Hemodynamic effects of positive end-expiratory pressure during abdominal hyperpression: A preliminary study in healthy volunteers

Hemodynamic effects of positive end-expiratory pressure during abdominal hyperpression: A preliminary study in healthy volunteers

Journal of Critical Care (2012) 27, 33–36 Hemodynamic effects of positive end-expiratory pressure during abdominal hyperpression: A preliminary study...

109KB Sizes 0 Downloads 48 Views

Journal of Critical Care (2012) 27, 33–36

Hemodynamic effects of positive end-expiratory pressure during abdominal hyperpression: A preliminary study in healthy volunteers☆ Jean-Luc Fellahi MD, PhD a,b,⁎, Vincent Caille MD c , Cyril Charron MD c , Georges Daccache MD d , Antoine Vieillard-Baron MD, PhD c,e a

Department of Anesthesiology and Critical Care Medicine, CHU de Caen, Caen, France Univ Caen, Faculty of Medicine, Caen, France c Intensive Care Unit, Centre Hospitalier Universitaire Ambroise Paré, Assistance Publique-Hôpitaux de Paris, Boulogne, France d Department of Anesthesiology, CHP Saint-Martin, Caen, France e University of Versailles Saint Quentin en Yvelines, Versailles, France b

Keywords: PEEP; Medical antishock trousers; Abdominal hyperpression; Left ventricular afterload

Abstract Purpose: An increase in abdominal pressure induces an increase in left ventricular afterload under clinical conditions. We tested the hypothesis that positive end-expiratory pressure (PEEP) could reverse the hemodynamic consequences of abdominal hyperpression by opposing the increase in left ventricular afterload. Materials and methods: Eight healthy volunteers were investigated during 3 experimental conditions: (1) baseline, (2) increase in abdominal pressure by means of medical antishock trousers (MAST) inflation, and (3) addition of PEEP +10 cm H2O. Heart loading conditions and left ventricular systolic and diastolic function were assessed by transthoracic echocardiography. Results: The application of PEEP significantly reduced the prior increase in end-systolic wall stress: 45 ± 11 vs 55 ± 14 kdyn/cm2, P b .05. Medical antishock trousers inflation significantly altered the deceleration time of mitral E wave: 199 ± 23 vs 156 ± 38 milliseconds, P b .05. Left ventricular preload and global systolic performance were unaffected by MAST and PEEP applications. Conclusions: The increase in left ventricular afterload induced by MAST inflation can be efficiently reduced by the use of a moderate PEEP. Potential clinical applications in the abdominal compartment syndrome or in the setting of laparoscopic surgery should be developed. © 2012 Elsevier Inc. All rights reserved.

☆ No conflicts of interest. ⁎ Corresponding author. Pôle Anesthésie-Réanimation-SAMUCoordination Hospitalière-Hémovigilance, CHU de Caen, Avenue de la Côte de Nacre, 14033 Caen Cedex 9, France. Tel.: +33 2 310 647 36; fax: +33 2 310 651 37. E-mail address: [email protected] (J.-L. Fellahi).

0883-9441/$ – see front matter © 2012 Elsevier Inc. All rights reserved. doi:10.1016/j.jcrc.2011.03.003

1. Introduction The increase in abdominal pressure induced by intraperitoneal gas insufflation has been found to increase cardiac afterload [1,2]. Similar results have been reported

34 when inflation of the medical antishock trousers (MAST) was used in critically ill patients [3,4] and in healthy volunteers [5]. The effects of positive end-expiratory pressure (PEEP) on heart loading conditions have been well documented for many years [6,7]. By an increase in pleural pressure, PEEP produces a decrease in left ventricular preload [7,8] and afterload [8,9]. Thus, the application of PEEP could counterbalance the effect of MAST and limit the hemodynamic consequences of abdominal hyperpression on left ventricular afterload. If it does, it could be applied in many medical or surgical situations where abdominal hyperpression occurs. The objective of the present study was to assess the effects of PEEP application in healthy volunteers undergoing a prior increase in left ventricular afterload by MAST inflation. We tested the hypothesis that PEEP could reverse the hemodynamic consequences of MAST on left ventricular afterload.

2. Methods Eight healthy volunteers were investigated at the Saint Martin Hospital (Caen, France). The study was approved by the local ethics committee, and all volunteers gave written informed consent. Subjects underwent complete physical examination, 12-lead electrocardiogram, and transthoracic echocardiography (TTE) before inclusion in the study. Inclusion criterion was age older than 18 years. Exclusion criteria were pregnancy, a body mass index of more than 30 kg/m2, a history of respiratory barotrauma and/or cardiac disease, any cardiac treatment, and poor quality of TTE images. At the time of the study, all volunteers were at rest in the supine position for at least 30 minutes and breathed spontaneously. Noninvasive systolic and diastolic arterial blood pressures were measured every 3 minutes by a plethysmographic method. Heart rate was obtained continuously from the 5-lead electrocardiogram monitoring. Doppler TTE was performed by a single trained cardiologist investigator with a Sequoia C 256 (Siemens Medical Solutions, Malvern, PA, USA). A transthoracic 2.5-MHz single-plane probe was positioned to obtain subcostal long-axis and short-axis views of the left ventricle, an apical 4- and 5-chamber view, and a parasternal long-axis view. Echocardiographic images were recorded on videotape during the protocol, and measurements were done by 2 blinded and trained observers unaware of the time of measurement. The end-diastolic frame was selected at the peak of the R wave on simultaneous electrocardiogram recording, and the end-systolic frame was defined as the smallest ventricular dimension during the last half of the T wave. Using a microcomputer interfaced with the videotape player, stop-motion frames at end-diastole and end-systole were displayed on the microcomputer screen to digitize the endocardial outlines of the left ventricle. From the apical 4-chamber view, end-diastolic and end-systolic areas were automatically processed, as well as the long axis

J.-L. Fellahi et al. of the left ventricle permitting the calculation of left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volumes. Left ventricular end-diastolic volume was used to approximate left ventricular preload. Intervariabilities and intravariabilities for LVEDV measurements were 7% ± 7% and 6% ± 6%, respectively. Left ventricular ejection fraction was calculated as (LVEDV − LVESV)/ LVEDV and provided global assessment of left ventricular systolic performance. From the apical 4-chamber view, Doppler mitral flow velocities were also recorded. The E/A ratio and the deceleration time of the E wave (DTE) were both calculated and used to approximate left ventricular diastolic function. Left ventricular end-diastolic and endsystolic diameters were measured from M-mode recording in the parasternal long-axis view. In the same view, left ventricular end-systolic wall thickness (WT) of the posterior wall was also measured via M-mode recording. Noninvasive left ventricular meridional end-systolic wall stress (ESWS) was calculated using the Reichek formula [10]: ESWS = 0.334 (SBP × ESD)/WT (1 ± WT/ESD), where SBP is systolic blood pressure and ESD is left ventricular endsystolic diameter. The ESWS provided a reliable indication of left ventricular afterload by reflecting the combined effects of peripheral loading conditions and intrinsic cardiac properties [11]. From the apical 5-chamber view, Doppler aortic velocity-time integral (VTI) was recorded at the level of the left ventricular outflow tract, together with aortic artery diameter (D), permitting calculation of left ventricular stroke volume as VTI × πD2/4. Cardiac index (CI) was then calculated using the following formula: CI = stroke volume × heart rate/body surface area. Intervariabilities and intravariabilities for CI measurements were 6% ± 4% and 5% ± 3%, respectively. Stroke index was computed as stroke volume/ body surface area. After completion of a baseline set of measurements for each volunteer, a mild lower body positive pressure by means of MAST inflated to 30 cm H2O in the abdominal compartment was applied, and measurements were repeated. Then, a PEEP of 10 cm H2O by means of a continuous positive airway pressure Boussignac system (Vygon, Ecouen, France) was applied for 10 minutes, and measurements were repeated again. These short stabilizing phases were sufficient because cardiovascular changes occur within seconds of PEEP [12] and MAST [3,4] applications. The global duration of the protocol was less than 1 hour per volunteer, suggesting that their volume status remained stable all along the study period.

2.1. Statistical analysis Data are expressed as mean ± SD. Absolute values and changes in hemodynamic parameters after MAST and PEEP applications were compared using 1-way analysis of variance for repeated measurements completed in case of statistical significance by the paired Wilcoxon test. P b .05 was considered statistically significant, and all P values were 2

Hemodynamic effects of PEEP during abdominal hyperpression tailed. Statistical analyses were performed using the Analyse-it Method Evaluation edition version 2.09 for Microsoft Excel Software (Analyse-it Software Ltd., Leeds, England).

3. Results We studied 4 men and 4 women. The mean age was 35 ± 6 years (extremes, 25-45 years), the body mass index was 22.9 ± 3.0 kg/m2 (extremes, 18.4-29.0 kg/m2), and the body surface area was 1.75 ± 0.17 m2 (extremes, 1.4-2.1 m2). Hemodynamic data at baseline and changes during MAST and MAST ± PEEP applications are indicated in Table 1. The application of MAST significantly increased ESWS from nearly 50%. This increase was mainly related to a simultaneous increase in left ventricular end-systolic diameter, whereas systolic blood pressure and end-systolic WT did not vary significantly. The application of PEEP reduced from more than 50% the prior increase in left ventricular afterload, whereas end-systolic diameter returned to baseline value. The significant increase in DTE suggested a MASTrelated acute diastolic dysfunction unmodified by PEEP application. Cardiac index significantly decreased when MAST and PEEP were simultaneously applied. Table 1 Hemodynamic effects of MAST and PEEP applications in healthy volunteers (n = 8)

Systolic blood pressure (mm Hg) Diastolic blood pressure (mm Hg) Heart rate (beats per minute) CI (L.min−1·m−2) Stroke index (mL·m−2) Left ventricular ejection fraction (%) LVEDV (mL·m−2) LVESV (mL·m−2) E/A ratio Deceleration time of E (ms) Left ventricular end-systolic diameter (mm) Left ventricular end-systolic WT (mm) ESWS (kdyn/cm2)

Baseline

MAST

MAST ± PEEP

112 ± 17

114 ± 8

118 ± 11

71 ± 5

76 ± 5

82 ± 9 ⁎†

76 ± 4

73 ± 5

70 ± 2 ⁎†

3.0 ± 0.4 40 ± 4

2.7 ± 0.2 37 ± 3

2.4 ± 0.4 ⁎ 35 ± 5

63 ± 7

65 ± 8

62 ± 5

66 ± 24 ± 1.45 ± 156 ±

11 65 ± 5 62 ± 11 7 23 ± 6 23 ± 4 0.32 1.50 ± 0.48 1.50 ± 0.41 38 199 ± 23 ⁎ 190 ± 32 ⁎

31 ± 2

12.2 ± 1.2

38 ± 8

Values are presented as mean ± SD. ⁎ P b .05 vs baseline. † P b .05 vs MAST.

35 ± 2 ⁎

10.9 ± 1.8 55 ± 14 ⁎

33 ± 3

11.4 ± 1.3 45 ± 11 †

35

4. Discussion The main finding of the present study is that a significant increase in left ventricular afterload induced by MAST can be reversed by addition of a moderate PEEP. The pressure gradient between the abdominal and thoracic compartments acts in a simple way on left ventricular afterload and in a complex way on left ventricular preload. The increase in pressure gradient induced by MAST inflation has previously been found to increase left ventricular afterload [3,4]. In the present study, a dramatic rise in ESWS was observed when MAST was inflated. Simultaneously, an increase in DTE by nearly 30% was observed. Then, the addition of a moderate PEEP of ±10 cm H2O induced a significant decrease in ESWS, which returned toward baseline values, meaning that PEEP could reduce the prior increase in pressure gradient and its consequences on left ventricular afterload. Nonetheless, DTE remained elevated after PEEP application. The effects of the pressure gradient on left ventricular preload are more complex and involve systemic venous return. Theoretically, venous return increases when the gradient is increased and decreases when the gradient is decreased or reversed, depending, however, on the intravascular volume of the abdominal venous compartment [13]. In the current study, neither MAST inflation nor PEEP application significantly modified LVEDV. A decrease in CI was, however, observed when MAST and PEEP were simultaneously applied because of both a significant decrease in heart rate and a trend toward a decrease in stroke index. Thus, even if nonsignificant (probably because of the small number of volunteers), a true decrease in preload, often seen with PEEP in patients with normal cardiac function, cannot be totally excluded and could limit the usefulness of PEEP under similar clinical conditions, MAST and PEEP potentially adding their negative effects on preload to further decrease cardiac output. It could, however, be different in patients with compromised cardiac function, much less sensitive to preload variations. As expected, no significant variation in global left ventricular systolic performance was observed in our healthy volunteers, but substantial hemodynamic deterioration has already been reported in patients with compromised cardiac function [3]. Some remarks must be included to indicate the limitations of the current study. First, we did not measure either intraabdominal or pleural pressures, so we do not know in what extent our MAST and PEEP load challenges could have influenced the pressure gradient. We previously showed that the mean increase in pleural pressure induced by a moderate PEEP was slight and probably trivial in terms of afterload changes in mechanically ventilated patients with normal left ventricular function [8]. It might, however, be significant in cardiac patients because a dilated ventricle is more sensitive to small afterload changes [14]. High levels of PEEP could further influence the pressure gradient and totally reverse MAST-induced increase in left ventricular afterload. Second, we cannot extrapolate our experimental results to critical

36 patients who develop an abdominal compartment syndrome [15] or patients undergoing laparoscopic surgery [2] because MAST inflation does not necessarily have similar hemodynamic consequences on heart loading conditions. Further studies are needed to estimate what clinical applications could be derived from our physiologic concept. In conclusion, the increase in left ventricular afterload induced by MAST inflation in healthy volunteers can be efficiently reduced by the use of a moderate PEEP. Potential clinical applications in the setting of critical abdominal compartment syndrome or in laparoscopic surgery with peritoneal gas insufflation could be developed in the future.

J.-L. Fellahi et al.

[6]

[7]

[8]

[9]

[10]

References [11] [1] Safran D, Sgambati S, Orlando R. Laparoscopy in high-risk cardiac patients. Surg Gynecol Obstet 1993;176:548-54. [2] Alfonsi P, Vieillard-Baron A, Coggia M, et al. Cardiac function during intraperitoneal CO2 insufflation for aortic surgery: a transesophageal echocardiographic study. Anesth Analg 2006;102:1304-10. [3] Fellahi JL, Valtier B, Beauchet A, et al. Hemodynamic effects of medical antishock trousers during mechanical ventilation. Can J Anesth 1999;46:423-8. [4] Loubieres Y, Vieillard-Baron A, Beauchet A, et al. Echocardiographic evaluation of left ventricular function in critically ill patients. Dynamic loading challenge using medical antishock trousers. Chest 2000;118: 1718-23. [5] Fellahi JL, Caille V, Charron C, et al. Non invasive assessment of cardiac index in healthy volunteers: a comparison between thoracic

[12]

[13]

[14]

[15]

impedance cardiography and Doppler echocardiography. Anesth Analg 2009;108:1553-9. Qvist J, Pontoppidan H, Wilson RS, et al. Hemodynamic responses to mechanical ventilation with PEEP: the effect of hypervolemia. Anesthesiology 1975;42:45-55. Jardin F, Farcot FJ, Boisante L, et al. Influence of positive endexpiratory pressure on left ventricular performance. N Engl J Med 1981;304:387-92. Fellahi JL, Valtier B, Beauchet A, et al. Does positive end-expiratory pressure ventilation improve left ventricular function? A comparative study by transesophageal echocardiography in cardiac and noncardiac patients. Chest 1998;114:556-62. Pinsky MR, Matuschak GM, Klain M. Determinants of cardiac augmentation by elevations in intrathoracic pressure. J Appl Physiol 1985;58:1189-98. Reichek N, Wilson J, St John Sutton M, et al. Noninvasive determination of left ventricular end-systolic stress: validation of the method and initial application. Circulation 1982;65:99-108. Lang RM, Borow KM, Neumann A, et al. Systemic vascular resistance: an unreliable index of left ventricular afterload. Circulation 1986;74:1114-23. Perschau RA, Pepine CJ, Nichols WW, et al. Instantaneous blood flow responses to positive end-expiratory pressure with spontaneous ventilation. Circulation 1979;59:1312-8. Takata M, Wise RA, Robotham JL. Effects of abdominal pressure on venous return: abdominal vascular zone conditions. J Appl Physiol 1990;69:1961-72. Scharf SM, Bianco JA, Tow DE, et al. The effects of large negative intrathoracic pressure on left ventricular function in patients with coronary artery disease. Circulation 1981;63:871-5. Cheatham ML, Malbrain ML. Cardiovascular implications of abdominal compartment syndrome. Acta Clin Belg Suppl 2007;1: 98-112.