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(Chest. 2003;124:1863-1870.)
© 2003 American College of Chest Physicians

Effects of Lung Volume Reduction Surgery on Left Ventricular Diastolic Filling and Dimensions in Patients With Severe Emphysema*

Kirsten Jörgensen, MD; Erik Houltz, MD, PhD; Ulla Westfelt, MD, PhD; Folke Nilsson, MD, PhD; Henrik Scherstén, MD, PhD and Sven-Erik Ricksten, MD, PhD

* From the Departments of Cardiothoracic Anesthesia and Intensive Care (Drs. Jörgensen, Houltz, Westfelt, and Ricksten), and Cardiothoracic Surgery (Drs. Nilsson and Scherstén), Sahlgrenska University Hospital, Gothenburg, Sweden.

Correspondence to: Sven-Erik Ricksten, MD, PhD, Department of Cardiothoracic Anesthesia and Intensive Care, Sahlgrenska University Hospital, S-413 45 Gothenburg, Sweden; e-mail: sven-erik.ricksten{at}aniv.gu.se


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Study objectives: Data on the influence of lung volume reduction surgery (LVRS) on cardiac function and hemodynamics are scarce and controversial. Previous studies have focused mainly on right ventricular function and pulmonary hemodynamics. Here, we evaluated the effects of LVRS on left ventricular (LV) end-diastolic filling pattern, dimensions, stiffness, and performance, as well as pulmonary and systemic hemodynamics.

Design: A prospective, open, controlled study.

Patients: Patients with severe emphysema undergoing LVRS (10 patients). Patients scheduled for pulmonary lobectomy due to carcinoma (ie, the lobectomy group) served as control subjects (10 patients).

Measurements: LV dimensions and mitral flow velocities were measured by transesophageal, two-dimensional, Doppler echocardiography, and central hemodynamics were measured by a pulmonary artery thermodilution catheter. Measurements were performed during anesthesia in the supine position, before and after surgery, without and with passive leg elevation.

Results: Baseline cardiac index (CI) [- 21%], stroke volume index (SVI) [- 31%], stroke work index (SWI) [- 26%], and LV end-diastolic area index (EDAI) [- 15%] were significantly (p < 0.001) lower, whereas LV end-diastolic stiffness (LVEDS) did not differ in the LVRS group compared to the lobectomy group. The time from peak early diastolic filling to zero flow (E-dec time) [58%] and the deceleration slope of early diastolic filling (E-dec slope) [45%] were significantly higher (p < 0.01), whereas peak early diastolic filling velocity (E-max) [- 31%; p < 0.01] and the proportion of E-max vs peak late diastolic filling velocity (A-max) [ie, the E/A ratio] (- 27%; p < 0.001) were significantly lower compared to the lobectomy group. LVRS significantly increased CI (40%; p < 0.001), SVI (34%; p < 0.001), SWI (58%; p < 0.001), LV EDAI (18%; p < 0.001), E-max (44%; p < 0.01), A-max (15%; p < 0.05) and E/A ratio (28%; p < 0.01), decreased E-dec time (- 31%; p < 0.05) and E-dec slope (- 98%; p < 0.01), and had no effect on LVEDS. In the lobectomy group, surgery affected none of these variables.

Conclusions: LV function is impaired in patients with severe emphysema due to small end-diastolic dimensions. LVRS increases LV end-diastolic dimensions and filling, and improves LV function.

Key Words: diastole • emphysema • hemodynamics • left ventricular function • lung volume reduction surgery


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 Conclusion
 References
 
Lung volume reduction surgery (LVRS) for the treatment of severe emphysema was described as early as in the late 1950s by Brantigan et al.1 These investigators suggested that reducing the volume of hyperinflated, functionless parts of a diseased lung allows improved function of the more normal parts of the lung. Because of high perioperative mortality, LVRS was later abandoned. It was reintroduced in 1994 by Cooper and coworkers.2

In some randomized, controlled, prospective studies,3 4 5 6 it has been demonstrated that LVRS improves dyspnea, lung function, exercise tolerance, and quality of life in patients with severe emphysema. This improvement seems to reach a maximum after 36 months and thereafter decreases as the disease progresses.7 Although the effects of LVRS have been attributed to several possible mechanisms (ie, enhanced pulmonary elastic recoil, correction of ventilation-perfusion mismatch, and improved efficiency of respiratory musculature), the physiologic basis of reported improvements is not fully understood.8 9 It also has been difficult to link the improvement in lung function test results to decreased dyspnea or increased quality of life after LVRS.10

Improved cardiac function may contribute to the increased exercise capacity seen in patients after LVRS. However, data on the effects of LVRS on systemic and pulmonary hemodynamics are scarce and controversial, and have not been fully investigated.8 To our knowledge, the potential effects of LVRS on left ventricular (LV) performance have not been discussed in detail. From the LV point of view, diastolic LV function would be affected if the emphysematous lungs were considered as "intrathoracic space-occupying processes." Thus, if LV diastolic filling was abnormal in patients with severe emphysema, LVRS could be expected to relieve this "pulmonary tamponade."

To address this question, the present study was undertaken using invasive hemodynamic measurements, together with two-dimensional Doppler echocardiography, to investigate the effects of LVRS on pulmonary and systemic hemodynamics, LV dimensions, performance, stiffness, and diastolic filling pattern in a group of 10 patients with emphysema. Ten patients undergoing lung resection due to malignancy served as a control group.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 Conclusion
 References
 
Patients
The local Ethics Committee of the Medical Faculty of Göteborg University approved the study protocol. Twenty patients were included in the study. The LVRS group consisted of 10 consecutive patients who were scheduled for LVRS due to severe pulmonary emphysema (ie, the LVRS group), whereas 10 patients scheduled for lobectomy due to pulmonary carcinoma served as control subjects (ie, the control group).

The criteria for inclusion in the LVRS group were as follows: a diagnosis of emphysema based on physical examination, chest radiographs, high-resolution CT scan, lung perfusion scan, and pulmonary function tests; FEV1 between 20% and 35% of the predicted value; residual volume of > 200%; total lung capacity of > 120% of predicted; and age < 75 years. Exclusion criteria were PCO2 > 7.5 kPa breathing room air, the presence of cardiac disease, and pulmonary hypertension, ie, systolic pulmonary artery pressure (SPAP) of > 55 mm Hg. All patients had a history of smoking, and two patients also had {alpha}1-antitrypsin deficiency. All patients in the LVRS group were considered by the referring pulmonologists to be receiving optimal medical treatment with inhaled steroids and bronchodilators. Inclusion criteria in the control group were a diagnosis of malignancy based on lung biopsy, a tumor location suitable for lobectomy, and no complicating cardiac or systemic disease.

Anesthesia
The patients were premedicated with flunitrazepam (1 mg), and the patients in the LVRS group also received morphine (5 to 10 mg) and scopolamine (0.2 to 0.4 mg). A thoracic epidural catheter was inserted prior to the induction of anesthesia. After an epidural bolus injection with sufentanil (10 to 25 µg) and bupivacaine (15 to 20 mg), a continuous infusion of sufentanil (1 µg/mL) and bupivacaine (1 mg/mL) was initiated at a rate of 3 to 4 mL/h. Anesthesia was induced with thiopental (3 to 5 mg/kg), fentanyl (1 to 2 µg/kg), and pancuronium (0.1 mg/kg). The patients were intubated with a left-angled double-lumen tube. Anesthesia was maintained with enflurane in oxygen/air with a fraction of inspired oxygen necessary to keep the PO2 at > 20 kPa. Ventilation was volume-controlled to maintain the PCO2 between 5.0 and 7.0 kPa during surgery. The patients were actively warmed by the use of warm-air blankets. The hemoglobin level was kept at > 10 g/dL by the infusion of erythrocyte-enriched blood products when necessary.

Surgery
Bilateral LVRS was performed by median sternotomy, as described by Cooper et al.2 The most emphysematous areas, targeted by chest CT scanning and ventilation/perfusion scanning, were excised by use of various mechanical staplers. To minimize air leaks, the staple lines were reinforced with bovine pericardial tissue or substitute. The excised lung volume was visually estimated to be approximately 20 to 30%.

Hemodynamic Measurements
A cannula was placed in the left radial artery. A pulmonary artery thermodilution catheter (model 131HF7; TD Baxter Healthcare Corporation; Irvine, CA) was inserted through the right internal jugular vein and was guided into the pulmonary artery. Continuous recordings of heart rate (HR), systolic arterial BP, diastolic arterial BP, and mean arterial pressure (MAP), together with SPAP, diastolic pulmonary artery pressure, mean pulmonary artery pressure (MPAP), and central venous pressure (CVP), were performed. The pressure transducers were zeroed against atmospheric pressure and were maintained at the mid-axillary level throughout the experimental procedure. Thermodilution cardiac output measurements (in triplicate) and pulmonary capillary wedge pressure (PCWP) measurements were performed at each measuring point. Stroke volume, stroke work, systemic vascular resistance, and pulmonary vascular resistance were calculated and indexed to the patient's body surface area.

Two-Dimensional Echocardiography
A multiplane transesophageal echocardiographic transducer (ACUSON; ACUSON Corp; Mountain View, CA) was positioned in the esophagus and adjusted until mid-papillary, short-axis images of the LV were obtained using an echocardiography system (model 128XP; ACUSON Corp). Images were stored on super-VHS videotape and later were transferred to a computer system by means of a video framegrabber (VISIONplus-AT; Imaging Technology Inc; Bedford, MA). Using a digitizing tablet, the endocardial border was outlined in systole and diastole, and end-systolic and end-diastolic areas were calculated together with area ejection fraction (AEF), as previously described by Houltz et al.11 End-systolic and end-diastolic areas were indexed to the patient's body surface area.

Mitral Doppler Measurements
When the LV short-axis measurements were completed, the transducer was withdrawn until a long-axis image was obtained. A pulsed Doppler line was positioned with the measuring caliper at the tips of the mitral leaflets and adjusted to be as parallel as possible to the mitral flow. The Doppler flow profiles were recorded on super-VHS videotape. These flow profiles were later transferred to a computer and independently evaluated using a digitizing tablet by means of a PC-based analysis system, as previously described.11 Three consecutive beats were digitized, and the mean values of these were used for analysis.

The following variables were derived from the mitral Doppler tracings: peak early diastolic filling velocity (E-max); peak late diastolic filling velocity (A-max); deceleration slope of early diastolic filling (E-dec slope); and time from peak early diastolic flow to zero flow (E-dec time). The ratio E-max/A-max (E/A) ratio was calculated.

Experimental Protocol
After the induction of anesthesia, pulmonary hemodynamic and echocardiographic measurements were performed before and after the end of surgery, with the patient in the supine position and with passive leg elevation (ie, 60° to 90°) to increase ventricular preload, which was confirmed by an increase in CVP and PCWP.

LV End-Diastolic Stiffness
End-diastolic pressure-area curves were constructed for each patient, using the indexed end-diastolic LV short-axis areas and the PCWPs obtained with patients in the supine position, with and without passive leg elevation. The end-diastolic pressure-area relation is approximately exponential in shape and can be described by the following equation:

where the relation between LV end-diastolic pressure (P) and LV end-diastolic area (A) is described by the two constants B and S.12 This exponential equation was transformed to its logarithmic form, a linear relation where the coefficient S, signifying the LV end-diastolic stiffness (LVEDS), describes the slope of the end-diastolic pressure-area curve. The coefficient can be solved using the values obtained with the patient in the supine position and with the legs elevated, using the following relation:

where ln (PCWP1) and ln (PCWP2) are the natural logarithms of the PCWPs, and EDAI1 and EDAI2 are the LV end-diastolic area indexes, before and after volume loading, respectively.

Statistical Analysis
The differential effects of surgery between the two groups were evaluated by a two-way analysis of variance (ANOVA) for repeated measurements. The effects of surgery within groups and the differences between groups at baseline (before surgery) were analyzed by an analysis of interactions generated by a two-way hierarchic ANOVA followed by contrast analyses. The results are presented as the mean ± SEM. Mean differences with a p value < 0.05 were considered to be significant.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 Conclusion
 References
 
Patients
The patients in the LVRS group consisted of five men and five women, whereas six women and four men were included in the control group. There were no differences between the groups regarding age, height, or weight (Table 1 ). As shown in Table 2 , the patients undergoing LVRS had the typical functional features of severe pulmonary emphysema, consisting of severe obstruction to expiratory airflow and considerable hyperinflation. The mean SPAP was 34 ± 3 mm Hg, and the mean LV AEF was 62 ± 2%, as assessed by preoperative transthoracic two-dimensional Doppler echocardiography in the LVRS group. The lung function data of the control group are provided in Table 2 . None of these patients had localized or diffuse emphysema on preoperative CT scans of the chest. Three patients underwent left-sided thoracotomies, and seven patients underwent right-sided thoracotomies. The duration of surgery was longer for the LVRS group than for the control group (125 ± 6 vs 103 ± 10 min, respectively).


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  		Table 1. Patient Characteristics*

 

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  		Table 2. Lung Function Data and Gas Exchange at Baseline*

 
Pulmonary and Systemic Hemodynamics
At baseline (ie, before surgery), there were no differences between the LVRS group and the control subjects regarding MAP, MPAP, CVP, or PCWP (Table 3 ). However, cardiac index (CI), stroke volume index (SVI), and stroke work index (SWI) were significantly lower, whereas HR was significantly higher in the LVRS group compared to the control group. Both the pulmonary vascular resistance index (PVRI) as well as the systemic vascular resistance index (SVRI) were significantly higher in the LVRS group compared to the control group at baseline.


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  		Table 3. Effects of LVRS or Lobectomy on Central Hemodynamic Variables*

 
In the control group undergoing pulmonary lobectomy for carcinoma, the surgical procedure affected no hemodynamic variables, while LVRS significantly improved CI, SVI, and SWI in the emphysema patients. Both PVRI and SVRI were significantly lower after LVRS, whereas HR was unchanged.

Two-Dimensional Doppler-Echocardiographic Variables
The baseline values for EDAI and end-systolic area index were significantly lower in the LVRS group compared to the control group, whereas the groups did not differ with respect to AEF (Table 4 ). Pulmonary lobectomy did not affect LV dimensions or AEF in the control group, whereas LVRS significantly increased EDAI in the emphysema patients. The two groups did not differ with regard to LVEDS. Surgery did not affect LVEDS in any of the groups.


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  		Table 4. Effects of LVRS and Lobectomy on LV Dimensions and Stiffness*

 
At baseline, the E-dec slope was significantly less pronounced and the E-dec time was significantly longer in the LVRS group compared to the control group (Table 5 ). E-max and the E/A ratio were significantly lower in the LVRS group, whereas the groups did not differ with respect to A-max at baseline. Pulmonary lobectomy affected none of these variables in the control group. LVRS significantly improved the E-dec slope, shortened the E-dec time, and increased significantly the transmitral flow velocities as well as the E/A ratio (Fig 1 ).


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  		Table 5. Effects of LVRS and Lobectomy on Mitral Doppler Variables*

 


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  		Figure 1. The mitral Doppler flow profile in one patient with severe emphysema before LVRS (top) and after LVRS (bottom). Note the low E-max and the abnormally low E/A ratio before surgery, which are partly normalized after LVRS. Stroke volume as well as LV end-diastolic area increased after LVRS (stroke volume increase, 39 to 54 mL; end-diastolic area increase, 11.0 to 13.6 cm2).

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
Conclusion
 References
 
We investigated LV performance in a group of patients with severe pulmonary emphysema who were undergoing LVRS. To compare these patients to nonemphysematous patients with regard to central hemodynamics and LV function, and to exclude the surgical procedure per se as the source of potential effects, we included a control group of patients undergoing lobectomy for pulmonary carcinoma (ie, the lobectomy group). Preoperative LV performance was depressed in patients with severe pulmonary emphysema undergoing LVRS, as demonstrated by lower values for CI, SVI, and SWI, when compared to patients undergoing lobectomy for lung carcinoma. A lower preload of the LV, as indicated by a lower EDAI, could result in this impaired preoperative LV performance in the LVRS group. The main finding of the present study was that LVRS improved postoperative LV performance, which was associated with an increase in EDAI. In contrast, neither central hemodynamics nor LV preload was affected by surgery in the lobectomy group.

To our knowledge, this is the first study comparing patients with severe pulmonary emphysema to nonemphysematous control patients with respect to pulmonary and systemic hemodynamics, as well as LV dimensions, performance, stiffness, and diastolic filling. LV systolic function, as judged by the LV AEF did not appear to be different from that of the control group, and LV systolic dysfunction probably did not cause the lower SVI and SWI in the LVRS group. Patients with good LV systolic function are not particularly sensitive to changes in LV outflow impedance,13 and the higher SVRI in the LVRS group is therefore probably not the main mechanism behind the lower values for SVI and SWI in the LVRS group. A lower preload (ie, a lower EDAI) is the most probable cause for the impaired LV performance in the LVRS group. A lower EDAI in combination with an apparently normal PCWP would suggest an increased LVEDS in the LVRS group, which in turn is caused by external compression (ie, pulmonary tamponade) from the hyperinflated lungs. However, LVEDS did not differ significantly between the two groups. PCWP estimates intracavitary left atrial pressure and LV end-diastolic pressure, whereas the true LV transmural pressures were not assessed in the present study. Due to the low elastic recoil of the lungs in pulmonary emphysema, and the less negative intrathoracic pressure,14 15 16 17 transmural LV pressures were probably lower in the LVRS group compared to the control group.

The reduced LV diastolic dimensions as well as the reduced LV systolic dimensions in the LVRS group could be due to a reduced intrathoracic blood volume, which in turn is caused by the dynamic hyperinflation and, hence, the generation of intrinsic positive end-expiratory pressure (PEEP).9 15 16 17 Tschernko and colleagues16 17 have shown that preoperative minimal intrinsic PEEP levels range between 5 and 7.5 cm H2O in patients with severe emphysema. In patients and volunteers, positive-pressure respiration with PEEP depletes the intrathoracic vascular bed and the heart, decreasing pulmonary vascular, right right ventricular RV and LV end-diastolic dimensions.18 19 20 21 22 23 24 The results of the preoperative mitral Doppler recordings of the LVRS group with a decrease in E-max, E/A ratio, and E-dec slope, and an increase in E-dec time are also suggestive of a decrease in LV preload when compared to the control group.25 26 Furthermore, positive pressure-respiration with PEEP induces similar changes in the mitral Doppler-derived indexes of LV filling.20 21 27

To our knowledge, there are no previous data on the immediate effects of LVRS on pulmonary and systemic hemodynamics. In the present study, myocardial performance was improved by LVRS, as indicated by an increase in SVI and SWI. This could be because of a decrease in RV and LV outflow impedance due to the decrease in PVRI and SVRI seen after LVRS. On the other hand, a selective dilation of systemic and pulmonary resistance vessels, unloading the RV and LV, usually increases both E-max and A-max with no change in the E/A ratio, and is accompanied by no change in E-dec time.11 In the present study, however, the E-max and E/A ratio, in particular, increased (44% and 28%, respectively) and the E-dec time decreased. There was a comparably less pronounced increase in A-max (15%). These LVRS-induced changes of the mitral Doppler flow pattern, are expected when LV preload is increased.25 26 The increase in A-max could be due to an increase in left atrial preload by LVRS. The decrease in both SVRI and PVRI after LVRS might be attributed to a flow-dependent pulmonary and systemic vasodilation.28 Another explanation for the increase in cardiac output after LVRS is the relief of the external compression (ie, pulmonary tamponade) from the hyperinflated lungs and a decrease in LVEDS. However, LVEDS was not affected by LVRS in the present study. Thus, the most likely explanation for the improved LV performance after LVRS is an increase in LV preload. It has been shown that LVRS decreases esophageal pressure at end-expiration and intrinsic PEEP,14 15 16 17 which would cause an increase in intrathoracic blood volume (see above). This is supported by the finding of an increase in LV dimensions after LVRS in the present study. Furthermore, the LVRS-induced changes in the mitral Doppler variables, increases in E-dec slope, E-max, and the E/A ratio, and the decrease in E-dec time, also indicates the presence of an increase in LV preload after LVRS.25 26

The results of previous studies on the effects of LVRS on late pulmonary and systemic hemodynamics are somewhat controversial. Kubo et al29 and Mineo et al30 showed that CI increased 6 months after LVRS both at rest and during exercise, findings that were not confirmed by other investigators.31 32 33 Sciurba et al14 showed that LVRS increased RV AEF, an indicator of systolic function. Although the authors did not measure RV outflow impedance, this finding was interpreted as an indication of an LVRS-induced reduction in pulmonary vascular resistance. Kubo et al29 suggested that the increase in CI after LVRS was caused by capillary recruitment of the previously compressed lung zones. Mineo et al30 demonstrated that RV end-diastolic volume increased after LVRS and ascribed the increase in CI after LVRS to improved RV filling, which in turn was caused by a decrease in intrathoracic pressure. Thus, the findings of Mineo et al30 and the results of the present study strongly suggest that LVRS in patients with severe emphysema has the potential to increase both the RV and LV dimensions after surgery. Such an increase in RV and LV preload could account for the improved cardiac function after LVRS. One could speculate that the mechanism behind this increase in cardiac dimensions after LVRS is a decrease in intrathoracic pressure and intrinsic PEEP with a redistribution of the blood volume to the intrathoracic compartment.


   Conclusion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
References
 
In the present study, we evaluated the immediate effects of LVRS for severe emphysema on LV end-diastolic filling, dimensions, and stiffness as well as pulmonary and systemic hemodynamics in comparison with pulmonary lobectomy for lung cancer. Before surgery, the LVRS group had a lower LV performance, as demonstrated by lower values for SVI, SWI, and CI when compared with the lobectomy group. This was due to a lower baseline LV preload, as indicated by the presence of a lower LV EDAI and mitral Doppler flow indexes of impaired LV filling when compared to those of the lobectomy group. There were no differences in preoperative LVEDS or systolic function (ie, AEF) between groups. LVRS improved LV performance in the emphysematous patients with increases in SVI, SWI, and CI, which were accompanied by an increase in LV EDAI and mitral Doppler flow indexes of improved LV filling. Lobectomy induced no changes in any of these variables. LVEDS or LV AEF was not influenced by surgery in either the LVRS group or the lobectomy group. The improvement in LV function in this group of patients with severe emphysema after LVRS could tentatively be explained by an alleviation of intrinsic PEEP, with a consequent increase in intrapulmonary and intracardiac blood volumes. It remains to be explained, however, whether or not this improvement in LV preload is related to the previously described improvement in exercise performance after LVRS in patients with severe emphysema.


   Footnotes
 
Abbreviations: AEF = area ejection fraction; A-max = peak late diastolic filling velocity; ANOVA = analysis of variance; CI = cardiac index; CVP = central venous pressure; E/A = ratio of peak early diastolic filling velocity to peak late diastolic filling velocity; EDAI = end-diastolic area index; E-dec slope = deceleration slope of early diastolic filling; E-dec time = time from peak early diastolic flow to zero flow; E-max = peak early diastolic filling velocity; HR = heart rate; LV = left ventricle, ventricular; LVEDS = left ventricular end-diastolic stiffness; LVRS = lung volume reduction surgery; MAP = mean artery pressure; MPAP = mean pulmonary artery pressure; PCWP = pulmonary capillary wedge pressure; PEEP = positive end-expiratory pressure; PVRI = pulmonary vascular resistance index; RV = right ventricle, ventricular; SPAP = systolic pulmonary artery pressure; SVI = stroke volume index; SVRI = systemic vascular resistance index; SWI = stroke work index

This study was supported by grant No. 13156 from the Swedish Medical Research Council and by the Medical Faculty of Gothenburg (LUA).

This study was partly presented at the ninth Annual Meeting of the European Society of Anaesthesiologists, Gothenburg, Sweden, April 7–10, 2001, and at the Annual Meeting of the International Society of Heart and Lung Transplantation, Washington, DC, April 10–13, 2002.

Received for publication December 31, 2002. Accepted for publication April 7, 2003.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 Conclusion
 References
 

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