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CRITICAL CARE AND TRAUMA

The Effects of Different Mouth-to-Mouth Ventilation Tidal Volumes on Gas Exchange During Simulated Rescue Breathing

Angelika Stallinger, MD^*, Volker Wenzel, MD^*, Stephan Oroszy, MD^*, Viktoria D. Mayr, MD^*, Ahamed H. Idris, MD, Karl H. Lindner, MD^*, and Christoph Hörmann, MD^*

*Department of Anesthesiology and Critical Care Medicine, Leopold-Franzens-University, Innsbruck, Austria; and Department of Emergency Medicine, University of Florida College of Medicine, Gainesville, Florida

Address correspondence to Dr. Angelika Stallinger, and reprint requests to Dr. Karl H. Lindner, Leopold-Franzens-University, Department of Anesthesiology and Critical Care Medicine, Anichstrasse 35, 6020 Innsbruck, Austria. Address e-mail to Angelika. Stallinger{at}uibk.ac.at

	Abstract

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The American Heart Association recommends tidal volumes of 700 to 1000 mL during mouth-to-mouth ventilation, but smaller tidal volumes of 500 mL may be of advantage to decrease the likelihood of stomach inflation. Because mouth-to-mouth ventilation gas contains only 17% oxygen, but 4% carbon dioxide, it is unknown whether 500-mL tidal volumes given during rescue breathing may result in insufficient oxygenation and inadequate carbon dioxide elimination. In a university hospital research laboratory, 20 fully conscious volunteer health care professionals were randomly assigned to breathe tidal volumes of 500 or 1000 mL of mouth-to-mouth ventilation gas (17% oxygen, 4% carbon dioxide, 79% nitrogen), or room air control (21% oxygen, 79% nitrogen) for 5 min. Arterial blood gases were taken immediately before, and after breathing 5 min of the experimental gas composition. When comparing 500 versus 1000 mL of mouth-to-mouth ventilation tidal volumes with 500 mL of room air, 500 mL of mouth-to-mouth ventilation tidal volume resulted in significantly (P < 0.05) lower mean ± SEM arterial oxygen partial pressure (70 ± 1 versus 85 ± 2 versus 92 ± 3 mm Hg, respectively), and lower oxygen saturation (94 ± 0.4 versus 97 ± 0.2 versus 98 ± 0.2%), but increased arterial carbon dioxide partial pressure (46 ± 1 versus 40 ± 1 versus 39 ± 1 mm Hg, respectively). Sixteen of 20 volunteers had to be excluded from the experiment with 500 mL of mouth-to-mouth ventilation gas after about 3 min instead of after 5 minutes as planned because of severe nervousness, sweating, and air hunger. We conclude that during simulated mouth-to-mouth ventilation, only large (approximately 1000 mL), but not small (approximately 500 mL) tidal volumes were able to maintain both sufficient oxygenation and adequate carbon dioxide elimination.

IMPLICATIONS: To provide efficient mouth-to-mouth ventilation, it is important to administer tidal volumes of 1000 mL; tidal volumes of 500 mL were not adequate.

	Introduction

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When ventilating a tracheally unintubated patient, the distribution of gas between lungs and stomach depends on the lower esophageal sphincter pressure, respiratory mechanics [respiratory system compliance and degree of airway obstruction (1)], and the technique of the rescuer performing basic life support (inspiratory flow rate, peak airway pressure, and tidal volume) (2). Stomach inflation is a complex problem that may cause regurgitation, aspiration, pneumonia, and possibly, death (3). Stomach inflation may also increase intragastric pressure, push up the diaphragm, restrict lung movements, and thereby decrease the respiratory system compliance (4). Decreased respiratory system compliance may force even more gas into the stomach, thereby inducing a vicious respiratory cycle with each tidal volume of increasing stomach inflation, and decreasing lung ventilation (5). A few studies showed that by providing reasonable ventilation while avoiding significant stomach inflation (6), a tidal volume of 500 mL instead of 800–1200 mL may be a good compromise when ventilating a tracheally unintubated patient. Studies performed in both bench (7) and clinical (8) settings during respiratory arrest and cardiopulmonary resuscitation (CPR) (9) have confirmed the beneficial effects of small (approximately 500 mL/approximately 7.5 mL/kg) instead of large (800 to 1200 mL/approximately 15 mL/kg) tidal volumes as long as oxygen supplementation is used (FIO₂ 0.4).

Small tidal volumes of approximately 500 mL containing room air (21% oxygen) were not sufficient to maintain adequate oxygenation and carbon dioxide elimination in anesthetized, paralyzed, supine adults (10), suggesting that mouth-to-mouth ventilation gas, which contains only approximately 17% oxygen, but approximately 4% carbon dioxide (11), may not be safe and effective for basic life support ventilation. If this were the case, large tidal volumes during mouth-to-mouth ventilation would be needed, although the risk of stomach ventilation would be increased. Accordingly, the purpose of the present study was to assess the effects of small (approximately 500 mL) versus large (approximately 1000 mL) tidal volumes with 17% oxygen and 4% carbon dioxide on gas exchange during simulated mouth-to-mouth ventilation. Our hypothesis was that there would be no difference in study endpoints between groups.

	Methods

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The experimental protocol of this study was approved by the IRB of the Leopold-Franzens University, Innsbruck, Austria. Health care professionals (physicians and medical students) volunteered as participants in this study, and provided written informed consent. Before the actual experiment, the volunteers were allowed to familiarize themselves with the experimental setup consisting of an anesthesia machine, noseclip, and arterial blood gas sampling kit. Namely, the breathing circuit and pneumotachometer of this anesthesia machine (Fabius; Dräger, Lübeck, Germany) were explained in detail to ensure proper compliance with the experimental protocol. The nitrous oxide outlet of this anesthesia machine was connected to a custom-made bottle of gas containing mouth-to-mouth ventilation gas (17% oxygen, 4% carbon dioxide, 79% nitrogen) (11); room air connections were not replaced. Because this anesthesia machine is fresh-gas independent, the simulated mouth-to-mouth ventilation gas could be readily adjusted with the regular oxygen controls of fresh gas flow. Thus, volunteers could breath through a mouthpiece connected via an airway filter with the regular ventilator tubing using either simulated mouth-to-mouth ventilation gas or room air to be set randomly by the investigators. We removed the absorption chalk of the anesthesia machine to ensure that exhaled carbon dioxide was not eliminated out of the breathing circuit. Furthermore, fresh gas flow was adjusted at 12 L/min, which is at or above the entitled minute ventilation of 6 L/min and 12 L/min, respectively.

The volunteers were placed on an operation table in the supine position, and the experimental setup and protocol were explained in detail. Namely, the ventilation rate was prescribed at 12/min, tidal volume at 500 or 1000 mL, and a noseclip was used to prevent inhaling room air through the nose during the experiment, and to ensure that all expired air was being measured. A subsequent test run ensured that all volunteers were willing and able to breathe tidal volumes and had respiration rates as prescribed by the experimental protocol. The volunteers were then randomized to breathe for 5 min either 500 mL of room air (21% oxygen, 79% nitrogen), or 500 mL or 1000 mL of simulated mouth-to-mouth ventilation gas (17% oxygen, 4% carbon dioxide, 79% nitrogen), respectively. Both the volunteers and the data recording investigator were blinded during the experiment to the ventilation gas being used. During the experiment, one investigator monitored and coached the volunteers to remain with their breathing pattern within the experimental protocol, while another investigator recorded ventilation variables. While breathing the experimental tidal volume of the gas mixtures, exhaled tidal volume, end-tidal carbon dioxide, and respiratory rate were measured with the pneumotachometer of the anesthesia machine; blood pressure, oxygen saturation, and heart rate were measured with a patient monitor (AS 3 Compact; Datex Ohmeda, Helsinki, Finland). Arterial blood gas samples were taken after 5 min of every ventilation attempt, respectively, before the experiment was terminated and were analyzed with a blood gas analyzer (Rapidlab 860; Chiron Diagnostics, East Walpol, MA). If oxygen saturation decreased below 90%, the experiment was concluded immediately, and 100% oxygen was given. Also, each volunteer was allowed to stop the experiment by themselves at any time point if adverse effects, such as severe nausea or sweating, air hunger, or dizziness, were felt; management was then performed as above.

All values were expressed as mean ± SEM. Comparisons were made with one-factor and repeated mea-sure analysis of variance, and with Newman-Keuls multiple comparison procedure. Was set at 0.05 for statistical significance.

	Results

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Twenty volunteer participants (7 women [35%], 13 men [65%]; age range 22 to 38 yr; none had underlying cardiac or respiratory disease) were enrolled in this study. Comparing 500 mL versus 1000 mL of mouth-to-mouth ventilation gas versus 500 mL of room air tidal volumes, there was a significant (P < 0.05) decrease of mean ± SEM oxygen saturation and arterial oxygen partial pressure values, and significant increase of arterial carbon dioxide partial pressure when breathing 500 mL of mouth-to-mouth ventilation tidal volume (Table 1, Fig. 1). In the 500-mL mouth-to-mouth ventilation gas group, 16 of 20 volunteers (80%) discontinued the trial after about 3 min because of severe nervousness, dizziness, sweating, or air hunger instead of after 5 min as planned. In contrast, 20 of 20 volunteers in both the 1000-mL mouth-to-mouth ventilation and 500-mL room air groups successfully completed the 5-min study period, respectively. When compared with 500 mL of room air, both 500 and 1000 mL of mouth-to-mouth ventilation tidal volumes had significantly higher arterial carbon dioxide partial pressure and end-tidal carbon dioxide, and significantly lower oxygen saturation, arterial oxygen partial pressure, and pH values (Table 1). No differences were observed in blood pressure or heart rate throughout the experiment.

View larger version (15K): [in this window] [in a new window]   Figure 1. PaO2 and PaCO2 while breathing 500 mL of room air versus 500 or 1000 mL of mouth-to-mouth ventilation gas.

	Discussion

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Measuring respiratory variables such as tidal volumes or even gas mixtures in a clinical investigation of basic life support ventilation is extremely difficult. Also, performing mouth-to-mouth ventilation reflects a hypoxic and hypercarbic gas mixture; this is the only circumstance in medicine of continuously administering a ventilation gas of which each component may result in life-threatening cardiocirculatory collapse (12). Accordingly, this experiment was not deemed ethical to perform in fully anesthetized patients by the IRB of our institution. Although the present data were obtained in fully conscious healthy, spontaneously breathing supine adults, the question arises whether information derived from this experiment can be extrapolated to the cardiopulmonary arrest setting as well. During low rates of blood flow similar to those rates found in shock and CPR, alterations in minute ventilation significantly influenced end-tidal carbon dioxide and both arterial and mixed venous saturation, pH, and carbon dioxide (13). In fact, when using an FIO₂ of 0.4, at a flow of 12% of baseline cardiac output, arterial oxygen partial pressure was maintained at 96 mm Hg despite the fact that ventila-tion was at 50% of the control minute ventilation. Although that study (13) suggests that ventilation-perfusion conditions with normal cardiac output versus normal minute ventilation compared with decreased cardiac output versus decreased minute ventilation may be actually comparable, the mechanisms involved, such as changes in cardiac output, and/or increases in pulmonary shunt attributed to hypercapnia, are most likely more complex (14). Systemic oxygen use during CPR becomes flow dependent; thus, if systemic perfusion is approximately 15% of normal, there may be less need for supplemental oxygen. However, marked increases in the pulmonary venous admixture may require higher inspired oxygen tension to overcome increases in the alveolar-arterial oxygen gradient (15). Accordingly, it is unknown whether this may indicate that 500-mL tidal volumes of mouth-to-mouth ventilation gas may be sufficient for oxygenation and carbon dioxide elimination during low-flow states such as during CPR, and thus further investigation may be warranted and our results may only apply to a beating heart.

The clinical importance of our results may be more important than anticipated. For example, whereas our healthy volunteers were enrolled into the study with normal oxygenation and carbon dioxide levels, a cardiac arrest victim is usually fully deoxygenated, indicating that the oxygen binding effects of hemoglobin are in the steep part of the rightward-shifted curve because of hypercapnia. Accordingly, an approximately 10% change in oxygen saturation at approximately 97%, such as in our volunteers, may indicate significantly less changes in oxygen partial pressure than at approximately 50% oxygen saturation in cardiac arrest patients. Also, carbon dioxide increases cardiac afterload and pulmonary vascular resistance, both of which are not beneficial during cardiac resuscitation.

During recent conferences intended to update the CPR guidelines, an effort was made to simplify the recommendations as much as possible (16). For example, it would be highly desirable to recommend a single tidal volume regardless of the ventilation device and/or technique being used. Several clinical and laboratory studies confirmed that small (approxi-mately 500 mL/7.5 mL/kg) instead of large (approximately 800–1200 mL/15 mL/kg) tidal volumes with an FIO₂ >0.4 during basic life support ventilation provide reasonable oxygenation and carbon dioxide elimination while significantly decreasing the risk of stomach ventilation (6–9). The present study adds important knowledge to the aforementioned guidelines—suggesting not to recommend 500-mL, but 1000-mL tidal volumes during mouth-to-mouth ventilation because of the apparent risk of further deteriorating the degree of both hypoxia and hypercarbia in an apneic patient. Accordingly, although the trade-off to achieve less stomach inflation with 500-mL tidal volumes with oxygen is readily available during bag-valve-mask ventilation, this strategy with mouth-to-mouth ventilation gas and 500-mL tidal volumes would be obtained, according to our data, most likely with hypoxia and hypercarbia. Our observation is in full agreement with the pioneer work of Safar (17) who demonstrated excellent efficacy of mouth-to-mouth ventilation in anesthetized and paralyzed volunteer adults, but showed that tidal volumes were consistently larger than 1000 mL.

The mechanism of gas exchange in our study may be partially explained by extrapolating experience of apneic ventilation. For example, during apneic ventilation for brain-death diagnosis, the patient’s lungs are filled with 100% oxygen, while the endotracheal tube is subsequently disconnected from the ventilator, but connected to an oxygen reservoir. Thus, if a patient with brain death does not breath, arterial carbon dioxide usually increases at a rate of approximately 2.5 to 4 mm Hg/minute (18). This is comparable to our volunteers, in whom breathing mouth-to-mouth ventilation gas caused an increase of arterial carbon dioxide of approximately 2 mm Hg/minute. Interestingly, these two maneuvers with apnea and endogenous carbon dioxide production versus spontaneous ventilation with endogenous carbon dioxide production and additional exogenous carbon dioxide inhalation resulted in comparable arterial carbon dioxide. Because arterial oxygen levels of approximately 70 mm Hg in our volunteers were nonhypoxic, an arterial carbon dioxide level of approximately 46 mm Hg may suggest that increased carbon dioxide levels induced an air hunger, nervousness, sweating, tachycardia, and subsequent discontinuation of the experiment by most volunteers. However, this would be in disagreement with an experiment in which conscious volunteers breathing 100% oxygen with an approximate arterial oxygen level of 450 mm Hg were able to hold their breath for approximately 14 minutes, while easily tolerating arterial carbon dioxide levels of approximately 91 mm Hg (19). Accordingly, if arterial oxygen is not >400 mm Hg as during apneic ventilation, but only approximately 70 mm Hg, and further decreasing as in our volunteers, increasing arterial carbon dioxide levels may not be well tolerated, which may be the most likely explanation of our observation. This is in full agreement with a historic experiment performed in 1908 demonstrating excellent efficacy of apneic ventilation for 1 to 2 hours in dogs with 100% oxygen, but not with room air (20).

Some limitations of the present model need to be noted. First, our fully conscious volunteers were spontaneously breathing, which does not simulate positive pressure ventilation such as during mouth-to-mouth ventilation. Thus, although we did not measure pulmonary ventilation/perfusion ratios, our volunteers most likely had less dead space ventilation, and a better ventilation/perfusion distribution than a patient receiving mouth-to-mouth ventilation. Accordingly, had we performed the present study in anesthetized patients, the differences would have likely been even greater. Interestingly, the 4 of 20 volunteers who were able to breathe the small mouth-to-mouth ventilation tidal volumes for 5 minutes were either smokers or those who reported episodes of sleep apnea, suggesting a better tolerance for increased levels of arterial carbon dioxide. Finally, our volunteers had normal cardiac output; accordingly, our results may have been different in patients with severely decreased cardiac output such as during CPR or shock.

In conclusion, during simulated mouth-to-mouth ventilation, only large (approximately 1000 mL), but not small (approximately 500 mL) tidal volumes were able to maintain both sufficient oxygenation and adequate carbon dioxide elimination.

	Acknowledgments

 
This project was supported, in part, by the Austrain Science Foundation Grant P14169-MED, Vienna, Austria, the Founders Grant of the Society of Critical Care Medicine, Anaheim, CA, and departmental funds.

	References

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