scholarly journals Non-invasive Monitoring of Core Body Temperature for Targeted Temperature Management in Post-Cardiac Arrest Care

2021 ◽  
Author(s):  
Kyle Fiorini ◽  
Tanya Tamasi ◽  
Justin Dorie ◽  
Ahmed F. Hegazy ◽  
Ting-Yim Lee ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Body Temperature ◽  
Core Body Temperature ◽  
Pearson Correlation ◽  
Targeted Temperature Management ◽  
Temperature Management ◽  
Invasive Monitoring ◽  
Limits Of Agreement ◽  
Non Invasive ◽  
Core Body

Abstract BackgroundAccurate monitoring of core body temperature is integral to targeted temperature management (TTM) following cardiac arrest. However, there are no reliable non-invasive methods for monitoring temperature during TTM. We compared the accuracy and precision of a novel non-invasive Zero-Heat Flux Thermometer (SpotOnä) to a standard invasive esophageal probe in a cohort of patients undergoing TTM post cardiac arrest. MethodsWe prospectively enrolled 20 patients undergoing post-cardiac arrest care in the intensive care units at the London Health Sciences Centre in London, Canada. A SpotOnä probe was applied on each patient’s forehead, while an esophageal temperature probe was inserted, and both temperature readings were recorded at 1-minute intervals for the duration of TTM. We compared the SpotOnä and esophageal monitors using Bland-Altman analysis and Pearson correlation, with accuracy set as a primary outcome. Secondary outcomes included precision and correlation. Bias exceeding 0.1°C and limits of agreement exceeding 0.5°C were considered clinically important.ResultsSixteen (80%) of patients had complete data used in the final analysis. The median (interquartile range) duration of recording was 38 (12-56) hours. Compared to the esophageal probe, SpotOnä had a bias of 0.05 ± 0.35ºC and 95% limits of agreement of -0.64 to 0.74 ºC. Pearson correlation coefficient was 0.98 (95% confidence interval 0.9796-0.9805), with a two-tailed p-value of <0.0001. ConclusionThe SpotOnä is an accurate method that may enable non-invasive monitoring of core body temperature during TTM, although its precision is slightly worse than the pre-defined 0.5°C when compared to invasive esophageal probe.

scholarly journals Cerebral autoregulation in anoxic brain injury patients treated with targeted temperature management

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Ilaria Alice Crippa ◽  
Jean-Louis Vincent ◽  
Federica Zama Cavicchi ◽  
Selene Pozzebon ◽  
Filippo Annoni ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Body Temperature ◽  
Hospital Discharge ◽  
Core Body Temperature ◽  
Targeted Temperature Management ◽  
Temperature Management ◽  
Anoxic Brain Injury ◽  
Shockable Rhythm ◽  
Core Body

Abstract Background Little is known about the prevalence of altered CAR in anoxic brain injury and the association with patients’ outcome. We aimed at investigating CAR in cardiac arrest survivors treated by targeted temperature management and its association to outcome. Methods Retrospective analysis of prospectively collected data. Inclusion criteria: adult cardiac arrest survivors treated by targeted temperature management (TTM). Exclusion criteria: trauma; sepsis, intoxication; acute intra-cranial disease; history of supra-aortic vascular disease; severe hemodynamic instability; cardiac output mechanical support; arterial carbon dioxide partial pressure (PaCO2) > 60 mmHg; arrhythmias; lack of acoustic window. Middle cerebral artery flow velocitiy (FV) was assessed by transcranial Doppler (TCD) once during hypothermia (HT) and once during normothermia (NT). FV and blood pressure (BP) were recorded simultaneously and Mxa calculated (MATLAB). Mxa is the Pearson correlation coefficient between FV and BP. Mxa > 0.3 defined altered CAR. Survival was assessed at hospital discharge. Cerebral Performance Category (CPC) 3–5 assessed 3 months after CA defined unfavorable neurological outcome (UO). Results We included 50 patients (Jan 2015–Dec 2018). All patients had out-of-hospital cardiac arrest, 24 (48%) had initial shockable rhythm. Time to return of spontaneous circulation was 20 [10–35] min. HT (core body temperature 33.7 [33.2–34] °C) lasted for 24 [23–28] h, followed by rewarming and NT (core body temperature: 36.9 [36.6–37.4] °C). Thirty-one (62%) patients did not survive at hospital discharge and 36 (72%) had UO. Mxa was lower during HT than during NT (0.33 [0.11–0.58] vs. 0.58 [0.30–0.83]; p = 0.03). During HT, Mxa did not differ between outcome groups. During NT, Mxa was higher in patients with UO than others (0.63 [0.43–0.83] vs. 0.31 [− 0.01–0.67]; p = 0.03). Mxa differed among CPC values at NT (p = 0.03). Specifically, CPC 2 group had lower Mxa than CPC 3 and 5 groups. At multivariate analysis, initial non-shockable rhythm, high Mxa during NT and highly malignant electroencephalography pattern (HMp) were associated with in-hospital mortality; high Mxa during NT and HMp were associated with UO. Conclusions CAR is frequently altered in cardiac arrest survivors treated by TTM. Altered CAR during normothermia was independently associated with poor outcome.

Forced-air pre-warming prevents peri-anaesthetic hypothermia and shortens recovery in adult rats

2017 ◽  
Vol 52 (2) ◽  
pp. 142-151 ◽  
Author(s):  
C J Schuster ◽  
D S J Pang
Keyword(s):  
Body Temperature ◽  
Core Temperature ◽  
Rectal Temperature ◽  
Core Body Temperature ◽  
Temperature Management ◽  
Limits Of Agreement ◽  
Adult Rats ◽  
Air Exposure ◽  
Core Body ◽  
The Impact

General anaesthesia disrupts thermoregulation in mammals, which can cause hypothermia. Decreases in core body temperature of 1℃ cause significant postoperative complications in humans, and peri-anaesthetic hypothermia in mice increases data variability, which can potentially increase animal use. In rats, the impact of different temperature management strategies on the incidence and severity of hypothermia, and the accuracy of different temperature measurement methods, is unknown. Eighteen adult male and female SD rats were block-randomized to one of three treatment groups: no-warming (NW), limited-warming (LW, heat pad during anaesthesia), and pre-warming (PW, warm air exposure before anaesthesia, followed by heat pad). Anaesthesia (isoflurane) duration was for 40 min. Core body temperature (intra-abdominal telemetric temperature capsule) was recorded during anaesthesia and recovery. During anaesthesia, rectal, skin, and tail temperatures were also recorded. In the PW group, core temperature was maintained during anaesthesia and recovery. By contrast, the NW group was hypothermic (11% temperature decrease) during anaesthesia. The LW group showed a decrease in temperature during recovery. Recovery to sternal recumbency was significantly faster in the PW (125 [70–186] s, P = 0.0003) and the LW (188 [169–420] s, P = 0.04) groups than in the NW group (525 [229–652] s). Rectal temperature underestimated core temperature (bias −0.90℃, 95% limits of agreement −0.1 to 1.9℃). Skin and tail temperatures showed wide 95% limits of agreement, spanning 6 to 15℃, respectively. The novel strategy of PW was effective at maintaining core temperature during and after anaesthesia. Rectal temperature provided an acceptable proxy for core body temperature.

Effects of Propofol on Hemodynamic Profile in Adults Receiving Targeted Temperature Management

2021 ◽  
pp. 001857872110323
Author(s):  
W. Anthony Hawkins ◽  
Jennifer Y. Kim ◽  
Susan E. Smith ◽  
Andrea Sikora Newsome ◽  
Ronald G. Hall
Keyword(s):  
Cardiac Arrest ◽  
Body Temperature ◽  
Multivariate Regression ◽  
Primary Outcome ◽  
Targeted Temperature Management ◽  
Temperature Management ◽  
Hemodynamic Changes ◽  
Failure Assessment ◽  
Hemodynamic Profile ◽  
Median Change

Background: Propofol is a key component for the management of sedation and shivering during targeted temperature management (TTM) following cardiac arrest. The cardiac depressant effects of propofol have not been described during TTM and may be especially relevant given the stress to the myocardium following cardiac arrest. The purpose of this study is to describe hemodynamic changes associated with propofol administration during TTM. Methods: This single center, retrospective cohort study evaluated adult patients who received a propofol infusion for at least 30 minutes during TTM. The primary outcome was the change in cardiovascular Sequential Organ Failure Assessment (cvSOFA) score 30 minutes after propofol initiation. Secondary outcomes included change in systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate (HR), and vasopressor requirements (VR) expressed as norepinephrine equivalents at 30, 60, 120, 180, and 240 minutes after propofol initiation. A multivariate regression was performed to assess the influence of propofol and body temperature on MAP, while controlling for vasopressor dose and cardiac arrest hospital prognosis (CAHP) score. Results: The cohort included 40 patients with a median CAHP score of 197. The goal temperature of 33°C was achieved for all patients. The median cvSOFA score was 1 at baseline and 0.5 at 30 minutes, with a non-significant change after propofol initiation ( P = .96). SBP and MAP reductions were the greatest at 60 minutes (17 and 8 mmHg; P < .05 for both). The median change in HR at 120 minutes was −9 beats/minute from baseline. This reduction was sustained through 240 minutes ( P < .05). No change in VR were seen at any time point. In multivariate regression, body temperature was the only characteristic independently associated with changes in MAP (coefficient 4.95, 95% CI 1.6-8.3). Conclusion: Administration of propofol during TTM did not affect cvSOFA score. The reductions in SBP, MAP, and HR did not have a corresponding change in vasopressor requirements and are likely not clinically meaningful. Propofol appears to be a safe choice for sedation in patients receiving targeted temperature management after cardiac arrest.

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.

Measuring core body temperature with a non-invasive sensor

2017 ◽  
Vol 66 ◽  
pp. 17-20 ◽  
Author(s):  
Savyon Mazgaoker ◽  
Itay Ketko ◽  
Ran Yanovich ◽  
Yuval Heled ◽  
Yoram Epstein
Keyword(s):  
Body Temperature ◽  
Core Body Temperature ◽  
Non Invasive ◽  
Core Body
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