A deep learning-based real-time hypothermia and hyperthermia monitoring system with a simple body sensor.

A real-time hypothermia and hyperthermia monitoring system with a simple body sensor based on a Convolutional Neural Network (CNN) is presented. The sensor is produced with 3D-printed thermochromic material. Due to the color change feature of thermochromic materials with temperature, 3D-printed thermochromic Polylactic Acid (PLA) material was used to monitor temperature changes visually. In this paper, we have used the transfer learning technique and fine-tuned the AlexNet CNN. Thirty images for each temperature class between 28-44°C and 510 image data were used in the algorithm. We used 80% and 20% of the data for training and validation. We achieved 96.1% accuracy of validation with a fine-tuned AlexNet CNN. The material's characteristics suggest that it could be employed in delicate temperature sensing and monitoring applications, particularly for hypothermia and hyperthermia.

A critically prolonged avalanche burial with recorded cardiac electrical activity and complete recovery - a case report.

The probability of survival in avalanche accidents is time-dependent. Critically buried victims who undergo a long burial duration (over 60 min) face a possible mortality rate of over 80%. Understanding the physiological response during critical avalanche burial is crucial for improving rescue strategies and outcomes. We present the case of a 55-year-old male skier buried under an avalanche for 4 h and 51 min in the Italian Alps. Continuous heart rate monitoring revealed distinct phases of cardiac activity during burial. Despite severe hypothermia, the victim survived without extracorporeal rewarming. This case highlights the importance of continuous monitoring and appropriate on-site management in avalanche accidents. Factors such as the presence of an air pocket may positively influence survival. This case underscores the importance of comprehensive resuscitative measures and guidelines for managing avalanche victims with prolonged burial durations.

ß-adrenergic stimulation after rewarming does not mitigate hypothermia-induced contractile dysfunction in rat cardiomyocytes.

Victims of severe accidental hypothermia are frequently treated with catecholamines to counteract the hemodynamic instability associated with hypothermia-induced cardiac contractile dysfunction. However, we previously reported that the inotropic effects of epinephrine are diminished after hypothermia and rewarming (H/R) in an intact animal model. Thus, the goal of this study was to investigate the effects of Epi treatment on excitation-contraction coupling in isolated rat cardiomyocytes after H/R. In adult male rats, cardiomyocytes isolated from the left ventricle were electrically stimulated at 0.5 Hz and evoked cytosolic [Ca2+] and contractile responses (sarcomere length shortening) were measured. In initial experiments, the effects of varying concentrations of epinephrine on evoked cytosolic [Ca2+] and contractile responses at 37 °C were measured. In a second series of experiments, cardiomyocytes were cooled from 37 °C to 15 °C, maintained at 15 °C for 2 h, then rewarmed to 37 °C (H/R protocol). Immediately after rewarming, the effects of epinephrine treatment on evoked cytosolic [Ca2+] and contractile responses of cardiomyocytes were determined. At 37 °C, epinephrine treatment increased both cytosolic [Ca2+] and contractile responses of cardiomyocytes in a concentration-dependent manner peaking at 25-50 nM. The evoked contractile response of cardiomyocytes after H/R was reduced while the cytosolic [Ca2+] response was slightly elevated. The diminished contractile response of cardiomyocytes after H/R was not mitigated by epinephrine (25 nM) and epinephrine treatment reduced the exponential time decay constant (Tau), but did not increase the cytosolic [Ca2+] response. We conclude that epinephrine treatment does not mitigate H/R-induced contractile dysfunction in cardiomyocytes.

INTERPLAY BETWEEN BRAIN OXYGENATION AND THE DEVELOPMENT OF HYPOTHERMIA IN ENDOTOXIC SHOCK.

ABSTRACT: There is evidence to suggest that the hypothermia observed in the most severe cases of systemic inflammation or sepsis is a regulated response with potential adaptive value, but the mechanisms involved are poorly understood. Here, we investigated the interplay between brain oxygenation (assessed by tissue P o2 ) and the development of hypothermia in unanesthetized rats challenged with a hypotension-inducing dose of bacterial LPS (1 mg/kg i.v.). At an ambient temperature of 22°C, oxygen consumption (V̇O 2 ) began to fall only a few minutes after the LPS injection, and this suppression in metabolic rate preceded the decrease in core temperature. No reduction in brain P o2 was observed prior to the development of the hypometabolic, hypothermic response, ruling out the possibility that brain hypoxia served as a trigger for hypothermia in this model. Brain P o2 was even increased. Such an improvement in brain oxygenation could reflect either an increased O 2 delivery or a decreased O 2 consumption. The former explanation seems unlikely because blood flow (cardiac output) was being progressively decreased during the recording period. On the other hand, the decrease in V̇O 2 usually preceded the rise in P o2 , and an inverse correlation between V̇O 2 and brain P o2 was consistently observed. These findings do not support the existence of a closed-loop feedback relationship between brain oxygenation and hypothermia in systemic inflammation. The data are consistent with a feedforward mechanism in which hypothermia is triggered (possibly by cryogenic inflammatory mediators) in anticipation of changes in brain oxygenation to prevent the development of tissue hypoxia.

Effect of active forced air warming during the first hour after anesthesia induction and intraoperation avoids hypothermia in elderly patients.

BACKGROUND: The study aimed at exploring an optimal temperature model of forced air warming during the first hour after induction and intraoperation to prevent hyperthermia for elderly patients undergoing laparoscopic abdominal surgery. METHODS: There were 218 patients that were randomly divided into 3 groups warmed with a forced-air warmer during surgery: Group L (intraoperative warming set to 38 °C, n = 63), Group H (intraoperative warming set to 42 °C, n = 65) and Group LH (intraoperative warming set to 42 °C for the first hour then set to 38 °C, n = 65). Core temperature in the preoperative room and PACU was measured by a tympanic membrane thermometer and in the operation room, a nasopharyngeal temperature probe was recorded. The rate of perioperative hypothermia, defined as a reduction in body temperature to < 36 °C was recorded as the primary outcome. Intraoperative anesthetic dosage, recovery time, adverse events, thermal comfort and satisfaction score were measured as secondary outcome. RESULTS: The incidence of intraoperative and postoperative hypothermia was significantly lower in Group LH and Group H than Group L (18.75 and 15.62% vs 44.44%, P<0.001; 4.69 and 4.69% vs 20.63%, P<.05). Anesthetic dosage of rocuronium was lower in Group L than other two groups, with the opposite result of recovery time. The number of patients with shivering was higher in Group L but sweating was higher in Group H. Both of the thermal comfort and satisfaction score was highest in Group LH. CONCLUSION: A temperature pattern of forced air warming set at 42 °C during the first hour after anesthesia induction and maintained with 38 °C was a suitable choice for elderly patients undergoing laparoscopic abdominal surgery lasting for more than 120 min. TRIAL REGISTRATION: Chictr.org.cn ChiCTR-2,100,053,211.

Soluble thrombomodulin ameliorates aberrant hemostasis after rewarming in a rat accidental hypothermia model.

BACKGROUND: Accidental hypothermia (AH) sometimes leads to coagulation disorder, especially in severe AH. We previously demonstrated that intrasplenic platelet activation caused aberrant hemostasis and thrombus formation after rewarming in a murine AH model. However, no study has focused on the appropriate management of platelets causing coagulation activation after rewarming of AH. We investigated whether or not recombinant soluble thrombomodulin (rTM) can suppress thrombosis formation after rewarming using a rat AH model. METHODS: Wistar rats were exposed to an ambient temperature of -20 °C under general anesthesia until their rectal temperature decreased to 26 °C. The Hypo group rats (n = 5) were immediately euthanized, while the Hypo/Re group (n = 5) and rTM group rats (n = 5), which were administered rTM (1 mg/kg) via the tail vein, were rewarmed until the rectal temperature returned to 34 °C and then euthanized 6 h later. Tissue and blood samples were collected from all rats for histopathological and coagulation analyses at euthanasia. RESULTS: There was no significant change in the D-dimer level in the Hypo group rats, while the D-dimer level was significantly elevated at 6 h after rewarming in the Hypo/Re group rats (P = 0.015), and histopathology detected both fibrin and platelets in the renal glomerulus. However, the rTM group rats did not show any elevation of the D-dimer levels at 6 h after rewarming, and no fibrin was noted on histopathology. CONCLUSIONS: rTM may be useful as an appropriate anticoagulant in cases of aberrant hemostasis after rewarming of AH.

Left Ventricular Function Changes Induced by Moderate Hypothermia Are Rapidly Reversed After Rewarming-A Clinical Study.

OBJECTIVES: Targeted temperature management (32-36°C) is used for neuroprotection in cardiac arrest survivors. The isolated effects of hypothermia on myocardial function, as used in clinical practice, remain unclear. Based on experimental results, we hypothesized that hypothermia would reversibly impair diastolic function with less tolerance to increased heart rate in patients with uninsulted hearts. DESIGN: Prospective clinical study, from June 2015 to May 2018. SETTING: Cardiothoracic surgery operation room, Oslo University Hospital. PATIENTS: Twenty patients with left ventricular ejection fraction greater than 55%, undergoing ascending aorta graft-replacement connected to cardiopulmonary bypass were included. INTERVENTIONS: Left ventricular function was assessed during reduced cardiopulmonary bypass support at 36°C, 32°C prior to graft-replacement, and at 36°C postsurgery. Electrocardiogram, hemodynamic, and echocardiographic recordings were made at spontaneous heart rate and 90 beats per minute at comparable loading conditions. MEASUREMENTS AND MAIN RESULTS: Hypothermia decreased spontaneous heart rate, and R-R interval was prolonged (862 ± 170 to 1,156 ± 254 ms, p < 0.001). Although systolic and diastolic fractions of R-R interval were preserved (0.43 ± 0.07 and 0.57 ± 0.07), isovolumic relaxation time increased and diastolic filling time was shortened. Filling pattern changed from early to late filling. Systolic function was preserved with unchanged myocardial strain and stroke volume index, but cardiac index was reduced with maintained mixed venous oxygen saturation. At increased heart rate, systolic fraction exceeded diastolic fraction (0.53 ± 0.05 and 0.47 ± 0.05) with diastolic impairment. Strain and stroke volume index were reduced, the latter to 65% of stroke volume index at spontaneous heart rate. Cardiac index decreased, but mixed venous oxygen saturation was maintained. After rewarming, myocardial function was restored. CONCLUSIONS: In patients with normal left ventricular function, hypothermia impaired diastolic function. At increased heart rate, systolic function was subsequently reduced due to impeded filling. Changes in left ventricular function were rapidly reversed after rewarming.

Changes in breathing pattern during severe hypothermia and autoresuscitation from hypothermic respiratory arrest in anesthetized mice.

Some evidence suggests that both hypothermia and anesthesia can exert similar effects on metabolism and ventilation. This study examined the synergistic effects of anesthesia and hypothermia on ventilation in spontaneously breathing adult mice under three different conditions, that is, (1) pentobarbital group (n = 7) in which mice were anesthetized with intraperitoneal pentobarbital of 80 mg/kg, (2) sevoflurane-continued group (n = 7) in which mice were anesthetized with 1 MAC sevoflurane, and (3) sevoflurane-discontinued group (n = 7) in which sevoflurane was discontinued at a body temperature below 22˚C. We cooled mice in each group until breathing ceased and followed this with artificial rewarming while measuring changes in respiratory variables and heart rate. We found that the body temperature at which respiration arrested is much lower in the sevoflurane-discontinued group (13.8 ± 2.0˚C) than that in the sevoflurane-continued group (16.7 ± 1.2˚C) and the pentobarbital group (17.0 ± 1.4˚C). Upon rewarming, all animals in all three groups spontaneously recovered from respiratory arrest. There was a considerable difference in breathing patterns between sevoflurane-anesthetized mice and pentobarbital-anesthetized mice during progressive hypothermia in terms of changes in tidal volume and respiratory frequency. The changes in the respiratory pattern during rewarming are nearly mirrored images of the changes observed during cooling in all three groups. These observations indicate that adult mice are capable of autoresuscitation from hypothermic respiratory arrest and that anesthesia and hypothermia exert synergistic effects on the occurrence of respiratory arrest while the type of anesthetic affects the breathing pattern that occurs during progressive hypothermia leading to respiratory arrest.

Effects of rewarming with extracorporeal membrane oxygenation to restore oxygen transport and organ blood flow after hypothermic cardiac arrest in a porcine model.

We recently documented that cardiopulmonary resuscitation (CPR) generates the same level of cardiac output (CO) and mean arterial pressure (MAP) during both normothermia (38 °C) and hypothermia (27 °C). Furthermore, continuous CPR at 27 °C provides O2 delivery (DO2) to support aerobic metabolism throughout a 3-h period. The aim of the present study was to investigate the effects of extracorporeal membrane oxygenation (ECMO) rewarming to restore DO2 and organ blood flow after prolonged hypothermic cardiac arrest. Eight male pigs were anesthetized and immersion cooled to 27 °C. After induction of hypothermic cardiac arrest, CPR was started and continued for a 3-h period. Thereafter, the animals were rewarmed with ECMO. Organ blood flow was measured using microspheres. After cooling with spontaneous circulation to 27 °C, MAP and CO were initially reduced to 66 and 44% of baseline, respectively. By 15 min after the onset of CPR, there was a further reduction in MAP and CO to 42 and 25% of baseline, respectively, which remained unchanged throughout the rest of 3-h CPR. During CPR, DO2 and O2 uptake (V̇O2) fell to critical low levels, but the simultaneous small increase in lactate and a modest reduction in pH, indicated the presence of maintained aerobic metabolism. Rewarming with ECMO restored MAP, CO, DO2, and blood flow to the heart and to parts of the brain, whereas flow to kidneys, stomach, liver and spleen remained significantly reduced. CPR for 3-h at 27 °C with sustained lower levels of CO and MAP maintained aerobic metabolism sufficient to support DO2. Rewarming with ECMO restores blood flow to the heart and brain, and creates a "shockable" cardiac rhythm. Thus, like continuous CPR, ECMO rewarming plays a crucial role in "the chain of survival" when resuscitating victims of hypothermic cardiac arrest.

Delta QRS distinguishes Ito -mediated J waves from pseudo J waves produced by conduction delay on body surface electrocardiographic.

BACKGROUND: On surface electrocardiographic (ECGs), it is difficult to differentiate Ito -mediated J waves, a repolarization phenomenon seen in J wave syndromes (JWS) from terminal QRS deflections that mimic J waves (pseudo J waves) in intraventricular conduction delay (IVCD), an abnormality in depolarization. We hypothesize that the difference between the "maximum QRS duration" inclusive of J point or terminal QRS deflections and the minimum QRS duration identified across a 12-lead ECG is significantly larger in Ito -mediated J waves, and can serve as a marker to make this distinction. METHODS: A retrospective analysis was performed on adults with ECGs consisting of one of the four following manifestations: J waves associated with hypothermia and early repolarization, and pseudo J waves associated with right bundle branch block (RBBB) and non-specific intraventricular conduction delay (NS-IVCD). All ECGs were assessed individually and the maximum and minimum discrete QRS deflections on 12-lead tracings, defined as "QRSmax " and QRSmin , were identified. The difference between "QRSmax " and QRSmin , designated as ∆QRS, was calculated and compared across the studied populations. RESULTS: A total of 60 patients consisting of 15 patients in each arm were included in the study. ΔQRS was significantly larger in the hypothermia and early repolarization groups, compared to RBBB and NS-IVCD (p < .0001), with the following mean ∆QRS: hypothermia 54.3 ± 13.7 ms, early repolarization pattern 47.3 ± 15.3 ms, RBBB 19.3 ± 6.5 ms, and NS-IVCD 16.0 ± 6.6 ms. CONCLUSION: ∆QRS may serve as a reliable ECG parameter for distinguishing Ito -mediated J waves from pseudo J waves produced by delayed intraventricular conduction.

Naturally occurring hypothermia promotes survival in severe anaphylaxis.

Although hypothermia has received substantial attention as an indicator of severity in anaphylaxis, it has been neglected from the perspective of whether it could act as a disease-modifying factor in this condition. Here, the impact of naturally occurring (spontaneous) hypothermia on anaphylaxis was evaluated in a murine model of ovalbumin (OVA)-induced allergy. Nonextreme changes in the ambient temperature (Ta) were used to modulate the magnitude of spontaneous hypothermia. At a Ta of 24°C, challenge with OVA intraperitoneally or intravenously resulted in a rapid, transient fall in body core temperature, which reached its nadir 4-6°C below baseline in 30 min. This hypothermic response was largely attenuated when the mice were kept at a Ta of 34°C. The Ta-dependent attenuation of hypothermia resulted in a survival rate of only 30%, as opposed to survival of 100% in the condition that favored the development of hypothermia. The protective effect of hypothermia did not involve changes in the rate of mast cell degranulation, as assessed by the concentration of mast cell protease-1 in bodily fluids. On the other hand, hypothermia improved oxygenation of the brain and kidneys, as indicated by higher NAD+/NADH ratios. Therefore, it is plausible to propose that naturally occurring hypothermia makes organs more resistant to the anaphylactic insult.

Central GABAA receptor mediates taurine-induced hypothermia and possibly reduces food intake in thermo-neutral chicks and regulates plasma metabolites in heat-exposed chicks.

The aim of this study was to examine the central action of taurine on body temperature and food intake in neonatal chicks under control thermoneutral temperature (CT) and high ambient temperature (HT). Intracerebroventricular injection of taurine caused dose-dependent hypothermia and reduced food intake under CT. The mRNA expression of the GABAA receptors, GABAAR-α1 and GABAAR-γ, but not that of GABABR, significantly decreased in the diencephalon after central injection of taurine. Subsequently, we found that picrotoxin, a GABAAR antagonist, attenuated taurine-induced hypothermia. Central taurine significantly decreased the brain concentrations of 3-methoxy-4-hydroxyphenylglycol, a major metabolite of norepinephrine; however, the concentrations of serotonin, dopamine, and the epinephrine metabolites, 3,4-hydroxyindoleacetic acid and homovanillic acid, were unchanged. Although hypothermia was not observed under HT after central injection of taurine, plasma glucose and uric acid levels were higher, and plasma sodium and calcium levels were lower, than those in chicks under CT. In conclusion, brain taurine may play a role in regulating body temperature and food intake in chicks through GABAAR. The changes in plasma metabolites under heat stress suggest that brain taurine may play an important role in maintaining homeostasis in chicks.

Pharmacological torpor prolongs rat survival in lethal normobaric hypoxia.

Resistance to hypoxia is one of the most prominent features of natural hibernation and is expected to be present in the pharmacological torpor (PT) that simulates hibernation. We studied resistance to lethal hypoxia (3.5% oxygen content) in rats under PT. To initiate PT, we used the previously developed pharmacological composition (PC) which, after a single intravenous injection, can induce a daily decrease in Tb by 7 °C-8 °C at the environmental temperature of 22 °C-23 °C. Half-survival (median) time of rats in lethal hypoxia was found to increase from 5 ± 0.8 min in anesthetized control rats to 150 ± 12 min in rats injected with PC, which is a 30-fold increase. Behavioral tests after PT and hypoxia, including the traveling distance, the number of rearing and grooming episodes, revealed that animal responses are significantly restored within a week. It is assumed that the discovered unprecedented resistance of artificially torpid rats to lethal hypoxia may open up broad prospects for the therapeutic use of PT for preconditioning to various damaging factors, treatment of diseases, and extend the so-called "golden hour" for lifesaving interventions.

Posterior subthalamic nucleus (PSTh) mediates innate fear-associated hypothermia in mice.

The neural mechanisms of fear-associated thermoregulation remain unclear. Innate fear odor 2-methyl-2-thiazoline (2MT) elicits rapid hypothermia and elevated tail temperature, indicative of vasodilation-induced heat dissipation, in wild-type mice, but not in mice lacking Trpa1-the chemosensor for 2MT. Here we report that Trpa1-/- mice show diminished 2MT-evoked c-fos expression in the posterior subthalamic nucleus (PSTh), external lateral parabrachial subnucleus (PBel) and nucleus of the solitary tract (NTS). Whereas tetanus toxin light chain-mediated inactivation of NTS-projecting PSTh neurons suppress, optogenetic activation of direct PSTh-rostral NTS pathway induces hypothermia and tail vasodilation. Furthermore, selective opto-stimulation of 2MT-activated, PSTh-projecting PBel neurons by capturing activated neuronal ensembles (CANE) causes hypothermia. Conversely, chemogenetic suppression of vGlut2+ neurons in PBel or PSTh, or PSTh-projecting PBel neurons attenuates 2MT-evoked hypothermia and tail vasodilation. These studies identify PSTh as a major thermoregulatory hub that connects PBel to NTS to mediate 2MT-evoked innate fear-associated hypothermia and tail vasodilation.

Effect of Preoperative Oral Carbohydrate Loading on Body Temperature During Combined Spinal-Epidural Anesthesia for Elective Cesarean Delivery.

BACKGROUND: Intraoperative hypothermia is a common complication after neuraxial block in cesarean delivery. At least 1 animal study has found that carbohydrate loading can maintain the body temperature of rats during general anesthesia, but it is unclear whether carbohydrate loading is beneficial for body temperature maintenance in parturient women during combined spinal-epidural anesthesia (CSEA) for elective cesarean delivery. METHODS: Women undergoing elective cesarean delivery were randomized into a control group (group C), an oral carbohydrate group (group OC), or an oral placebo group (group OP), with 40 women in each group. Core body temperature (Tc) and body surface temperature (Ts) before and after cesarean delivery, changes in Tc (ΔTc) and Ts (ΔTs), and the incidence of side effects (eg, intraoperative shivering) were compared among the groups. RESULTS: The postoperative Tc (core body temperature after cesarean delivery [Tc2]) of group OC (36.48 [0.48]°C) was higher than those of group C (35.95 [0.55]°C; P < .001), and group OP (36.03 [0.49]°C; P = .001). The ΔTc (0.30 [0.39]°C) in group OC was significantly smaller than those in group C (0.73 [0.40]°C; P = .001) and group OP (0.63 [0.46]°C; P = .0048). CONCLUSIONS: Oral carbohydrate loading 2 hours before surgery facilitated body temperature maintenance during CSEA for elective cesarean delivery.