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Effects of stomach inflation on haemodynamic and pulmonary function during cardiopulmonary resuscitation in pigs
Resuscitation 80 (2009) 365–371
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Experimental paper
Effects of stomach inflation on haemodynamic and pulmonary function during cardiopulmonary resuscitation in pigs夽 Peter Paal ∗ , Andreas Neurauter, Michael Loedl a , Daniel Pehböck, Holger Herff, Achim von Goedecke, Karl H. Lindner, Volker Wenzel Department of Anesthesiology and General Critical Care Medicine, Innsbruck Medical University, Innsbruck, Austria
a r t i c l e
i n f o
Article history: Received 25 July 2008 Received in revised form 27 November 2008 Accepted 1 December 2008 Keywords: Advanced life support (ALS) Basic life support (BLS) Cardiac arrest Cardiopulmonary resuscitation (CPR) Ventilation
a b s t r a c t Aim: Stomach inflation during cardiopulmonary resuscitation (CPR) is frequent, but the effect on haemodynamic and pulmonary function is unclear. The purpose of this study was to evaluate the effect of clinically realistic stomach inflation on haemodynamic and pulmonary function during CPR in a porcine model. Methods: After baseline measurements ventricular fibrillation was induced in 21 pigs, and the stomach was inflated with 0 L (n = 7), 5 L (n = 7) or 10 L air (n = 7) before initiating CPR. Results: During CPR, 0, 5, and 10 L stomach inflation resulted in higher mean pulmonary artery pressure [median (min–max)] [35 (28–40), 47 (25–50), and 51 (49–75) mmHg; P < 0.05], but comparable coronary perfusion pressure [10 (2–20), 8 (4–35) and 5 (2–13) mmHg; P = 0.54]. Increasing (0, 5, and 10 L) stomach inflation decreased static pulmonary compliance [52 (38–98), 19 (8–32), and 12 (7–15) mL/cmH2 O; P < 0.05], and increased peak airway pressure [33 (27–36), 53 (45–104), and 103 (96–110) cmH2 O; P < 0.05). Arterial oxygen partial pressure was higher with 0 L when compared with 5 and 10 L stomach inflation [378 (88–440), 58 (47–113), and 54 (43–126) mmHg; P < 0.05). Arterial carbon dioxide partial pressure was lower with 0 L when compared with 5 and 10 L stomach inflation [30 (24–36), 41(34–51), and 56 (45–68) mmHg; P < 0.05]. Return of spontaneous circulation was comparable between groups (5/7 in 0 L, 4/7 in 5 L, and 3/7 in 10 L stomach inflation; P = 0.56). Conclusions: Increasing levels of stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome in this CPR model. © 2008 Elsevier Ireland Ltd. All rights reserved.
Introduction In cardiac arrest patients, ventilation of an unprotected airway is a common manoeuvre during cardiopulmonary resuscitation (CPR) before intubation. When the airway is unprotected, the combination of peak inspiratory flow rate, respiratory system compliance, airway resistance, and especially lower oesophageal sphincter pressure determines whether assisted ventilation produces lung ventilation, or causes stomach inflation.1,2 In a patient undergoing routine induction of anaesthesia, normal lower oesophageal sphincter pressure is ∼20 cmH2 O, thus minimis-
夽 A Spanish translated version of the summary of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2008.12.001. ∗ Corresponding author at: Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. Tel.: +43 512 504 80448; fax: +43 512 504 22450. E-mail addresses: [email protected], [email protected] (P. Paal). a Died in July 2008. 0300-9572/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2008.12.001
ing stomach inflation in the unprotected airway.3 In a cardiac arrest patient, lower oesophageal sphincter pressure decreases to ∼5 cmH2 O within a few minutes, thus facilitating stomach inflation.4 Accordingly, in almost half of CPR patients ventilation with an unprotected airway results in stomach inflation-mediated regurgitation and subsequent pulmonary aspiration.5 While stomach inflation-mediated pneumonia is an obvious problem, another stomach inflation-mediated problem may be less obvious. A recent study demonstrated that excessive ventilation rates decreased coronary perfusion pressure during CPR efforts, and subsequently decreased outcome.6 Similarly, excessive stomach inflation might impair haemodynamic and pulmonary function during CPR, with possibly adverse effects on survival from cardiac arrest. The purpose of this study was to evaluate the effect of clinically realistic stomach inflation on haemodynamic and pulmonary function during CPR and the post-resuscitation period in an established porcine model. The null hypothesis was that there would be no differences in haemodynamic and pulmonary parameters between groups.
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Materials and methods This project was approved by the Austrian Federal Animal Investigation Committee, and animals were managed in accordance with the American Physiologic Society, institutional, and Utstein-style guidelines,7 and the position of the American Heart Association on Research Animal Use. Animal care and use were performed by qualified individuals, supervised by veterinarians. All facilities and transportation comply with current legal requirements and meet the standards of the American Association for Accreditation of Laboratory Animal Care. Anaesthesia was used in all surgical interventions, all suffering was avoided, and research would have been terminated if pain or fear resulted. This study was performed on 21 healthy, 12- to 16-week-old pigs of either gender weighing 30–50 kg. The animals were fasted overnight, but had free access to water. The pigs were premedicated with azaperone (4 mg/kg IM; Jansen, Vienna, Austria), and atropine (0.01 mg/kg IM) 1 h before surgery. Anaesthesia was induced with a single bolus dose of ketamine (25 mg/kg IM), propofol (1–2 mg/kg IV), and piritramid (30 mg, IV, Janssen, Vienna, Austria) given via an ear vein. The animals were placed in supine position, and their trachea and oesophagus were intubated during spontaneous ventilation; both cuffs were blocked to simulate excessive stomach inflation. After intubation of the trachea, pigs were ventilated with volume-controlled ventilation (Evita 2, Draeger, Lübeck, Germany) and 100% inspiratory oxygen at 20 breaths/min. Tidal volume was adjusted to maintain normocapnia (35–45 mmHg), maximum peak airway pressure was set to 100 cmH2 O, and positive end expiratory pressure was set to 5 cmH2 O during preparation. Anaesthesia was maintained with propofol (6–8 mg/kg/h IV) and an injection of piritramid (30 mg IV); neuromuscular blockade was achieved with 0.3 mg/kg/h pancuronium after tracheal intubation to prevent spontaneous breathing or gasping. Body temperature was maintained between 38.0◦ and 39.0 ◦ C. A standard lead II electrocardiogram was used to monitor cardiac rhythm; depth of anaesthesia was judged according to arterial blood pressure and heart rate. If haemodynamic variables during the preparation phase indicated a reduced depth of anaesthesia, additional propofol and piritramid were administered. Lactated Ringer’s solution (10 mL/kg/h IV) was administered in the preparation and experimental protocol phase.8 A 7.0-Fr saline-filled pulmonary artery catheter (Edwards Life Sciences, Irvine, CA) was placed in the pulmonary artery via right jugular vein cut-down to measure right atrial and pulmonary artery pressure, cardiac output and core temperature. A 6.0-Fr saline-filled arterial catheter (Arrow, Reading, PA) was advanced via the right carotid artery to measure aortic blood pressure. The intravascular catheters were attached to pressure transducers (1290A, Hewlett Packard, Böblingen, Germany), which were aligned at the level of the right atrium. All pressure tracings were recorded with a data acquisition system (Datex AS/3, Fairfield, CT and Dewetron 2000, Graz, Austria). Respiratory vari-
ables were measured and analysed using an established pulmonary monitor (CP-100, Bicore System, Irvine, CA)9 attached to a variable orifice pneumotachograph (Varflex, Allied Health Products, Riverside, CA), which was connected to the proximal end of the tracheal tube. Blood gases were analysed with a blood gas analyser (Bayer Rapidlab 865, Leverkusen, Germany); end-tidal carbon dioxide was measured using an infrared absorption analyser (Cardiocap 2, Datex, Fairfield, CT). After preparation, the animals were paralysed with additional pancuronium 0.3 mg/kg to avoid gasping during CPR, and 5000 IU of unfractioned heparin was administered to prevent intracardiac clot formation. PEEP was reduced to 0 cmH2 O 10 min before starting the experimental protocol (Figure 1). In a pilot study, 5 L stomach inflation was the critical threshold for haemodynamic and pulmonary failure. In this model of stomach inflation during spontaneous circulation cardiovascular collapse and pulmonary dysfunction started with 5 L, resembling an abdominal compartment syndrome. Therefore, animals were randomly assigned to receive either 0 L (control group, n = 7), 5 L (n = 7), or 10 L (n = 7) stomach inflation. After assessing baseline haemodynamic values, ventilation parameters, and blood gases were measured; the propofol infusion was then switched off. After induction of ventricular fibrillation (60 V, 50 Hz) stomach inflation was performed using a calibrated syringe (Rudolph, Kansas City, MO), which remained connected to the proximal end of the oesophageal tube during the study. The oesophageal tube was clamped between inflations, impeding air to leave the stomach. After 4 min of ventricular fibrillation, chest compressions and ventilations with a 30:2 ratio were initiated (basic life support). Chest compressions were performed by the same investigator, blinded to haemodynamic and end-tidal carbon dioxide monitor tracings, in all animals at a rate of 100/min guided by acoustic audiotones. We employed an established CPR model,10 after 3 min of basic life support 45 g/kg epinephrine were administered. Two minutes after the first epinephrine administration a shock (Heartstart 4000SP defibrillator, 150J biphasic, Laerdal, Stavanger, Norway) was given, and shocks (150J biphasic) were repeated every minute, if appropriate. If cardiac arrest persisted, epinephrine 45 g/kg and vasopressin 0.4 IU/kg were administered 2 min after the first epinephrine dosage. If cardiac arrest persisted epinephrine (45 g/kg) and vasopressin (0.4 IU/kg) were repeated after another 5 min; if cardiac arrest then still persisted epinephrine (45 g/kg) and vasopressin (0.8 IU/kg) were administered after another 5 min. All drugs were diluted to 10 mL with normal saline and injected intravenously followed by a 20 mL saline flush. The experiment was terminated if cardiac arrest was still present 5 min after the last drug administration. The propofol infusion was restarted if return of spontaneous circulation occurred. Return of spontaneous circulation was defined as a pulse with a systolic arterial pressure of ≥ 80 mmHg for ≥ 5 min. Haemodynamic parameters were registered continuously; respiratory parameters and blood gases were measured at baseline,
Figure 1. Flowchart of the study protocol; ALS indicating advanced life support; BLS, basic life support; CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation.
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Figure 2. Aortic and right atrial blood pressure before and after onset of stomach inflation, showing a gradual increase of parameters with stomach inflation, and a decrease after termination of stomach inflation. X-axis shows time elapsed after cardiac arrest. Note that scales do not start at zero.
Figure 3. Diastolic aortic blood pressure (DABP), diastolic right atrial blood pressure (DRABP), and coronary perfusion pressure (CPP) before cardiac arrest at baseline (BL), during basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that the CPP scale does not start at zero.
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Figure 4. Mean pulmonary artery pressure (MPAP) before cardiac arrest at baseline (BL), during basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Stroke volume index (SVI) and pulmonary capillary wedge pressure (PCWP) at baseline (BL), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that the SVI scale does not start at zero.
at 1 min of basic life support and advanced life support, and 5, 15 and 30 min after return of spontaneous circulation. After the experimental protocol was finished, the animals were sacrificed with an overdose of piritramid, propofol and potassium chloride. Statistical analysis Data are reported as absolute and median values. Data for respiratory, circulatory parameters and blood gases was tested with the Kruskal-Wallis-test, survival with the Chi Square test; P < 0.05 was considered to be statistically significant. All statistical analysis was performed using SPSS, version 13.0 for Windows and MATLAB R14 SP3 (Mathworks, Natwick, MA) with Statistics toolbox. Results Haemoglobin (9.4 vs. 9.2 vs. 9.3 g/dL, respectively) and weight (39 vs. 35 vs. 37 kg, respectively) were comparable between 0, 5, and 10 L stomach inflation groups. Before induction of cardiac arrest, there were no differences between groups. During cardiac arrest, stomach inflation increased both aortic pressure and right atrial pressure; representative tracings are given in Figure 2. Increasing stomach inflation increased diastolic aortic, diastolic right atrial, and mean pulmonary artery pressure (P < 0.05; Figures 3 and 4), additionally mean pulmonary artery pressure was higher with 10 L when compared to 0 and 5 L stomach inflation (P < 0.05; Figure 4), indicating impaired haemodynamic function. However, coronary perfusion pressure (P = 0.54) and stroke volume index (P = 0.28) were comparable between groups (Figures 3 and 4). Increasing stomach inflation decreased static pulmonary compliance, also
increasing peak and mean airway pressures (0 L vs. 5 and 10 L, P < 0.05; Figure 5). Similarly increasing stomach inflation decreased arterial pH and oxygen partial pressure (0 L vs. 5 and 10 L, P < 0.05), and increased arterial carbon partial dioxide pressure (0 L vs. 5 and 10 L, P < 0.05; Figure 6), indicating impaired pulmonary function. Stomach inflation also decreased oxygen delivery (0 L vs. 10 L, P < 0.05; Figure 6). Return of spontaneous circulation was comparable between groups (5/7 in 0 L, 4/7 in 5 L, and 3/7 in 10 L stomach inflation; P = 0.56). Discussion In this CPR model, increasing levels of stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome. In a cardiac arrest patient with an unprotected airway more than 50% of minute ventilation enters into the stomach.11 Thus, in a 70 kg patient being ventilated with ∼5 L/min (i.e. 0.5 L tidal volume, 10/min), 2.5 L/min stomach inflation will result. Extrapolating this to a 35 kg pig ∼1.25 L/min would be inflating the stomach. To simulate different stomach inflation degrees, we included a modest (5 L) and a severe (10 L) stomach inflation group. The 5 L and 10 L of stomach inflation were extrapolated from a mechanical model simulating respiratory mechanics of a cardiac arrest victim with an unprotected airway.11 While it is unclear if this observation can be directly extrapolated to the clinical setting since gas in the stomach may get exhaled again in an unprotected airway, recent observations in a case of inadvertent oesophageal intubation reveal that gas passed through the pylorus to a large degree remains in the gut.12 With these limitation in mind, we suggest that our model may be a realistic model to assess stomach inflation related adverse effects.
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Figure 5. Peak airway pressure (PAP), mean airway pressure (MAP), and static pulmonary compliance (Cstat) before cardiac arrest at baseline (BL), during basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that scales, except Cstat, do not start at zero.
Surprisingly, coronary perfusion pressure was comparable between 0, 5, and 10 L stomach inflation groups throughout basic and advanced life support CPR, and also in the post-resuscitation period. This may be due to simultaneous and comparable increases in both diastolic aortic and diastolic right atrial blood pressure during stomach inflation, resulting in comparable coronary perfusion pressure. Another possible mechanism may be that excessive stomach inflation impeded perfusion of the distal body half substantially, similar to previous experiments with selective aortic arch perfusion.13 For example, if intra-abdominal pressure during CPR was higher than diastolic aortic blood pressure, no diastolic perfusion would occur, indicating ischaemia which was suggested by severely cyanotic skin of the distal body half in our stomach-inflated pigs. Our findings of increased pulmonary airway pressures with stomach inflation correspond to previous observations, and suggest that even a modest amount of 5 L stomach inflation may trigger pulmonary failure.14 Additionally, increased peak airway pressure may lead to severe barotrauma of the lung15 and the stomach,16 and may even contribute to multi-organ failure.17 When extrapolating a critical 5 L stomach inflation in a 35 kg pig to a 70 kg patient, cumulative 10 L stomach inflation may be a critical threshold in an adult patient. While 10 L may sound substantial, this amount may be rapidly achieved since lower oesophageal sphincter pressure is ∼5 cm H2 O during cardiac arrest.4 Thus, by the time tracheal intubation is performed by an advanced life support team in a cardiac arrest patient at the scene, a critical level of stomach inflation may have already occurred that poses substantial problems during the CPR attempt18 and the post-resuscitation period.
Arterial oxygenation and carbon dioxide elimination worsened with increasing levels of stomach inflation. Despite the lungs of our animals being ventilated with 100% oxygen during the entire study, arterial oxygen partial pressure dropped from ∼500 to ∼50 mmHg during CPR in the stomach inflation groups compared with a ∼500 to ∼300 mHg drop in the animals without stomach inflation, indicating severe oxygenation failure and impaired oxygen delivery. Similarly arterial pH, base excess and oxygen delivery decreased more in the stomach inflation groups than in the control group, suggesting insufficient oxygenation and resulting metabolic acidosis. Similarly, arterial carbon dioxide partial pressure in the stomach inflation groups increased from ∼35 to ∼50 mmHg in the CPR phase when compared to the 0 L stomach inflation group, indicating again severely impaired pulmonary gas exchange. Animals in our study were ventilated with volume-controlled ventilation, which ensured adequate tidal volumes even with critical stomach inflation and a peak airway pressure of up to ∼100 cmH2 O. However, tidal volumes might have been somewhat curbed due to the maximum pressure setting, and peak airway pressure at or above ∼100 cmH2 O. With pressure-controlled ventilation or even bag-valve-mask ventilation, hypoventilation could have resulted in even more hypoxia and diminished survival. Although limited numbers of surviving animals and wide standard deviation preclude exact statistical analysis of study end points in the post-resuscitation phase, some observations may be valuable. Increased pulmonary artery blood pressure is in agreement with decreased stroke volume index, suggesting acute right heart failure. While coronary perfusion pressure normalised, pulmonary failure persisted in the post-resuscitation period.
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Figure 6. Arterial pH (pHa), arterial oxygen partial pressure (PaO2 ), arterial carbon dioxide partial pressure (PaCO2 ), mixed venous oxygen partial pressure (PsvO2 ), oxygen delivery (DO2 ), and arterial base excess (BEa) before cardiac arrest at baseline (BL), basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that scales, except PaO2 , do not start at zero.
Stomach inflation may have triggered an acute abdominal compartment syndrome,19 in our pigs as indicated by compromised haemodynamic and pulmonary function. Although we did not directly measure intra-abdominal pressure, some findings are important. Stomach inflation increased abdominal diameter and abdominal wall tension, decreased static pulmonary compliance from ∼55 to ∼20 ml/cmH2 O and increased peak airway pressure from ∼20 to ∼100 cm H2 O. An increased intra-abdominal pressure reduces abdominal perfusion pressure, and may lead to subsequent haemodynamic, pulmonary, renal, splanchnic organ, and subsequent multi-organ failure.20,21 Recently, we described a case of gut ischaemia due to excessive stomach inflation.12 Therefore, an abdominal compartment syndrome and gut ischaemia should be suspected in cardiac arrest patients being excessively ventilated with an unprotected airway. Possibly, these combined potential adverse effects from stomach inflation may partially explain why chest compression only bystander CPR seems to be as effective as chest compressions plus rescue breathing, and why emergency medical service (EMS) minimally interrupted cardiac resuscitation without rescue breathing may be more effective than EMS CPR with rescue breathing. It is unclear to which degree stomach inflation is self-limited by gas flowing out of the gastrointestinal tract again. While this is possible during bag-valve mask ventilation, a recent case report suggests substantial gas in the entire gastrointestinal tract after inadvertent oesophageal intubation.12 This is plausible since the lower oesophageal sphincter pressure is extremely low after cardiac
arrest, thus pathophysiology may be similar. The Oslo group found high end-tidal carbon dioxide with unrecognised oesophageal intubation disappearing after a few ventilations as the stomach carbon dioxide from previous mouth-to-mouth ventilation disappears,22 and also found rhythmic changes in transthoracic impedance with oesophageal ventilations, though less than for tracheal ventilation, indicating that air moves into and out of the stomach.23 Some limitations of this study should be noted, including the small sample size, which limits evaluation of survival outcome. We used young and healthy animals with flexible ribcages; it may be possible that the observed effects may be more profound in the elderly with a more rigid chest wall. Moreover, cardiac arrest in pigs was due to ventricular fibrillation; in cardiac arrest caused by profound shock, stomach inflation mediated haemodynamic failure may be more pronounced. Also, data suggesting that 50% of minute ventilation enters the stomach is derived from a manikin study,11 and has not been validated against human data. Additionally, the lower oesophageal sphincter is not a one-way valve, and is it not likely that all the inflated air will stay in the stomach during CPR. Only a part of the air may stay in the stomach or further down the alimentary tract, the rest escaping between ventilations resulting in regurgitation. Finally, the use of potent anaesthetics and vasopressors may have influenced haemodynamic parameters. In conclusion, increasing levels of clinically realistic stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome in this CPR model.
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Conflict of interest No author has any financial or personal relationships with other people or organisations that could inappropriately influence this work. Acknowledgements Supported, in part, by the Science foundation of the Austrian National Bank grant 11448, Vienna, Austria. We are indebted to Fritz Zschiegner; Christian Gritsch, MSc (died in March 2008); and Thomas Niederklapfer, MSc; for their technical expertise. References 1. Stallinger A, Wenzel V, Wagner-Berger H, et al. Effects of decreasing inspiratory flow rate during simulated basic life support ventilation of a cardiac arrest patient on lung and stomach tidal volumes. Resuscitation 2002;54:167–73. 2. Wenzel V, Idris AH, Banner MJ, et al. Respiratory system compliance decreases after cardiopulmonary resuscitation and stomach inflation: impact of large and small tidal volumes on calculated peak airway pressure. Resuscitation 1998;38:113–8. 3. von Goedecke A, Wagner-Berger HG, Stadlbauer KH, et al. Effects of decreasing peak flow rate on stomach inflation during bag-valve-mask ventilation. Resuscitation 2004;63:131–6. 4. Gabrielli A, Wenzel V, Layon AJ, et al. Lower esophageal sphincter pressure measurement during cardiac arrest in humans: potential implications for ventilation of the unprotected airway. Anesthesiology 2005;103:897–9. 5. Virkkunen I, Kujala S, Ryynanen S, et al. Bystander mouth-to-mouth ventilation and regurgitation during cardiopulmonary resuscitation. J Intern Med 2006;260:39–42. 6. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109: 1960–5. 7. Idris AH, Becker LB, Ornato JP, et al. Utstein-style guidelines for uniform reporting of laboratory CPR research. Circulation 1996;94:2324–36. 8. Wenzel V, Padosch SA, Voelckel WG, et al. Survey of effects of anesthesia protocols on hemodynamic variables in porcine cardiopulmonary resuscitation laboratory models before induction of cardiac arrest. Comp Med 2000;50:644–8.
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9. von Goedecke A, Voelckel WG, Wenzel V, et al. Mechanical versus manual ventilation via a face mask during the induction of anesthesia: a prospective, randomized, crossover study. Anesth Analg 2004;98:260–3. 10. Meybohm P, Cavus E, Dorges V, et al. Revised resuscitation guidelines: adrenaline versus adrenaline/vasopressin in a pig model of cardiopulmonary resuscitationA randomised, controlled trial. Resuscitation 2007;75:380–8. 11. Wenzel V, Idris AH, Banner MJ, et al. Influence of tidal volume on the distribution of gas between the lungs and stomach in the nonintubated patient receiving positive-pressure ventilation. Crit Care Med 1998;26:364–8. 12. Paal P, Herff H, Mitterlechner T, et al. Excessive stomach inflation causing gut ischaemia. Resuscitation 2009;80:142. 13. Manning JE, Katz LM, Pearce LB, et al. Selective aortic arch perfusion with hemoglobin-based oxygen carrier-201 for resuscitation from exsanguinating cardiac arrest in swine. Crit Care Med 2001;29:2067–74. 14. Toens C, Schachtrupp A, Hoer J, et al. A porcine model of the abdominal compartment syndrome. Shock 2002;18:316–21. 15. Gajic O, Frutos-Vivar F, Esteban A, et al. Ventilator settings as a risk factor for acute respiratory distress syndrome in mechanically ventilated patients. Intensive Care Med 2005;31:922–6. 16. Reiger J, Eritscher C, Laubreiter K, et al. Gastric rupture-an uncommon complication after successful cardiopulmonary resuscitation: report of two cases. Resuscitation 1997;35:175–8. 17. Imai Y, Parodo J, Kajikawa O, et al. Injurious mechanical ventilation and endorgan epithelial cell apoptosis and organ dysfunction in an experimental model of acute respiratory distress syndrome. JAMA 2003;289:2104–12. 18. Berg MD, Idris AH, Berg RA. Severe ventilatory compromise due to gastric distention during pediatric cardiopulmonary resuscitation. Resuscitation 1998;36:71–3. 19. Malbrain ML, Cheatham ML, Kirkpatrick A, et al. Results from the International Conference of Experts on Intra-abdominal Hypertension and Abdominal Compartment Syndrome. I. Definitions. Intensive Care Med 2006;32:1722–32. 20. Meldrum DR, Moore FA, Moore EE, et al. Prospective characterization and selective management of the abdominal compartment syndrome. Am J Surg 1997;174:667–72. 21. Sugrue M, Jones F, Deane SA, et al. Intra-abdominal hypertension is an independent cause of postoperative renal impairment. Arch Surg 1999;134:1082–5. 22. Kramer-Johansen J, Dorph E, Steen PA. Detection of carbon dioxide in expired air after oesophageal intubation; the role of bystander mouth-to-mouth ventilation. Acta Anaesthesiol Scand 2008;52:155–7. 23. Kramer-Johansen J, Eilevstjonn J, Olasveengen TM, et al. Transthoracic impedance changes as a tool to detect malpositioned tracheal tubes. Resuscitation 2008;76:11–6.
Contents lists available at ScienceDirect
Resuscitation journal homepage: www.elsevier.com/locate/resuscitation
Experimental paper
Effects of stomach inflation on haemodynamic and pulmonary function during cardiopulmonary resuscitation in pigs夽 Peter Paal ∗ , Andreas Neurauter, Michael Loedl a , Daniel Pehböck, Holger Herff, Achim von Goedecke, Karl H. Lindner, Volker Wenzel Department of Anesthesiology and General Critical Care Medicine, Innsbruck Medical University, Innsbruck, Austria
a r t i c l e
i n f o
Article history: Received 25 July 2008 Received in revised form 27 November 2008 Accepted 1 December 2008 Keywords: Advanced life support (ALS) Basic life support (BLS) Cardiac arrest Cardiopulmonary resuscitation (CPR) Ventilation
a b s t r a c t Aim: Stomach inflation during cardiopulmonary resuscitation (CPR) is frequent, but the effect on haemodynamic and pulmonary function is unclear. The purpose of this study was to evaluate the effect of clinically realistic stomach inflation on haemodynamic and pulmonary function during CPR in a porcine model. Methods: After baseline measurements ventricular fibrillation was induced in 21 pigs, and the stomach was inflated with 0 L (n = 7), 5 L (n = 7) or 10 L air (n = 7) before initiating CPR. Results: During CPR, 0, 5, and 10 L stomach inflation resulted in higher mean pulmonary artery pressure [median (min–max)] [35 (28–40), 47 (25–50), and 51 (49–75) mmHg; P < 0.05], but comparable coronary perfusion pressure [10 (2–20), 8 (4–35) and 5 (2–13) mmHg; P = 0.54]. Increasing (0, 5, and 10 L) stomach inflation decreased static pulmonary compliance [52 (38–98), 19 (8–32), and 12 (7–15) mL/cmH2 O; P < 0.05], and increased peak airway pressure [33 (27–36), 53 (45–104), and 103 (96–110) cmH2 O; P < 0.05). Arterial oxygen partial pressure was higher with 0 L when compared with 5 and 10 L stomach inflation [378 (88–440), 58 (47–113), and 54 (43–126) mmHg; P < 0.05). Arterial carbon dioxide partial pressure was lower with 0 L when compared with 5 and 10 L stomach inflation [30 (24–36), 41(34–51), and 56 (45–68) mmHg; P < 0.05]. Return of spontaneous circulation was comparable between groups (5/7 in 0 L, 4/7 in 5 L, and 3/7 in 10 L stomach inflation; P = 0.56). Conclusions: Increasing levels of stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome in this CPR model. © 2008 Elsevier Ireland Ltd. All rights reserved.
Introduction In cardiac arrest patients, ventilation of an unprotected airway is a common manoeuvre during cardiopulmonary resuscitation (CPR) before intubation. When the airway is unprotected, the combination of peak inspiratory flow rate, respiratory system compliance, airway resistance, and especially lower oesophageal sphincter pressure determines whether assisted ventilation produces lung ventilation, or causes stomach inflation.1,2 In a patient undergoing routine induction of anaesthesia, normal lower oesophageal sphincter pressure is ∼20 cmH2 O, thus minimis-
夽 A Spanish translated version of the summary of this article appears as Appendix in the final online version at doi:10.1016/j.resuscitation.2008.12.001. ∗ Corresponding author at: Department of Anesthesiology and Critical Care Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. Tel.: +43 512 504 80448; fax: +43 512 504 22450. E-mail addresses: [email protected], [email protected] (P. Paal). a Died in July 2008. 0300-9572/$ – see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.resuscitation.2008.12.001
ing stomach inflation in the unprotected airway.3 In a cardiac arrest patient, lower oesophageal sphincter pressure decreases to ∼5 cmH2 O within a few minutes, thus facilitating stomach inflation.4 Accordingly, in almost half of CPR patients ventilation with an unprotected airway results in stomach inflation-mediated regurgitation and subsequent pulmonary aspiration.5 While stomach inflation-mediated pneumonia is an obvious problem, another stomach inflation-mediated problem may be less obvious. A recent study demonstrated that excessive ventilation rates decreased coronary perfusion pressure during CPR efforts, and subsequently decreased outcome.6 Similarly, excessive stomach inflation might impair haemodynamic and pulmonary function during CPR, with possibly adverse effects on survival from cardiac arrest. The purpose of this study was to evaluate the effect of clinically realistic stomach inflation on haemodynamic and pulmonary function during CPR and the post-resuscitation period in an established porcine model. The null hypothesis was that there would be no differences in haemodynamic and pulmonary parameters between groups.
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Materials and methods This project was approved by the Austrian Federal Animal Investigation Committee, and animals were managed in accordance with the American Physiologic Society, institutional, and Utstein-style guidelines,7 and the position of the American Heart Association on Research Animal Use. Animal care and use were performed by qualified individuals, supervised by veterinarians. All facilities and transportation comply with current legal requirements and meet the standards of the American Association for Accreditation of Laboratory Animal Care. Anaesthesia was used in all surgical interventions, all suffering was avoided, and research would have been terminated if pain or fear resulted. This study was performed on 21 healthy, 12- to 16-week-old pigs of either gender weighing 30–50 kg. The animals were fasted overnight, but had free access to water. The pigs were premedicated with azaperone (4 mg/kg IM; Jansen, Vienna, Austria), and atropine (0.01 mg/kg IM) 1 h before surgery. Anaesthesia was induced with a single bolus dose of ketamine (25 mg/kg IM), propofol (1–2 mg/kg IV), and piritramid (30 mg, IV, Janssen, Vienna, Austria) given via an ear vein. The animals were placed in supine position, and their trachea and oesophagus were intubated during spontaneous ventilation; both cuffs were blocked to simulate excessive stomach inflation. After intubation of the trachea, pigs were ventilated with volume-controlled ventilation (Evita 2, Draeger, Lübeck, Germany) and 100% inspiratory oxygen at 20 breaths/min. Tidal volume was adjusted to maintain normocapnia (35–45 mmHg), maximum peak airway pressure was set to 100 cmH2 O, and positive end expiratory pressure was set to 5 cmH2 O during preparation. Anaesthesia was maintained with propofol (6–8 mg/kg/h IV) and an injection of piritramid (30 mg IV); neuromuscular blockade was achieved with 0.3 mg/kg/h pancuronium after tracheal intubation to prevent spontaneous breathing or gasping. Body temperature was maintained between 38.0◦ and 39.0 ◦ C. A standard lead II electrocardiogram was used to monitor cardiac rhythm; depth of anaesthesia was judged according to arterial blood pressure and heart rate. If haemodynamic variables during the preparation phase indicated a reduced depth of anaesthesia, additional propofol and piritramid were administered. Lactated Ringer’s solution (10 mL/kg/h IV) was administered in the preparation and experimental protocol phase.8 A 7.0-Fr saline-filled pulmonary artery catheter (Edwards Life Sciences, Irvine, CA) was placed in the pulmonary artery via right jugular vein cut-down to measure right atrial and pulmonary artery pressure, cardiac output and core temperature. A 6.0-Fr saline-filled arterial catheter (Arrow, Reading, PA) was advanced via the right carotid artery to measure aortic blood pressure. The intravascular catheters were attached to pressure transducers (1290A, Hewlett Packard, Böblingen, Germany), which were aligned at the level of the right atrium. All pressure tracings were recorded with a data acquisition system (Datex AS/3, Fairfield, CT and Dewetron 2000, Graz, Austria). Respiratory vari-
ables were measured and analysed using an established pulmonary monitor (CP-100, Bicore System, Irvine, CA)9 attached to a variable orifice pneumotachograph (Varflex, Allied Health Products, Riverside, CA), which was connected to the proximal end of the tracheal tube. Blood gases were analysed with a blood gas analyser (Bayer Rapidlab 865, Leverkusen, Germany); end-tidal carbon dioxide was measured using an infrared absorption analyser (Cardiocap 2, Datex, Fairfield, CT). After preparation, the animals were paralysed with additional pancuronium 0.3 mg/kg to avoid gasping during CPR, and 5000 IU of unfractioned heparin was administered to prevent intracardiac clot formation. PEEP was reduced to 0 cmH2 O 10 min before starting the experimental protocol (Figure 1). In a pilot study, 5 L stomach inflation was the critical threshold for haemodynamic and pulmonary failure. In this model of stomach inflation during spontaneous circulation cardiovascular collapse and pulmonary dysfunction started with 5 L, resembling an abdominal compartment syndrome. Therefore, animals were randomly assigned to receive either 0 L (control group, n = 7), 5 L (n = 7), or 10 L (n = 7) stomach inflation. After assessing baseline haemodynamic values, ventilation parameters, and blood gases were measured; the propofol infusion was then switched off. After induction of ventricular fibrillation (60 V, 50 Hz) stomach inflation was performed using a calibrated syringe (Rudolph, Kansas City, MO), which remained connected to the proximal end of the oesophageal tube during the study. The oesophageal tube was clamped between inflations, impeding air to leave the stomach. After 4 min of ventricular fibrillation, chest compressions and ventilations with a 30:2 ratio were initiated (basic life support). Chest compressions were performed by the same investigator, blinded to haemodynamic and end-tidal carbon dioxide monitor tracings, in all animals at a rate of 100/min guided by acoustic audiotones. We employed an established CPR model,10 after 3 min of basic life support 45 g/kg epinephrine were administered. Two minutes after the first epinephrine administration a shock (Heartstart 4000SP defibrillator, 150J biphasic, Laerdal, Stavanger, Norway) was given, and shocks (150J biphasic) were repeated every minute, if appropriate. If cardiac arrest persisted, epinephrine 45 g/kg and vasopressin 0.4 IU/kg were administered 2 min after the first epinephrine dosage. If cardiac arrest persisted epinephrine (45 g/kg) and vasopressin (0.4 IU/kg) were repeated after another 5 min; if cardiac arrest then still persisted epinephrine (45 g/kg) and vasopressin (0.8 IU/kg) were administered after another 5 min. All drugs were diluted to 10 mL with normal saline and injected intravenously followed by a 20 mL saline flush. The experiment was terminated if cardiac arrest was still present 5 min after the last drug administration. The propofol infusion was restarted if return of spontaneous circulation occurred. Return of spontaneous circulation was defined as a pulse with a systolic arterial pressure of ≥ 80 mmHg for ≥ 5 min. Haemodynamic parameters were registered continuously; respiratory parameters and blood gases were measured at baseline,
Figure 1. Flowchart of the study protocol; ALS indicating advanced life support; BLS, basic life support; CPR, cardiopulmonary resuscitation; VF, ventricular fibrillation.
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Figure 2. Aortic and right atrial blood pressure before and after onset of stomach inflation, showing a gradual increase of parameters with stomach inflation, and a decrease after termination of stomach inflation. X-axis shows time elapsed after cardiac arrest. Note that scales do not start at zero.
Figure 3. Diastolic aortic blood pressure (DABP), diastolic right atrial blood pressure (DRABP), and coronary perfusion pressure (CPP) before cardiac arrest at baseline (BL), during basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that the CPP scale does not start at zero.
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Figure 4. Mean pulmonary artery pressure (MPAP) before cardiac arrest at baseline (BL), during basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Stroke volume index (SVI) and pulmonary capillary wedge pressure (PCWP) at baseline (BL), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that the SVI scale does not start at zero.
at 1 min of basic life support and advanced life support, and 5, 15 and 30 min after return of spontaneous circulation. After the experimental protocol was finished, the animals were sacrificed with an overdose of piritramid, propofol and potassium chloride. Statistical analysis Data are reported as absolute and median values. Data for respiratory, circulatory parameters and blood gases was tested with the Kruskal-Wallis-test, survival with the Chi Square test; P < 0.05 was considered to be statistically significant. All statistical analysis was performed using SPSS, version 13.0 for Windows and MATLAB R14 SP3 (Mathworks, Natwick, MA) with Statistics toolbox. Results Haemoglobin (9.4 vs. 9.2 vs. 9.3 g/dL, respectively) and weight (39 vs. 35 vs. 37 kg, respectively) were comparable between 0, 5, and 10 L stomach inflation groups. Before induction of cardiac arrest, there were no differences between groups. During cardiac arrest, stomach inflation increased both aortic pressure and right atrial pressure; representative tracings are given in Figure 2. Increasing stomach inflation increased diastolic aortic, diastolic right atrial, and mean pulmonary artery pressure (P < 0.05; Figures 3 and 4), additionally mean pulmonary artery pressure was higher with 10 L when compared to 0 and 5 L stomach inflation (P < 0.05; Figure 4), indicating impaired haemodynamic function. However, coronary perfusion pressure (P = 0.54) and stroke volume index (P = 0.28) were comparable between groups (Figures 3 and 4). Increasing stomach inflation decreased static pulmonary compliance, also
increasing peak and mean airway pressures (0 L vs. 5 and 10 L, P < 0.05; Figure 5). Similarly increasing stomach inflation decreased arterial pH and oxygen partial pressure (0 L vs. 5 and 10 L, P < 0.05), and increased arterial carbon partial dioxide pressure (0 L vs. 5 and 10 L, P < 0.05; Figure 6), indicating impaired pulmonary function. Stomach inflation also decreased oxygen delivery (0 L vs. 10 L, P < 0.05; Figure 6). Return of spontaneous circulation was comparable between groups (5/7 in 0 L, 4/7 in 5 L, and 3/7 in 10 L stomach inflation; P = 0.56). Discussion In this CPR model, increasing levels of stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome. In a cardiac arrest patient with an unprotected airway more than 50% of minute ventilation enters into the stomach.11 Thus, in a 70 kg patient being ventilated with ∼5 L/min (i.e. 0.5 L tidal volume, 10/min), 2.5 L/min stomach inflation will result. Extrapolating this to a 35 kg pig ∼1.25 L/min would be inflating the stomach. To simulate different stomach inflation degrees, we included a modest (5 L) and a severe (10 L) stomach inflation group. The 5 L and 10 L of stomach inflation were extrapolated from a mechanical model simulating respiratory mechanics of a cardiac arrest victim with an unprotected airway.11 While it is unclear if this observation can be directly extrapolated to the clinical setting since gas in the stomach may get exhaled again in an unprotected airway, recent observations in a case of inadvertent oesophageal intubation reveal that gas passed through the pylorus to a large degree remains in the gut.12 With these limitation in mind, we suggest that our model may be a realistic model to assess stomach inflation related adverse effects.
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Figure 5. Peak airway pressure (PAP), mean airway pressure (MAP), and static pulmonary compliance (Cstat) before cardiac arrest at baseline (BL), during basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that scales, except Cstat, do not start at zero.
Surprisingly, coronary perfusion pressure was comparable between 0, 5, and 10 L stomach inflation groups throughout basic and advanced life support CPR, and also in the post-resuscitation period. This may be due to simultaneous and comparable increases in both diastolic aortic and diastolic right atrial blood pressure during stomach inflation, resulting in comparable coronary perfusion pressure. Another possible mechanism may be that excessive stomach inflation impeded perfusion of the distal body half substantially, similar to previous experiments with selective aortic arch perfusion.13 For example, if intra-abdominal pressure during CPR was higher than diastolic aortic blood pressure, no diastolic perfusion would occur, indicating ischaemia which was suggested by severely cyanotic skin of the distal body half in our stomach-inflated pigs. Our findings of increased pulmonary airway pressures with stomach inflation correspond to previous observations, and suggest that even a modest amount of 5 L stomach inflation may trigger pulmonary failure.14 Additionally, increased peak airway pressure may lead to severe barotrauma of the lung15 and the stomach,16 and may even contribute to multi-organ failure.17 When extrapolating a critical 5 L stomach inflation in a 35 kg pig to a 70 kg patient, cumulative 10 L stomach inflation may be a critical threshold in an adult patient. While 10 L may sound substantial, this amount may be rapidly achieved since lower oesophageal sphincter pressure is ∼5 cm H2 O during cardiac arrest.4 Thus, by the time tracheal intubation is performed by an advanced life support team in a cardiac arrest patient at the scene, a critical level of stomach inflation may have already occurred that poses substantial problems during the CPR attempt18 and the post-resuscitation period.
Arterial oxygenation and carbon dioxide elimination worsened with increasing levels of stomach inflation. Despite the lungs of our animals being ventilated with 100% oxygen during the entire study, arterial oxygen partial pressure dropped from ∼500 to ∼50 mmHg during CPR in the stomach inflation groups compared with a ∼500 to ∼300 mHg drop in the animals without stomach inflation, indicating severe oxygenation failure and impaired oxygen delivery. Similarly arterial pH, base excess and oxygen delivery decreased more in the stomach inflation groups than in the control group, suggesting insufficient oxygenation and resulting metabolic acidosis. Similarly, arterial carbon dioxide partial pressure in the stomach inflation groups increased from ∼35 to ∼50 mmHg in the CPR phase when compared to the 0 L stomach inflation group, indicating again severely impaired pulmonary gas exchange. Animals in our study were ventilated with volume-controlled ventilation, which ensured adequate tidal volumes even with critical stomach inflation and a peak airway pressure of up to ∼100 cmH2 O. However, tidal volumes might have been somewhat curbed due to the maximum pressure setting, and peak airway pressure at or above ∼100 cmH2 O. With pressure-controlled ventilation or even bag-valve-mask ventilation, hypoventilation could have resulted in even more hypoxia and diminished survival. Although limited numbers of surviving animals and wide standard deviation preclude exact statistical analysis of study end points in the post-resuscitation phase, some observations may be valuable. Increased pulmonary artery blood pressure is in agreement with decreased stroke volume index, suggesting acute right heart failure. While coronary perfusion pressure normalised, pulmonary failure persisted in the post-resuscitation period.
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Figure 6. Arterial pH (pHa), arterial oxygen partial pressure (PaO2 ), arterial carbon dioxide partial pressure (PaCO2 ), mixed venous oxygen partial pressure (PsvO2 ), oxygen delivery (DO2 ), and arterial base excess (BEa) before cardiac arrest at baseline (BL), basic life support (BLS), advanced life support (ALS), and 5, 15 and 30 min after return of spontaneous circulation (5 , 15 and 30 ). Significant differences (P < 0.05) between 0 and 5 L are marked with §, between 0 and 10 L with ||, and between 5 and 10 L with #, respectively. Note that scales, except PaO2 , do not start at zero.
Stomach inflation may have triggered an acute abdominal compartment syndrome,19 in our pigs as indicated by compromised haemodynamic and pulmonary function. Although we did not directly measure intra-abdominal pressure, some findings are important. Stomach inflation increased abdominal diameter and abdominal wall tension, decreased static pulmonary compliance from ∼55 to ∼20 ml/cmH2 O and increased peak airway pressure from ∼20 to ∼100 cm H2 O. An increased intra-abdominal pressure reduces abdominal perfusion pressure, and may lead to subsequent haemodynamic, pulmonary, renal, splanchnic organ, and subsequent multi-organ failure.20,21 Recently, we described a case of gut ischaemia due to excessive stomach inflation.12 Therefore, an abdominal compartment syndrome and gut ischaemia should be suspected in cardiac arrest patients being excessively ventilated with an unprotected airway. Possibly, these combined potential adverse effects from stomach inflation may partially explain why chest compression only bystander CPR seems to be as effective as chest compressions plus rescue breathing, and why emergency medical service (EMS) minimally interrupted cardiac resuscitation without rescue breathing may be more effective than EMS CPR with rescue breathing. It is unclear to which degree stomach inflation is self-limited by gas flowing out of the gastrointestinal tract again. While this is possible during bag-valve mask ventilation, a recent case report suggests substantial gas in the entire gastrointestinal tract after inadvertent oesophageal intubation.12 This is plausible since the lower oesophageal sphincter pressure is extremely low after cardiac
arrest, thus pathophysiology may be similar. The Oslo group found high end-tidal carbon dioxide with unrecognised oesophageal intubation disappearing after a few ventilations as the stomach carbon dioxide from previous mouth-to-mouth ventilation disappears,22 and also found rhythmic changes in transthoracic impedance with oesophageal ventilations, though less than for tracheal ventilation, indicating that air moves into and out of the stomach.23 Some limitations of this study should be noted, including the small sample size, which limits evaluation of survival outcome. We used young and healthy animals with flexible ribcages; it may be possible that the observed effects may be more profound in the elderly with a more rigid chest wall. Moreover, cardiac arrest in pigs was due to ventricular fibrillation; in cardiac arrest caused by profound shock, stomach inflation mediated haemodynamic failure may be more pronounced. Also, data suggesting that 50% of minute ventilation enters the stomach is derived from a manikin study,11 and has not been validated against human data. Additionally, the lower oesophageal sphincter is not a one-way valve, and is it not likely that all the inflated air will stay in the stomach during CPR. Only a part of the air may stay in the stomach or further down the alimentary tract, the rest escaping between ventilations resulting in regurgitation. Finally, the use of potent anaesthetics and vasopressors may have influenced haemodynamic parameters. In conclusion, increasing levels of clinically realistic stomach inflation had adverse effects on haemodynamic and pulmonary function, indicating an acute abdominal compartment syndrome in this CPR model.
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Conflict of interest No author has any financial or personal relationships with other people or organisations that could inappropriately influence this work. Acknowledgements Supported, in part, by the Science foundation of the Austrian National Bank grant 11448, Vienna, Austria. We are indebted to Fritz Zschiegner; Christian Gritsch, MSc (died in March 2008); and Thomas Niederklapfer, MSc; for their technical expertise. References 1. Stallinger A, Wenzel V, Wagner-Berger H, et al. Effects of decreasing inspiratory flow rate during simulated basic life support ventilation of a cardiac arrest patient on lung and stomach tidal volumes. Resuscitation 2002;54:167–73. 2. Wenzel V, Idris AH, Banner MJ, et al. Respiratory system compliance decreases after cardiopulmonary resuscitation and stomach inflation: impact of large and small tidal volumes on calculated peak airway pressure. Resuscitation 1998;38:113–8. 3. von Goedecke A, Wagner-Berger HG, Stadlbauer KH, et al. Effects of decreasing peak flow rate on stomach inflation during bag-valve-mask ventilation. Resuscitation 2004;63:131–6. 4. Gabrielli A, Wenzel V, Layon AJ, et al. Lower esophageal sphincter pressure measurement during cardiac arrest in humans: potential implications for ventilation of the unprotected airway. Anesthesiology 2005;103:897–9. 5. Virkkunen I, Kujala S, Ryynanen S, et al. Bystander mouth-to-mouth ventilation and regurgitation during cardiopulmonary resuscitation. J Intern Med 2006;260:39–42. 6. Aufderheide TP, Sigurdsson G, Pirrallo RG, et al. Hyperventilation-induced hypotension during cardiopulmonary resuscitation. Circulation 2004;109: 1960–5. 7. Idris AH, Becker LB, Ornato JP, et al. Utstein-style guidelines for uniform reporting of laboratory CPR research. Circulation 1996;94:2324–36. 8. Wenzel V, Padosch SA, Voelckel WG, et al. Survey of effects of anesthesia protocols on hemodynamic variables in porcine cardiopulmonary resuscitation laboratory models before induction of cardiac arrest. Comp Med 2000;50:644–8.
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