turned to the left-lateral position. The upper arm was supported 24 ± 4 cm above the midsternal line; the dependent arm was supported 24 ± 2 cm below the midsternal line. Padding was positioned under the rib cage to avoid compression of the brachial artery and consequent flow restriction to the dependent arm.
Mean skin temperature was then abruptly decreased to 31°C with a circulating-water mattress (Cincinnati Sub-Zero, Cincinnati, OH) and a forced-air cooler (Augustine Medical, Inc., Eden Prairie, MN). This produced a gradual, but progressive, decrease in tympanic membrane temperature. The study ended when further reduction in core temperature no longer decreased finger blood flow. Throughout the protocol, arms were protected from active warming and cooling to avoid locally mediated vasomotion (14). However, all other skin below the neck was similarly manipulated throughout the study day.
Core temperature was recorded from the tympanic membrane by use of Mon-a-Therm thermocouples (Tyco, Inc., St. Louis, MO). The volunteers inserted the aural probes until they felt the thermocouple touching the tympanic membrane; appropriate placement was confirmed when volunteers easily detected a gentle rubbing of the attached wire. The aural canal was occluded with cotton, the probe was securely taped in place, and a gauze bandage was positioned over the external ear.
Mean skin-surface temperature was calculated from measurements at 15 area-weighted sites (15). All temperatures were displayed at 1-s intervals and were recorded at 1-min intervals from thermocouples connected to calibrated Iso-Thermex (Columbus Instruments Corp., Columbus, OH) thermometers, which have an accuracy of 0.1°C and a precision of 0.01°C.
Absolute middle fingertip blood flow on each hand was quantified with venous occlusion volume plethysmography at 1-min intervals (16). Arterial blood pressure was determined oscillometrically from each upper arm in the supine position and in the lateral position in each arm before and after vasoconstriction. (Modulus CD; Ohmeda Inc., Salt Lake City, UT).
Thresholds were defined by the core temperatures triggering various intensities of vasoconstriction. Mild vasoconstriction was defined as a sustained fingertip blood flow of <1 mL/min, which corresponds to a forearm minus fingertip skin-temperature gradient near 0°C. This degree of constriction is sufficient to initiate a core temperature plateau during general anesthesia (17). Intense vasoconstriction was defined as a sustained fingertip blood flow of <0.25 mL/min, which corresponds to a skin-temperature gradient near 4°C. Very intense vasoconstriction was defined as a sustained fingertip blood flow of <0.1 mL/min.
The effect of core cooling on plethysmographic finger blood flow was determined in three steps. The core temperatures at flows of 1.0 mL/min on the upper and dependent arm were designated the thresholds in each subject. The effect of additional core cooling on finger blood flows was then calculated relative to the 1.0 mL/min individual threshold temperatures. Because flow measurements were taken at specific time intervals rather than fixed temperature intervals, data from each volunteer within 0.05°C core temperature increments were averaged. Subsequently, the population means were calculated from these individual averages. Finally, the average flow values for the population were plotted relative to the mean thresholds for the upper and dependent arm. This is similar to the analysis method we used in previous studies of vasoconstriction gain (7).
As previously reported, finger blood flows from 0.15 to 1.0 mL/min are roughly linear functions of core temperature during desflurane administration (7). Furthermore, these values define the clinically important range from mild to very intense vasoconstriction. The gain of vasoconstriction in each arm was thus considered to be the slope of the population flow versus core temperature linear regression in the flow range from 1.0 to 0.15 mL/min. Gains in each arm were then compared by using analysis of covariance.
The vasoconstriction thresholds in each arm were compared by using two-tailed, paired Student’s t-tests. Arterial blood pressures in each arm before and after vasoconstriction were similarly compared. Parametric results are expressed as mean ± SD; other data are reported as median and interquartile range. Differences were considered statistically significant when P < 0.05.
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Results |
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Arterial blood pressure in the supine position was comparable in each arm (93 ± 20 mm Hg [left arm] versus 93 ± 20 mm Hg [right arm]; P = 0.96). In the lateral position, though, mean arterial blood pressure in the dependent arm was significantly greater (80 ± 20 mm Hg) than in the upper arm (62 ± 18 mm Hg; P = 0.003).
The vasoconstriction threshold (with a flow of 1.0 mL/min) was slightly, but significantly, less in the dependent arm (36.2°C ± 0.3°C) than in the upper arm (36.5°C ± 0.3°C). Intense vasoconstriction (flow of 0.25 mL/min) and very intense vasoconstriction (flow <0.1 mL/min) were also slightly, but significantly, less in the dependent arm (Table 1).
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Discussion |
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The mean blood pressure in our volunteers in the lateral position was approximately 20 mm Hg greater in the dependent than in the upper arm; this is consistent with previous reports. The vasoconstriction threshold in the dependent arm was reduced, as predicted, by 0.4°C ± 0.4°C. This observation is consistent with our theory that greater intraluminal pressure in the dependent arm would help maintain flow even after hypothermia-triggered central thermoregulatory vasoconstriction. Baroreceptor unloading similarly reduces the vasoconstriction threshold (13), but that response is presumably centrally mediated and thus unlikely to explain differences between the upper and dependent arms in this study.
However, we also predicted that greater blood pressure in the dependent arm would reduce the gain of vasoconstriction. It is interesting that we observed just the opposite effect: gain in the dependent arm was 2.3-fold greater than in the upper arm. Why gain was augmented in the dependent arm remains unclear, but it is presumably the result of direct thermoregulatory vasomotor control. These data suggest that thermoregulatory vasomotion is more complex than previously believed.
Because the threshold was lower in the dependent arm but the gain was greater, the flow regressions intersected at a flow near 0.15 mL/min—-a value consistent with intense vasoconstriction. It remains unknown whether the flow regressions would similarly intersect at intense vasoconstriction with other anesthetics and other anesthetic doses. However, an intriguing possibility is that the thermoregulatory system recognized the fact that hydrostatic forces reduced the vasoconstriction threshold and compensated by augmenting gain sufficiently to produce intense vasoconstriction at a similar core temperature in each arm.
In conclusion, the threshold for cold-induced vasoconstriction is reduced in the dependent arm. However, the gain of vasoconstriction is increased. The consequence is that the core temperature triggering intense vasoconstriction (a fingertip blood flow of only 0.15 mL/min) was similar in each arm. These data suggest the intriguing possibility that the thermoregulatory system is able to compensate for the hydrostatic effects of lateral positioning.
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Acknowledgments |
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We appreciate the assistance of Nancy Alsip, PhD.
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References |
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arms. Flow values were averaged over 0.05°C increments in each volunteer. Data are presented as medians with 25th and 75th percentile error bars. The first flows <1.0 ml/min identify the vasoconstriction threshold. The slopes of the flow versus core temperature regressions identify the gain of vasoconstriction in each arm. The gain was reduced by a factor of 2.3 in the upper arm, from 3.0 to 1.3 mL · min-1 · °C-1 (P < 0.05).
