Oxygenation and ventilation during prolonged experimental cardiopulmonary resuscitation with either continuous or 30:2 compression-to-ventilation ratios together with 10 cmH20 positive end-expiratory pressure.

BACKGROUND: In refractory out-of-hospital cardiac arrest, the patient is commonly transported to hospital with mechanical continuous chest compressions (CCC). Limited data are available on the optimal ventilation strategy. Accordingly, we compared arterial oxygenation and haemodynamics during manual asynchronous continuous ventilation and compressions with a 30:2 compression-to-ventilation ratio together with the use of 10 cmH2O positive end-expiratory pressure (PEEP). METHODS: Intubated and anaesthetized landrace pigs with electrically induced ventricular fibrillation were left untreated for 5 min (n = 31, weight ca. 55 kg), after which they were randomized to either the CCC group or the 30:2 group with the the LUCAS® 2 piston device and bag-valve ventilation with 100% oxygen targeting a tidal volume of 8 ml/kg with a PEEP of 10 cmH2O for 35 min. Arterial blood samples were analysed every 5 min, vital signs, near-infrared spectroscopy and electrical impedance tomography (EIT) were measured continuously, and post-mortem CT scans of the lungs were obtained. RESULTS: The arterial blood values (median + interquartile range) at the 30-min time point were as follows: PaO2: 180 (86-302) mmHg for the 30:2 group; 70 (49-358) mmHg for the CCC group; PaCO2: 41 (29-53) mmHg for the 30:2 group; 44 (21-67) mmHg for the CCC group; and lactate: 12.8 (10.4-15.5) mmol/l for the 30:2 group; 14.7 (11.8-16.1) mmol/l for the CCC group. The differences were not statistically significant. In linear mixed models, there were no significant differences between the groups. The mean arterial pressures from the femoral artery, end-tidal CO2, distributions of ventilation from EIT and mean aeration of lung tissue in post-mortem CTs were similar between the groups. Eight pneumothoraces occurred in the CCC group and 2 in the 30:2 group, a statistically significant difference (p = 0.04). CONCLUSIONS: The 30:2 and CCC protocols with a PEEP of 10 cmH2O resulted in similar gas exchange and vital sign outcomes in an experimental model of prolonged cardiac arrest with mechanical compressions, but the CCC protocol resulted in more post-mortem pneumothoraces.

Ventilation during continuous compressions or at 30:2 compression-to-ventilation ratio results in similar arterial oxygen and carbon dioxide levels in an experimental model of prolonged cardiac arrest.

BACKGROUND: In refractory out-of-hospital cardiac arrest, transportation to hospital with continuous chest compressions (CCC) from a chest compression device and ventilation with 100% oxygen through an advanced airway is common practice. Despite this, many patients are hypoxic and hypercapnic on arrival, possibly related to suboptimal ventilation due to the counterpressure caused by the CCC. We hypothesized that a compression/ventilation ratio of 30:2 would provide better ventilation and gas exchange compared to asynchronous CCC during prolonged experimental cardiopulmonary resuscitation (CPR). METHODS: We randomized 30 anaesthetized domestic swine (weight approximately 50 kg) with electrically induced ventricular fibrillation to the CCC or 30:2 group and bag-valve ventilation with a fraction of inspired oxygen (FiO2) of 100%. We started CPR after a 5-min no-flow period and continued until 40 min from the induction of ventricular fibrillation. Chest compressions were performed with a Stryker Medical LUCAS® 2 mechanical chest compression device. We collected arterial blood gas samples every 5 min during the CPR, measured ventilation distribution during the CPR using electrical impedance tomography (EIT) and analysed post-mortem computed tomography (CT) scans for differences in lung aeration status. RESULTS: The median (interquartile range [IQR]) partial pressure of oxygen (PaO2) at 30 min was 110 (52-117) mmHg for the 30:2 group and 70 (40-171) mmHg for the CCC group. The median (IQR) partial pressure of carbon dioxide (PaCO2) at 30 min was 70 (45-85) mmHg for the 30:2 group and 68 (42-84) mmHg for the CCC group. No statistically significant differences between the groups in PaO2 (p = 0.40), PaCO2 (p = 0.79), lactate (p = 0.37), mean arterial pressure (MAP) (p = 0.47) or EtCO2 (p = 0.19) analysed with a linear mixed model were found. We found a deteriorating trend in PaO2, EtCO2 and MAP and rising PaCO2 and lactate levels through the intervention. There were no differences between the groups in the distribution of ventilation in the EIT data or the post-mortem CT findings. CONCLUSIONS: The 30:2 and CCC protocols resulted in similar gas exchange and lung pathology in an experimental prolonged mechanical CPR model.

The use of 100% compared to 50% oxygen during ineffective experimental cardiopulmonary resuscitation improves brain oxygenation.

INTRODUCTION: Perfusion pressure and chest compression quality are generally considered key determinants of brain oxygenation during cardiopulmonary resuscitation (CPR) and the impact of oxygen administration is less clear. We compared ventilation with 100% and 50% oxygen during ineffective manual chest compressions and hypothesized that 100% oxygen would improve brain oxygenation. METHODS: Ventricular fibrillation (VF) was induced electrically in anaesthetized pigs and left untreated for 5 minutes, followed by randomization to ineffective manual CPR with ventilation of 50% or 100% oxygen. The first defibrillation was performed 10 minutes after induction of VF, and CPR continued with mechanical chest compressions (LUCAS2™) and defibrillation every 2 minutes until 36 minutes or return of spontaneous circulation (ROSC). Brain oxygenation was measured with near-infrared spectroscopy (rSO2) and invasive brain tissue oxygen (PbtO2) with a probe (NEUROVENT-PTO, RAUMEDIC) inserted into frontal brain tissue. Cerebral oxygenation was compared between groups with Mann-Whitney U tests and linear mixed models. RESULTS: Twenty-eight pigs were included in the study: 14 subjects in each group. During ineffective chest compressions relative PbtO2 was higher in the group ventilated with 100% compared to 50% oxygen (5.2 mmHg [1.4-20.5] vs 2.2 [0.8-6.8], p = 0.001), but there was no difference in rSO2 (22% [16-28] vs 18 [15-25], p = 0.090). The use of 50% or 100% oxygen showed no difference in relative PbtO2 (p = 1.00) and rSO2 (p = 0.206) during mechanical CPR. CONCLUSIONS: The use of 100% compared to 50% oxygen during ineffective manual CPR improved brain oxygenation measured invasively in brain tissue, but there was no difference in rSO2.

Intravenous lipid emulsion given to volunteers does not affect symptoms of lidocaine brain toxicity.

Intravenous lipid emulsion has been suggested as treatment for local anaesthetic toxicity, but the exact mechanism of action is still uncertain. Controlled studies on the effect of lipid emulsion on toxic doses of local anaesthetics have not been performed in man. In randomized, subject-blinded and two-phase cross-over fashion, eight healthy volunteers were given a 1.5 ml/kg bolus of 20% Intralipid(®) (200 mg/ml) or Ringer's acetate solution intravenously, followed by a rapid injection of lidocaine 1.0 mg/kg. Then, the same solution as in the bolus was infused at a rate of 0.25 ml/kg/min. for 30 min. Electroencephalography (EEG) was recorded, and 5 min. after lidocaine injection, the volunteers were asked to report subjective symptoms. Total and un-entrapped lidocaine plasma concentrations were measured from venous blood samples. EEG band power changes (delta, alpha and beta) after the lidocaine bolus were similar during lipid and during Ringer infusion. There were no differences between infusions in the subjective symptoms of central nervous system toxicity. Lidocaine was only minimally entrapped in the plasma by lipid emulsion, but the mean un-entrapped lidocaine area under concentration-time curve from 0 to 30 min. was clearly smaller during lipid than Ringer infusion (16.4 versus 21.3 mg × min/l, p = 0.044). Intravenous lipid emulsion did not influence subjective toxicity symptoms nor affect the EEG changes caused by lidocaine.

Intravenous lipid emulsion entraps amitriptyline into plasma and can lower its brain concentration--an experimental intoxication study in pigs.

Intravenous lipid emulsion has been suggested as treatment for severe intoxications caused by lipophilic drugs, including tricyclic antidepressants. We investigated the effect of lipid infusion on plasma and tissue concentrations of amitriptyline and haemodynamic recovery, when lipid was given after amitriptyline distribution into well-perfused organs. Twenty anaesthetized pigs received amitriptyline intravenously 10 mg/kg for 15 min. Thirty minutes later, in random fashion, 20% Intralipid(®) (Lipid group) or Ringer's acetate (Control group) was infused 1.5 ml/kg for 1 min. followed by 0.25 ml/kg/min. for 29 min. Arterial and venous plasma amitriptyline concentrations and haemodynamics were followed till 75 min. after amitriptyline infusion. Then, frontal brain and heart apex samples were taken for amitriptyline measurements. Arterial plasma total amitriptyline concentrations were higher in the Lipid than in the Control group (p < 0.03) from 20 min. on after the start of the treatment infusions. Lipid emulsion reduced brain amitriptyline concentration by 25% (p = 0.038) and amitriptyline concentration ratios brain/arterial plasma (p = 0.016) and heart/arterial plasma (p = 0.011). There were no differences in ECG parameters and no severe cardiac arrhythmias occurred. Two pigs developed severe hypotension during the lipid infusion and were given adrenaline. In conclusion, lipid infusion, given not earlier than after an initial amitriptyline tissue distribution, was able to entrap amitriptyline back into plasma from brain and possibly from other highly perfused, lipid-rich tissues. In spite of the entrapment, there was no difference in haemodynamics between the groups.