Abstract 100: Neuroprotection Provided by Transnasal Airflow-Induced Brain Cooling in a Model of Pediatric Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Zeng-Jin Yang ◽  
C. Danielle Hopkins ◽  
Shawn Adams ◽  
Ewa Kulikowicz ◽  
Harikrishna S Tandri ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Sensorimotor Cortex ◽  
Brain Temperature ◽  
Low Cost ◽  
Venous Blood ◽  
Swine Model ◽  
Brain Cooling ◽  
Surface Cooling ◽  
Arterial Blood ◽  
Normothermic Group

Introduction: High transnasal airflow at ambient temperature increases evaporative cooling of the nasal passages and drives a countercurrent heat exchange between cooled venous blood draining the nasal turbinates with cephalic arterial blood. Hypothesis: High transnasal airflow is not inferior to standard surface cooling in protecting the brain in an infant swine model of asphyxic cardiac arrest. Methods: Arterial O2 saturation was decreased to ~35% for 45 min followed by 7 min airway occlusion to produce asphyxic cardiac arrest in 2-week-old anesthetized piglets (4 kg). Viable neuronal counts were assessed at 6 days of recovery in 6 groups (n=5-9): 1) sham surgery, 2) normothermic recovery, 3) surface cooling to decrease rectal temperature from 38.5 to 34C between 10-120 min 4) transnasal cooling with airflow of 32 L/min from 10-120 min, 5) surface cooling onset delayed until 120 min ROSC, and 6) transnasal cooling delayed by 120 min ROSC. In all 4 cooling groups, hypothermia was sustained at 34C with surface cooling until 20 h ROSC followed by 6-8 h of rewarming. Results: Nasal airflow of 32 L/min decreased brain temperature from 38.3±0.3°C to 33.8±0.6 within 60 min without spatial temperature gradients in these 45-g brains. Surface cooling and transnasal airflow rescued the number of viable neurons in putamen from 38±23% (% of sham viable neurons; ±SD) in the normothermic group to 67±33% and 76±36%, respectively, when initiated at 10 min ROSC, and to 72±30% and 61±25%, respectively, when initiated at 120 min. In sensorimotor cortex, surface cooling and transnasal airflow rescued neurons from 56±36% in the normothermic group to 89±37% and 89±29%, respectively, when initiated at 10 min ROSC, and to 84±19% and 81±28%, respectively, when initiated at 120 min. Conclusions: The use of a high transnasal airflow is as effective as standard surface cooling when initiated at 10 or 120 min after ROSC in protecting vulnerable putamen and sensorimotor cortex from asphyxic cardiac arrest in infant piglets. Because of its simplicity, portability, and low cost, we postulate that transnasal cooling potentially could be deployed in the field by first responders for early initiation of brain cooling prior to maintenance with standard surface cooling after pediatric cardiac arrest.

Abstract 246: Therapeutic Hypothermia Mimicking Peptide Administration During Cardiopulmonary Resuscitation Improved Cardiac Arrest Survival in Swine

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Matt Oberdier ◽  
Jing Li ◽  
Dan Ambinder ◽  
Xiangdong Zhu ◽  
Sarah Fink ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Sudden Cardiac Arrest ◽  
The United States ◽  
Rapid Onset ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Swine Model

Background: Out-of-hospital sudden cardiac arrest is a leading cause of death in the United States, affecting over 350,000 people per year with an overall survival rate around 10%. CPR, defibrillation, and therapeutic hypothermia are common resuscitation strategies, but hypothermia is difficult to implement timely to achieve survival benefit. A cell-permeable peptide TAT-PHLPP9c has been shown to alter metabolic pathways similar to hypothermia, and decreases the release of two biomarkers, taurine and glutamate, during the high osmotic stress of heart stunning and brain injury in a mouse arrest model. Hypothesis: TAT-PHLPP9c, given during CPR, enhances 24-hour survival in a swine ventricular fibrillation (VF) model. Methods: In 14 (8 controls and 6 treated) sedated, intubated, and mechanically ventilated swine, after 5 min of VF, ACLS with vest CPR and periodic defibrillations was performed. Venous blood samples were collected at baseline, after 2 min of CPR, and at 2 and 30 min after return of spontaneous circulation (ROSC). The animals were survived up to 24 hrs and plasma samples were analyzed for glutamate and taurine in 2 controls and 1 animal given peptide. Results: Three of the control animals had ROSC, but none survived for 24 hrs, while 4 of 6 treated animals achieved neurologically intact survival at 24 hrs (p < 0.02). Compared to baseline, both taurine and glutamate plasma concentrations increased in the control group, but the increase was reduced substantially by the peptide treatment at 30 min after ROSC (Figure). Conclusion: The use of the cooling mimicking peptide TAT-PHLPP9c administered during CPR significantly improved 24-hour survival in this swine model of cardiac arrest. It reduced the increase of cerebral and myocardial metabolic biomarkers, which encourages utilizing a strategy of cell-permeable peptides for intravenous administration for more rapid onset of hypothermia-like salutary effects than are possible with current CPR cooling devices.

Rectal temperature measurement results in artifactual evidence of selective brain cooling

2001 ◽  
Vol 281 (1) ◽  
pp. R108-R114 ◽  
Author(s):  
Shane K. Maloney ◽  
Andrea Fuller ◽  
Graham Mitchell ◽  
Duncan Mitchell
Keyword(s):  
Rectal Temperature ◽  
Brain Temperature ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
Blood Temperature ◽  
Arterial Blood ◽  
The Status ◽  
Conscious Sheep ◽  
Surrogate Measures ◽  
Arterial Blood Temperature

Selective brain cooling (SBC) is defined as a brain temperature cooler than the temperature of arterial blood from the trunk. Surrogate measures of arterial blood temperature have been used in many published studies on SBC. The use of a surrogate for arterial blood temperature has the potential to confound proper identification of SBC. We have measured brain, carotid blood, and rectal temperatures in conscious sheep exposed to 40, 22, and 5°C. Rectal temperature was consistently higher than arterial blood temperature. Brain temperature was consistently cooler than rectal temperature during all exposures. Brain temperature only fell below carotid blood temperature during the final few hours of 40°C exposure and not at all during the 5°C exposure. Consequently, using rectal temperature as a surrogate for arterial blood temperature does not provide a reliable indication of the status of the SBC effector. We also show that rapid suppression of SBC can result if the animals are disturbed.

Dehydration increases the magnitude of selective brain cooling independently of core temperature in sheep

2007 ◽  
Vol 293 (1) ◽  
pp. R438-R446 ◽  
Author(s):  
Andrea Fuller ◽  
Leith C. R. Meyer ◽  
Duncan Mitchell ◽  
Shane K. Maloney
Keyword(s):  
Drinking Water ◽  
Brain Temperature ◽  
Heat Exposure ◽  
Plasma Osmolality ◽  
Threshold Temperature ◽  
Evaporative Heat Loss ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
Blood Temperature ◽  
Arterial Blood

By cooling the hypothalamus during hyperthermia, selective brain cooling reduces the drive on evaporative heat loss effectors, in so doing saving body water. To investigate whether selective brain cooling was increased in dehydrated sheep, we measured brain and carotid arterial blood temperatures at 5-min intervals in nine female Dorper sheep (41 ± 3 kg, means ± SD). The animals, housed in a climatic chamber at 23°C, were exposed for nine days to a cyclic protocol with daytime heat (40°C for 6 h). Drinking water was removed on the 3rd day and returned 5 days later. After 4 days of water deprivation, sheep had lost 16 ± 4% of body mass, and plasma osmolality had increased from 290 ± 8 to 323 ± 9 mmol/kg ( P < 0.0001). Although carotid blood temperature increased during heat exposure to similar levels during euhydration and dehydration, selective brain cooling was significantly greater in dehydration (0.38 ± 0.18°C) than in euhydration (−0.05 ± 0.14°C, P = 0.0008). The threshold temperature for selective brain cooling was not significantly different during euhydration (39.27°C) and dehydration (39.14°C, P = 0.62). However, the mean slope of lines of regression of brain temperature on carotid blood temperature above the threshold was significantly lower in dehydrated animals (0.40 ± 0.31) than in euhydrated animals (0.87 ± 0.11, P = 0.003). Return of drinking water at 39°C led to rapid cessation of selective brain cooling, and brain temperature exceeded carotid blood temperature throughout heat exposure on the following day. We conclude that for any given carotid blood temperature, dehydrated sheep exposed to heat exhibit selective brain cooling up to threefold greater than that when euhydrated.

Selective regulation of brain and body temperatures in the squirrel monkey

1983 ◽  
Vol 245 (2) ◽  
pp. R293-R297 ◽  
Author(s):  
C. A. Fuller ◽  
M. A. Baker
Keyword(s):  
Squirrel Monkey ◽  
Brain Temperature ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Body Core Temperature ◽  
Saimiri Sciureus ◽  
Brain Cooling ◽  
The Face ◽  
Body Core

Many panting mammals can cool the brain below body core temperature during heat stress. Studies on human subjects suggest that primates may also be able selectively to regulate brain temperature. We examined this possibility by measuring hypothalamic (Thy) and colonic (Tco) temperatures of unanesthetized squirrel monkeys (Saimiri sciureus) in two different experiments. First, Thy and Tco were examined at four different ambient temperatures (Ta) between 20 and 36 degrees C. Over this range of Ta, Thy was regulated within a narrower range than Tco. In the cold Ta, Tco was lower than Thy; whereas in warm Ta, Tco was higher than Thy. Second, monkeys maintained at 35 degrees C Ta were acutely exposed to cool air blown on the face or abdomen. Air directed at the face cooled Thy more and faster than Tco, whereas air directed at the abdomen cooled Tco and Thy at the same rate. The second experiment was repeated in anesthetized animals with a thermocouple in the right atrium, and the results showed that this brain cooling was not produced by cooling of blood in the body core. These data demonstrate that the squirrel monkey is capable of selectively regulating Thy. Further the results suggest that venous blood returning from the face may be involved in selective brain cooling in warm environments.

Abstract P139: A Paradoxical Increase in Brain Temperature Occurs Early During Cardiopulmonary Arrest.

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Manuel C Boller ◽  
Joseph M Katz ◽  
Lance B Becker
Keyword(s):  
Cardiac Arrest ◽  
Brain Temperature ◽  
Cardiopulmonary Arrest ◽  
Heat Removal ◽  
External Heat ◽  
Brain Cooling ◽  
The Face ◽  
The Brain ◽  
Domestic Swine ◽  
Recorded Temperature

Introduction : In patients with cardiac arrest, brain cooling is a powerful intervention to improve neurological outcome. However, brain temperature variation during the initial phase of untreated cardiac arrest has not been well characterized. Objective : To describe passive changes in brain temperature in early untreated cardiac arrest. Methods : Eleven domestic swine (35 kg) were anesthetized and routine respiratory and cardiovascular parameters were monitored and recorded. Temperature was recorded from various sites including the forebrain. External heat support was adjusted to maintain rectal temperature at 37±0.5 °C at baseline, but was discontinued thereafter. Ventricular fibrillation was then induced and cardiac arrest remained untreated for 15 minutes. During this phase, forebrain temperature was recorded every 60 seconds. Results : The brain temperature increased in all animals after induction of cardiac arrest and remained above baseline for the duration of the study period. Peak mean (±SEM) increase above baseline was 0.26 (±0.03) °C and was reached after 9 minutes. Brain temperature slowly declined thereafter. The maximum and minimum temperature increase in individual animals was 0.42 °C and 0.13 °C, respectively. Conclusions : Brain temperature consistently and rapidly increases in the early phase of untreated cardiac arrest in anesthetized swine. This may parallel ongoing, yet diminishing, heat production from cerebral metabolic activity in the face of cessation of convective heat removal via cerebral blood flow.

Blood and brain temperatures of free-ranging black wildebeest in their natural environment

1994 ◽  
Vol 267 (6) ◽  
pp. R1528-R1536 ◽  
Author(s):  
C. Jessen ◽  
H. P. Laburn ◽  
M. H. Knight ◽  
G. Kuhnen ◽  
K. Goelst ◽  
...  
Keyword(s):  
Brain Temperature ◽  
Natural Habitat ◽  
Radiant Heat ◽  
Brain Cooling ◽  
Selective Brain Cooling ◽  
Blood Temperature ◽  
Arterial Blood ◽  
Data Loggers ◽  
Free Ranging ◽  
Arterial Blood Temperature

Using miniature data loggers, we measured the temperatures of carotid blood and brain in four wildebeest (Connochaetes gnou) every 2 min for 3 wk and every 5 min, in two of the animals, for a further 6 wk. The animals ranged freely in their natural habitat, in which there was no shelter. They were subject to intense radiant heat (maximum approximately 1,000 W/m2) during the day. Arterial blood temperature showed a circadian rhythm with low amplitude (< 1 degree C) and peaked in early evening. Brain temperature was usually within 0.2 degrees C of arterial blood temperature. Above a threshold between 38.8 and 39.2 degrees C, brain temperature tended to plateau so that the animals exhibited selective brain cooling. However, selective brain cooling sometimes was absent even when blood temperature was high and present when it was low. During helicopter chases, selective brain cooling was absent, even though brain temperature was near 42 degrees C. We believe that selective brain cooling is controlled by brain temperature but is modulated by sympathetic nervous system status. In particular, selective brain cooling may be abolished by high sympathetic activity even at high brain temperatures.

scholarly journals Point-of-Care Testing in Out-of-Hospital Cardiac Arrest: A Retrospective Analysis of Relevance and Consequences

2021 ◽  
Author(s):  
Tobias Gruebl ◽  
Birgit Ploeger ◽  
Erich Wranze-Bielefeld ◽  
Markus Mueller ◽  
Willi Schmidbauer ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Treatment Time ◽  
Point Of Care ◽  
Venous Blood ◽  
Hospital Setting ◽  
Hospital Treatment ◽  
Point Of Care Testing ◽  
Study Region ◽  
Probability Of Survival ◽  
Arterial Blood

Abstract BackgroundMetabolic and electrolyte imbalances are some of the reversible causes of cardiac arrest and can be diagnosed even in the pre-hospital setting with a mobile analyser for point-of-care testing (POCT).MethodsWe conducted a retrospective observational study, which included analysing all pre-hospital resuscitations in the study region between October 2015 and December 2016. A mobile POCT analyser (Alere epoc®) was available at the scene of each resuscitation. We analysed the frequency of use of POCT, the incidence of pathological findings, the specific interventions based on POCT as well as every patient’s eventual outcome.ResultsN=263 pre-hospital resuscitations were included and in n=98 of them, the POCT analyser was used. Of these measurements, 64% were performed using venous blood and 36% using arterial blood. The results of POCT showed that 63% of tested patients had severe metabolic acidosis (pH<7.2+BE<-5mmol/l). Of these patients, 82% received buffering treatment with sodium bicarbonate. Potassium levels were markedly divergent normal (>6.0mmol/l / <2.5mmol/l) in 17% of tested patients and 14% of them received a potassium infusion. On average, the pre-hospital treatment time between arrival of the first emergency medical responders and the beginning of transport was 54 (+/- 20) min without POCT and 60 (+/- 17) min with POCT (p=0.07). Overall, 21% of patients survived to hospital discharge (POCT 30% vs no POCT 16%, p=0.01).Conclusions Using a POCT analyser in pre-hospital resuscitation allows rapid detection of pathological acid-base imbalances and potassium concentrations and often leads to specific interventions on scene and could improve the probability of survival.

scholarly journals Point-of-care testing in out-of-hospital cardiac arrest: a retrospective analysis of relevance and consequences

2021 ◽  
Vol 29 (1) ◽  
Author(s):  
Tobias Gruebl ◽  
B. Ploeger ◽  
E. Wranze-Bielefeld ◽  
M. Mueller ◽  
W. Schmidbauer ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Treatment Time ◽  
Point Of Care ◽  
Venous Blood ◽  
Hospital Setting ◽  
Hospital Treatment ◽  
Point Of Care Testing ◽  
Study Region ◽  
Probability Of Survival ◽  
Arterial Blood

Abstract Background Metabolic and electrolyte imbalances are some of the reversible causes of cardiac arrest and can be diagnosed even in the pre-hospital setting with a mobile analyser for point-of-care testing (POCT). Methods We conducted a retrospective observational study, which included analysing all pre-hospital resuscitations in the study region between October 2015 and December 2016. A mobile POCT analyser (Alere epoc®) was available at the scene of each resuscitation. We analysed the frequency of use of POCT, the incidence of pathological findings, the specific interventions based on POCT as well as every patient’s eventual outcome. Results N = 263 pre-hospital resuscitations were included and in n = 98 of them, the POCT analyser was used. Of these measurements, 64% were performed using venous blood and 36% using arterial blood. The results of POCT showed that 63% of tested patients had severe metabolic acidosis (pH < 7.2 + BE <  − 5 mmol/l). Of these patients, 82% received buffering treatment with sodium bicarbonate. Potassium levels were markedly divergent normal (> 6.0 mmol/l/ < 2.5 mmol/l) in 17% of tested patients and 14% of them received a potassium infusion. On average, the pre-hospital treatment time between arrival of the first emergency medical responders and the beginning of transport was 54 (± 20) min without POCT and 60 (± 17) min with POCT (p = 0.07). Overall, 21% of patients survived to hospital discharge (POCT 30% vs no POCT 16%, p = 0.01, Φ = 0.16). Conclusions Using a POCT analyser in pre-hospital resuscitation allows rapid detection of pathological acid–base imbalances and potassium concentrations and often leads to specific interventions on scene and could improve the probability of survival.

Abstract 129: Gasping During Cardiac Arrest Before Cardiopulmonary Resuscitation Increases Cerebral Oximetry in a Swine Model

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Nelly Rojas-Salvador ◽  
Bayert Salverda ◽  
Johanna C Moore ◽  
Michael Lick ◽  
Guillaume P Debaty ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Near Infrared ◽  
Venous Blood ◽  
Intrathoracic Pressure ◽  
Aortic Pressure ◽  
Cerebral Oximetry ◽  
Right Atrial ◽  
Swine Model ◽  
Therapeutic Implications ◽  
The Impact

Introduction: Spontaneous gasping (SG) during cardiac arrest is associated with favorable neurological outcomes. SG lowers intrathoracic pressure (ITP), enhancing flow of respiratory gases to the lungs and venous blood to the heart, while simultaneously lowering intracranial pressure (ICP). The impact of SG on regional cerebral oximetry (rSO2) is unknown. Hypothesis: During untreated ventricular fibrillation (VF), SG will increase rSO2 until the gasping effort declines. Methods: Swine (~40 kg) were intubated and anesthetized with isoflurane. After 8 min of untreated VF, conventional mechanical CPR at 100 compressions/min was performed. Intrathoracic pressure (ITP), mean aortic pressure (MAP), ICP, right atrial pressure (RAP) and calculated cerebral perfusion pressure (CerPP) were measured continuously. rSO2 was measured continuously with near-infrared spectroscopy (Equanox 7600, Nonin Medical). These parameters were assessed before and during SG, and during CPR. Data are expressed as mean ± SD. A paired Student’s t- test was used. Results: SG occurred in 19/22 pigs during untreated VF, with 9.2 ± 4.3 gasps/pig. For pigs that gasped, the individual gasp duration was 1.74 ± 0.52 sec and the maximum negative ITP (mmHg) was -3.24 ± 1.93 mmHg. rSO2 increased in 9/19 (47%) pigs from 54.7% ± 4.1 to 57.8% ± 4.8 during SG (p<0.001). Figure 1 shows rSO2 from 2 representative pigs, A) with and B) without SG. SG also decreased ITP (p<0.001), RAP (p=0.02) and ICP (p<0.001), and increased MAP (p<0.001) and CerPP (p<0.001). After 8 min of untreated VF, rSO2 for all 22 pigs was 49.3% ± 3.7. After 30 and 60 sec of CPR, rSO2 values were 54.6% ± 3.8 and 57.8% ± 3.8, respectively. Conclusions: rSO2 values increased in nearly half of animals with SG. This increase in rSO2 with SG was equal to the level of rSO2 achieved after 1 minute of CPR. Further study is warranted to determine potential prognostic and therapeutic implications of SG-induced increases rSO2 during cardiac arrest.

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