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Anesth Analg 2007;104:887-892
© 2007 International Anesthesia Research Society
doi: 10.1213/01.ane.0000258020.27849.6b

CRITICAL CARE AND TRAUMA

Left Ventricular Performance and Dimensions in Patients with Severe Emphysema

Kirsten Jörgensen, MD, Erik Houltz, MD, PhD, Ulla Westfelt, MD, PhD, and Sven-Erik Ricksten, MD, PhD

From the Department of Cardiothoracic Anesthesia and Intensive Care, Sahlgrenska University Hospital, Gothenburg, Sweden.

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


   Abstract
Top
 Abstract
Introduction
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
BACKGROUND: Concomitant heart dysfunction during the course of chronic obstructive pulmonary disease is well recognized. The prevailing view is that mainly the right side of the heart is involved. We evaluated left ventricular (LV) function and dimensions in patients with severe emphysema.

METHODS: Patients with severe emphysema undergoing lung volume reduction surgery were studied after anesthesia induction (n = 10). Non-emphysematous patients scheduled for lobectomy served as controls (n = 10). LV dimensions were measured with patients in the supine position by transesophageal two-dimensional echocardiography and systemic hemodynamics by a pulmonary artery thermodilution catheter, before and during central blood volume expansion by passive leg elevation.

RESULTS: Baseline cardiac index (–25%), stroke volume index (SVI, –32%) stroke work index (–34%) and LV end-diastolic area index (EDAI, –33%) were significantly (P < 0.001) lower in the emphysema group. Passive leg elevation increased SVI and LV area ejection fraction more in the emphysema group than in controls (P < 0.05). The {Delta}SVI/{Delta} pulmonary capillary wedge pressure and the {Delta}SVI/{Delta}EDAI relationships were significantly (P < 0.05) higher in the emphysema group compared to controls (2.2 ± 0.71 vs 0.6 ± 0.2 mL/mm Hg x m2 and 5.8 ± 0.89 vs 2.8 ± 0.8 mL/cm2 x m2, respectively). Preload-recruitable stroke work ({Delta}stroke work index/{Delta}EDAI), a load-independent index of systolic LV function, did not differ between the two groups.

CONCLUSION: The LV in patients with severe emphysema is hypovolemic, and operates on a steeper portion of the LV function curve, while indices of systolic function are not significantly impaired compared to non-emphysematous controls.


   Introduction
Top
 Abstract
 Introduction
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Patients with severe lung emphysema have poor quality of life because of impaired lung function and significant reduction in exercise tolerance (1). The functional features consist of severe expiratory airflow obstruction and considerable hyperinflation due to destruction of lung parenchyma and loss of lung elasticity. Intrathoracic (intrapleural) pressure is increased (less negative) due to generation of a high intrinsic positive end-expiratory pressure (PEEPi) (2,3). Concomitant heart disease during the course of chronic obstructive pulmonary disease is well recognized. The prevailing view is that mainly the right side of the heart is involved (4); the issue of left ventricular (LV) involvement is controversial. Load-dependent indices of LV function have been used in previous studies to evaluate LV function in patients with emphysema. Two studies showed no abnormality of LV function (5,6), while one study (7) demonstrated abnormal LV function curves in the majority of patients with chronic obstructive lung disease. Others have suggested that LV systolic dysfunction, assessed by LV area ejection fraction (AEF), is unusual in patients with severe parenchymal lung disease without pulmonary hypertension (4,8,9), but LV area ejection fraction may be decreased in patients with emphysema and pulmonary hypertension because of ventricular interaction (10).

The aim of the present study was to further evaluate LV function and dimensions in patients with severe emphysema. To assess LV function, a load-independent estimate was used, the so-called "preload-recruitable stroke work." LV dimensions and performance were assessed by pulmonary artery catheterization and transesophageal two-dimensional echocardiography, before and during intravascular volume loading, in anesthetized patients with severe emphysema scheduled for lung volume reduction surgery. Anesthetized non-emphysematous patients scheduled for lobectomy due to malignancy served as a control group.


   METHODS
Top
 Abstract
 Introduction
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
The local Ethics Committee of the Medical Faculty of Gothenburg University approved the study protocol. Twenty patients were included in the study. The emphysema group consisted of 10 consecutive patients scheduled for lung volume reduction surgery due to severe pulmonary emphysema, while 10 patients scheduled for lobectomy due to pulmonary carcinoma served as controls (control group). All patients gave written informed consent before being enrolled in the study. Criteria for inclusion in the emphysema group were as follows: a diagnosis of emphysema based on physical examination, chest radiographs, high-resolution computed tomography scan, lung perfusion scan, and pulmonary function tests; forced expiratory volume in the first second between 20% and 35% of the expected value; residual volume over 200%; total lung capacity over 120% of the expected value; and age <75 yr. Exclusion criteria were Pco2 higher than 58 mm Hg breathing room air, cardiac disease, and pulmonary hypertension, i.e., systolic pulmonary artery pressure >55 mm Hg. Criteria for inclusion 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
All patients were premedicated with flunitrazepam (1 mg), and the patients in the emphysema group also received morphine (5–10 mg) and scopolamine (0.2–0.4 mg). Anesthesia was induced with thiopental (3–5 mg/kg), fentanyl (1–2 µg/kg), and pancuronium (0.1 mg/kg). The patients were tracheally intubated with a left-angled double-lumen tube. Anesthesia was maintained with enflurane in oxygen/air with a Fio2 necessary to keep Po2 >150 kPa. Ventilation was volume-controlled (6–7 mL/kg tidal volume) at a frequency of 15/min and a 1:3 inspiratory/expiratory ratio, to maintain arterial Pco2 between 40 and 55 mm Hg. PEEP was not applied. The patients were actively warmed with warm-air blankets. The patients did not receive IV fluids during the induction or maintenance of anesthesia.

Hemodynamic Measurements
A cannula was placed in the left radial artery. A pulmonary artery thermodilution catheter (131HF7, TD Baxter Healthcare Corporation, Irvine, CA) was inserted through the right internal jugular vein and guided into the pulmonary artery. Continuous recordings of heart rate (HR), systolic, diastolic and mean arterial blood pressures, together with systolic, diastolic and mean pulmonary artery pressures (MPAP) and central venous pressure were performed. Pulmonary capillary wedge pressure (PCWP) measurements and thermodilution cardiac output measurements (in triplicate) were performed at each measuring point. Stroke volume (SV), stroke work (SW), systemic vascular resistance (SVR), and pulmonary vascular resistance (PVR) were calculated according to standard formulas and indexed to the patient’s body surface area (stroke volume index (SVI), stroke work index (SWI), systemic vascular resistance index (SVRI), and pulmonary vascular resistance index (PVRI), respectively).

Two-Dimensional Echocardiography
A multiplane transesophageal echocardiographic transducer (ACUSONTM, ACUSON, Mountain View, CA) was positioned in the esophagus and adjusted until mid-papillary short axis images of the LV were obtained using an ACUSON 128XP echocardiography system. The endocardial border was outlined in systole and diastole, and end-systolic and end-diastolic areas were calculated together with AEF, as described by Houltz et al. (11). Mean values of at least five consecutive beats were used for estimation of LV areas. End-systolic areas (ESA) and end-diastolic areas (EDA) were indexed to the patient’s body surface area (end-systolic area index (ESAI), end-diastolic area index (EDAI)).

Protocol
After induction of anesthesia, systemic hemodynamic and echocardiographic measurements were performed with the patient in the supine position before and during passive leg elevation (60–90 degrees) to increase ventricular preload. The increase in SVI to a certain increase in preload, assessed by the change in PCWP and change in EDAI, was estimated as: {Delta}SVI/{Delta}PCWP (mL/mm Hg x m2) and {Delta}SVI/{Delta}EDAI (mL/cm2 x m2), respectively. The preload-recruitable stroke work was assessed as: {Delta}SWI/{Delta}EDAI (g/cm2 x 10–2). LV EDAI was used as a surrogate variable for LV end-diastolic volume.

Data Analysis
The differential effects of passive leg elevation between the two groups were evaluated by an analysis of interactions generated by a two-way analysis of variance (ANOVA) for repeated measurements. Differences between groups at baseline were analyzed by Student’s t-test. The results are presented as means and standard error of the mean (SEM). Mean differences with a P value below 0.05 were considered significant.


   RESULTS
Top
 Abstract
 Introduction
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
The patients in the emphysema 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 groups regarding age, height or weight (Table 1). As shown in Table 2, the emphysema patients had the typical functional features of severe pulmonary emphysema, consisting of severe obstruction to expiratory airflow and considerable hyperinflation. Control group lung function data are provided in Table 2.


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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 (Table 3)


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  		Table 3. Effects of Passive Leg Elevation on Central Hemodynamic Variables

 
At baseline there were no differences between the emphysema group and the controls regarding mean arterial blood pressure, MPAP, central venous pressure or PCWP. However, cardiac index (CI), SVI, and SWI were significantly lower in the emphysema group, whereas HR was significantly higher compared to controls. Both PVRI and SVRI were significantly higher in the emphysema group compared to controls at baseline. Passive leg elevation induced a more pronounced increase in SVI in the emphysema group and a decrease in SVRI when compared to the control group.

Two-Dimensional Echocardiographic Variables (Table 4)


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  		Table 4. Effects of Passive Leg Elevation on Left Ventricular Dimensions

 
None of the patients in the emphysema group had obvious signs of right ventricular hypertrophy and/or dilation, and in none of the patients was there a permanent bulging of the septum towards the LV. Baseline EDAI and ESAI were significantly lower in the emphysema group compared to controls, whereas the groups did not differ with respect to LV AEF. Passive leg elevation caused an increase in LV AEF in the emphysema group, which was not seen in the control group. EDAI increased to a similar extent in the two groups, while ESAI increased to a lesser extent in the emphysema group, during passive leg elevation.

LV Function (Table 5)


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  		Table 5. Left Ventricular Function Indices

 
The {Delta}SVI/{Delta}PCWP and the {Delta}SVI/{Delta}EDAI relationships were significantly (P < 0.05) higher in the emphysema group compared to controls (2.2 ± 0.7 vs 0.7 ± 0.2 mL/mm Hg x m2 and 5.8 ± 0.9 vs 2.8 ± 0.8 mL/cm2 x m2, respectively). Preload-recruitable stroke work ({Delta}SWI/{Delta}EDAI) did not differ between the two groups.


   DISCUSSION
Top
 Abstract
 Introduction
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
We investigated systemic hemodynamics and LV performance and dimensions in a group of anesthetized patients with severe emphysema without pulmonary hypertension. To compare these patients to non-emphysematous patients, we included a control group of patients undergoing lobectomy for pulmonary carcinoma. LV performance was impaired in patients with severe pulmonary emphysema, as demonstrated by a lower CI, SVI and SWI, when compared to non-emphysematous patients. LV AEF was normal in the emphysema group, and the impaired LV performance in the emphysema patients is therefore most likely explained by a lower preload of the LV, as indicated by a lower EDAI.

Indirect evidence that the LVs of emphysema patients seem to be hypovolemic in diastole was provided by our finding that a certain increase in LV preload (PCWP or EDAI) caused a more pronounced increase in SVI and LV AEF, indicating that the LV operates on a steeper portion of the (normal) Frank– Starling relationship in these patients and thus has a less than optimal diastolic stretch of the myocardial sarcomers at baseline.

Another explanation for this vigorous hemodynamic response to a standardized increase in preload in emphysema patients could be a higher inotropic state of their left ventricles, operating on leftward-shifted and steeper LV function curves. However, the relationship between SWI and LV end-diastolic dimensions (EDAI), the so-called preload-recruitable stroke work, which is supposed to be a relatively load-independent variable sensitive to changes in alterations in inotropic state (12), was not significantly different between the two groups, indicating no significant differences in LV contractile state between the two groups. This is further supported by the fact that baseline LV AEF did not differ significantly between the two groups. The two indices of LV systolic performance were, if anything, slightly lower in the emphysema group.

As a formal power analysis was not performed prior to the study, we cannot exclude the possibility that LV systolic function is slightly depressed in patients with emphysema. If so, one would have expected that the LV of the emphysema patients operates on a more flat LV function during an intravascular volume challenge and not a steeper one, as shown in the present study.

Another possible mechanism for the decreased SV in the emphysema patients is a higher LV outflow impedance, as SVRI was 33% higher compared to the control group. Patients with good LV systolic function are, however, not particularly sensitive to changes in LV outflow impedance (13), and the higher SVRI in the lung volume reduction surgery group is therefore probably not the main mechanism behind the lower SVI and SWI in the emphysema group.

Cardiac preload of the LV is defined by the Frank–Starling relationship as the ventricular muscle fiber length at end-diastole, and is measured clinically as the LV end-diastolic volume. In clinical practice, LV preload is routinely assessed by the PCWP. However, it is increasingly evident that PCWP is a poor predictor of LV preload, particularly in patients ventilated with high intrathoracic pressures (14–16). This also seems to be likely for patients with severe emphysema with high intrinsic PEEP, since PCWP in patients with emphysema does not differ from that seen in patients undergoing lobectomy, as shown in the present study and by Haniuda et al., (17) despite the lower LV end-diastolic dimension in the former group. Due to the low elastic recoil of the lungs in pulmonary emphysema, and less negative intrathoracic pressure (3,4,18), transmural LV pressures were probably lower in the emphysema group compared to controls.

One limitation of the present study was that the intrathoracic pressure was not assessed, and LV transmural filling pressures could therefore not be established. To overcome this problem, LV preload was also assessed by LV EDA, as a surrogate variable for LV end-diastolic volume.

The reduced LV diastolic as well as systolic dimensions in the lung volume reduction surgery group could have been due to reduced intrathoracic blood volume, in turn caused by the dynamic hyperinflation and hence the generation of PEEPi (2,3,18,19). Tschernko et al. (3) showed that preoperative minimal PEEPi levels range between 5 and 7.5 cm H2O during spontaneous breathing in patients with severe emphysema scheduled for lung volume reduction surgery (18).

A major limitation of the present study is that we did not measure PEEPi. However, our patient characteristics and lung function data were identical to those described by Tschernko et al (3). It would therefore seem reasonable that PEEPi levels were also high in the present study, particularly as our patients were studied during positive pressure ventilation, which further aggravates dynamic hyperinflation and PEEPi in patients with severe emphysema (20). In patients with normal lung function, and in volunteers, positive pressure-respiration with PEEP depletes the intrathoracic vascular bed and the heart, decreasing both pulmonary, right ventricular (RV) and LV end-diastolic dimensions (21–27).

Another mechanism for the impaired filling of the LV in patients with emphysema could be LV diastolic dysfunction caused by LV hypertrophy. However, LV wall mass is not increased in these patients with emphysema, as shown by Vonk-Noordegraaf et al. (10,28).

A third explanation for the low LV end-diastolic dimensions in these patients with severe emphysema could be pulmonary hypertension and chronic pressure overload of the RV accompanied by RV hypertrophy and dilation, causing flattening of the interventricular septum and impaired filling of the LV, as has been shown in patients with primary pulmonary hypertension (29). However, none of the patients in the present study had severe pulmonary hypertension. Patients with severe pulmonary hypertension (systolic pulmonary artery pressure >55 mm Hg) were not included, and there was no significant difference in MPAP between the two groups (22 mm Hg vs 26 mm Hg, Table 3). Furthermore, none of the patients in the emphysema group had obvious echocardiographic signs of RV hypertrophy and/or dilation and bulging of the septum towards the LV. Ventricular interaction is therefore probably not a major factor explaining the low LV end-diastolic dimensions in patients with severe emphysema, as demonstrated in the present study. The hypothesis that intrathoracic hypovolemia, due to dynamic hyperinflation of the lungs, explains the low LV preload and low SV in emphysematous patients without cor pulmonale remains, however, to be proven.

The significantly higher SVR and HR, as shown in the present study, might be the adaptive cardiovascular sympathetic reflex response to low SV seen in patients with severe emphysema. Lower SV and LV end-diastolic volumes would unload arterial baroreceptors and cardiopulmonary volume receptors (30), respectively, inducing a reflex increase in sympathetic nerve activity, which would explain, to some extent, the increase in plasma catecholamines (31), SVR and HR seen in these patients.

In summary, we have shown that CI, SVI, and SWI are 25%–35% lower in anesthetized mechanically ventilated patients with severe emphysema compared to non-emphysematous control patients. This is most likely caused by the apparent decreased LV end-diastolic dimensions and not by systolic dysfunction, as indices of systolic function, LV AEF, and preload-recruitable stroke work did not differ significantly between the groups. These findings might have clinical implications in the perioperative hemodynamic management of these patients with respect to IV fluid therapy and with respect to the hemodynamic response to positive pressure ventilation.


   Footnotes
 
Accepted for publication December 28, 2006.

Supported by Swedish Medical Research Council Grant 13156 and the Medical Faculty of Gothenburg (LUA).


   REFERENCES
Top
 Abstract
 Introduction
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press