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Original Articles – General

Comparison of three modes of positive pressure mask ventilation during induction of anaesthesia: a prospective, randomized, crossover study

Seet, Mustafa Ma; Soliman, Khalid Mb; Sbeih, Zuhair Fc

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European Journal of Anaesthesiology: November 2009 - Volume 26 - Issue 11 - p 913-916
doi: 10.1097/EJA.0b013e328329b0ab
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Mask ventilation is a procedure routinely used in anaesthesia and emergency medicine to maintain alveolar ventilation and arterial oxygenation. In a study in which simulated emergency ventilation in apnoeic patients employing four different airway devices that used small tidal volumes, Dörges et al.[1] have shown that bag-valve-mask ventilation was the most simple and successful strategy.

Some of the potential hazards of mask ventilation are inadequate alveolar ventilation and inflation of the stomach with air, leading to subsequent regurgitation and aspiration [2].

During bag-valve-mask ventilation if peak airway pressure exceeds lower esophageal sphincter pressure, gas volume will not be directed completely towards the lungs but may induce a certain degree of stomach inflation. Although lower esophageal sphincter pressure in awake volunteers was shown to be approximately 16 cmH2O, it may be less during induction of anaesthesia and during cardiac arrest [3]. Thus, if peak airway pressure during ventilation in an unprotected airway is kept as low as possible, stomach inflation may be less likely.

Silent gastroesophageal reflux also may occur when facemask is used in patients undergoing general anaesthesia. Associated tracheal aspiration may result in a chemical pneumonitis and increase morbidity and mortality. The incidence of reflux reported in the literature ranges from 4.5 to 26% [4].

One approach to make mask ventilation safer in an unprotected airway is to limit tidal volume [5]; another one might be to limit peak airway pressure [5,6].

This study was designed to compare the effect of three modes of positive pressure mask ventilation during induction of anaesthesia regarding ventilatory variables and gastric insufflation in apnoeic patients with unprotected airway.


The study had the approval of the Hospital Research and Ethics Committee.

Ninety patients ASA physical status I or II undergoing elective surgical procedures, which ordinarily involved tracheal intubation, were enrolled in the study. Exclusion criteria were BMI more than 30 kg m−2, gastroesophageal diseases, facial and upper airway abnormalities that would make mask ventilation or tracheal intubation difficult, or both, and pregnancy. Informed consent was obtained from each patient.

Patients were premedicated 20 min prior to the induction of anaesthesia with intravenous injection of 2 mg of midazolam, 10 mg of metoclopramide, 50 mg of ranitidine, and 1 mg kg−1 of tramadol.

In the operating room, standard monitors (ECG, NIBP, ETCO2 and SpO2) and a peripheral nerve stimulator were used. Low compliance, wide bore tubing were used, and all connections were checked for leaks.

After baseline measurements of blood pressure, oxygen saturation and heart rate, patients were preoxygenated with 100% oxygen for 3 min and anaesthesia was induced with 1 μg kg−1 of fentanyl and 2.5–3.0 mg kg−1 propofol administered over 30 s. Rocuronium 0.6 mg kg−1 was used to provide neuromuscular blockade.

After induction of anaesthesia, ventilation by a well fitting standard anatomical anaesthesia face mask (size #4 or #5, depending on sex and size of patient) with a Guedel oropharyngeal airway with oxygen 100% (oxygen flow 6 l min−1) was performed until neuromuscular blockade was established. Neuromuscular blockade was assessed with train-of-four stimulation.

Airway management, insertion of the oropharyngeal airway and placement of the anaesthesia mask were performed by a single experienced anaesthesiologist. The mask was fixed using a single hand.

Gastric insufflation was assessed by another anaesthesiologist blinded to the ventilating mode by listening over the stomach with a stethoscope during ventilation.

Each patient received the three modes of ventilation under study. Patients were divided into three groups of 30 as follows:

  1. Group (MVP) received MCV, VCV and PCV.
  2. Group (VPM) received VCV, PCV and MCV.
  3. Group (PMV) received PCV, MCV and VCV.

Each mode of ventilation lasted for 1 min. Patients were randomized to groups according to a computer generated randomization allocation.

During MCV, the oxygen flow meter was adjusted to 1 l min−1, respiratory rate of 15 breaths min−1 as indicated by a metronome, providing an inspiratory to expiratory (I/E) ratio of 1: 1. The APL valve adjusted to 20 cmH2O. The anaesthesiologist delivers the tidal volume through the circle system producing a visible chest rise. During volume-controlled ventilation the oxygen flow meter was adjusted to 1 l min−1, tidal volume of 7–8 ml kg−1, respiratory rate of 15 breaths min−1, and an I/E ratio of 1: 1. In pressure-controlled ventilation, the oxygen flow meter was adjusted to 1 l min−1, peak airway pressure (Paw) was adjusted to deliver a tidal volume of 7–8 ml kg−1, respiratory rate of 15 breaths min−1, and an I/E ratio of 1: 1.

Haemodynamic variables measurements were measured using Datex-Ohmeda S/5 ADU monitor. The following variables were recorded: heart rate (HR) (beats m−1), mean arterial blood pressure (MABP) (mmHg), (SPO2) (%), (ETCO2) (mmHg), respiratory rate (RR) (beats m−1), inspiratory tidal volume (iVt)(ml), expiratory tidal volume (eVt) (ml), minute ventilation (MV) (l/m), peak airway pressure (Paw) (Cm H2O), plateau Paw (CmH2O) respiratory compliance (ml/CmH2O), auto PEEP (CmH2O), inspiratory time (seconds), and expiratory time (seconds).

Sample size was selected to detect 25% difference in between groups with respect to peak airway pressure for a type 1 error of 0.05 and a power of 0.09. This power analysis was based on data from previous studies [7,8].

Results are presented as mean ± SD and ranges. Statistical analysis was done using the SPSS 14.0 software (SPSS Inc, Chicago, Illinois, USA). Statistical analysis was performed using one-way Analysis Of Variance ‘ANOVA’ tests. Post Hoc-Dunnett T3, multiple comparisons was used with 95% confidence interval to compare between each pair of the three modes. Data were considered statistically significant when P < 0.05.


Ninety patients were enrolled in this study. The mean (range) age and weight were 29 (15–51) years, 69.8 (44–95) kg male to female ratio (2: 1), BMI range [17–30 kg m–2], ASA I to II ratio (29: 16). There were no significant differences in patient characteristics among the groups.

PCV was associated with lower peak airway pressures (11.4 ± 1.2 cmH2O) compared with MCV and VCV (14.3 ± 1.7 cm H2O and 13.3 ± 1.5 cm H2O, respectively; P < 0.0001). Inspiratory tidal volume showed no significant differences between the three modes (500.9 ± 60.7), (496.3 ± 57.9) and (496.4 ± 59.7). Expiratory tidal volume was comparable in the three modes (483.4 ± 57.4), (486.2 ± 54.1) and (485.11 ± 58.0).

Minute ventilation was not different among the three different modes of ventilation used in this study. End-tidal carbon dioxide was comparable in PCV and VCV modes (33.6 ± 1.9 and 33.4 ± 2.7 mmHg) and low in MCV (30.7 ± 3.2 mmHg; P < 0.0001). Gastric insufflation was positive in one patient (1.1%) receiving PCV compared with three patients (3.3%) in MCV and three patients (3.3%) in VCV (Table 1).

Table 1
Table 1:
Haemodynamic and respiratory data

No regurgitation or pulmonary aspiration occurred in any patient including those who were showing positive gastric insufflations.


Comparable minute ventilation was achieved in all individuals with all forms of ventilations. The peak airway pressure, however, was significantly lower in pressure-controlled ventilation compared with volume-controlled ventilation and manual-controlled ventilation (11, 13, 14 cmH2O respectively) (P < 0.0001).

Peak airway pressure of 27 cmH2O has been shown to result in stomach ventilation in approximately 71% of patients during mask ventilation with Magill system [6]. The author of the study suggested limiting inspiratory pressures to 20 cmH2O to prevent stomach insufflations.

In our study, none of the patients peak airway pressures exceeded 19 cmH2O. However, in seven patients (2.5%) stomach insufflation occurred; one (1.1%) in the pressure-controlled ventilation group (Paw = 16 cmH2O), three (3.3%) in volume-controlled ventilation (average Paw = 16.3 cmH2O) group and three (3.3%) in the manual-controlled ventilation (average Paw = 16.3 cmH2O). Limiting peak airway pressure to less than 16 cmH2O may thus provide additional patient safety through eliminating gastric insufflation.

In our study we used a stethoscope placed in the epigastric area to detect gastric insufflation. This method of detecting gastric insufflation has been shown to be reliable in detecting as little as 5 ml of air insufflation of the stomach [9]. None of the earlier-mentioned incidents has resulted in regurgitation of stomach content or aspiration.

In order to reduce the peak airway pressure, we increased the I: E ratio to 1: 1 and, with a respiratory rate of 15 breath min−1, the inspiratory time was approximately 2 s.

The peak airway pressure can further be reduced by decreasing the tidal volume. In our study, we used a tidal volume of 7–8 ml kg−1. Dörges et al.[10] have shown that, when using 100% oxygen, tidal volume can be safely reduced to at least 350 ml. Small tidal volumes applied with a paediatric self-inflating bag and 100% oxygen resulted in adequate oxygenation and ventilation.

Apart from providing an extra level of patient safety through reducing peak airway pressure, pressure-controlled ventilation has the added advantage of providing the anaesthesiologist with free hands to hold a tight mask in case of difficulty with mask ventilation.

Our data are comparable to those previously reported by von Goedecke et al.[7] in which he showed that pressure-controlled ventilation resulted in reduced inspiratory peak flow rates and peak airway pressures when compared with manual circle system ventilation. However, to our knowledge, there were no studies that compared the respiratory effects of pressure-controlled ventilation in apnoeic patients to manual and volume-controlled ventilation during induction of anaesthesia.

Some limitations in our study should be noted. First, we used a qualitative method to determine gastroesophageal insufflation as we were unable to quantitate the amount of air entering the stomach with our technique. Second, only healthy ASA physical status I–II patients without underlying respiratory disease, gastroesophageal diseases, and fascial and upper airway abnormalities were enrolled into the study. Third, we did not measure arterial blood gases.

In conclusion, our study has shown that automatic pressure-controlled ventilation of apnoeic patients during induction of anaesthesia delivered by built-in ventilators of modern anaesthesia machines resulted in significant reduction of peak airway pressure in comparison to automatic volume-controlled ventilation and the more established manual circle system ventilation, which may confer an additional safety profile.


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© 2009 European Society of Anaesthesiology