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Ann Thorac Surg 2008;85:1355-1360. doi:10.1016/j.athoracsur.2007.10.002
© 2008 The Society of Thoracic Surgeons
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Right arrow Cardiac - physiology

Original Articles: Adult Cardiac

Use of Negative Extrathoracic Pressure to Improve Hemodynamics After Cardiac Surgery

Rakesh K. Chaturvedi, MD, PhDa, Arnold A. Zidulka, MD, FRCPc, Peter Goldberg, MD, FRCPb, Benoit deVarennes, MD, FRCSa, Sameena Iqbal, MD, FRCPd, Elham Rahme, PhDe, Kevin Lachapelle, MD, FRCSa,*

a Division of Cardiac Surgery, Royal Victoria Hospital, Montreal, Quebec, Canada
b Division of Critical Care, Royal Victoria Hospital, Montreal, Quebec, Canada
c Division of Respiratory Medicine, Montreal General Hospital, McGill University Health Center, Montreal, Quebec, Canada
d Division of Nephrology, Montreal General Hospital, McGill University Health Center, Montreal, Quebec, Canada
e Division of Clinical Epidemiology and Biostatistics, Montreal General Hospital, McGill University Health Center, Montreal, Quebec, Canada

Accepted for publication October 1, 2007.

* Address correspondence to Dr Lachapelle, Division of Cardiac Surgery, 687 Pine Ave West, Room S8.30, Royal Victoria Hospital, Montreal, PQ H3A 1A3, Canada (Email: kevin.lachapelle{at}muhc.mcgill.ca).


   Abstract
Top
 Abstract
Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Background: Little attention is given to the mode of mechanical ventilation after cardiac surgery. Positive pressure ventilation with positive end-expiratory pressure (PEEP) has been shown to reduce cardiac output. We hypothesized that positive pressure ventilation with continual negative pressure applied to the chest through a cuirass would increase cardiac output in coronary artery bypass graft patients immediately after surgery.

Methods: Twenty patients with a normal left ventricular ejection fraction were studied 2 hours after coronary artery bypass graft surgery. The patients were ventilated with synchronized intermittent mandatory ventilation (SIMV) and PEEP. Hemodynamic variables and blood gases were studied using four modes of ventilation after 15 minutes in each mode: A (baseline 1) = SIMV and 5 cmH2O of PEEP; B = SIMV without PEEP; C = SIMV without PEEP and with continuous negative pressure applied to the thorax at –20 cmH2O; D (baseline 2) = SIMV and 5 cmH2O of PEEP. The results of the two baselines were averaged.

Results: All patients were hemodynamically stable during the trial. Heart rate, blood pressure, and gas exchange were not affected by the changes in ventilatory modes. With continual negative pressure, the stroke volume index and cardiac index were significantly increased relative to ventilation with SIMV and PEEP by 3.21 mL · min–1 · m–2 (9.0%) and 0.45 L · min–1 · m–2 (13.8%), respectively. Continual negative pressure also reduced venous and wedge pressure.

Conclusions: Continual negative pressure attenuates the negative effects of positive pressure ventilation on cardiac output. Although the improvement in this cohort with normal ventricular function is modest, this pilot study demonstrates that the mode of ventilation may have potentially important effects on cardiac output.


   Introduction
Top
 Abstract
 Introduction
Material and Methods
 Results
 Comment
 Acknowledgments
 References
 
Patients undergoing cardiac surgery most commonly receive positive pressure ventilation with positive end-expiratory pressure (PEEP) in the immediate postoperative period. Little consideration, however, is given to the mode of ventilation used in the postoperative period. Positive end-expiratory pressure can improve gas exchange by increasing functional residual capacity thereby decreasing right-to-left shunting and can also reduce left ventricular afterload [1]. Positive end-expiratory pressure, however, may decrease cardiac output by reducing venous return [2], increasing right ventricular afterload [3], and decreasing left ventricular distensibility [4].

Continual negative pressure (CNP) can cause lung expansion similar to PEEP with improvement in gas exchange and can cause improvement in cardiac output by increasing venous return. On the other hand, CNP can increase pulmonary blood volume [5] and may increase left ventricular afterload [6]. These might worsen gas exchange and cardiac output. In dogs with normal lungs receiving positive pressure ventilation, the application of CNP by chest cuirass has been shown to improve cardiac output when compared with PEEP [2] while preserving adequate gas exchange. Similar results have been obtained in both dogs and patients with low pressure [7–9] and high pressure [10] pulmonary edema.

For the immediate postoperative coronary artery bypass graft surgery (CABG) patient receiving mechanical ventilation, we hypothesized that the application of CNP as compared with PEEP would improve cardiac output while safeguarding adequate gas exchange. This was done as part of a pilot project on alternate modes of ventilation in the postoperative period.


   Material and Methods
Top
 Abstract
 Introduction
 Material and Methods
Results
 Comment
 Acknowledgments
 References
 
A prospective study was done to determine the effect of CNP applied through chest cuirass relative to PEEP. The protocol was approved by the Office of Research Ethics (Protocol SUR-02-060). Consent for the protocol was obtained from each patient (n = 30) before surgery between March 2003 and May 2004.

Characteristics of the patients studied are listed in Table 1. All patients underwent elective first-time CABG surgery. In all patients, the left internal mammary artery was used in addition to other bypass vessels.


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  		Table 1 Characteristics of Patients Studied
 
Enrollment criteria included a preoperative left ventricular ejection fraction (LVEF) greater than 40% (the mean LVEF was 56.5% ± 6.9 SD), absence of chronic obstructive pulmonary disease or congestive heart failure, and absence of recent abdominal surgery, neurologic deficits, or psychiatric problems.

Patients who were too large or too small were excluded from the study as this resulted in the inability of the cuirass (Model F, 277; Technicon-Huxley, New York, NY) to achieve a seal for the creation of negative pressure. The cuirass is a rigid shell covering the anterior thorax and upper abdomen. When in position, it covers an area bounded by the sternal notch, the mid axillary line, and the umbilicus.

Once the patient was deemed stable (approximately 2 hours after leaving the operating room), the study was initiated. Stability was defined by the following: (1) an uncomplicated operative course without the use of an intra-aortic balloon pump, (2) the requirement of a stable dose of vasoactive medication throughout the study, (3) core temperature more than 36°C, (4) mediastinal bleeding less than 125 cc per hour, (5) blood pressure greater than 100 mm Hg systolic, and (6) cardiac index greater than 2.0 L · min–1 · m–2. Ten patients were excluded from the study before starting the protocol because of one or more of the above exclusion criteria.

Upon entry into the intensive care unit and into the study (baseline 1), all patients were placed on synchronized intermittent mandatory ventilation (SIMV) of 12 to 16 breaths per minute, tidal volume of 500 to 700 mL (6 to 8 mL/kg), PEEP of 5 cm H2O, and pressure support ventilation of 10 cm H2O. Given that none of the patients triggered the ventilator during the course of the study owing to the sedation and narcotics given, the respiratory rate and tidal volume remained constant throughout the study period. Therefore, pressure support ventilation was not included in describing the mode of ventilation. Patients were given meperidine for shivering and midazolam for sedation as required. During the entire study period, the infusion rates of vasoactive drugs and fluids was kept constant.

All the patients were positioned supine. All had a pulmonary artery catheter placed intraoperatively after induction of anesthesia. Each mode of ventilation was maintained for 20 minutes, and the following measurements were taken at the end of 15 minutes: heart rate, central venous pressure, pulmonary artery occlusion pressure, and cardiac output (the mean of two consecutive values within 5% of each other) by thermodilution [11]. The cardiac index was derived. The mean blood pressure and mean pulmonary arterial blood pressure were mathematically derived by multiplying the diastolic pressure by 2, adding that product to the systolic pressure, and dividing that sum was by 3. The systemic vascular resistance index and pulmonary vascular resistance index were derived according to standard formulas, as was the stroke volume index. Arterial blood gases and mixed venous blood gases were measured by co-oximeter (Model 865; Bayer Diagnostics, Sudbury, United Kingdom) in 17 of the 20 patients, providing measurement of partial pressure of oxygen (pO2), partial pressure of carbon dioxide (pCO2), and pH and oxygen saturation.

The sequence of changes in the ventilatory modes were done in each patient in the following order: (A) baseline 1: SIMV with PEEP 5 cm H2O; (B) SIMV with PEEP removed; (C) SIMV with the addition of CNP of –20 cm H2O; and (D) baseline 2: SIMV with PEEP 5 cm H2O.

Continual negative pressure was applied to the chest and upper part of the abdomen through a modified Emerson In-exsufflator (Model 2-CMH; J.H. Emerson, Cambridge, Massachusetts). The level of negative pressure was measured by a catheter under the cuirass.

Given that there was no significant difference between baseline 1 and baseline 2, an average of the two was used for all statistical comparisons. The mean baseline (mean of baseline 1 and baseline 2, ie, beginning and end of the experiment) was derived to try and obviate any continual improvement or deterioration in the condition of the patient that might have been independent of the mode of ventilation.

Always the actual values of each patient were used as input for the statistical program (InStat; GraphPad Software, San Diego, California). Percentage increase or decrease were never used to perform the statistical analyses. Using a one-group repeated measures of analysis of variance (ANOVA), with a sample size of 20 and at a significance level of 0.05, the study has a power of 86% to detect a difference of 19% across three levels of repeated measures, assuming a standard deviation of 0.65 and a correlation level of 0.6. For the paired t test analysis, the sample size of 20 provides a power of 81% to detect a difference in the means of 0.44, assuming a standard deviation of 0.65 and using a two-sided significance level of 0.05.

Group data are presented in the form of mean ± SD and repeated measures of ANOVA was used for statistical purposes.


   Results
Top
 Abstract
 Introduction
 Material and Methods
 Results
Comment
 Acknowledgments
 References
 
All results are presented in Table 2. During the different modes of ventilation, no significant changes were found in heart rate, mean blood pressure, mean pulmonary artery pressure or pulmonary venous resistance index, arterial or venous pH, partial pressure of oxygen (pO2), partial pressure of carbon dioxide (pCO2), or O2 saturation.


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  		Table 2 Summary of Results for All Patients: Hemodynamics and Blood Gas During Different Modes of Ventilation
 
With positive pressure ventilation, removal of PEEP did not result in any change in measured or derived variables (mean baseline versus B). The institution of CNP when compared with SIMV without PEEP (B versus C) did not result in any change in the heart rate, blood pressure, or blood gases but did result in a significant increase in cardiac index, by a mean of 0.28 L · min–1 · m–2 or 8.1% (Fig 1). In addition, there was a significant reduction in pulmonary artery occlusion pressure.


Figure 1
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  		Fig 1. Mean ± SD of cardiac index with different modes of ventilation. (CNP = continuous negative pressure; PEEP = positive end-expiratory pressure.)

 
When compared with mean baseline, the application of CNP (mean baseline versus C) resulted in a significant increase in stroke volume index (by a mean of 3.21 mL · min–1 · m–2, or 9.0%; Fig 2) and cardiac index (by a mean of 0.45 L · min–1 · m–2, or 13.8%; Fig 1) and a significant decrease in systemic vascular resistance index. Additionally, CNP caused a significant decrease in central venous pressure (by 2.73 mm Hg, or 28.6%) and pulmonary artery occlusion pressure (by 1.58 mm Hg, or 16.1%). The arterial-venous O2 saturation difference increased from a mean of 23.1% to 23.9% (p = 0.5568).


Figure 2
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  		Fig 2. Mean ± SD of stroke volume index with different modes of ventilation. (CNP = continuous negative pressure; PEEP = positive end-expiratory pressure.)

 
Of interest, 3 patients (4, 11, and 14) were receiving inotrops. In these 3 patients, the mean change in cardiac index compared with mean baseline was 1.02 L · min–1 · m–2 with continual negative pressure. In the other 17 patients who were not receiving inotropes, the mean change in cardiac index was 0.40 L · min–1 · m–2. Although these differences were not statistically significantly different, these results may suggest that CNP was more effective in improving cardiac index in the patients requiring inotropic support.


   Comment
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
Acknowledgments
 References
 
In the immediate postoperative period, CABG patients receiving positive pressure ventilation and CNP (applied to the chest and upper abdomen) resulted in a significant improvement in both cardiac index and stroke volume index as compared with positive pressure ventilation and PEEP, while demonstrating no change in gas exchange. Both the stroke volume index and cardiac index improved with continual CNP and returned to baseline once CNP was removed.

These results are similar to previous studies in dogs with normal lungs [2] as well as in dogs [7] and patients with acute lung injury [8, 9] and in dogs with left heart failure [10]. Furthermore, Shekerdemian and coworkers [12–14] reported increases in both cardiac output and stroke volume in pediatric patients undergoing surgery for congenital heart diseases. However, in that study, the investigators used negative pressure ventilation with a cuirass rather than CNP and compared their results with intermittent positive pressure ventilation.

As there was no change in heart rate during the application of CNP, it is assumed the increase in the stroke volume that resulted in the increased cardiac output in the present study. Most likely, that increase was a result of an increase in venous return, which was a result of a decrease in intrathoracic pressure (signaled by the significant falls in both central venous pressure and pulmonary artery occlusion pressure). The changes in stroke volume and cardiac output are what one would expect according to the Frank-Starling mechanism [15].

Another factor that may have contributed to the increase in stroke volume index was the lack of pericardial constraint in this patient population. During the standard operation for CABG, the pericardium is left open or loosely approximated with 1 or 2 stitches. Elzinga and colleagues [16] have elegantly demonstrated that when the pericardium is removed, cardiac output increases under conditions of increased preload to the right ventricle (similar to CNP).

Although CNP, in the presence of a constant mean blood pressure, will increase left ventricular afterload [6], it appears that the increase in preload predominated over that increase in afterload. That was due, in all likelihood, to the normal baseline left ventricular ejection fractions of these subjects [17].

Additionally, there was a significant fall in systemic vascular resistance index that accompanied the application of CNP. As the mean blood pressure did not change with CNP while the cardiac index increased, the systemic vascular resistance index would be predicted to decrease and did so, likely in a reflex manner. It is interesting to note, in this regard, that Kumar and colleagues [18] recently documented a similarly significant decrease in systemic vascular resistance index after the a 3-L saline challenge in normal volunteers, whereas Torelli and coworkers [9] documented a similar finding in trauma victims undergoing CNP.

While gas exchange appeared to be unaffected by the application of CNP in the present study (a result similar to that found in dogs with low [5, 7] and high [10] pressure pulmonary edema) the effect of increasing lung volumes on extravascular lung water remains controversial. In dogs with acute lung injury, Skaburskis and coworkers [19] found, by measuring the wet to dry weight ratio and correcting for blood volume, that CNP increases extravascular lung water in an amount similar to that produced by the application of PEEP. Conversely, Kudoh and colleagues [5], using a double-indicator dilution method, found that extravascular lung water increased with CNP but not with PEEP. However, unlike the former study [19], CNP resulted in higher transmural lung pressures relative to PEEP [5], and may have therefore resulted in increased surface area available for fluid transudation. Therefore, given this continuing controversy, the potential for increased lung water and worsening gas exchange exists as result of negative intrathoracic pressure in patients with high or low pressure pulmonary edema [20].

When a cuirass is used, there is chest wall distortion as the sides of the cuirass press against the sides of the thorax resulting in a decrease in the compliance of the respiratory system. One could expect that a higher negative pressure around the anterior chest would be necessary to match the increase in functional residual capacity provided by PEEP, as PEEP acts on the entire undistorted respiratory system. Although we did not measure changes in functional residual capacity in our study because of difficulties in obtaining this measurement, we used 5 cm H2O of PEEP and –20 cm H2O of CNP. These differences in absolute levels of PEEP and CNP are similar to that obtained in dogs with normal lungs [2] to match the changes in functional residual capacity. There exists negative pressure devices that surround the entire thorax (rather than pressing on the side of the thorax) that will not distort the chest wall as much. The cuirass did not interfere with nursing the patient. To achieve an adequate seal, a plastic sheet is attached to the cuirass as a skirt to cover the mediastinal and pleural tubes as well as the abdomen, thereby giving a very good seal and allowing for the delivery of negative pressure.

It is of interest that some of the greatest increases in cardiac index occurred in the 3 patients receiving inotropic support (although this was not statistically significant).

In conclusion, CNP counteracts the effects of positive pressure in the thorax with or without PEEP. It caused an increased cardiac output and stroke volume in the immediate postoperative period in CABG patients. This study was undertaken to observe the physiologic effects of continual negative pressure in patients with relatively preserved cardiac function. Although the improvement in cardiac index and stroke volume was modest, the application of CNP may have a greater benefit in patients with reduced ventricular function. Further exploration of CNP for postoperative patients with low cardiac output should be done.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
References
 
The authors gratefully acknowledge the clinical assistance from Royal Victoria Hospital intensive care unit nursing staff and support from our office managers Jocelyne Prince, Connie Vaccarom and Line Desssureault. This work was performed at the Royal Victoria Hospital intensive care unit.


   References
Top
 Abstract
 Introduction
 Material and Methods
 Results
 Comment
 Acknowledgments
 References
 

  1. Pinsky MR, Summer WR, Wise RA, Bromberger-Bernea B. Augmentation of cardiac function by elevation of intrathoracic pressure J Appl Physiol 1983;54:950-955.[Abstract/Free Full Text]
  2. Krumpe PE, Zidulka A, Urbanetti J, Anthonisen NR. Comparison of the effects of continuous negative external chest pressure and positive end-expiratory pressure on cardiac index in dogs Am Rev Respir Dis 1977;115:39-45.[Medline]
  3. Whittenberger JL, McGregor M, Berglund E, Borst HG. Influence of state of inflation of the lung on pulmonary vascular resistance J Appl Physiol 1960;15:878-882.[Abstract/Free Full Text]
  4. Dorinsky P, Whitcomb M. The effect of PEEP on cardiac output Chest 1983;84:210-216.[Medline]
  5. Kudoh I, Andoh T, Doi H, Kazuhiro K, Okutsu Y, Okumura F. Continuous negative extrathoracic pressure ventilation, lung water volume, and central blood volume. Studies in dogs with pulmonary edema induced by oleic acid. Chest 1992;101:530-533.[Medline]
  6. Hausknecht MJ, Kenneth PB, Weisfeldt ML, Permutt S, Yin FCP. Effect of left ventricular loading by negative intrathoracic pressure in dogs Circ Res 1988;62:620-631.[Abstract/Free Full Text]
  7. Skaburkis M, Helal R, Zidulka A. Hemodynamic effect of external continuous negative pressure ventilation compared with those of continuous positive pressure ventilation in dogs with acute lung injury Am Rev Respir Dis 1987;136:866-891.
  8. Borelli M, Benini A, Denkewitz T, Costanza A, Giuseppe F, Pesenti A. Effect of continuous negative extra-thoracic pressure versus positive end-expiratory pressure in acute lung injury Crit Care Med 1998;26:1025-1031.[Medline]
  9. Torelli L, Zoccali G, Casarin M, Dalla Zuanna F, Lieta E, Conti G. Comparative evaluation of the haemodynamic effects of continuous negative external pressure (CNEP) and positive end-expiratory pressure (PEEP) in mechanically ventilated trauma patients Int Care Med 1995;21:67-70.[Medline]
  10. Skaburskis M, Rivero A, Fitchett D, Zidulka A. Hemodynamic effects of continuous negative chest pressure ventilation in heart failure Am Rev Respir Dis 1990;141:938-943.[Medline]
  11. Ganz W, Donoso R, Marcus HS, Forrester JS, Swan HJC. A new technique for measurement of cardiac output by thermodilution in man Am J Cardiol 1971;27:392-396.[Medline]
  12. Shekerdemian LS, Bush A, Lincoln C, Shore DF, Petros A, Redington AN. Cardiopulmonary interaction in healthy children and children after simple cardiac surgery: the effect of positive and negative pressure ventilation Heart 1997;78:587-593.[Abstract/Free Full Text]
  13. Shekerdemian LS, Bush A, Shore DF, Lincoln C, Redington AN. Cardio-pulmonary interactions after Fontan operations: augmentation of cardiac output using negative pressure ventilation Circulation 1997;96:3934-3942.[Abstract/Free Full Text]
  14. Shekerdemian LS, Bush A, Shore DF, Lincoln C, Redington AN. Cardiorespiratory response to negative pressure ventilation after tetralogy of Fallot repair: a hemodynamic tool for patients with low-output state J Am Coll Cardiol 1999;33:549-555.[Abstract/Free Full Text]
  15. Hoffman JIE, Guz A, Charlier AA, Wilcken DEL. Stroke volume in conscious dogs: effect of respiration, posture, and vascular occlusion J Appl Physiol 1965;20:865-877.[Abstract/Free Full Text]
  16. Elzinga G, van Grondelle R, Westerhof N, van den Bos GC. Ventricular interference Am J Physiol 1974;226:941-947.[Free Full Text]
  17. Fessler HE, Brower RG, Wise RA, Permutt S. Effects of systolic and diastolic positive pleural pressure pulses with altered cardiac contractility J Appl Physiol 1992;73:498-505.[Abstract/Free Full Text]
  18. Kumar A, Anel R, Bunnel E, et al. Effect of large volume infusion of left ventricular volumes, performance and contractility parameters in normal volunteers Int Care Med 2004;30:1361-1369.[Medline]
  19. Skaburskis M, Michel RP, Gatensby A, Zidulka A. Effect of negative-pressure ventilation on lung water in permeability pulmonary edema J Appl Physiol 1989;66:2223-2230.[Abstract/Free Full Text]
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