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Study objectives To determine the relationships between partial pressure of arterial carbon dioxide (PaCO 2 ), prescribed minute ventilation (MV), and neurologic outcome in patients resuscitated from cardiac arrest. Methods This was a retrospective cohort study utilizing a multicenter database of adult patients with return of spontaneous circulation (ROSC) after cardiac arrest. The primary outcome was neurologic status at hospital discharge, defined by Cerebral Performance Category (CPC) score: CPC 1–2 was favorable, CPC 3–5 was poor. We compared rates of initial normocarbia (PaCO 2 31–49mmHg) and mean sequential PaCO 2 measurements obtained over the first 24h. We also assessed the influence of MV on the PaCO 2 at initial, 6, 12, 18, and 24h after cardiac arrest using univariate linear regression. Results One hundred and fourteen patients from 3 institutions met inclusion criteria. Overall, 46/114 (40.4%, 95% CI: 31.4–49.4%) patients survived to hospital discharge, and 33/114 (28.9%, 20.6–37.2%) had CPC 1–2 at the time of discharge. A total of 38.9% (95% CI: 29.9–47.9%) of patients had initial normocarbia; 43.2% (28.6–57.8%) of these patients were discharged with CPC 1–2, compared with 20.3% (10.8–29.8%) of dyscarbic patients. By 6h, neurologic outcomes were not significantly associated with PaCO 2 . Prescribed MV was not associated with PaCO 2 at any time point with the exception of a weak correlation at hour 18. Conclusion Initial normocarbia was associated with favorable neurological outcome in patients resuscitated from cardiac arrest. This relationship was not seen at subsequent time points. There was no significant association between prescribed MV and PaCO 2 or neurologic outcome.

Aim of the study: To evaluate in an established porcine post cardiac arrest model the effect of a mild hypercapnic ventilatory strategy on outcome. Methods: The left anterior descending coronary artery was occluded in 14 pigs and ventricular fibrillation induced and left untreated for 12 min. Cardiopulmonary resuscitation was performed for 5 min prior to defibrillation. After resuscitation, pigs were assigned to either normocapnic (end-tidal carbon dioxide (EtCO2) target: 35-40 mmHg) or hypercapnic ventilation (EtCO2 45-50 mmHg). Hemodynamics was invasively measured and EtCO2 was monitored with an infrared capnometer. Blood gas analysis, serum neuron-specific enolase (NSE) and high sensitive cardiac troponin T (hs-cTnT) were assessed. Survival and functional recovery were evaluated up to 96 h. Results: Twelve pigs were successfully resuscitated and eight survived up to 96 h, with animals in the hypercapnic group showing trend towards a longer survival. EtCO2 and arterial partial pressure of CO2 were higher in the hypercapnic group compared to the normocapnic one (p

Contains fulltext : 152328.pdf (Publisher’s version ) (Closed access) AIM: Pulmonary ventilation remains an important part of cardiopulmonary resuscitation, affecting gas exchange and haemodynamics. We designed and studied an improved method of ventilation for CPR, constructed specifically to support both gas exchange and haemodynamics. This method uses continuous insufflation of oxygen at three levels of pressure, resulting in tri-level pressure ventilation (TLPV). We hypothesized that TLPV improves gas exchange and haemodynamics compared to manual gold standard ventilation (GSV). METHODS: In 14 pigs, ventricular fibrillation was induced and automated CPR performed for 10min with either TLPV or GSV. After defibrillation, CPR was repeated with the other ventilation method. Gas exchange and haemodynamics were monitored. Data are presented as mean+/-standard error of the mean. RESULTS: TLPV was superior to GSV for PaO2 (163+/-36mmHg difference; P=0.001), and peak AWP (-20+/-2cmH2O difference; P=0.000) and higher for mean AWP (8+/-0.2cmH2O difference; P=0.000). TLPV was comparable to GSV for CPP (5+/-3mmHg difference; P=0.012), VCO2 (0.07+/-0.3mL/min/kg difference; P=0.001), SvO2 (4+/-3%-point; P=0.001), mean carotid flow (-0.5+/-4mL/min difference; P=0.016), and pHa (0.00+/-0.03 difference; P=0.002). The PaCO2 data do not provide a conclusive result (4+/-4mmHg difference). CONCLUSION: We conclude that the ventilation strategy with a tri-level pressure cycle performs comparable to an expert, manual ventilator in an automated-CPR swine model.

Optimum cardiopulmonary resuscitation (CPR) for both basic and advanced cardiac life support depends on a compromise between the number of chest compressions delivered and the amount of ventilation provided. This study used theoretical models of blood flow and both arterial and venous blood gas values to investigate the influence of different compression to ventilation ratios on CPR efficiency, as well as the effects of different inspired oxygen concentrations. With mouth-to-mouth ventilation, greater numbers of compressions between each ventilation provided progressively greater blood flow. However, a greater the number of compressions, reduced the arterial oxygen levels and carbon dioxide clearance. There was an optimum ratio, in terms of both oxygen delivery and carbon dioxide clearance, of around 20:1 compressions to ventilation. Optimum oxygen delivery was 0.19 L/min at 20:1, which was better than the oxygen delivery for standard CPR based on a ratio of 15:2 (0.13 L/min). When patients were ventilated with supplemental oxygen (either 50 or 85%) the lungs rapidly became saturated with oxygen, and oxygen delivery depended more on blood flow. Higher numbers of compressions provided greater oxygen delivery, but at the cost of increasing hypercarbia, which is thought to affect resuscitation success rates adversely. The simulation results suggested ratios around 20:1 would be the best compromise between blood flow, oxygen delivery (0.25 L/min) and avoidance of hypercarbia. The best results were provided by continuous chest compressions and simultaneous, asynchronous ventilation in an intubated patient. Arterial and venous oxygen and carbon dioxide levels were well maintained, with very good oxygen delivery (0.32 L/min). Intubation with continuous chest compressions and asynchronous ventilation can therefore significantly improve the quality of CPR as a whole, and not just ventilation.

The optimal tidal and minute ventilation during cardiopulmonary resuscitation (CPR) is not known. In the present study seven adult, non-traumatic, out-of-hospital cardiac arrest patients were intubated and mechanically ventilated at 12 min(-1) with 100% oxygen and a tidal volume of 700 ml (10 +/- 2 ml kg(-1)). Arterial blood gas samples were analysed after 6-8 min of unsuccessful resuscitation and mechanical ventilation. Mean PaCO2 was 5.2 +/- 1.3 kPa and mean PaO2 30.7 +/- 17.2 kPa. The patient with the highest (14 ml kg(-1)) and lowest (8 ml kg(-1)) tidal volumes per kg had the lowest and highest PaCO2 values of 2.6 and 6.8 kPa, respectively. Linear regression analysis confirmed a significant correlation between arterial pCO2 and tidal volume in ml/kg, r2 = 0.87. We conclude that aiming for an estimated ventilation of 10 ml kg(-1) tidal volume at frequency of 12 min(-1) might be expected to achieve normocapnia during ALS.

The European Resuscitation Council has recommended decreasing tidal volume during basic life support ventilation from 800 to 1200 ml, as recommended by the American Heart Association, to 500 ml in order to minimise stomach inflation. However, if oxygen is not available at the scene of an emergency, and small tidal volumes are given during basic life support ventilation with a paediatric self-inflatable bag and room-air (21% oxygen), insufficient oxygenation and/or inadequate ventilation may result. When apnoea occurred after induction of anaesthesia, 40 patients were randomly allocated to room-air ventilation with either an adult (maximum volume, 1500 ml) or paediatric (maximum volume, 700 ml) self-inflatable bag for 5 min before intubation. When using an adult (n=20) versus paediatric (n=20) self-inflatable bag, mean +/-SEM tidal volumes and tidal volumes per kilogram were significantly (P

The aim of this study was to investigate the influence of acid-base management (pH stat or alpha stat) on hemodynamics and oxygen metabolism during long-term hypothermia in the pig. Seventeen female pigs were anesthetized, slowly cooled to 28 degrees C with cooling mats and kept at this temperature for 36 h. Thereafter, slow rewarming was performed with inhalation of a 40 degrees C warm air/oxygen mixture and insulation. Eight of the 17 pigs were ventilated according to the pH stat strategy and 9 according to the alpha stat strategy. Both groups were compared 4 times each for hemodynamics and metabolism during cooling, hypothermia and rewarming. The 2 strategies showed no significant difference in cardiac output, heart rate or mean arterial pressure. The only difference in hemodynamics was observed in mean pulmonary artery pressure and pulmonary artery resistance during hypothermia, showing higher values in pH stat animals. As for oxygen metabolism, oxygen consumption during hypothermia was significantly higher in alpha stat animals. Long-term hypothermia with spontaneous circulation revealed significant differences in oxygen metabolism and pulmonary artery pressure as well as resistance between alpha and pH stat acid-base management. These differences may be of importance when using moderate hypothermia in a clinical or experimental setting.

Aim: Mild hypothermia is increasingly applied in the intensive care unit. Knowledge on the effects of hypothermia on respiratory parameters during mechanical ventilation is limited. In this retrospective study, we describe the effect of hypothermia on gas exchange in patients cooled for 24 h after a cardiac arrest. Methods: Respiratory parameters were derived from electronic patient files from 65 patients at the start and end of the hypothermic phase and at every centigrade increase in body temperature until normo-temperature, including tidal volume, positive end expiratory pressure (PEEP), plateau pressure, respiratory rate, exhaled CO2 concentrations (etCO(2)) and FIO2. Static compliance was calculated as V-T/P-plateau - PEEP. Dead space ventilation was calculated as (PaCO2-etCO(2))/PaCO2. Results: During hypothermia, PaCO2 decreased, at unchanged PaCO2-etCO(2) gap and minute ventilation. During rewarming, PaCO2 did not change, while etCO(2) increased at unchanged minute ventilation. Dead space ventilation did not change during hypothermia, but lowered during rewarming. During hypothermia, PaO2/FIO2 ratio increased at unchanged PEEP levels. Respiratory static compliance did not change during hypothermia, nor during rewarming. Conclusion: Hypothermia possibly improves oxygenation and ventilation in mechanically ventilated patients. Results may accord with the hypothesis that reducing metabolism with applied hypothermia may be beneficial in patients with acute lung injury, in whom low minute ventilation results in severe hypercapnia. (C) 2010 Elsevier Ireland Ltd. All rights reserved

The authors studied the effects of hypocapnic-hyperventilation on cerebral blood flow (CBF) (study 1) and on cerebral oxygenation (study 2) during mechanical ventilation in 8 patients, 4 with hepatic (HE) and 4 with septic encephalopathy (SE). In study 1, a positive linear relationship between CBF(y) and PaCO2 (x) was observed (y = 2.44x - 55.5, r = 0.6276, P less than 0.01, n = 18). In the study 2, hypocapnic-hyperventilation produced a reduction in CBF below the level required to meet the demand in 4 of 8 patients. A good linear relationship was observed between CBF/CMRO2 (CMRO2 = cerebral oxygen consumption, y) and jugular venous PO2 (PjVO2, x) (y = 0.99x - 15.53, r = 0.8962, P less than 0.01, n = 18). It is concluded that cerebrovascular reactivity to CO2 was preserved in these patients, therefore, intentional or inadvertant hyperventilation may produce cerebral ischemia. Moreover, JPVO2 may be useful in monitoring cerebral oxygenation in such patients.

We studied a new rescue breathing device consisting of a mouthcap and a "glossopalatinal" tube reaching between tongue and palate (the "GPT"), with a connector for a bag, ventilator or rescuers mouth. By tilting the connector in a cranial direction, the tongue can be "scooped" out of the hypopharynx. The study was to test the efficacy and the ease of application of the GPT in anaesthetised patients. It was compared with a conventional face mask with and without an oropharyngeal (OP) airway.19 patients (ethics committee approval, informed consent) anaesthetised for elective surgery were ventilated using an anaesthesia circuit and Ventilog (Draeger) through the GPT and via a face mask (Laerdal) with and without an OP tube. Flow and pressures at the airway opening, in the hypopharynx and the trachea were measured, and the resistance was derived. In addition, the relations of the devices to the anatomical structures were visualised by fibrescope, and ease of operation and fit on the face were scored.Inspiratory resistance with the GPT and mask did not differ (1.31+/-0.96 vs. 1.38+/-0.66 kPa s/l at 1 l/s, mean+/-standard deviation (S.D.); reduction of resistance by "scooping" the tongue through angulation of the GPT (to 0.64+/-0.32; P0.05 vs. GPT without angulation) was equivalent to that by an OP tube used with the mask (to 0.68+/-0.26; P0.05 vs. mask solo). Pharyngoscopy showed that the effectiveness of the GPT depended on the individual anatomy. The angulating motion caused some fatigue. The GPT is an alternative to established breathing adjuncts; despite not protruding into the pharynx it can enhance airway patency like an OP.

Current adult basic cardiopulmonary resuscitation (CPR) guidelines recommend a 2:15 ventilation:compression ratio, while the optimal ratio is unknown. This study was designed to compare arterial and mixed venous blood gas changes and cerebral circulation and oxygen delivery with ventilation:compression ratios of 2:15, 2:50 and 5:50 in a model of basic CPR. Ventricular fibrillation (VF) was induced in 12 anaesthetised pigs, and satisfactory recordings were obtained from 9 of them. A non-intervention interval of 3 min was followed by CPR with pauses in compressions for ventilation with 17% oxygen and 4% carbon dioxide in a randomised, cross-over design with each method being used for 5 min. Pulmonary gas exchange was clearly superior with a ventilation:compression ratio of 2:15. While the arterial oxygen saturation stayed above 80% throughout CPR for 2:15, it dropped below 40% during part of the ventilation:compression cycle for both the other two ratios. On the other hand, the ratio 2:50 produced 30% more chest compressions per minute than either of the two other methods. This resulted in a mean carotid flow that was significantly higher with the ratio of 2:50 than with 5:50 while 2:15 was not significantly different from either. The mean cerebrocortical microcirculation was approximately 37% of pre-VF levels during compression cycles alone with no significant differences between the methods. The oxygen delivery to the brain was higher for the ratio of 2:15 than for either 5:50 or 2:50. In parallel the central venous oxygenation, which gives some indication of tissue oxygenation, was higher for the ratio of 2:15 than for both 5:50 and 2:50. As the compressions were done with a mechanical device with only 2–3 s pauses per ventilation, the data cannot be extrapolated to laypersons who have great variations in quality of CPR. However, it might seem reasonable to suggest that basic CPR by professionals should continue with ratio of 2:15 at present if it can be shown that similar brief pauses for ventilation can be achieved in clinical practice.

The 'Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - International Consensus on Science' recommend an artificial ventilation volume of 10 ml/kg bodyweight (equivalent to a tidal volume of 700-1000 ml) without the use of supplemental oxygen in adults with respiratory arrest. For first aid providers using the mouth-to-mouth or mouth-to-nose-ventilation technique, respectively, a ventilation volume of approximately 9.6 l/min results. Additionally, a deep breath is recommended before each ventilation to increase the end-expiratory oxygen concentration of the air exhaled by the first aid provider. To investigate the effects of these recommendations in healthy volunteers, test persons were asked to ventilate an artificial lung model for a period of up to 10 min. The tidal volume was set at 800 ml at a breathing rate of 12/min. End-tidal carbon dioxide, oxygen saturation (measured by pulse oximetry), and heart rate were measured continuously. Capillary blood gas samples were collected and non-invasive blood pressure readings were recorded prior to the start of ventilation and immediately after the end of the measuring period. The data reveal a statistically significant and clinically relevant decrease in end-tidal carbon dioxide pressure (P0.001, median decrease 14 mmHg), and the occurrence of hyperventilation-associated symptoms such as paraesthesia, dizziness, and carpopedal spasms in more than 75% of the participants. Clinically and statistically significant hyperventilation results in first aid providers performing artificial ventilation according to the guidelines. This artificial ventilation is associated with a significant decrease in capillary and end-tidal carbon dioxide pressure as well as with multiple symptoms of an acute hyperventilation syndrome. Ventilation performed according to these guidelines may cause injury to the health of the first aid provider. Rescuers ventilating the victim should be replaced at regular intervals and the recommendation to take a deep breath before each ventilation should not be upheld in order to minimise the risk of hyperventilation.

The application of percutaneous transtracheal jet ventilation for emergency ventilation depends on special equipment which is often not available outside the operating room. The oxygen flow modulator is a new specially designed device for emergency ventilation using a low pressure oxygen supply. We studied the effects of the new device in comparison with a hand triggered emergency jet injector on oxygenation and ventilation in six pigs (21±1 kg). The animals were anaesthetized, tracheally intubated, and mechanically ventilated. Following central venous and pulmonary artery catheterization, a Paratrend 7 sensor was placed in the left femoral artery for continuous measurements of PaO 2 and PaCO 2 . Then an emergency transtracheal airway catheter was inserted into the trachea after surgical exposure. In randomized order each animal was ventilated via the transtracheal airway catheter with the hand triggered emergency jet injector (inspiratory/expiratory ( I / E ) ratio of 1:1; respiratory rate of 60 min −1 ; driving pressure 1.5 bar; FjetO 2 1.0) and the oxygen flow modulator (FiO 2 1.0 at an oxygen flow of 15 l min −1 ; respiratory rate of 60 min −1 ; I / E ratio of approximately 1:1) for 15 min each. After each phase of the experiment respiratory and hemodynamic variables were measured. Whereas PaO 2 was not significantly different between the two devices, PaCO 2 was higher during the hand-triggered jet ventilation. Thus, the efficacy of the oxygen flow modulator during the experiment was comparable with the efficacy of the hand triggered emergency jet injector.

End tidal CO2 measurement may be helpful in detecting the efficacy of thrombolysis after a massive pulmonary embolism. We report the case of a 76-year-old man with a massive pulmonary embolism, who required early intubation and mechanical ventilation. Thrombolysis with rtpA (total dosage: 60 mg) was initiated. During this procedure, clinical data, arterial blood gases and end-tidal CO, with a capnograph were recorded. Before thrombolysis the P(a-ET)CO2 gradient was raised to 25 mmHg. During thrombolysis, the clinical data improved and the P(a-ET) gradient fell to 14 mmHg. We postulate that the P(a-ET)CO2 gradient seems to be a reasonable indicator of efficacy of thrombolysis in this setting. However. the gradient did not return to normal values(45 mmHg). The possible reasons for this may be that during mechanical ventilation there was a large ventilation- perfusion ratio and the cardiac output may have still reduced. With these limitations, we conclude that the P(a-ET)CO2 gradient should be evaluated as an indicator of pulmonary reperfusion in massive pulmonary embolism. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

In the clinical literature there are reports of patients failing to breathe and becoming comatose when supplied with 100% oxygen for respiratory distress. This effect has been attributed to a loss of respiratory drive. Recent studies have established that this explanation is incorrect, but have left the phenomenon unexplained. We propose that the apnea and coma reported is due to carbon dioxide narcosis. We have reproduced this effect in an animal model and have documented PCO2 values in excess of 250 mmHg during the apneic period. Our results suggest that this level of PCO2 suppresses both brainstem auditory evoked potentials and spontaneous respiration. The high PCO2 is due to inadequate gas exchange, and is easily remedied by provision of adequate ventilation.

End-tidal carbon dioxide concentration in the expired air (ETCO 2 ) is measured with different technologies. ETCO 2 allows the global evaluation of three main body functions: metabolism, circulation and ventilation. If two of these parameters are held constant, changes in ETCO 2 reflect a variation of the third. Thus, ETCO 2 is now widely used as a reliable monitoring device in various clinical settings. In the past years several studies proposed ETCO 2 as a non-invasive monitor for the evaluation of therapeutic efforts during low-flow states, and especially during cardiopulmonary resuscitation. However, recent laboratory and clinical investigations demonstrated that various pharmacological and physical interventions may influence ETCO 2 . Especially, the use of the CO 2 generating buffer NaHCO 3 increase and α-adrenergic agents constantly decrease ETCO 2 . Thus, although ETCO 2 remains a necessary tool during anaesthesia, it may loose the potential for prediction of survival when monitoring the resuscitative efforts during cardiopulmonary resuscitation.

This study examined the effect of carbon dioxide, lidoflazine and deferoxamine therapy upon the 10-day survival incidence and subsequent neurologic function of rats subjected to 7 min of cardiorespiratory arrest with resuscitation. Cardiac arrest (asystole) was induced at time zero by injection of cold, 1% KCl into the left ventricle of ketamine-anesthetized rats pretreated with succinylcholine. Positive pressure ventilation was discontinued at time zero. Cardiopulmonary resuscitation (CPR) was begun at 7 min, and animals with return of spontaneous circulation were entered into the study. Twenty treated rats were ventilated for 1 h with 7% carbon dioxide-93% oxygen and given lidoflazine (2.0 mg/kg, i.v.) and deferoxamine (50 mg/kg, i.v.) 5 min after CPR. Twenty control rats were ventilated for 1 h with 100% oxygen and given lidoflazine vehicle and deferoxamine vehicle. Lidoflazine treatment (1.0 mg/kg) for the treated group, or lidoflazine vehicle for the control group, was repeated at 8 h postresuscitation. At 2 days postresuscitation, 75% of treated rats vs. 25% of control rats were alive (CHI2 = 10.0, d.f. = 1, P less than 0.01), and at 10 days, 60% of treated rats vs. 25% of control rats were alive (CHI2 = 5.01, d.f. = 1, P less than 0.05). There was no detectable neurologic deficit among survivors in either group at 15 days. The combination of carbon dioxide, lidoflazine and deferoxamine, administered after return of spontaneous circulation, is a simple and easily administered treatment regimen that improves the survival incidence without neurologic deficits in this animal model of cardiorespiratory arrest and CPR.