Cerebral tissue oxygen saturation during therapeutic hypothermia in post-cardiac arrest patients

Aim of the study

This observational study was performed to assess the cerebral tissue oxygen saturation during and after therapeutic hypothermia in comatose patients after out-of-hospital cardiac arrest.

Methods

We performed a prospective observational study on the cerebral tissue oxygen saturation (SctO₂) in post-cardiac arrest patients treated with therapeutic hypothermia (TH) between March 2011 and April 2012. SctO₂ (measured by near-infrared spectroscopy) was non-invasively and continuously measured in 28 post-cardiac arrest patients during hypothermia and active rewarming.

Results

At the start of mechanically induced TH, SctO₂ was 68% (65–72) and PaCO₂ was 47.2 mmHg (36.9 – 51.4). SctO₂ and PaCO₂ significantly decreased to 59% (57–64; p = 0.006) and 36.6 mmHg (33.9–44.7; p = 0.002), respectively, within the first 3 h of mechanically induced TH. Cerebral tissue oxygen saturation was significantly lower in non-survivors (n = 10) compared with survivors (n = 18) at 3 h after induction of hypothermia (p = 0.02) while the decrease in PaCO₂ was similar in both groups. During TH maintenance, SctO₂ gradually returned to baseline values (69% (63–72)) at 24 h, with no differences between survivors and non-survivors (p = 0.65). Carbon dioxide remained within the range of mild hypocapnia (32–38 mmHg) throughout the hypothermic period. During rewarming, SctO₂ further increased to 71% (67–78).

Conclusions

Induction of TH in comatose post-CA patients changes the balance between oxygen delivery and supply. The decrease in SctO₂ was less pronounced in patients surviving to hospital discharge.     

Body temperature effects on lung injury in ventilated preterm lambs

Aims

Mechanical ventilation causes lung injury in premature infants. Hypothermia may protect against and hyperthermia may augment lung injury. We tested the effects of hypo- and hyperthermia on ventilation induced acute lung injury in preterm lambs.

Methods

Twin sheep fetuses at 128 d GA (term 150 d) were surgically delivered and randomized to unventilated control (UVC), normothermia (38-39 °C) without lung injury (NTNI), or to 1 of 3 injurious ventilation groups: hypothermic (33-34 °C, LT), normothermic (38-39 °C, NT) or hyperthermic (40-41 °C, HT). NT, LT and HT groups had 15 min of injurious ventilation (PEEP 0 cmH₂O, V_T escalation to 15 mL/kg) following delivery and prior to surfactant. The animals were then gently ventilated (PEEP 5 cmH₂O, V_T 7.5 mL/kg) for 2 h 45 min. NTNI lambs received surfactant at birth prior to gentle ventilation. The lambs were then euthanized, and bronchoalveolar lavage (BAL) fluid and lung tissue were used to evaluate lung injury, inflammatory cell counts, inflammatory markers and cytokine mRNA.

Results

Target temperatures were achieved by 15 min of age and maintained for 3 h. All ventilated groups had increased BAL protein, lung inflammation and increased cytokine mRNA. HT animals developed acidosis, premature death, pneumothoraces, impaired lung function and increased inflammatory mRNA expression. LT animals remained clinically stable without pneumothoraces or death, had improved ventilatory efficiency and trended toward lower inflammatory mRNA expression than NT animals.

Conclusion

Hyperthermia exacerbated ventilator induced lung injury, while hypothermia may protect against lung injury in the preterm lamb.     

Changing gas flow during neonatal resuscitation: a manikin study

Introduction

When using a T-piece device, resuscitators may try to improve airway pressures by increasing gas flow instead of correcting face mask position.

Aim

To measure the effects of changing gas flow during positive pressure ventilation (PPV) on peak inspiratory pressure (PIP), positive end expiratory pressure (PEEP), expiratory tidal volume (V_Te) and mask leak.

Methods

Using a Neopuff T-piece device, 20 neonatal staff members delivered PPV to a modified, leak-free manikin. Resuscitation parameters were recorded. Study A: PPV for 4 min at PIP 30 cm H₂O and PEEP 5 cm H₂O. Each minute gas flow was increased (5, 8, 10, and 15 L/min). PIP and PEEP settings were unchanged. Study B: same pressure settings; PPV for 1 min with 5, 8, 10, and 15 L/min in a random order, at a rate of ∼60/min. The pressures were adjusted to maintain the same PIP and PEEP after each flow change.

Results

Study A: As gas flow increased (5, 8, 10 and 15 L/min) the median PEEP increased from 4.7 to 26.4 cm H₂O (p < 0.002). Median V_Te decreased from 10.0 to 0.8 mL (p < 0.001). PIP increased slightly from 30 cm H₂O to 36 cm H₂O at 15 L/min (p < 0.005). Mask leak increased from 14% to 98% (p < 0.001) because mask pressure increased. Study B: when PIP and PEEP were maintained there were no significant differences in V_Te (p = 0.42) or mask leak (p = 0.51) with changing gas flow.

Conclusion

During PPV increasing gas flow dramatically increased PEEP and mask leak and in consequence reduced V_Te. Gas flow should rarely be changed during T-piece resuscitation.     

Effect of speed of rewarming and administration of anti-inflammatory or anti-oxidant agents on acute lung injury in an intestinal ischemia model treated with therapeutic hypothermia

Aim of the study

Acute lung injury (ALI) develops in various clinical situations and is associated with high morbidity and mortality and therapeutic hypothermia (HT) has been studied to attenuate the ALI. However, the optimal method of rewarming has not been determined. We determined the effect of speed of rewarming and the administration of anti-inflammatory or anti-oxidant agents on ALI in an intestinal ischemia and reperfusion (I/R) model treated with HT.

Materials and methods

A Sprague-Dawley rat model of intestine ischemia and reperfusion was used. Two parallel animal experiments were conducted. In the survival study, rats (n = 5 per group) underwent normothermic intestinal ischemia (60 min, 36-38 °C) and then randomized into 7 groups with reperfusion: normothermia (NT), HT without rewarming (30-32 °C, HT), 2 h HT + rewarming for 1 h (RW1), 2 h HT + rewarming for 2 h (RW2), RW1 + N-acetyl cysteine (RW-NAC), RW1 + ethylpyruvate (RW-EP), and RW1 + dexamethasone (RW + Dexa). In the second experiment, we investigated the histological and biochemical effects on the lung 4 h after reperfusion (n = 8 per group).

Results

The survival rate was lowest after NT. The HT, RW2, and RW-Dexa groups survived longer than the RW1, RW-NAC, and RW-EP groups. ALI scores were lower in the HT, RW2, and RW-Dexa groups than RW1. Lung malondialdehyde content was also lower in these groups. Interleukin (IL)-6 was significantly higher in the RW1 group. Inducible NO synthase gene expression in lung was lower in the HT, RW2, and RW-Dexa than RW1, and serum NO was lower in the RW2 and RW-Dexa than RW1.

Conclusion

Gradual rewarming and administration of dexamethasone improved survival and attenuated ALI after intestinal I/R injury treated with HT in rats.     

Therapeutic hypothermia attenuates acute lung injury in paraquat intoxication in rats

Aim of the study

Paraquat intoxication induces acute lung injury and numerous fatalities have been reported. The mechanism of toxic effect of paraquat is oxidative injury and inflammation. Therapeutic hypothermia has been known to have antioxidant and anti-inflammatory effects. This study was designed to evaluate the effect of therapeutic hypothermia on paraquat intoxication.

Methods

Male Sprague-Dawley rats were given 50 mg/kg of paraquat intraperitoneally and divided into the normothermia (36-38 °C) group and the hypothermia (30-32 °C) group after 1 h of paraquat administration. The hypothermia group underwent 2 h of hypothermia followed by 2 h of rewarming. In the survival study, mortality was observed for 24 h after paraquat administration. An in the second experiment, lung tissues and plasma were harvested at 6 h after paraquat administration.

Results

The 12 h survival rate was significantly higher in the hypothermia group than in the normothermia group (100% vs. 50%, p < 0.05), but survival rates for 24 h were not different. Acute lung injury score was lower in the hypothermia group than in the normothermia group (p < 0.05). Thmalondialdehyde contents of lung tissues, plasma interleukin-6 and nitrite/nitrate concentrations were significantly decreased in the HT group compared to the NT group (p < 0.05).

Conclusion

Therapeutic hypothermia delayed early mortality and attenuated acute lung injury in paraquat intoxication.     

Accidental hypothermia: Rewarming treatments, complications and outcomes from one university medical centre

Aim of the study

Accidental hypothermia (AH) is a complex and life threatening condition. Knowledge about epidemiology, rewarming treatments, complications and outcome is limited. This study was initiated to obtain data on causes, rewarming treatments and complications.

Methods

A retrospective cohort study of all patients with a body temperature ≤35 °C admitted to the Emergency Department (ED) of the VU university medical centre, Amsterdam, The Netherlands, between January 1, 2000 and August 31, 2008. A predefined set of epidemiological and clinical data was retrieved.

Results

Eighty-four patients were included (median age: 47 years). Categories of hypothermia included immersion (18), submersion (29) and exposure to cold (37); concomitant factors were intoxication (26), trauma (40) and homelessness (7). Temperature at admission in the ED was 31.6 ± 2.6 °C (mean ± SD), lowest temperature 24.2 °C. Fourteen different rewarming treatments were used resulting in a wide range of rewarming speeds. Seventy-nine complications occurred: pulmonary, renal and neurological complications in 20, 17 and 10 patients respectively. Seventeen patients had 2 or more late complications. Twenty-four patients (28.6%) died: 10 during rewarming and 14 after rewarming was completed. Prognosis was poor in older and colder patients and after indoor exposure and submersion.

Conclusion

AH is a rare diagnosis in an inhomogeneous population, treated with a large variety of rewarming techniques. Most complications and death occurred late, after rewarming was completed. Because individual teams gain little clinical experiences, we suggest multiple centre data collection as a first step towards an evidence-based standard of care.     

Cold saline infusion and ice packs alone are effective in inducing and maintaining therapeutic hypothermia after cardiac arrest

Aim of the study

Hypothermia treatment with cold intravenous infusion and ice packs after cardiac arrest has been described and used in clinical practice. We hypothesised that with this method a target temperature of 32-34 °C could be achieved and maintained during treatment and that rewarming could be controlled.

Materials and methods

Thirty-eight patients treated with hypothermia after cardiac arrest were included in this prospective observational study. The patients were cooled with 4 °C intravenous saline infusion combined with ice packs applied in the groins, axillae, and along the neck. Hypothermia treatment was maintained for 26 h after cardiac arrest. It was estimated that passive rewarming would occur over a period of 8 h. Body temperature was monitored continuously and recorded every 15 min up to 44 h after cardiac arrest.

Results

All patients reached the target temperature interval of 32-34 °C within 279 ± 185 min from cardiac arrest and 216 ± 177 min from induction of cooling. In nine patients the temperature dropped to below 32 °C during a period of 15 min up to 2.5 h, with the lowest (nadir) temperature of 31.3 °C in one of the patients. The target temperature was maintained by periodically applying ice packs on the patients. Passive rewarming started 26 h after cardiac arrest and continued for 8 ± 3 h. Rebound hyperthermia (>38 °C) occurred in eight patients 44 h after cardiac arrest.

Conclusions

Intravenous cold saline infusion combined with ice packs is effective in inducing and maintaining therapeutic hypothermia, with good temperature control even during rewarming.     

Perfluorocarbon induced intra-arrest hypothermia does not improve survival in a swine model of asphyxial cardiac arrest

Background

Pulseless electrical activity is an important cause of cardiac arrest. Our purpose was to determine if induction of hypothermia with a cold perfluorocarbon-based total liquid ventilation (TLV) system would improve resuscitation success in a swine model of asphyxial cardiac arrest/PEA.

Methods

Twenty swine were randomly assigned to control (C, no ventilation, n = 11) or TLV with pre-cooled PFC (n = 9) groups. Asphyxia was induced by insertion of a stopper into the endotracheal tube, and continued in both groups until loss of aortic pulsations (LOAP) was reached, defined as a pulse pressure less than 2 mmHg. The TLV animals underwent asphyxial arrest for an additional 2 min after LOAP, followed by 3 min of hypothermia, prior to starting CPR. The C animals underwent 5 min of asphyxia beyond LOAP. Both groups then underwent CPR for at least 10 min. The endpoint was the resumption of spontaneous circulation maintained for 10 min.

Results

Seven of 9 animals achieved resumption of spontaneous circulation (ROSC) in the TLV group vs. 5 of 11 in the C group (p = 0.2). The mean pulmonary arterial temperature was lower in total liquid ventilation animals starting 4 min after induction of hypothermia (TLV 36.3 ± 0.2 °C vs. C 38.1 ± 0.2 °C, p < 0.0001). Arterial pO₂ was higher in total liquid ventilation animals at 2.5 min of CPR (TLV 76 ± 12 mmHg vs. C 44 ± 2 mmHg; p = 0.03).

Conclusion

Induction of moderate hypothermia using perfluorocarbon-based total liquid ventilation did not improve ROSC success in this model of asphyxial cardiac arrest.     

Therapeutic hypothermia after cardiac arrest: A retrospective comparison of surface and endovascular cooling techniques

Objectives

Therapeutic hypothermia (32-34 °C) is recommended for comatose survivors of cardiac arrest; however, the optimal technique for cooling is unknown. We aimed to compare therapeutic hypothermia using either surface or endovascular techniques in terms of efficacy, complications and outcome.

Design

Retrospective cohort study.

Setting

Thirty-bed teaching hospital intensive care unit (ICU).

Patients

All patients (n = 83) undergoing therapeutic hypothermia following cardiac arrest over a 2.5-year period. The mean age was 61 ± 16 years; 88% of arrests occurred out of hospital, and 64% were ventricular fibrillation/tachycardia.

Interventions

Therapeutic hypothermia was initiated in the ICU using iced Hartmann's solution, followed by either surface (n = 41) or endovascular (n = 42) cooling; choice of technique was based upon endovascular device availability. The target temperature was 32-34 °C for 12-24 h, followed by rewarming at a rate of 0.25 °C h⁻¹.

Measurements and main results

Endovascular cooling provided a longer time within the target temperature range (p = 0.02), less temperature fluctuation (p = 0.003), better control during rewarming (0.04), and a lower 48-h temperature load (p = 0.008). Endovascular cooling also produced less cooling-associated complications in terms of both overcooling (p = 0.05) and failure to reach the target temperature (p = 0.04). After adjustment for known confounders, there were no differences in outcome between the groups in terms of ICU or hospital mortality, ventilator free days and neurological outcome.

Conclusion

Endovascular cooling provides better temperature management than surface cooling, as well as a more favorable complication profile. The equivalence in outcome suggested by this small study requires confirmation in a randomized trial.     

Accuracy of End-Tidal Co2 Capnometers in Post-Cardiac Surgery Patients During Controlled Mechanical Ventilation

Background

The determination of end-tidal carbon dioxide (etCO₂₎ is very helpful in cardiac resuscitation for confirmation and monitoring of endotracheal tube placement and as an indicator of return of circulation and effectiveness of chest compressions. There is now also widespread use of capnometry on-site at emergency and trauma fields.

Objective

We studied the accuracy and correlation of three capnometers (EMMA, Medtronic, and Evita) with partial pressure of arterial CO₂ (PaCO₂) measurements.

Methods

The three capnometers were placed in-line in the ventilator tubing of the patient. Forty sedated and mechanically ventilated post-cardiac surgery patients were studied. Twenty consecutive etCO₂ values were collected simultaneously from all three monitors while drawing an arterial blood sample. Paired sample t-test and Pearson correlation were used to compare the capnometers and their correlation with PaCO₂.

Results

The correlation of etCO₂ measurements between all three capnometers was good (Emma vs. Evita: 0.874, Emma vs. Medtronic: 0.949, Evita vs. Medtronic: 0.878). The correlation of PaCO₂ with the Evita is the lowest (0.671) as compared to the EMMA (0.693) and the Medtronic (0.727). The lowest dispersion of the difference between etCO₂ and PaCO₂ was seen in EMMA (3.30), the highest in Evita (3.98).

Conclusions

A good correlation between etCO₂ and PaCO₂ was shown with the three capnometers in the present study. However, etCO₂ measurements were not valid to estimate PaCO₂ in these patients. Therefore, capnometry cannot be used to replace serial blood gas analyses completely, but may be a good cardiopulmonary trend monitor and alerting system in catastrophic events.     

Tetramethylammonium ion causes respiratory failure related mortality in a rat model

Aim of the study

Tetramethylammonium ion (TMA) is an emerging industrial chemical and has caused mortalities in humans. The present study was conducted to evaluate the effects of subcutaneously injected TMA on heart rate (HR), mean arterial blood pressure (MAP) and arterial blood gases (ABG) and to determine whether pretreatment using mechanical ventilation (MV) or atropine could prevent the mortality caused by TMA.

Methods

Male Wistar rats were anesthetized and catheterized in the femoral arterials for monitoring. We injected 25, 50, 100, and 200 μmol/kg of TMA s.c. in four groups of rats respectively and compared them to a control group. The effects of MV and atropine (1 mg/kg, s.c.) pretreatment were evaluated by comparing the treatment groups with the 200 μmol/kg group. The primary outcome was survival curve, and the secondary endpoints included the changes of HR, MAP, and ABG, such as arterial pH, PaO₂, PaCO₂ and calculated HCO₃⁻.

Results

TMA decreased HR, MAP, pH, and PaO₂, increased PaCO₂ and calculated HCO₃⁻ and resulted in death of all animals in the 200 μmol/kg group by 15 min. All animals pretreated with MV survived. Although all animals receiving atropine died, the mean survival time increased by 37 min. Both MV and atropinization improved HR, MAP, and ABG.

Conclusion

This rat model suggests that acute respiratory failure is responsible for the mortality caused by TMA, and therefore first aid should emphasize respiratory support. Atropinization prolonged survival time in the present study that possibly bought time for further management.     

Therapeutic hypothermia after cardiac arrest - cerebral perfusion and metabolism during upper and lower threshold normocapnia

Background

During cardiac arrest and after successful resuscitation a continuum of ischaemia-reperfusion injury develops. Mild hypothermia exerts protective effects in the postresuscitation phase but also alters CO₂ production and solubility, which may lead to deleterious effects if overlooked when adjusting the ventilation of the resuscitated patient. Using a multimodality approach, the effects of different carbaemic states on cerebral perfusion and metabolism were evaluated during therapeutic hypothermia.

Methods

Eight comatose survivors of prehospital cardiac arrest were cooled to 33 °C for 24 h and underwent a 60 min phase of interventional lower threshold normocapnia according to temperature non-corrected pCO₂ (4.2 kPa) and higher threshold normocapnia according to corrected pCO₂ (6.0 kPa) in a random order. Prior to, during and after each phase, cerebral perfusion and metabolites via a microdialysis catheter were measured.

Results

During upper-threshold pCO₂, an increase in middle cerebral artery mean flow velocity (MFV) and jugular bulb oxygen saturation (jSvO₂) were observed with a concomitant decrease in cerebral lactate concentration. Lower threshold normocapnia was associated with a decrease in MFV in most patients. In all patients jSvO₂ decreased but no change in cerebral lactate was observed. In seven patients jSvO₂ decreased below 55%. These changes were not reflected to intracranial pressure or cerebral oximetry.

Conclusions

During induced hypothermia, lower threshold normocapnia was associated with decreased cerebral perfusion/oxygenation but not reflected to interstitial metabolites. Upper threshold pCO₂ increased cerebral perfusion and reduced cerebral lactate. Vigilance over the ventilatory and CO₂ analysis regimen is mandatory during mild hypothermia.     

Mechanical ventilators in the hot zone: Effects of a CBRN filter on patient protection and battery life

Objective

In a contaminated environment, respiratory protection for ventilator dependent patients can be achieved by attaching a chemical, biological, radiological, or nuclear (CBRN) filter to the air intake port of a portable ventilator. We evaluated the effect of the filter on battery performance of four portable ventilators in a laboratory setting.

Methods

Each ventilator was attached to a test lung. Ventilator settings were: assist control (AC) mode, respiratory rate 35 bpm, tidal volume 450 ml, positive end-expiratory pressure (PEEP) 10 cm H₂O, inspiratory time 0.8 s, and FIO₂ 0.21. Ventilators were operated until the battery was fully discharged. We also evaluated the ventilators’ ability to deliver all the gas through the CBRN filter and analyzed the pressures required to breathe through the anti-asphyxiation valve of a failed device.

Results

The range of battery life varied widely across different ventilator models (99.8-562.6 min). There was no significant difference in battery life (p < 0.01) when operating with or without the CBRN filter attached. Only the Impact 731 routed all inspired gases through the CBRN filter. The pressure required to breathe though the failed device was −4 cm H₂O to −9 cm H₂O.

Conclusions

Duration of operation from the internal battery was not altered by attachment of the CBRN filter. The use of a CBRN filter is necessary for protection of ventilator dependent patients when environmental contamination is present, although conditions exist where all gas does not pass through the filter with some ventilators under normal operating conditions.     

A structural model of perfusion and oxygenation in low-flow states

Background

Recent investigations underscore the critical importance of ventilation strategies on resuscitation outcomes. In low perfusion states, such as cardiac arrest and traumatic shock, the rise in intrathoracic pressure that accompanies positive-pressure ventilation can significantly impede venous return and lead to a decrease in cardiac output. The optimal ventilation strategy in these “low-flow” states remains unclear.

Objective

To create a mathematical model of perfusion and oxygenation to predict the effects of PPV with both normotension and hypotension.

Methods

The lung pressure-volume relationship was modeled using a novel formula allowing manipulation of various lung characteristics. A separate formula was then derived to predict mean intrathoracic pressure (MITP) for specific minute ventilation values using the pressure-volume formula. The addition of positive end-expiratory pressure was also modeled. Finally, a formula was derived to model oxygen absorbance as a function of alveolar surface area and flow based on ventilation rate and MITP.

Results

Mathematical models of the lung pressure-volume relationship, MITP, and absorbance were successfully derived. Manipulation of total lung capacity, compliance, upper and lower inflection points, positive end-expiratory pressure, and minute ventilation allowed prediction of optimal ventilation rate and tidal volume for a normal lung and with various abnormal characteristics to simulate particular disease states, such as acute respiratory distress syndrome (ARDS). For a normal lung, ventilation rates of 4-6 breaths/min with higher tidal volumes (15-20 mL/kg) resulted in the lowest predicted MITP values (5 cm H₂O) and the highest absorbance. The input of lung parameters that would simulate ARDS resulted in optimal ventilation rates of 10-12 breaths/min with lower tidal volumes (8-10 mL/kg) and higher predicted MITP values (10-15 cm H₂O).

Conclusions

A mathematical model of ventilation was successfully derived allowing manipulation of multiple pulmonary physiological variables to predict MITP and potentially identify optimal ventilation strategies. This model suggests the use of lower ventilation rates and larger tidal volumes to minimize the hemodynamic effects of positive pressure ventilation in patients with hypoperfusion but normal lung characteristics.     

Hypothermic protection in an acute hypoxia model in rats: Acid-base and oxidant/antioxidant profiles

Aim of the study

Recent works demonstrate the benefits of hypothermia when used to preserve brain, cardiac, hepatic, and intestinal function against hypoxic-ischemic injury. However, it is also known that hypothermia affects systemic parameters and also induces the generation of reactive oxygen species in cells and tissues. Here we studied the acid-base related parameters and the antioxidant-oxidant effects of deep hypothermia induction before an acute hypoxic insult in rats.

Methods

Acid-base indicators and parameters related to oxidative stress were analyzed in hypothermic rats (21-22 °C) breathing room air during 2 h (control hypothermia), and hypothermic animals switched to hypoxic air (10% O₂) during the second hour (hypothermia hypoxia group), and they were compared with corresponding normothermia groups maintained at 37 °C (control normothermia and normothermia hypoxia groups).

Results

Mild metabolic acidosis appeared early in arterial blood during hypothermia. After exposure to hypoxia, evidence of tissue injury (plasma transaminases and blood lactate) and oxidative stress (increase in lipid peroxidation, decrease in glutathione levels and in the glutathione reduction potential in liver) was found. In contrast, in the hypothermia hypoxia group, plasmatic parameters remained as the control values, and the hepatic glutathione reduction potential were significantly more negative when compared with the normothermia hypoxia group.

Conclusions

We propose that acidosis induced by hypothermia contributes to the maintenance of intracellular reduction potential in liver, regarding the GSSG/2GSH couple and may help to increase plasmatic antioxidant pool. Our findings provide new insights into the protective effects of hypothermia in vivo.     

Continuous tracheal gas insufflation during protective mechanical ventilation in juvenile piglets with acute lung injury induced by endotoxin

BACKGROUND:

Low tidal volume mechanical ventilation is difficult to correct hypoxemia, and prolonged inhalation of pure oxygen can lead to oxygen poisoning. We suggest that continuous tracheal gas insufflation (TGI) during protective mechanical ventilation could improve cardiopulmonary function in acute lung injury.

METHODS:

Totally 12 healthy juvenile piglets were anesthetized and mechanically ventilated at PEEP of 2 cmH₂O with a peak inspiratory pressure of 10 cmH₂O. The piglets were challenged with lipopolysaccharide and randomly assigned into two groups (n=6 each group): mechanical ventilation (MV) alone and TGI with continuous airway flow 2 l/min. FIO₂ was set at 0.4 to avoid oxygen toxicity and continuously monitored with an oxygen analyzer.

RESULTS:

Tidal volume, ventilation efficacy index and mean airway resistant pressure were significantly improved in the TGI group (P<0.01 or P<0.05). At 4 hours post ALI, pH decreased to below 7.20 in the MV group, and improved in the TGI group (P<0.01). Similarly, PaCO₂ was stable and was significantly lower in the TGI group than in the MV group (P<0.01). PaO₂ and PaO₂/FIO₂ increased also in the TGI group (P<0.05). There was no significant difference in heart rate, respiratory rate, mean artery pressure, central venous pressure, dynamic lung compliance and mean resistance of airway between the two groups. Lung histological examination showed reduced inflammation, reduced intra-alveolar and interstitial patchy hemorrhage, and homogenously expanded lungs in the TGI group.

CONCLUSION:

Continuous TGI during MV can significantly improve gas exchange and ventilation efficacy and may provide a better treatment for acute lung injury.KEY WORDS: Acute lung injury, Tracheal gas insufflation, Lung protective strategy, Mechanical ventilation     

Facilitation of hypothermia by quinpirole and 8-OH-DPAT in a rat model of cardiac arrest

Aim of the study

Therapeutic hypothermia improves outcome after cardiac arrest. Dopamine D₂ agonists and serotonin 5-HT_1A agonists lower body temperature by decreasing the set-point. We investigated the effect of these drugs on temperature and cerebral recovery of rats after cardiac arrest.

Methods

Male Wistar-Han rats were subjected to 6 min of cardiac arrest due to ventricular fibrillation. Following restoration of circulation, 1 mg quinpirole, 1 mg 8-OH-DPAT or vehicle were injected subcutaneously. Body temperature was monitored for 48 h. One additional group was kept normothermic. Animals were neurologically tested by a tape removal test. After 7 days, histology of hippocampal CA-1 sector was analysed with Nissl and TUNEL staining.

Results

Rats became spontaneously hypothermic after cardiac arrest. Induction of hypothermia was facilitated by both quinpirole (−0.033 ± 0.008 °C/min) and 8-OH-DPAT (−0.029 ± 0.010 °C/min) when compared to vehicle (−0.020 ± 0.005 °C/min). Total ‘dose’ of hypothermia (area under the curve) was not different. All animals showed a neurological deficit, which improved with time; after 7 days, test results of the normothermic group (30 [11-88] s) still tended to be worse than those of the hypothermic groups (vehicle 8 [6-14] s, quinpirole 9 [4-17] s, 8-OH-DPAT 10 [8-22] s). There were no clear differences in Nissl or TUNEL histology after 7 days.

Conclusion

Both quinpirole and 8-OH-DPAT led to faster induction of hypothermia. However, the outcome was not different from spontaneous hypothermia, probably because the total ‘dose’ of hypothermia was not influenced.     

Two-thumb technique is superior to two-finger technique during lone rescuer infant manikin CPR

Objective

Infant CPR guidelines recommend two-finger chest compression with a lone rescuer and two-thumb with two rescuers. Two-thumb provides better chest compression but is perceived to be associated with increased ventilation hands-off time. We hypothesized that lone rescuer two-thumb CPR is associated with increased ventilation cycle time, decreased ventilation quality and fewer chest compressions compared to two-finger CPR in an infant manikin model.

Design

Crossover observational study randomizing 34 healthcare providers to perform 2 min CPR at a compression rate of 100 min⁻¹ using a 30:2 compression:ventilation ratio comparing two-thumb vs. two-finger techniques.

Methods

A Laerdal™ Baby ALS Trainer manikin was modified to digitally record compression rate, compression depth and compression pressure and ventilation cycle time (two mouth-to-mouth breaths). Manikin chest rise with breaths was video recorded and later reviewed by two blinded CPR instructors for percent effective breaths. Data (mean ± SD) were analyzed using a two-tailed paired t-test. Significance was defined qualitatively as p ≤ 0.05.

Result

Mean % effective breaths were 90 ± 18.6% in two-thumb and 88.9 ± 21.1% in two-finger, p = 0.65. Mean time (s) to deliver two mouth-to-mouth breaths was 7.6 ± 1.6 in two-thumb and 7.0 ± 1.5 in two-finger, p < 0.0001. Mean delivered compressions per minute were 87 ± 11 in two-thumb and 92 ± 12 in two-finger, p = 0.0005. Two-thumb resulted in significantly higher compression depth and compression pressure compared to the two-finger technique.

Conclusion

Healthcare providers required 0.6 s longer time to deliver two breaths during two-thumb lone rescuer infant CPR, but there was no significant difference in percent effective breaths delivered between the two techniques. Two-thumb CPR had 4 fewer delivered compressions per minute, which may be offset by far more effective compression depth and compression pressure compared to two-finger technique.     

Therapeutic hypothermia is associated with a decrease in urine output in acute stroke patients

Aims

It is unclear what effect therapeutic hypothermia may have on renal function, because its effect has so far been primarily evaluated in settings in which there may be possible confounding perturbations in cardiovascular and renal physiology, such deep intraoperative hypothermia, general anesthesia, and post-cardiac arrest. We sought to determine if therapeutic hypothermia affects renal function in awake patients with normal renal function who were enrolled into a clinical trial of hypothermia plus intravenous thrombolysis for acute ischemic stroke.

Methods

Eleven patients with normal renal function were cooled to 33 °C for 24 h using an endovascular catheter, and then re-warmed over 12 h to 36.5 °C, while hourly temperature, blood pressure, and fluid status data was recorded. Blood samples for blood urea nitrogen (BUN), creatinine, and hematocrit were drawn prior to treatment (baseline), immediately after hypothermia and re-warming (day 2), and again at day 7 or discharge, and values compared.

Results

On initiation of cooling, temperatures dropped from a median pre-treatment value of 36.1 °C (IQR: 35.8-36.4 °C) to 33.1 °C (IQR: 33.1-33.4 °C). Urine output decreased 5.1 ml/h for every 1 °C decrease in body temperature (p-value = 0.001), with no associated serious adverse events. There were no statistically significant changes in BUN, creatinine, or hematocrit in the hypothermia patients.

Conclusion

Inducing hypothermia in patients with relatively unperturbed renal physiology results in a decrease in urine output that is linearly correlated with the decrease in core temperature. This has important implications for fluid management in patients undergoing therapeutic hypothermia.     

Is enteral feeding tolerated during therapeutic hypothermia?

Objective

To determine whether patients undergoing therapeutic hypothermia following cardiac arrest tolerate early enteral nutrition.

Methods

We undertook a single-centre longitudinal cohort analysis of the tolerance of enteral feeding by 55 patients treated with therapeutic hypothermia following resuscitation from cardiac arrest. The observation period was divided into three phases: (1) 24 h at target temperature (32–34 °C); (2) 24 h rewarming to 36.5 °C; and (3) 24 h maintained at a core temperature below 37.5 °C.

Results

During period 1, patients tolerated a median of 72% (interquartile range (IQR) 68.7%; range 31.3–100%) of administered feed. During period 2 (rewarming phase), a median of 95% (IQR 66.2%; range 33.77–100%) of administered feed was tolerated. During period 3 (normothermia) a median of 100% (IQR 4.75%; range 95.25–100%) of administered feed was tolerated. The highest incidence of vomiting or regurgitation of feed (19% of patients) occurred between 24 and 48 h of therapy.

Conclusions

Patients undergoing therapeutic hypothermia following cardiac arrest may be able to tolerate a substantial proportion of their daily nutritional requirements. It is possible that routine use of prokinetic drugs during this period may increase the success of feed delivery enterally and this could usefully be explored.