ResusciTimer Studies
 

The new AHA guidelines quote a range of studies that too many breaths, too long a ventilation or too large a tidal volume during CPR may be harmful for several reasons. First, the positive pressure in the chest created by excessive rescue breaths or too long a breath actually decreases venous return to the heart and limits refilling of the heart, which therefore reduces the cardiac output created by subsequent chest compressions. Second, large tidal volumes / pressures, forceful breaths and excessive ventilations are also likely to cause gastric inflation and vomiting, with the potential to aspirate with disastrous consequences. If an unresponsive adult patient isn’t breathing but has a pulse, the AHA Guidelines recommend rescuers ventilate 10–12 times per minute (approximately one breath every five to six seconds). During CPR with an advanced airway in place, it’s recommended that health-care providers deliver eight to 10 rescue breaths per minute (approximately one breath every six to eight seconds). Studies as shown below confirm that whilst in training, health-care providers can correctly meet the AHA guidelines, multiple research studies show that during actual resuscitations, this is not the case.

The following studies review current failings by prehospital personal to maintain correct standards during resuscitations and the dangers of hyperventilation that often occurs during resuscitation and the care to the head injured patient.

 

 
J Trauma. 2007 Jun;62(6):1330-6; discussion 1336-8.

The impact of prehospital ventilation on outcome after severe traumatic brain injury.

Warner KJ, Cuschieri J, Copass MK, Jurkovich GJ, Bulger EM.

Department of Surgery, University of Washington, Harborview Medical Center, Seattle, Washington 98104, USA.

BACKGROUND: Prehospital intubation has been challenged on the grounds that it predisposes to hyperventilation, which is detrimental after traumatic brain injury (TBI), and impairs venous return in patients with hypovolemia. We sought to determine the incidence of hyperventilation among a cohort of trauma patients undergoing prehospital intubation and the impact of ventilation on outcome after severe TBI. METHODS: Data were prospectively collected for all intubated trauma patients transported directly from the field for a period of 14 months (n = 574). An arrival Pco2 <30 mm Hg was termed severe hypocapnea and considered a marker of hyperventilation. Patients with a Pco2 >45 mm Hg were considered severely hypercapneic. Targeted ventilation was defined as a Pco2 between 30 and 35 mm Hg based on the Brain Trauma Foundation guidelines. RESULTS: The rate of severe hypocapnea was 18% and women were more likely to be hyperventilated (p < 0.05). Patients with severe hypercapnia had higher Injury Severity Scores and were more likely hypotensive, hypoxic, and acidodic (p < 0.05). Patients in the targeted ventilation range were less likely to die than were those outside the range even after excluding the severe hypercapnea group (odds ratio, 0.57; 95% confidence interval, 0.33-0.99). This effect was even greater among patients with isolated TBI (odds ratio, 0.31; 95% confidence interval, 0.10-0.96). CONCLUSION: Targeted prehospital ventilation is associated with lower mortality after severe TBI.

 

Resuscitation. 2007 Apr;73(1):82-5.

 

Do we hyperventilate cardiac arrest patients?

 

O'Neill JF, Deakin CD.

 

North Hampshire Hospital, NHS Trust, Basingstoke RG24 9NA, UK.

 

 

INTRODUCTION: Hyperventilation during cardiopulmonary resuscitation is detrimental to survival. Several clinical studies of ventilation during hospital and out-of-hospital cardiac arrest have demonstrated respiratory rates far in excess of the 10 min(-1) recommended by the ERC. We observed detailed ventilation variables prospectively during manual ventilation of 12 cardiac arrest patients treated in the emergency department of a UK Hospital. METHODS: Adult cardiac arrest patients were treated according to ERC guidelines. Ventilation was provided using a self-inflating bag. A COSMOplus monitor (Respironics Inc.) was inserted into the ventilation circuit at the beginning of the resuscitation from which ventilation data were downloaded to a laptop. RESULTS: Data were collected from 12 patients (7 male; age 47-82 years). The maximum respiratory rate was 9-41 breaths per minute (median 26). The median tidal volume was 619 ml (374-923 ml) and the median respiratory rate was 21 min(-1) (7-37 min(-1)). The corresponding median minute volume was 13.0 l/min (4.6-21.3 min(-1)). Median peak inspiratory pressures were 60.6 cmH(2)O (range 46-106). Airway pressure was positive for 95.3% of the respiratory cycle (range 87.9-100%). CONCLUSIONS: Hyperventilation was common, mostly through high respiratory rates rather than excessive tidal volumes. This is the first study to document tidal volumes and airway pressures during resuscitation. The persistently high airway pressures are likely to have a detrimental effect on blood flow during CPR. Guidelines on respiratory rates are well known, but it would appear that in practice they are not being observed.

 

 
J Emerg Med. 2006 Jan;30(1):63-7.

Effects of face mask ventilation in apneic patients with a resuscitation ventilator in comparison with a bag-valve-mask.

von Goedecke A, Wenzel V, Hörmann C, Voelckel WG, Wagner-Berger HG, Zecha-Stallinger A, Luger TJ, Keller C.

Department of Anesthesiology and Critical Care Medicine, Medical University of Innsbruck, Innsbruck, Austria.

Bag-valve-mask ventilation in an unprotected airway is often applied with a high flow rate or a short inflation time and, therefore, a high peak airway pressure, which may increase the risk of stomach inflation and subsequent pulmonary aspiration. Strategies to provide more patient safety may be a reduction in inspiratory flow and, therefore, peak airway pressure. The purpose of this study was to evaluate the effects of bag-valve-mask ventilation vs. a resuscitation ventilator on tidal volume, peak airway pressure, and peak inspiratory flow rate in apneic patients. In a crossover design, 40 adults were ventilated during induction of anesthesia with either a bag-valve-mask device with room air, or an oxygen-powered, flow-limited resuscitation ventilator. The study endpoints of expired tidal volume, minute volume, respiratory rate, peak airway pressure, delta airway pressure, peak inspiratory flow rate and inspiratory time fraction were measured using a pulmonary monitor. When compared with the resuscitation ventilator, the bag-valve-mask resulted in significantly higher (mean+/-SD) peak airway pressure (15.3+/-3 vs. 14.1+/-3 cm H2O, respectively; p=0.001) and delta airway pressure (14+/-3 vs. 12+/-3 cm H2O, respectively; p<0.001), but significantly lower oxygen saturation (95+/-3 vs. 98+/-1%, respectively; p<0.001). No patient in either group had clinically detectable stomach inflation. We conclude that the resuscitation ventilator is at least as effective as traditional bag-valve-mask or face mask resuscitation in this population of very controlled elective surgery patients

 
Neurocrit Care. 2005;2(2):165-71. Links

Ventilation patterns in patients with severe traumatic brain injury following paramedic rapid sequence intubation.

Davis DP, Heister R, Poste JC, Hoyt DB, Ochs M, Dunford JV.

Department of Emergency Medicine, University of California-San Diego, San Diego, CA, USA. davismd@cox.net

INTRODUCTION: Inadvertent hyperventilation has been documented during aeromedical transports but has not been studied following paramedic rapid sequence intubation (RSI). The San Diego Paramedic RSI Trial was designed to study the impact of paramedic RSI on outcome in patients with severe head injury. This analysis explores ventilation patterns in a cohort of trial patients undergoing end-tidal CO2 (ETCO2) monitoring. METHODS: Adult patients with severe head injury (Glasgow Coma Score: 3-8) unable to be intubated without RSI were prospectively enrolled in the trial. Midazolam and succinylcholine were used for RSI; rocuronium was administered following tube confirmation. Standardized ventilation protocols were used by most paramedics; however, one agency instituted ETCO2 monitoring during the second trial year, with paramedics instructed to target ETCO2 values of 30 to 35 mmHg. The incidence and duration of inadvertent hyperventilation (ETCO2: <30 mmHg) and severe hyperventilation (ETCO2: <25 mmHg) were explored for patients undergoing ETCO2 monitoring. The initial, final, minimum, and maximum values for ETCO2 and the maximum and minimum ventilatory rate values were also calculated using descriptive statistics (95% confidence interval). The pattern of ETCO2 values over time and distribution of recorded ventilatory rate values were explored graphically. RESULTS: A total of 76 trial patients had adequate ETCO2 data for this analysis. The mean values for initial, final, maximum, and minimum ETCO2 were 40.8 (range: 37.5-44.2), 28.4 (range: 25.4-31.4), 45.1 (range: 41.4-48.8), and 23.5 mmHg (range: 21.4-25.5), respectively. The mean maximum and minimum ventilatory rate values were 36.0/minute (range: 33.5-38.5) and 12.8/minute (range: 11.9-13.7), respectively. ETCO2 values less than 30 and 25 mmHg were documented in 79% and 59% of patients, respectively, with mean durations of 485 (range: 378-592) and 390 seconds (range: 285-494). CONCLUSION: Inadvertent hyperventilation is common following paramedic RSI, despite ETCO2 monitoring and target parameters.

 

Respir Care. 2005 May;50(5):628-35

 

Reducing ventilation frequency during cardiopulmonary resuscitation in a porcine model of cardiac arrest.

 

Yannopoulos D, Tang W, Roussos C, Aufderheide TP, Idris AH, Lurie KG.

 

Minneapolis Medical Research Foundation, 914 South 8th Street, 3rd Floor, Minneapolis MN 55404, USA.

 

INTRODUCTION: American Heart Association/American College of Cardiology guidelines recommend a compression-to-ventilation ratio (C/V ratio) of 15:2 during cardiopulmonary resuscitation (CPR) for out-of-the-hospital cardiac arrest. Recent data have shown that frequent ventilations are unnecessary and may be harmful during CPR, since each positive-pressure ventilation increases intrathoracic pressure and may increase intracranial pressure and decrease venous blood return to the right heart and thereby decrease both the cerebral and coronary perfusion pressures. HYPOTHESIS: We hypothesized that reducing the ventilation rate by increasing the C/V ratio from 15:2 to 15:1 will increase vital-organ perfusion pressures without compromising oxygenation and acid-base balance. METHODS: Direct-current ventricular fibrillation was induced in 8 pigs. After 4 min of untreated ventricular fibrillation without ventilation, all animals received 4 min of standard CPR with a C/V ratio of 15:2. Animals were then randomized to either (A) a C/V ratio of 15:1 and then 15:2, or (B) a C/V ratio of 15:2 and then 15:1, for 3 min each. During CPR, ventilations were delivered with an automatic transport ventilator, with 100% oxygen. Right atrial pressure, intratracheal pressure (a surrogate for intrathoracic pressure), aortic pressure, and intracranial pressure were measured. Coronary perfusion pressure was calculated as diastolic aortic pressure minus right atrial pressure. Cerebral perfusion pressure was calculated as mean aortic pressure minus mean intracranial pressure. Arterial blood gas values were obtained at the end of each intervention. A paired t test was used for statistical analysis, and a p value < 0.05 was considered significant. RESULTS: The mean +/- SEM values over 1 min with either 15:2 or 15:1 C/V ratios were as follows: intratracheal pressure 0.93 +/- 0.3 mm Hg versus 0.3 +/- 0.28 mm Hg, p = 0.006; coronary perfusion pressure 10.1 +/- 4.5 mm Hg versus 19.3 +/- 3.2 mm Hg, p = 0.007; intracranial pressure 25.4 +/- 2.7 mm Hg versus 25.7 +/- 2.7 mm Hg, p = NS; mean arterial pressure 33.1 +/- 3.7 mm Hg versus 40.2 +/- 3.6 mm Hg, p = 0.007; cerebral perfusion pressure 7.7 +/- 6.2 mm Hg versus 14.5 +/- 5.5 mm Hg, p = 0.008. Minute area intratracheal pressure was 55 +/- 17 mm Hg . s versus 22.3 +/- 10 mm Hg . s, p < 0.001. End-tidal CO(2) with 15:2 versus 15:1 was 24 +/- 3.6 mm Hg versus 29 +/- 2.5 mm Hg, respectively, p = 0.001. Arterial blood gas values were not significantly changed with 15:2 versus 15:1 C/V ratios: pH 7.28 +/- 0.03 versus 7.3 +/- 0.03; P(aCO(2)) 37.7 +/- 2.9 mm Hg versus 37.6 +/- 3.5 mm Hg; and P(aO(2)) 274 +/- 36 mm Hg versus 303 +/- 51 mm Hg. CONCLUSIONS: In a porcine model of ventricular fibrillation cardiac arrest, reducing the ventilation frequency during CPR by increasing the C/V ratio from 15:2 to 15:1 resulted in improved vital-organ perfusion pressures, higher end-tidal CO(2) levels, and no change in arterial oxygen content or acid-base balance.

 

 

Resuscitation. 2005 Mar;64(3):321-5

 

Effects of decreasing inspiratory times during simulated bag-valve-mask ventilation.

 

von Goedecke A, Bowden K, Wenzel V, Keller C, Gabrielli A.

 

Department of Anesthesiology and Critical Care Medicine, Medical University Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria

 

During CPR, an inspiratory time of 2 s is recommended when the airway is unprotected; indicating that approximately 30% of the resuscitation attempt is spent on ventilation, but not on chest compressions. Since survival rates may not decrease when ventilation levels are relatively low, and uninterrupted chest compressions with a constant rate of approximately 100/min have been shown to be lifesaving, it may be beneficial to cut down the time spent on ventilation, and instead, increase the time for chest compressions. In an established bench model of a simulated unprotected airway, we evaluated if inspiratory time can be decreased from 2 to 1 s at different lower oesophageal sphincter pressure (LOSP) levels during ventilation with a bag-valve-mask device. In comparison with an inspiratory time of 2 s, 1 s resulted in significantly (p < 0.001) higher peak airway pressure and peak inspiratory flow rate, while lung tidal volumes at all LOSP levels were clinically comparable. Neither ventilation strategy produced stomach inflation at 20 cmH2O LOSP, and 1 s versus 2 s inspiratory time did not produce significantly higher (mean +/- S.D.) stomach inflation at 15 (8 +/-9 ml versus 0 +/- 0 ml; p < 0.01) and 10 cmH2O LOSP (69 +/- 20 ml versus 34 +/- 18 ml; p < 0.001), and significantly lower stomach inflation at 5 cmH2O LOSP (219 +/- 16 ml versus 308 +/- 21 ml; p < 0.001) per breath. Total cumulative stomach inflation volume over constantly decreasing LOSP levels with an inspiratory time of 2 s versus 1 s was higher (6820 ml versus 5920 ml). In conclusion, in this model of a simulated unprotected airway, a reduction of inspiratory time from 2 to 1 s resulted in a significant increase of peak airway pressure and peak inspiratory flow rate, while lung tidal volumes remained clinically comparable (up to approximately 15% difference), but statistically different due to the precise measurements. Theoretically, this may increase the time available for, and consequently the actual number of, chest compressions during CPR by approximately 25% without risking an excessive increase in stomach inflation.

 

 

Circulation. 2004 Apr 27;109(16):1960-5

 

Hyperventilation-induced hypotension during cardiopulmonary resuscitation.

 

Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen C, Sparks CW, Conrad CJ, Provo TA, Lurie KG.

 

Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee, USA.

 

 

BACKGROUND: A clinical observational study revealed that rescuers consistently hyperventilated patients during out-of-hospital cardiopulmonary resuscitation (CPR). The objective of this study was to quantify the degree of excessive ventilation in humans and determine if comparable excessive ventilation rates during CPR in animals significantly decrease coronary perfusion pressure and survival. METHODS AND RESULTS: In humans, ventilation rate and duration during CPR was electronically recorded by professional rescuers. In 13 consecutive adults (average age, 63+/-5.8 years) receiving CPR (7 men), average ventilation rate was 30+/-3.2 per minute (range, 15 to 49). Average duration per breath was 1.0+/-0.07 per second. No patient survived. Hemodynamics were studied in 9 pigs in cardiac arrest ventilated in random order with 12, 20, or 30 breaths per minute. Survival rates were then studied in 3 groups of 7 pigs in cardiac arrest that were ventilated at 12 breaths per minute (100% O2), 30 breaths per minute (100% O2), or 30 breaths per minute (5% CO2/95% O2). In animals treated with 12, 20, and 30 breaths per minute, the mean intrathoracic pressure (mm Hg/min) and coronary perfusion pressure (mm Hg) were 7.1+/-0.7, 11.6+/-0.7, 17.5+/-1.0 (P<0.0001), and 23.4+/-1.0, 19.5+/-1.8, and 16.9+/-1.8 (P=0.03), respectively. Survival rates were 6/7, 1/7, and 1/7 with 12, 30, and 30+ CO2 breaths per minute, respectively (P=0.006). CONCLUSIONS: Professional rescuers were observed to excessively ventilate patients during out-of-hospital CPR. Subsequent animal studies demonstrated that similar excessive ventilation rates resulted in significantly increased intrathoracic pressure and markedly decreased coronary perfusion pressures and survival rates.

 

 
Crit Care Med. 2004 Sep;32(9 Suppl):S345-51

Death by hyperventilation: a common and life-threatening problem during cardiopulmonary resuscitation.

Aufderheide TP, Lurie KG.

Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin, USA.

CONTEXT: This translational research initiative focused on the physiology of cardiopulmonary resuscitation (CPR) initiated by a clinical observation of consistent hyperventilation by professional rescuers in out-of-hospital cardiac arrest. This observation generated scientific hypotheses that could only ethically be tested in the animal laboratory. OBJECTIVE: To examine the hypothesis that excessive ventilation rates during performance of CPR by overzealous but well-trained rescue personnel causes a significant decrease in coronary perfusion pressure and an increased likelihood of death. DESIGN AND SETTING: In the in vivo human aspect of the study, we set out to objectively and electronically record rate and duration of ventilation during performance of CPR by trained professional rescue personnel in a prospective clinical trial in intubated, adult patients with out-of-hospital cardiac arrest. In the in vivo animal aspect of the study, to simulate the clinically observed hyperventilation, nine pigs in cardiac arrest were ventilated in a random order with 12, 20, or 30 breaths/min, and physiologic variables were assessed. Next, three groups of seven pigs in cardiac arrest were ventilated at 12 breaths/min with 100% oxygen, 30 breaths/min with 100% oxygen, or 30 breaths/min with 5% CO2/95% oxygen, and survival was assessed. MAIN OUTCOME MEASURES: Ventilation rate and duration in humans; mean intratracheal pressure, coronary perfusion pressure, and survival rates in animals. RESULTS: In 13 consecutive adults (average age, 63 +/- 5.8 yrs) receiving CPR (seven men) the average ventilation rate was 30 +/- 3.2 breaths/min (range, 15 to 49 breaths/min) and the average duration of each breath was 1.0 +/- 0.07 sec. The average percentage of time in which a positive pressure was recorded in the lungs was 47.3 +/- 4.3%. No patient survived. In animals treated with 12, 20, and 30 breaths/min, the mean intratracheal pressures and coronary perfusion pressures were 7.1 +/- 0.7, 11.6 +/- 0.7, 17.5 +/- 1.0 mm Hg/min (p < .0001) and 23.4 +/- 1.0, 19.5 +/- 1.8, 16.9 +/- 1.8 mm Hg (p = .03) with each of the different ventilation rates, respectively (p = comparison of 12 breaths/min vs. 30 breaths/min for mean intratracheal pressure and coronary perfusion pressure). Survival rates were six of seven, one of seven, and one of seven with 12, 30, and 30 + CO2 breaths/min, respectively (p = .006). CONCLUSIONS: Despite seemingly adequate training, professional rescuers consistently hyperventilated patients during out-of-hospital CPR. Subsequent hemodynamic and survival studies in pigs demonstrated that excessive ventilation rates significantly decreased coronary perfusion pressures and survival rates, despite supplemental CO2 to prevent hypocapnia. This translational research initiative demonstrates an inversely proportional relationship between mean intratracheal pressure and coronary perfusion pressure during CPR. Additional education of CPR providers is urgently needed to reduce these newly identified and deadly consequences of hyperventilation during CPR. These findings also have significant implications for interpretation and design of resuscitation research, CPR guidelines, education, the development of biomedical devices, emergency medical services quality assurance, and clinical practice

 
Circulation. 2004 Apr 27;109(16):1960-5.

Hyperventilation-induced hypotension during cardiopulmonary resuscitation.

Aufderheide TP, Sigurdsson G, Pirrallo RG, Yannopoulos D, McKnite S, von Briesen C, Sparks CW, Conrad CJ, Provo TA, Lurie KG.

Department of Emergency Medicine, Medical College of Wisconsin, Milwaukee, USA.

BACKGROUND: A clinical observational study revealed that rescuers consistently hyperventilated patients during out-of-hospital cardiopulmonary resuscitation (CPR). The objective of this study was to quantify the degree of excessive ventilation in humans and determine if comparable excessive ventilation rates during CPR in animals significantly decrease coronary perfusion pressure and survival. METHODS AND RESULTS: In humans, ventilation rate and duration during CPR was electronically recorded by professional rescuers. In 13 consecutive adults (average age, 63+/-5.8 years) receiving CPR (7 men), average ventilation rate was 30+/-3.2 per minute (range, 15 to 49). Average duration per breath was 1.0+/-0.07 per second. No patient survived. Hemodynamics were studied in 9 pigs in cardiac arrest ventilated in random order with 12, 20, or 30 breaths per minute. Survival rates were then studied in 3 groups of 7 pigs in cardiac arrest that were ventilated at 12 breaths per minute (100% O2), 30 breaths per minute (100% O2), or 30 breaths per minute (5% CO2/95% O2). In animals treated with 12, 20, and 30 breaths per minute, the mean intrathoracic pressure (mm Hg/min) and coronary perfusion pressure (mm Hg) were 7.1+/-0.7, 11.6+/-0.7, 17.5+/-1.0 (P<0.0001), and 23.4+/-1.0, 19.5+/-1.8, and 16.9+/-1.8 (P=0.03), respectively. Survival rates were 6/7, 1/7, and 1/7 with 12, 30, and 30+ CO2 breaths per minute, respectively (P=0.006). CONCLUSIONS: Professional rescuers were observed to excessively ventilate patients during out-of-hospital CPR. Subsequent animal studies demonstrated that similar excessive ventilation rates resulted in significantly increased intrathoracic pressure and markedly decreased coronary perfusion pressures and survival rates.

 
Prehosp Disaster Med. 2003 Jan-Mar;18(1):20-3. Links

Prehospital hyperventilation after brain injury: a prospective analysis of prehospital and early hospital hyperventilation of the brain-injured patient.

Lal D, Weiland S, Newton M, Flaten A, Schurr M.

Department of Surgery, Medical School, University of Wisconsin, Madison, Wisconsin 53792, USA.

BACKGROUND: The Brain Trauma Foundation's Guidelines for the Management of Severe Head Injury state that the use of prophylactic hyperventilation after traumatic brain injury (TBI) should be avoided because it can compromise cerebral perfusion. The objective of this study was to assess the prevalence of unintentional hyperventilation. METHODS: A prospective evaluation of all intubated trauma patients with a diagnosis of TBI was performed. Patients with signs of impending herniation were excluded. RESULTS: Forty patients were included in the study. The average Glasgow Coma Scale (GCS) was 6.3. Of these, 28 patients (70%) were unintentionally hyperventilated.

 

Resuscitation. 2002 Aug;54(2):167-73

 

Effects of decreasing inspiratory flow rate during simulated basic life support ventilation of a cardiac arrest patient on lung and stomach tidal volumes.

 

Stallinger A, Wenzel V, Wagner-Berger H, Schäfer A, Voelckel WG, Augenstein S, Dörges V, Idris AH, Lindner KH, Hörmann C.

 

Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University, Anichstrasse 35, 6020 Innsbruck, Austria. angelika.stallinger@uibk.ac.at

 

If the airway of a cardiac arrest patient is unprotected, basic life support with low rather than high inspiratory flow rates may reduce stomach inflation. Further, if the inspiratory flow rate is fixed such as with a resuscitator performance may improve; especially when used by less experienced rescuers. The purpose of the present study was to assess the effect of limited flow ventilation on respiratory variables, and lung and stomach volumes, when compared with a bag valve device. After institutional review board approval, and written informed consent was obtained, 20 critical care unit registered nurses volunteered to ventilate a bench model simulating a cardiac arrest patient with an unprotected airway consisting of a face mask, manikin head, training lung [with lung compliance, 50 ml/0.098 kPa (50 ml/cmH(2)O); airway resistance, 0.39 kPa/l/s (4 cmH(2)O/l/s)] oesophagus [lower oesophageal sphincter pressure, 0.49 kPa (5 cmH(2)O)] and simulated stomach. Each volunteer ventilated the model with a self-inflating bag (Ambu, Glostrup, Denmark; max. volume, 1500 ml), and a resuscitator providing limited fixed flow (Oxylator EM 100, CPR Medical devices Inc., Toronto, Canada) for 2 min; study endpoints were measured with 2 pneumotachometers. The self-inflating bag vs. resuscitator resulted in comparable mean +/- SD mask tidal volumes (945 +/- 104 vs. 921 +/- 250 ml), significantly (P < 0.05) higher peak inspiratory flow rates (111 +/- 27 vs. 45 +/- 21 l/min), and peak inspiratory pressure (1.2 +/- 0.47 vs. 78 +/- 0.07 kPa), but significantly shorter inspiratory times (1.1 +/- 0.29 vs. 1.6 +/- 0.35 s). Lung tidal volumes were comparable (337 +/- 120 vs. 309 +/- 61 ml), but stomach tidal volumes were significantly (P < 0.05) higher (200 +/- 95 vs. 140 +/- 51 ml) with the self-inflating bag. In conclusion, simulated ventilation of an unintubated cardiac arrest patient using a resuscitator resulted in decreased peak flow rates and therefore, in decreased peak airway pressures when compared with a self-inflating bag. Limited flow ventilation using the resuscitator decreased stomach inflation, although lung tidal volumes were comparable between groups.

 

 
J Trauma. 2002 Jan;52(1):47-52

Hyperventilation in traumatic brain injury patients: inconsistency between consensus guidelines and clinical practice.

Thomas SH, Orf J, Wedel SK, Conn AK.

Boston MedFlight Critical Care Transport Service, Boston, Massachusetts, USA. thomas.stephen@mgh.harvard.edu

BACKGROUND: This study assessed patients with traumatic brain injury (TBI) to determine whether prehospital and community hospital providers employed hyperventilation therapy inconsistent with consensus recommendation against its routine use. METHODS: This prospective analysis of 37 intubated TBI patients without herniation, undergoing helicopter transport to an urban Level I center, entailed flight crews' noting of assisted ventilation rate (AVR) and end-tidal carbon dioxide (ETCO2) upon their arrival at trauma scenes or community hospitals. A priori-set levels of AVR and ETCO2 were used to assess frequency of guideline-inconsistent hyperventilation, and Fisher's exact and Kruskal-Wallis tests assessed association between guideline-inconsistent hyperventilation and manual vs. mechanical ventilation mode. RESULTS: Inappropriately high AVR and low ETCO2 were seen in 60% and 70% of patients, respectively. Manual ventilation was associated with guideline-inconsistent hyperventilation assessed by AVR (p = 0.038) and ETCO2 (p = 0.022). CONCLUSION: Prehospital and community hospital hyperventilation practices are not consistent with consensus recommendations for limitation of hyperventilation therapy

 
Circulation. 2001;104:2465.

Adverse Hemodynamic Effects of Interrupting Chest Compressions for Rescue Breathing During Cardiopulmonary Resuscitation for Ventricular Fibrillation Cardiac Arrest

Robert A. Berg, MD; Arthur B. Sanders, MD; Karl B. Kern, MD; Ronald W. Hilwig, DVM, PhD; Joseph W. Heidenreich, BA; Matthew E. Porter, BA; Gordon A. Ewy, MD

From the University of Arizona College of Medicine, Steele Memorial Children’s Research Center and Department of Pediatrics (R.A.B.), Sarver Heart Center (all authors), Department of Surgery (A.B.S.), and Department of Medicine (K.B.K., G.A.E.), Tucson, Ariz.

Background— Despite improving arterial oxygen saturation and pH, bystander cardiopulmonary resuscitation (CPR) with chest compressions plus rescue breathing (CC+RB) has not improved survival from ventricular fibrillation (VF) compared with chest compressions alone (CC) in numerous animal models and 2 clinical investigations.

Methods and Results— After 3 minutes of untreated VF, 14 swine (32±1 kg) were randomly assigned to receive CC+RB or CC for 12 minutes, followed by advanced cardiac life support. All 14 animals survived 24 hours, 13 with good neurological outcome. For the CC+RB group, the aortic relaxation pressures routinely decreased during the 2 rescue breaths. Therefore, the mean coronary perfusion pressure of the first 2 compressions in each compression cycle was lower than those of the final 2 compressions (14±1 versus 21±2 mm Hg, P<0.001). During each minute of CPR, the number of chest compressions was also lower in the CC+RB group (62±1 versus 92±1 compressions, P<0.001). Consequently, the integrated coronary perfusion pressure was lower with CC+RB during each minute of CPR (P<0.05 for the first 8 minutes). Moreover, at 2 to 5 minutes of CPR, the median left ventricular blood flow by fluorescent microsphere technique was 60 mL · 100 g-1 · min-1 with CC+RB versus 96 mL · 100 g-1 · min-1 with CC, P<0.05. Because the arterial oxygen saturation was higher with CC+RB, the left ventricular myocardial oxygen delivery did not differ.

Conclusions— Interrupting chest compressions for rescue breathing can adversely affect hemodynamics during CPR for VF.

 

 
Ann Emerg Med. 1995 Aug;26(2):216-9.

Lower esophageal sphincter pressure during prolonged cardiac arrest and resuscitation.

 Bowman FP, Menegazzi JJ, Check BD, Duckett TM.

Center for Emergency Medicine of Western Pennsylvania, School of Medicine, University of Pittsburgh, USA.

STUDY OBJECTIVE: Unprotected airway ventilation models have been based on a lower esophageal sphincter (LES) pressure found in human beings under general anesthesia. Whether this assumption is applicable during cardiac arrest in human beings is unknown. We attempted to determine the effects of prolonged ventricular fibrillation (VF) on the tension of the LES in a swine model of cardiac arrest. DESIGN: Prospective experimental trial using 18 female mixed-breed domestic swine (mean weight, 21.9 +/- 2.0 kg). RESULTS: Animals were anesthetized, intubated, and fitted with instruments for the monitoring of LES pressure. LES tone was measured with a LECTRON 302 esophageal monitor (American Antec, Incorporated). VF was induced with a 3-second, 100 mA transthoracic shock and left untreated for 8 minutes; then resuscitation was attempted. LES tension was measured during the first 7 minutes of the arrest. If return of spontaneous circulation (ROSC) occurred, LES pressure was measured for 7 more minutes. The mean baseline LES pressure was 20.6 +/- 2.8 cm H2O. During minutes 1 through 7 of the arrest the LES tone (mean +/- SD) decreased from 18.0 +/- 3.0 to 3.3 +/- 4.2. ROSC occurred in 10 of the 18 trials. In the 7 minutes after ROSC, LES pressure increased from 4.7 +/- 3.8 to 9.8 +/- 3.0. CONCLUSION: This study demonstrated a rapid and severe decrease in LES tone during prolonged cardiac arrest. When ROSC occurred, LES tension increased quickly but did not return to baseline

 
Prehosp Disaster Med. 1995 Apr-Jun;10(2):101-5.

Assessment of pulmonary mechanics and gastric inflation pressure during mask ventilation.

 Weiler N, Heinrichs W, Dick W.

Johannes Gutenberg University Medical School, Clinic of Anesthesiology, Mainz, Germany.

INTRODUCTION: Mask ventilation is a procedure routinely used in emergency medicine. Potential hazards are inadequate alveolar ventilation and inflation of the stomach with air, leading to subsequent regurgitation and aspiration. The aim of this study was to measure lung function and gastric inflation pressures during mask ventilation. METHODS: For this purpose, 31 patients scheduled for routine urological procedures were studied during induction of anesthesia. Lung function was assessed by recording respiratory flow and pressure directly at the face mask. Gastric inflation was observed with a microphone taped to the epigastric area. RESULTS: Gastric inflation occurred in 22 of the 31 patients. Mean gastric inflation pressure was 27.5 +/- 6.55 cm H2O, mean compliance was 67 +/- 24.1 ml/cm H2O, mean resistance was 17.4 +/- 6.41 cm H2O/L/sec, and the mean respiratory time constant was 1.1 +/- 0.26 seconds. CONCLUSIONS: These data suggest that inspiratory pressure be limited to 20 cm H2O, and that an inspiratory time of at least four times the respiratory time constant be allowed. Monitoring airway pressure and gastric inflation is a simple technique that may improve the safe-ty of patients during mask ventilation.