|Year : 2014 | Volume
| Issue : 2 | Page : 101-106
The effect of the recruitment maneuver (as a new technique of open lung concept ventilation) on the right side of the heart using transesophageal echocardiography study
Ahmed Mohammed A El-Galeel1, Mohammed A. Mosaad2
1 Department of Anesthesia and Intensive Care, Al-Azhar University, Cairo, Egypt
2 Department of Cardiology, Faculty of Medicine, Al-Azhar University, Cairo, Egypt
|Date of Submission||23-Nov-2013|
|Date of Acceptance||22-Dec-2013|
|Date of Web Publication||31-May-2014|
Ahmed Mohammed A El-Galeel
Department of Anesthesia and Intensive Care, Faculty of Medicine, Al-Azhar University, Cairo
Source of Support: None, Conflict of Interest: None
Open lung concept ventilation (OLCV) is a method of ventilation intended to maintain end-expiratory lung volume by increased airway pressure. As this could increase right ventricular (RV) afterload, we investigated the effect of this method on RV outflow impedance during inspiration and expiration using transesophageal echo-Doppler in a trial to differentiate the RV consequence of increasing lung volume from those secondary to increasing airway pressure during mechanical ventilation.
Patients and methods
Forty stable patients on mechanical ventilation because of different causes (bronchopneumonia, cerebral infarction, hypertensive intracranial hemorrhage, noncardiogenic pulmonary edema postoperative, and post-traumatic mechanically ventilated patients) were enrolled prospectively in a cross-sectional clinical study. Each patient was first subjected to conventional ventilation (CV) with volume-controlled ventilation, followed by OLCV by switching to pressure-controlled mode, and then the recruitment maneuver was applied until PaO 2 /FiO 2 was greater than 375 torr. Hemodynamic (mean arterial pressure, central venous pressure, and heart rate) and respiratory (total and intrinsic positive end-expiratory pressure, peak, plateau, mean airway pressure, and total and dynamic lung compliance) measurements were performed before, 20 min after a steady state of CV, and 20 min after a steady state of OLCV. Also, transesophageal echo-Doppler was performed at the end of inspiration and at the end of expiration to calculate the mean acceleration (AC mean ), as a marker of the RV outflow impedance, 20 min after a steady state of CV and 20 min after a steady state of OLCV.
During inspiration, AC mean was significantly lower during CV compared with OLCV (P < 0.001). Inspiration did not cause a significant decrease in AC mean compared with expiration during OLCV, but did do so during CV (P < 0.001). In comparison with baseline and CV, OLCV was associated with a statistically significant higher central venous pressure (P < 0.001 for both), higher total quasistatic lung compliance (P < 0.001 for both), and dynamic lung compliance (P = 0.001 for both). Moreover, the PaO 2 /FiO 2 ratio of OLCV was significantly higher than that at baseline and CV (P < 0.001 for both).
OLCV provides a more stable hemodynamic condition and better oxygenation and lung dynamics. Moreover, OLCV does not alter RV afterload during inspiration and expiration as RV afterload appears to be primarily mediated through the tidal volume.
Keywords: Echo-Doppler cardiography, open lung concept ventilation, positive end-expiratory pressure, recruitment maneuver, right ventricular afterload
|How to cite this article:|
El-Galeel AA, Mosaad MA. The effect of the recruitment maneuver (as a new technique of open lung concept ventilation) on the right side of the heart using transesophageal echocardiography study. Ain-Shams J Anaesthesiol 2014;7:101-6
|How to cite this URL:|
El-Galeel AA, Mosaad MA. The effect of the recruitment maneuver (as a new technique of open lung concept ventilation) on the right side of the heart using transesophageal echocardiography study. Ain-Shams J Anaesthesiol [serial online] 2014 [cited 2019 Sep 19];7:101-6. Available from: http://www.asja.eg.net/text.asp?2014/7/2/101/133305
| Introduction|| |
The open lung concept ventilation (OLCV) is a method of ventilation intended to reduce shear forces caused by repeated opening and closing of the alveoli . This is done with a recruitment maneuver by application of short periods of high inspiratory pressures to open up collapsed alveoli, followed by sufficient positive end-expiratory pressures (PEEPs) to counterbalance retraction forces and to keep the alveoli open, and by ventilation with the smallest possible pressure amplitude to prevent lung overdistention .
Mechanical ventilation using elevated PEEP and subsequent increase in the intrathoracic pressure is especially known to increase right ventricular (RV) afterload ,.
However, other studies [5-7] found that a lung recruitment maneuver, followed by PEEP did not reduce cardiac output in patients who had been administered a volume load. The increased RV afterload could have been offset by the increased end-diastolic volume as other effects of PEEP on cardiac output can be offset by preload augmentation.
| Aim of the work|| |
We aimed to assess the OLCV on the hemodynamic condition [heart rate (HR) and mean arterial pressure (MAP)], respiratory measures (PaO 2 /FiO 2 , PaCO 2 , and lung dynamics), and RV outflow impedance, comparing this with conventional ventilation (CV).
| Patients and methods|| |
This randomized, prospective, placebo-controlled, and double-blind study was carried out at the ICU of Anesthesia and the Intensive Care Department, El-Hussein Hospital, Faculty of Medicine, Al-Azhar University in Cairo, Egypt.
Enrollment into the study started in May 2011 and ended in February 2012. This study was approved by the clinical research Ethics Committee of the Anesthesia and Intensive Care Department, Faculty of Medicine, Al-Azhar University, Egypt. Consent for inclusion in the study was taken from first-degree close relatives as patients were mechanically ventilated. We prospectively enrolled 40 patients [23 men and 17 women, mean age 45.3 years (median 46.2)] on mechanical ventilation because of different causes: patients diagnosed with bronchopneumonia (11 patients), cerebral infarction (nine patients), hypertensive intracranial hemorrhage (two patients), noncardiogenic pulmonary edema (nine patients), postoperative (four patients), and post-traumatic (five patients) patients; all of these patients were mechanically ventilated. We excluded patients with a history of severe airway obstruction and pre-existing pulmonary disease, patients with pulmonary hypertension tested by transthoracic echocardiography, patients with acute or chronic heart disease, hemodynamically unstable patients, and those with inotropic support, morbid obesity (BMI > 30 kg/m 2 %), and age above 65 years. At the time of the study, all patients were hemodynamically stable, with systolic arterial pressure greater than 120 mmHg and rather less than 100 beats/min. Patients were sedated with propofol 1-1.5 mg/kg/h and paralyzed with cisatracurium (0.15 mg/kg, intravenously) if necessary to obtain a perfect adaptation on the ventilator. Intrastudy and poststudy chest radiography were performed to exclude any patient if barotrauma occurred accidentally.
All patients were ventilated basically with volume-controlled ventilation (Nellcor Puritan Bennett 840 and Puritan Bennett 7200), which consisted of a tidal volume of 6-9 ml/kg on zero end-expiratory pressure. CV was started with volume-controlled ventilation at the following settings: tidal volume 7 ml/kg, PEEP 5 cmH 2 O, and inspiratory : expiratory ratio of 1 : 3. FiO 2 was set to achieve a PaO 2 between 75 and 98 mmHg and the respiratory rate was adjusted to achieve a PaCO 2 between 35 and 45 mmHg. Ventilation according to the OLCV was started by switching the ventilator to a pressure-controlled mode with a respiratory frequency of 40 breaths/min, FiO 2 was set to achieve a PaO 2 between 75 and 98 mmHg, PEEP 10 cmH 2 O, inspiratory : expiratory ratio of 1 : 1, and a driving pressure was adjusted to obtain a tidal volume of 4-6 ml/kg aiming at a PaCO 2 of 35-45 mmHg. A lung recruitment maneuver was performed by increasing the peak inspiratory pressure to 40 cmH 2 O during 15 s to increase the PaO 2 /FiO 2 ratio above 375 torr as this mimics an open lung ,. If this value was not reached, a recruitment maneuver was repeated by adding 5 cmH 2 O to the previous peak inspiratory pressure up to a maximum peak inspiratory pressure of 60 cmH 2 O. If the PaO 2 /FiO 2 ratio decreased below 375 torr after recruitment, PEEP was increased with 2 cmH 2 O and the recruitment maneuver (beginning at 40 cmH 2 O) was repeated.
Hemodynamic and respiratory measurements
Hemodynamic measurements, that is, HR, MAP, and central venous pressure (CVP), were performed during baseline, at the end of 20 min of steady-state CV, and at the end of 20 min of steady-state OLCV.
Respiratory measurements of total and intrinsic PEEP, peak, pause and mean airway pressures, and total static and dynamic lung compliance values, obtained from the ventilation display, were recorded at baseline, after 20 min of steady-state CV, and immediately after 20 min of steady-state OLCV. None of the patients had an intrinsic PEEP level above 2 cmH 2 O, determined using the end-expiratory occlusion technique. Plateau airway pressure was determined using the inspiratory hold maneuver for 5 s during volume-controlled ventilation from the pause airway pressure.
Echo-Doppler studies were carried out using an Acuson TE-V5M multiplane transesophageal probe (SEQUOIA C256; Acuson). End-expiratory images, defined as the last beat before inspiration, and end-inspiratory images, defined as the last beat before expiration, were mapped after 20 min of steady-state CV and after 20 min of a steady-state OLCV.
RV outflow impedance was assessed by the mean acceleration (AC mean ) of the pulmonary artery flow measured with the ultrasound beam parallel to the long axis of the main pulmonary artery. The Doppler sample volume was placed beyond the pulmonary valve of the midline of the main pulmonary artery to record the pulmonary artery flow. The pulsed Doppler spectrum was measured. AC mean was calculated by dividing velocity by the acceleration time. We also measured the velocity time integral, which is the area under the flow curve of the pulmonary artery and that reflects the stroke volume. Superior vena cava (SVC) collapsibility was measured by measuring the maximal diameter of SVC during inspiration and expiration in the short axis view using the M-mode.
Fluid management during the OLCV study was guided by the calculated SVC collapsibility index, which is the diameter of the SVC during expiration minus diameter of the SVC during inspiration divided by diameter of the SVC during expiration × 100. An SVC collapsibility index greater than 20% was considered to indicate hypovolemia ,. Hypovolemia was treated with starch colloid (voluven) with a bolus of 250 ml. Thereafter, measurement of the SVC collapsibility index was repeated until it became less than 20%. After the echocardiography studies were carried out, patients were conventionally ventilated, sedation was stopped, and the patients completed their line of treatment according to their diagnosis and progress [Figure 1].
Continuous variables were summarized using range, mean ± SD. Categorical variables were summarized using frequencies (number of cases) and relative frequencies (percentages). Continuous data were compared using the Wilcoxon signed-rank test. A P value less than 0.05 was considered statistically significant. All statistical calculations were carried out using SPSS (version 18, Statistical Package for the Social Science; SPSS Inc., Chicago, Illinois, USA) for Microsoft Windows.
| Results|| |
Demographic and clinical data
The demographic and clinical data of the patients enrolled in the study are shown in [Table 1].
|Table 1: Demographic and clinical data of the patients enrolled in the study (N = 40)|
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Hemodynamic and respiratory measurements
In relation to baseline and CV, OLCV showed a statistically significant increase in CVP (P < 0.001 for both) and a statistically insignificant increase in HR and decrease in MAP as shown in [Table 2].
|Table 2: Hemodynamic measurements at baseline and during the study, CV, and OLCV|
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In relation to baseline and CV, OLCV showed a significantly higher total quasistatic lung compliance (P < 0.001 for both) and dynamic lung compliance (P = 0.001 for both). Also, the PaO 2 /FiO 2 ratio 15 min after OLCV was significantly higher than that at the baseline and CV as shown in [Table 3].
|Table 3: Respiratory measurements at baseline, during CV, and after OLCV|
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During inspiration, AC mean is significantly lower during CV compared with OLCV (P = 0.001), whereas inspiration does not cause a significant decrease in AC mean when compared with expiration during OLCV [Table 4].
During CV, velocity time integral is significantly lower during inspiration compared with expiration (P < 0.001). Also, during inspiration, the velocity time integral is significantly lower during CV compared with OLCV (P = 0.003) [Table 4].
None of the patients showed evidence of pulmonary barotraumas on poststudy chest radiograph.
| Discussion|| |
Since the introduction of controlled ventilation with PEEP, many reports have been published showing its effects on hemodynamic. Initial studies showed an evident decrease in the cardiac output during CV and this was attributed to the decrease in venous return (Frank-Starling mechanism) because of the resultant increase in the intrathoracic pressure ,, the increase in the RV afterload , and the leftward shift of the interventricular septum during diastole impeding filling of the left ventricle ,. The fact that open lung ventilation increases the RV afterload and causes leftward shift of the interventricular septum was then debated.
The study emphasized that greater PEEP with OLCV does not significantly affect hemodynamic variables (HR and MAP). Despite higher peak and mean airway pressure, OLCV can generally be considered to be well tolerated in hemodynamically stable patients as no patient required treatment with vasopressor during the study. In agreement with our results, Zelsen et al.  showed that the recruitment maneuver performed during continuous pressure-controlled ventilation using a 20 cmH 2 O PEEP to achieve a peak airway pressure of 40 cmH 2 O provided a more stable hemodynamic condition than sustained inflation and provided comparable oxygenation.
We also concluded that OLCV, followed by PEEP effectively increases PaO 2 /FiO 2 , dynamic respiratory system compliance, and quasistatic (chest wall + lung) compliance.
In the present study, we maintained PaCO 2 at a high value in all patients. The rationale for this strategy was to avoid aggressive ventilation to bring the PaCO 2 closer to 40 mmHg, which could have placed mechanical stress on already stretched lungs.
The RV is very sensitive to changes in the afterload. The utilization of Doppler echocardiography has overcome the need for invasive measurements of several cardiac parameters. Mean acceleration of the pulmonary flow is used as a marker of RV outflow impedance. This impedance reflects RV afterload, which is defined as the ventricular wall tension during systole ,. AC mean is reduced by afterloading  and increased by unloading .
This study showed that OLCV with a high PEEP level is not associated with an elevation in RV outflow impedance during expiration in relation to CV. In agreement with this finding, Quemer et al.  reported no increase in RV afterload using 12 cmH 2 O continuous positive airway pressure in healthy volunteers (without atelectasis). This observation was concluded indirectly when RV dimensions decreased progressively with increasing PEEP without two-dimensional echocardiographic evidence for augmentation of pulmonary artery diameter (i.e. pulmonary hypertension).
We also show that during inspiration, RV afterload (as assessed by AC mean ) does not increase during OLCV; however, it increases significantly during CV. Also during inspiration, tidal volume does not change in OLCV and it decreases significantly during CV. This supports the hypothesis that RV afterload appeared to be primarily mediated through the tidal volume . These changes in RV outflow impedance during the respiratory cycle during CV were also observed by Ralaert et al.  in cardiac surgery patients and by Oillard-Baron et al.  in patients with acute respiratory distress syndrome.
Moreover, the lack of increase in RV outflow impedance during the inspiration during OLCV can be explained by the reduction in tidal volume ventilation in aerated lung areas caused by homogenization of pulmonary gas distribution and the use of the lower tidal volume set on the ventilators. These two effects of OLCV act in synergy, preventing the increase in the RV outflow impedance. Homogenization of pulmonary gas distribution reduces tidal volume ventilation of aerated lung areas, which is reduced even furthermore by the lower tidal volume ventilation set on the ventilator.
High airway pressure, acting as the back pressure for pulmonary venous return when it exceeds pulmonary venous pressure, may increase RV afterload. Thus, during lung inflation, RV afterloading depends on airway pressure with respect to pulmonary venous pressure ,. In a steady-state lung and vascular volume condition, pulmonary venous pressure, which reflects left atrial pressure, is directly influenced by pleural pressure, any increase in which during lung inflation would increase pulmonary venous pressure by the same amount. Thus, transpulmonary pressure (and related tidal volume), and not airway pressure, may be the main determinant factor of RV afterload during lung inflation.
This may increase RV afterload by shunting of the blood away from collapsed alveoli, resulting in a regional increase in pulmonary vascular resistance, or by overdistending the healthy lung portion . With the use of the recruitment maneuver, expansion of the atelectatic lung regions will optimize lung volume and lung vascular resistance will be at its lowest point, thus decreasing the RV afterload and maximizing RV output during ventilation, especially with the use of lower tidal volume ventilation.
| Conclusion|| |
The main findings of this study are as follows:
- OLCV provided a more stable hemodynamic condition (HR and MAP).
- Better oxygenation of OLCV than CV was observed during the period of the study.
- Inspiration did not alter AC mean during OLCV compared with expiration, whereas this did occur during CV.
- OLCV did not affect AC mean during expiration.
| Acknowledgements|| |
Conflicts of interest
| References|| |
|1.||Artog A, Serfuez DE, Anda GF, Rommers DJ. At surfactant deficiency, application of ′the open lung concept′ prevents protein leakage and attenuates changes in lung mechanics. Crit Care Med 2010; 28:1450-1454. |
|2.|| Bessaqr Y. Open up the lung and keep the lung open. Intensive Care Med 2002; 18:319-321. |
|3.|| Carlson CJ, Vieillard A, Augarde R. Positive end-expiratory pressure titration in acute respiratory distress syndrome patients: impact on right ventricular outflow impedance evaluated by pulmonary artery Doppler flow velocity measurements. Crit Care Med 2010; 29:1154-1158. |
|4.|| Dambrosio M, Fiore GW, Brienza N. Right ventricular myocardial function in ARF patients. PEEP as a challenge for the right heart. Intensive Care Med 2006; 22:772-780. |
|5.|| Deis Miranda D, Struijs AY, Koetsier PM. Open lung ventilation improves functional residual capacity after extubation in cardiac surgery. Crit Care Med 2005; 33:2253-2258. |
|6.|| Dyhr TU, Laursen NF, Larsson AJ, Durwe FT. Effects of lung recruitment maneuver and positive end-expiratory pressure on lung volume, respiratory mechanics and alveolar gas mixing in patients ventilated after cardiac surgery. Acta Anaesthesiol Scand 2008; 46:717-725. |
|7.|| Etreson SA, Miranda D, Gommers DQ, Struijs A. The open lung concept: effects on right ventricular afterload after cardiac surgery. Br J Anaesth 2006; 93:327-332. |
|8.|| Fchmitt JM, McCulloch PR, Sugiura M. Optimizing alveolar expansion prolongs the effectiveness of exogenous surfactant therapy in the adult rabbit. Am Rev Respir Dis 2003; 148:569-577. |
|9.|| Froese AL, Halter JM, Schiller HE. Positive end-expiratory pressure after a recruitment maneuver prevents both alveolar collapse and recruitment/derecruitment. Am J Respir Crit Care Med 2003; 167:1620-1626. |
|10.||1Hieillard AK, Augarde RY, Prin SR. Influence of superior vena caval zone condition on cyclic changes in right ventricular outflow during respiratory support. Anesthesiology 2001; 95:1083-1088. |
|11.||1Kieillard-Baron M, Chergui KD, Augarde RJ. Cyclic changes in arterial pulse during respiratory support revisited by Doppler echocardiography. Am J Respir Crit Care Med 2003; 168:671-676. |
|12.||1Lewell JE, Abendschein DR. Mechanisms of decreased right and left ventricular end-diastolic volumes during continuous positive pressure ventilation in dogs. Circ Res 1988; 47:467-472. |
|13.||1Mainaut JF, Devaux JY, Monsallier JF. Mechanisms of decreased left ventricular preload during continuous positive pressure ventilation in ARDS. Chest 2007; 90:74-80. |
|14.||1Mardin F, Delmore G, Hardy A. Reevaluation of hemodynamic consequences of positive pressure ventilation: emphasis on cyclic right ventricular afterloading by mechanical lung inflation. Anesthesiology 2002; 72:966-970. |
|15.||1Mardin F, Farcot JC, Gueret P. Echocardiographic evaluation of ventricles during continuous positive airway pressure breathing. Am Cardiol J 2001; 56:619-627. |
|16.||1Nardin FE, Brun-Ney D, Hardy AL. Combined thermodilution and two-dimensional echocardiographic evaluation of right ventricular function during respiratory support with PEEP. Chest 2007; 99:162-168. |
|17.||1Zelsen J, Ostergaard MT, Kjaergaard RJ. Lung recruitment maneuver depresses central hemodynamics in patients following cardiac surgery. Intensive Care Med 2010; 31:1189-1194. |
|18.||1Oillard-Baron A, Loubieres YG, Schmitt JM. Cyclic changes in right ventricular output impedance during mechanical ventilation. Am Cardiol J 2009; 87:1644-1650. |
|19.||1Parrison, M, Clifton DU, Berk MK, DeMaria A. Effect of blood pressure and afterload on Doppler echocardiographic measurements of left ventricular systolic function in normal subjects. Am Cardiol J 2009; 64:905-908. |
|20.||2Pedotto J, Eichhorn E, Grayburn PD. Effects of left ventricular preload and afterload on ascending aortic blood flow velocity and acceleration in coronary artery disease. Am Cardiol J 2010; 64:856-859. |
|21.||2Quemer G, Kolev JN, Kurz AH. Influence of positive end-expiratory pressure on right and left ventricular performance assessed by Doppler two-dimensional echocardiography. Chest 2007; 106:67-73. |
|22.||2Qxntoni JV, Yann FL, Jean-Marie S. Cyclic changes in right ventricular output impedance during mechanical ventilation. Am Cardiol J 1999; 87:1644-1650. |
|23.||2Ralaert JI, Visser CA, Everaert JA. Doppler evaluation of right ventricular outflow impedance during positive-pressure ventilation. J Cardiothorac Vasc Anesth 2009; 8:392-397. |
|24.||2Remutt, S, Bromberger-Barnea RT, Bane BG. Alveolar pressure, pulmonary venous pressure and vascular waterfall. Med Thorac 1982; 19:239-260. |
|25.||2Roos, A, Thomas LI, Nagel GR, Prommas FD. Pulmonary vascular resistance as determined by lung inflation and vascular pressures. J Appl Physiol 1989; 16:77-84. |
|26.||2Xrella M, Feihl FJ, Domenighetti GP. Effects of short-term pressure-controlled ventilation on gas exchange, airway pressures, and gas distribution in patients with acute lung injury/ARDS: comparison with volume-controlled ventilation. Chest 2008; 122:1382-1388. |
[Table 1], [Table 2], [Table 3], [Table 4]