scholarly journals A Human Thermoregulation Simulator for Calibrating Water-Perfused Cooling Pad Systems for Therapeutic Hypothermia

2017 ◽  
Vol 11 (3) ◽  
Author(s):  
Priya S. E. Chacko ◽  
Ali Seifi ◽  
Kenneth R. Diller
Keyword(s):  
Therapeutic Hypothermia ◽  
Core Temperature ◽  
Convective Transport ◽  
The Body ◽  
Body Core Temperature ◽  
Temperature Management ◽  
Thermal Mass ◽  
The Core ◽  
Highly Nonlinear ◽  
Human Thermoregulation

The induction of a mild reduction in body core temperature has been demonstrated to provide neuroprotection for patients who have suffered a medical event resulting in ischemia to the brain or vital organs. Temperatures in the range of 32–34 °C provide the required level of protection and can be produced and maintained by diverse means for periods of days. Rewarming from hypothermia must be conducted slowly to avoid serious adverse consequences and usually is performed under control of the thermal therapeutic device based on a closed-loop feedback strategy based on the patient's core temperature. Given the sensitivity and criticality of this process, it is important that the device control system be able to interact with the human thermoregulation system, which itself is highly nonlinear. The therapeutic hypothermia device must be calibrated periodically to ensure that its performance is accurate and safe for the patient. In general, calibration processes are conducted with the hypothermia device operating on a passive thermal mass that behaves much differently than a living human. This project has developed and demonstrated an active human thermoregulation simulator (HTRS) that embodies major governing thermal functions such as central metabolism, tissue conduction, and convective transport between the core and the skin surface via the flow of blood and that replicates primary dimensions of the torso. When operated at physiological values for metabolism and cardiac output, the temperature gradients created across the body layers and the heat exchange with both an air environment and a clinical water-circulating cooling pad system match that which would occur in a living body. Approximately two-thirds of the heat flow between the core and surface is via convection rather than conduction, highlighting the importance of including the contribution of blood circulation to human thermoregulation in a device designed to calibrate the functioning of a therapeutic hypothermia system. The thermoregulation simulator functions as anticipated for a typical living patient during both body cooling and warming processes. This human thermoregulatory surrogate can be used to calibrate the thermal function of water-perfused cooling pads for a hypothermic temperature management system during both static and transient operation.

Abstract 10475: Heat Loss Augmented by Extracorporeal Circulation is Associated with Overcooling in Cardiac Arrest Survivors Who Underwent Targeted Temperature Management

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Byungkook Lee ◽  
Dong Hun Lee
Keyword(s):  
Water Temperature ◽  
Core Temperature ◽  
Neurological Outcome ◽  
Temperature Management ◽  
Extracorporeal Circuit ◽  
Matched Cohort ◽  
Maintenance Period ◽  
Neurological Outcomes ◽  
The Core ◽  
Poor Neurological Outcome

Introduction: Extracorporeal circuit-based salvage therapy can affect targeted temperature management (TTM) in comatose out-of-hospital cardiac arrest (OHCA) survivors. We investigated the association of patients with extracorporeal device with TTM and neurological outcome. Methods: We performed a retrospective analysis using prospectively collected data from adult comatose OHCA survivors who underwent TTM between October 2015 and December 2020. We defined patients with ECMO and/or CRRT as the extracorporeal group. We calculated the cooling rate during the induction period; the minimum, maximum, and mean time-weighted core temperatures (TWCT), and the standard deviation (SD) of the core temperature and water temperature during the maintenance period based on the temperature measured every minute. We defined the sum of TWCT more and less than 33°C as positive and negative TWCT, respectively. The primary outcome was a poor neurological outcome, defined as cerebral performance category 3-5. We used propensity score (PS) matching to adjust the characteristics of patients who required an extracorporeal circuit device. Results: Of the 223 included patients, 140 (62.8%) patients had poor neurological outcome and 40 (17.9%) patients were categorized into the extracorporeal group. The extracorporeal group had a rapid cooling rate (2.08°C/h [1.13-3.73] vs. 1.24°C/h [0.77-1.79]; p < 0.001). The extracorporeal group had lower mean core temperature; higher core temperature SD; lower positive TWCT; higher negative TWCT; and higher maximum, minimum, and mean water temperature than the no-extracorporeal group. In PS matched cohort, the extracorporeal group had a lower minimum core temperature, lower mean core temperature, higher core temperature SD, higher negative TWCT, higher maximum water temperature, and higher mean water temperature. The neurological outcomes were not different between the two groups, in either the whole or PS-matched cohort. Conclusions: The extracorporeal group achieved the target temperature earlier. The core temperature distribution during the maintenance period was further skewed below 33°C in the extracorporeal group. The extracorporeal group had similar neurological outcomes to the no-extracorporeal group.

P0250COLD DIURESIS DURING TARGETED TEMPERATURE MANAGEMENT AFTER CARDIAC ARREST, MYTH OR FACT?

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Min-Jeong Lee ◽  
Minjung Kathy Chae
Keyword(s):  
Cardiac Arrest ◽  
Body Temperature ◽  
Therapeutic Hypothermia ◽  
Urine Output ◽  
The Body ◽  
Targeted Temperature Management ◽  
Neurologic Outcome ◽  
Temperature Management ◽  
Induction Phase ◽  
Target Temperature

Abstract Background and Aims Therapeutic hypothermia or targeted temperature management (TTM) has been standard treatment for cardiac arrest survivors with suspected hypoxic ischemic brain injury for improvement in both survival and neurological outcomes. TTM is consisted of an induction phase of quickly lowering the temperature to target temperature (ranging from 32°C -36°C) as soon as possible, a hypothermia maintenance phase of keeping the body temperature at target temperature for at least 24 hours, a rewarming phase of slowly rewarming the temperature to normothermia, and a normothermia phase of keeping the body temperature at normothermia. During the dynamic changes in body temperature, cold-diuresis is a commonly described phenomenon. However, limited studies have characterized cold-induced diuresis during TTM. In this study, we sought to determine urine output changes during post cardiac arrest therapeutic hypothermia. Method This retrospective cohort study included adult patients who underwent TTM after out-of-hospital cardiac arrest and were admitted to the intensive care unit for post cardiac arrest care between January 2012 and August 2018. The exclusion criteria of this study were as follows: 1) deceased status before the completion of all phase of TTM; 2) previous end stage kidney disease patients, 3) undergoing renal replacement therapy due to AKI within 48 hours of TTM termination; 4) terminal cancer less than 6 months of life expectancy or previously cerebral performance category (CPC) 3 or more. The neurologic outcome was assessed using the CPC score after 1 month. Good neurologic outcome was defined as a CPC score of 1, 2 and poor neurologic outcome as a CPC score of 3 to 5. The post cardiac arrest protocol recommends a target temperature of 33°C unless the patient is hemodynamically unstable or has a bleeding tendency or severe infection. Rewarming rate was 0.15°C/hr or 0.25°C/hr. TTM was conducted with the use of temperature managing devices with a feedback loop system (Artic Sun Energy Transfer Pads, Medivance Corp., Louisville, CO, USA; Cool Guard Alsius Icy Heat Exchange Catheter, Alsius Corporation, Irvine, CA, USA). We calculated the hourly IV fluid input and urine output rates for each TTM phase. To compare the mean of urine volume between each TTM phase, we used repeated measure analysis of variance (ANOVA). Results 178 Patients included in the analysis. We observed a increase in urine output rates during hypothermia induction. This effect persisted even after adjustment for variable clinical confounders, including intravenous fluid input rate, mean arterial pressure (MAP), initial shockable rhythm, SOFA score, body mass index, and IV furosemide use. However, we did not detect any evidence of urine output increases or decreases during the hypothermia maintenance or rewarming phases. By repeating measures ANOVA and a linear mixed model, it was confirmed that there is a difference in urine output for each TTM phase. Even after the post hoc analysis was calibrated with several variables, only the hypotheria induction phase differed significantly from the urine output of the phase. Conclusion Although our results are some limitations, the findings support the potential presence of cold-induced dieresis, but not rewarm anti-diuresis during TTM. Our study may not fully capture the extent of renal impairment in post cardiac arrest undergoing TTM. However, our objective was to characterize urine output during TTM in post cardiac arrest patients. This has important implications for fluid management in patients undergoing TTM.

Restoration of thermoregulation after exercise

2017 ◽  
Vol 122 (4) ◽  
pp. 933-944 ◽  
Author(s):  
Glen P. Kenny ◽  
Ryan McGinn
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Current Knowledge ◽  
Thermal Control ◽  
The Body ◽  
Body Core Temperature ◽  
Whole Body ◽  
Temperature Sensitive ◽  
Internal Core ◽  
Body Core

Performing exercise, especially in hot conditions, can heat the body, causing significant increases in internal body temperature. To offset this increase, powerful and highly developed autonomic thermoregulatory responses (i.e., skin blood flow and sweating) are activated to enhance whole body heat loss; a response mediated by temperature-sensitive receptors in both the skin and the internal core regions of the body. Independent of thermal control of heat loss, nonthermal factors can have profound consequences on the body’s ability to dissipate heat during exercise. These include the activation of the body’s sensory receptors (i.e., baroreceptors, metaboreceptors, mechanoreceptors, etc.) as well as phenotypic factors such as age, sex, acclimation, fitness, and chronic diseases (e.g., diabetes). The influence of these factors extends into recovery such that marked impairments in thermoregulatory function occur, leading to prolonged and sustained elevations in body core temperature. Irrespective of the level of hyperthermia, there is a time-dependent suppression of the body’s physiological ability to dissipate heat. This delay in the restoration of postexercise thermoregulation has been associated with disturbances in cardiovascular function which manifest most commonly as postexercise hypotension. This review examines the current knowledge regarding the restoration of thermoregulation postexercise. In addition, the factors that are thought to accelerate or delay the return of body core temperature to resting levels are highlighted with a particular emphasis on strategies to manage heat stress in athletic and/or occupational settings.

Thermal regulatory dysfunction of growth hormone in classical heat stroke?

1996 ◽  
Vol 134 (6) ◽  
pp. 727-730
Author(s):  
Abdulaziz Alzeer ◽  
Abdullah Al Arifi ◽  
Mohsen El-Hazmi ◽  
Arjumand S Warsy ◽  
Eric S Nylen
Keyword(s):  
Growth Hormone ◽  
Core Temperature ◽  
Heat Stroke ◽  
The Body ◽  
Body Core Temperature ◽  
Treatment Unit ◽  
Gh Secretion ◽  
Body Core ◽  
Time Of Admission ◽  
Regulatory Dysfunction

Alzeer A, Al Arifi A, El-Hazmi M, Warsy AS, Nylen ES. Thermal regulatory dysfunction of growth hormone in classical heat stroke? Eur J Endocrinol 1996;134:727–30. ISSN 0804–4643 Growth hormone (GH) secretion associated with classical (non-exertional) heat stroke (HS) was evaluated in 26 HS victims and 10 control (non heat-exhausted) subjects during the annual Hajj in Makkah, Saudi Arabia. On admission to the HS treatment unit, the GH level was 1.54 ± 0.14 ng/ml (approximately 3.5-fold higher in the HS victims compared to controls; p = 0.005). The GH levels subsequently declined by 78% by 24 h. The categorized GH response was significantly associated with survival for those subjects with a GH level of < 5.53 ng/ml by 6 h (chi-squared test; p = 0.06). In those patients who died (N = 6), there was a continued increase in GH levels from the time of admission, which peaked at 6 h. In those patients who survived, the GH levels peaked at the time of admission and declined rapidly thereafter. There was a direct correlation of age and GH level upon admission (p = 0.02), as well as to peak GH (p = 0.041). However, there was no relationship of GH level to either body core temperature or the cooling time. In summary, HS induced significant GH secretion. The degree of GH response was not related to the body core temperature and was more pronounced in older individuals and in those that died. Although patients with GH deficiency and HS are characterized by anhidrosis/hypohidrosis, there does not appear to be dysfunction of GH response to heat stress-associated HS. In contrast, a vigorous GH response at 6 h suggested a worse outcome. ES Nylen, Rm GE 246, VAMC, 50 Irving St, NW Washington, DC 20422, USA

Heat loss responses in rats acclimated to heat loaded intermittently

1990 ◽  
Vol 68 (1) ◽  
pp. 66-70 ◽  
Author(s):  
O. Shido ◽  
T. Nagasaka
Keyword(s):  
Skin Temperature ◽  
Heat Loss ◽  
Core Temperature ◽  
Thermal Conductance ◽  
Heat Acclimation ◽  
The Body ◽  
Body Core Temperature ◽  
Acclimation Temperature ◽  
Hypothalamic Temperature ◽  
Direct Body

The present study examined the heat loss response of heat-acclimated rats to direct body heating with an intraperitoneal heater or to indirect warming by elevating the ambient temperature (Ta). The heat acclimation of the rats was attained through exposure to Ta of 33 or 36 degrees C for 5 h daily during 15 consecutive days. Control rats were kept at Ta of 24 degrees C for the same acclimation period. Heat acclimation lowered the body core temperature at Ta of 24 degrees C, and the core temperature level was lowered as acclimation temperature increased. When heat was applied by direct body heating, the threshold hypothalamic temperature (Thy) for the tail skin vasodilation was also lower in heat-acclimated rats than in the control rats. However, the amount of increase in Thy from the resting level to the threshold was the same in all three groups. When heat was applied by indirect warming, threshold Thy was slightly higher in heat-acclimated than in control rats. The amount of increase in Thy from the resting level to the threshold was significantly greater in heat-acclimated rats. In addition, Ta and the skin temperature at the onset of skin vasodilation were significantly higher in heat-acclimated rats. The results indicate that heat-acclimated rats were less sensitive to the increase in skin temperature in terms of threshold Thy. The gain constant of nonevaporative heat loss response was assessed by plotting total thermal conductance against Thy.(ABSTRACT TRUNCATED AT 250 WORDS)

The Comparison between Different types of Cold Fluid Ingestion towards Endurance Exercise in Hot and Humid Condition

2019 ◽  
Vol 2 (1) ◽  
pp. 48-55
Author(s):  
Nur Marsya Amani Mohd Jamil ◽  
Muhamad Nur Fitri Azari ◽  
Norlena Salamuddin ◽  
Azrina Md Azhari ◽  
Nur Shakila Mazalan
Keyword(s):  
Core Temperature ◽  
Endurance Exercise ◽  
The Body ◽  
Body Core Temperature ◽  
Continuous Exercise ◽  
Fluid Ingestion ◽  
Cold Fluid ◽  
Significant Difference ◽  
Different Types ◽  
Cooling Methods

The rise in body core temperature associated with continuous exercise in hot and humid environments is known to possess a particularly stressful challenge to the maintenance of normal body temperature and fluid homeostasis. Recent evidence has shown that internal cooling methods, such as drinking cold fluids, are able to lower core temperature and enhance endurance performance in the heat. Pre-cooling (before exercise) and per-cooling (during exercise) methods were use, as ingesting cold fluids is easily implemented on site and provides additional benefit of hydration for athletes. Therefore, this study examines the effectiveness of pre-cooling and per-cooling methods on endurance exercise towards heart rate, rectal temperature, sweat rate, and power output of athletes ingesting different types of cold fluids. 3 female high-performance cyclists were asked to complete a 30km time trial on a cycle ergometer. The familiarisation and experimental sessions were identical, however application of fluid ingestion at 4-5°C before and during exercise differs (plain water = PW, Guava juice = GJ, isotonic drink = ID). Fluid is ingested every 15 minutes during the exercise sessions. As different athletes possess different work intensities, results showed that there is no significant difference on the effects of different types of cold fluid ingestion towards thermoregulation of the body as each fluid succeeded in enhancing athletes’ performance. Therefore, it is suggested that the consumption of any types of fluid at cold temperature could help in body thermoregulation as well as enhancing continuous exercise performance.

Keeping a Cool Head

Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 41-44 ◽  
Author(s):  
M Cabanac
Keyword(s):  
Heat Stress ◽  
Core Temperature ◽  
Heat Exchangers ◽  
The Body ◽  
Body Core Temperature ◽  
Mammalian Brain ◽  
Poor Tolerance ◽  
Selective Cooling ◽  
Body Core ◽  
The Brain

The mammalian brain has poor tolerance to increased temperature. However, when body core temperature rises during exercise or heat stress, the temperature of the brain can remain at a lower level, somewhat independent of the rest of the body. In several mammals the cooling of the brain is related to anatomically well-defined countercurrent heat exchangers. Humans lack these distinct anatomic structures, but significant cooling of the brain can nevertheless occur. Such selective cooling of the brain may have important medical implicantions.

Control of respiratory evaporative heat loss in exercising goats

1979 ◽  
Vol 46 (5) ◽  
pp. 978-983 ◽  
Author(s):  
J. B. Mercer ◽  
C. Jessen
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Exchangers ◽  
The Body ◽  
Body Core Temperature ◽  
Evaporative Heat Loss ◽  
Hypothalamic Temperature ◽  
Body Core ◽  
Total Body ◽  
Rest And Exercise

Investigations were carried out to determine whether a nonthermal input is involved in the control of respiratory evaporative heat loss (REHL) in exercising goats. Two goats were implanted with hypothalamic perfusion thermodes and three goats were implanted with intravascular heat exchangers to clamp hypothalamic temperature and total body core temperature, respectively. At 30 degrees C air temperature REHL was measured while the animals were resting or walking on a treadmill (3 km.h-1, 5 degrees gradient). When the hypothalamic temperature was clamped between 33.0 and 43.0 degrees C the slopes of the responses relating increased REHL to hypothalamic temperature were similar during rest and exercise. However, the threshold hypothalamic temperatures for the increased REHL responses were lower during exercise than at rest, presumably due to higher extrahypothalamic temperatures. When the body core temperature was clamped between 37.0 and 40.4 degrees C the slopes of the responses relating increased REHL to total body core temperature during exercise showed only minor differences compared to those at rest, none of them conclusively indicating nonthermal influences.

Heat Balance and Distribution during the Core-Temperature Plateau in Anesthetized Humans

1995 ◽  
Vol 83 (3) ◽  
pp. 491-499. ◽  
Author(s):  
Andrea Kurz ◽  
Daniel I. Sessler ◽  
Richard Christensen ◽  
Martha Dechert
Keyword(s):  
Heat Loss ◽  
Core Temperature ◽  
Heat Production ◽  
Heat Balance ◽  
Thermal Flux ◽  
The Body ◽  
Metabolic Heat Production ◽  
The Core ◽  
Metabolic Heat ◽  
Temperature Plateau

Background Once triggered, intraoperative thermoregulatory vasoconstriction is remarkably effective in preventing further hypothermia. Protection results from both vasoconstriction-induced decrease in cutaneous heat loss and altered distribution of body heat. However, the independent contributions of each mechanism have not been quantified. Accordingly, we evaluated overall heat balance and distribution of heat within the body during the core-temperature plateau. Methods Nine minimally clothed male volunteers were anesthetized with propofol and isoflurane and maintained in an approximately 22 degrees C environment. They were monitored for approximately 2 h before vasoconstriction and for 3 h subsequently. Overall heat balance was determined from the difference between cutaneous heat loss (thermal flux transducers) and metabolic heat production (oxygen consumption). Arm and leg tissue heat contents were determined from 19 intramuscular temperatures, ten skin temperatures, and "deep" foot temperature. Heat constrained by vasoconstriction to the trunk and head was calculated by subtracting the expected change in that region (overall heat balance multiplied by the fractional weight of the trunk and head) from the actual change (change in distal esophageal temperature multiplied by the specific heat of human tissue and the weight of the trunk and head); the result represents the amount by which core heat exceeded that which would be expected based on overall heat balance, assuming that the change was evenly distributed throughout the body. Results Vasoconstriction and passive tissue cooling decreased heat loss but not to the level of heat production. Consequently, heat loss exceeded metabolic heat production throughout the study. Core temperature decreased approximately 1.3 C during the 2-h prevasoconstriction period; however, core temperature remained virtually constant during the subsequent 3 h. In the 3 h after vasoconstriction, arm and leg heat content decreased 57 +/- 9 kcal, and vasoconstriction constrained 22 +/- 8 kcal to the trunk and head. Conclusions These results confirm the efficacy of thermo-regulatory vasoconstriction in preventing additional core hypothermia. Decreased cutaneous heat loss and constraint of metabolic heat to the core thermal compartment contributed to the plateau.

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