Chest ACCP Career Connection
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Guest Access | Sign In via User Name/Password
doi:10.1378/chest.06-2245
(Chest. 2007; 131:1050-1057)
© 2007 American College of Chest Physicians
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jörgensen, K.
Right arrow Articles by Ricksten, S.-E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jörgensen, K.
Right arrow Articles by Ricksten, S.-E.

Reduced Intrathoracic Blood Volume and Left and Right Ventricular Dimensions in Patients With Severe Emphysema*

An MRI Study

Kirsten Jörgensen, MD; Markus F. Müller, MD, PhD; Jacqueline Nel, RN, MRT; Richard N. Upton, BSc, PhD; Erik Houltz, MD, PhD and Sven-Erik Ricksten, MD, PhD

* From the Departments of Cardiothoracic Anesthesia and Intensive Care (Drs. Jörgensen, Houltz, and Ricksten) and Radiology (Dr. Müller and Ms. Nel), Sahlgrenska University Hospital, Gothenburg, Sweden; and Department of Anesthesia and Intensive Care (Dr. Upton), Royal Adelaide Hospital and University of Adelaide, Adelaide, Australia.

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

Background: Left ventricular (LV) filling is impaired in patients with severe emphysema manifesting in small end-diastolic dimensions. We hypothesized that the hyperinflated lungs of these patients with high intrinsic positive end-expiratory pressure will decrease intrathoracic blood volume (ITBV) and ventricular preload. We therefore measured ITBV, and LV and right ventricular (RV) dimensions and function using MRI techniques in patients with severe emphysema.

Methods: Patients with severe emphysema (n = 13) and matched healthy volunteers (n = 11) were included. The magnetic resonance (MR) examination consisted of three parts: (1) evaluation of RV and LV dimensions and function and interventricular septum curvature using cine MRI; (2) quantification of aortic flow using MR phase velocity mapping; and (3) calculation of the cardiopulmonary peak transit time (PTT) from the pulmonary artery to the ascending aorta using contrast-enhanced, time-resolved, two-dimensional MR angiography.

Results: There were no differences between the groups regarding age, height, or weight. In the emphysema patients, ITBV index (– 35%), LV end-diastolic volume index (LVEDVI) [– 21%], RV end-diastolic volume index (– 20%), cardiac index (– 22%), and stroke volume index (SVI) [– 40%] were lower compared to control subjects. LV and RV end-systolic volumes, LV wall mass, septal curvature, and PTT did not differ between the groups. LVEDVI (r = 0.83) as well as SVI (r = 0.82) correlated closely to ITBV index. SVI correlated closely to LVEDVI (r = 0.84).

Conclusions: LV and RV performance is impaired in patients with severe emphysema because of small end-diastolic dimensions. One possible explanation for the decreased biventricular preload in these patients is intrathoracic hypovolemia caused by hyperinflated lungs.

Key Words: biventricular end-diastolic volumes • biventricular function • cardiac output • emphysema • intrathoracic blood volume • mean transit time • MRI

Patients with severe lung emphysema have poor quality of life because of impaired lung function and considerable 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 due to generation of a high intrinsic positive end-expiratory pressure (PEEPi).23

We have studied4 left ventricular (LV) diastolic and systolic function in patients with severe emphysema and found that LV function is impaired in patients with severe emphysema due to small LV end-diastolic dimensions, ie, a decrease in LV preload. The present investigation is an extension of that study, and the aim was to evaluate whether or not the hyperinflated lungs in patients with severe emphysema will cause blood to pool peripherally and thus decrease intrathoracic blood volume (ITBV) and LV and right ventricular (RV) end-diastolic volumes (preload), stroke volume (SV), and stroke work.5 We therefore measured ITBV and LV and RV dimensions and function in patients with severe emphysema using MRI techniques.

Materials and Methods

The local Ethics Committee of the Medical Faculty of Göteborg University approved the study protocol, written informed consent was obtained from all subjects, and the study complied with the recommendations found in the Declaration of Helsinki.6 Criteria for inclusion in the emphysema group (n = 13) were a history of lung emphysema based on physical examination, chest radiography, and pulmonary function test results: FEV1 from 15 to 30% of predicted value; total lung capacity > 120% of predicted value; and residual volume > 200% of predicted value. Furthermore, the emphysema patients should have no history of cardiac disease, a normal echocardiographic examination (LV ejection fraction > 50% and systolic pulmonary artery [PA] pressure < 55 mm Hg). These criteria are in concordance with commonly accepted guidelines for single-lung transplantation.7 The control group consisted of healthy volunteers (n = 11) with no history of cardiopulmonary disease and were matched for age, gender, and body size.

Imaging Protocol
Each subject underwent a single magnetic resonance (MR) examination (1.5-T MR system, Philips Intera, R9.3; Philips Medical Systems; Best, the Netherlands). [Figs 123456 ]. Heart rate was continuously recorded, and systolic and diastolic arterial BPs (by sphygmomanometer) were recorded before the start of imaging. Subjects in the emphysema group were allowed to breathe oxygen-enriched air during the entire examination.


Figure 1
View larger version (118K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 1.. Short-axis MRI of the heart in a healthy subject and a patient with severe emphysema. Note the smaller end-diastolic volumes of the emphysema patient.

 

Figure 2
View larger version (19K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 2.. Typical recording of contrast intensity vs time for the calculation of PTT. Full-line square symbols indicate original values from the PA (left arrow) and AO (right arrow). Superimposed with full-line/circles are fitted curves according to pharmacokinetic models. PTT is calculated as the temporal distance between maximum values of intensity in the PA and AO fitted curves.

 

Figure 3
View larger version (14K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 3.. Bland-Altman analysis on the agreement of the two methods for estimating ITBVI: qf-ITBVI by MR phase velocity mapping for qf and NONMEM for calculation of ITBVI (NM-ITBVI). Filled circles represent emphysema patients, and open circles represents control subjects.

 

Figure 4
View larger version (10K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 4.. Individual data on calculated ITBVI by MR phase velocity mapping for qf measurements in the control and emphysema groups. Statistical bars show mean value (diamond), SD, and SEM. Filled circles represent emphysema patients, and open circles represents control subjects.

 

Figure 5
View larger version (17K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 5.. Linear regression showing the close correlation between qf-ITBVI and LVEDVI. Filled circles represent emphysema patients, and open circles represents control subjects.

 

Figure 6
View larger version (16K):
[in this window]
[in a new window]
[Download PPT slide]
  		Figure 6.. Linear regression showing the close correlation between LVEDVI and LVSVI (cine-SVI). Filled circles represent emphysema patients, and open circles represents control subjects.

 
Cardiac Volumes and Function by Cine MRI
Values for cardiac volume and function by cine MRI were obtained once in all participants. During the examination, multiple slices through the heart were acquired to encompass completely the ventricle in multiple phases within the cardiac cycle by using ECG triggering. The images were acquired during breath-hold in expiration with approximately 12 sections through the left ventricle in the short-axis view. In the short axis, the contours describing the endocardial and epicardial border of the myocardium were delineated, and the following LV and RV parameters were evaluated using commercially available software (Easy Vision 5.1; Philips Medical Systems): ejection fraction, end-diastolic volume, end-systolic volume, and SV. Endocardial contours were traced on the diastolic and systolic images, and the ventricular volume (diastolic or systolic) equals the sum of all the endocardial areas (of the diastolic or systolic images, respectively) multiplied by the slice thickness. The LV wall mass was calculated by tracing the epicardial borders in diastole to obtain an epicardial volume. The volume of the myocardium was defined as the epicardial volume minus LV end-diastolic volume (LVEDV). Multiplication of this value by the specific gravity for muscle (1.05 g/mL) yields the myocardial mass.89 Papillary muscles were included in the volume and excluded in the mass determination.10 Septal bowing was measured in the short-axis image plane as the septal curvature, defined as 1/septal radius in centimeters, as described by Roeleveld et al.11 The cine image with the lowest septal curvature was used for quantification.

Quantification of Aortic Flow Using MR Phase Velocity Mapping
Quantification of aortic flow using MR phase velocity mapping was performed once during breath-holding using a phase-contrast ECG-triggered two-dimensional fast-field echo sequence at the level of the PA, perpendicularly to the ascending aorta (AO). SV was evaluated using the Easy Vision 5.1. Circular regions of interest (ROI) were placed over the AO. The contours of the ROI were delineated around the internal border of the vessel of interest on all images by automated contour detection. SV (quantitative aortic flow [qf]-SV) was computed by integrating the flow over a complete cardiac cycle.

Contrast-Enhanced, Time-Resolved, Two-Dimensional MR Angiography of the Heart and Lungs for Calculation of the Peak Transit Time
Contrast-enhanced, time-resolved, two-dimensional MR angiography of the heart and lungs for calculation of the peak transit time (PTT) was performed twice in each patient for evaluation of reproducibility. A two-dimensional, T1-weighted, flow-compensated fast-field echo sequence was applied at the level of the pulmonary trunk and AO during IV gadolinium bolus injection (2 mL bolus of gadopentetate dimeglumine; Magnevist; Berlex Laboratories; Wayne, NJ), followed by 20 mL of saline solution, injected at a rate of 5 mL/s using an automated power injector (Spectris Solaris; Medrad; Indianola, PA). Two-dimensional data sets were acquired at 0.559- to 1.1-s intervals (approximately 2 Hz) for 25 to 30 s after contrast material injection. Subjects were requested to hold their breath in expiration during the MR angiographic examination for at least 30 s or as long as was comfortable. Time-intensity curves were generated for bolus transit through the ROI (Intera R 9.3; Philips Medical Systems): the outflow part of the PA and the AO. The PA and AO curves were fitted to functions describing peak/pulse curves (PA) and multicompartment impulse response exponential decay curves (AO) using software (Origin Version 7; Origin Lab Corporation; Northampton, MA). The PA-to-AO PTT was calculated by subtracting the time of peak signal intensity of the PA curve from that of the AO curve (Fig 2).

All hemodynamic data and data on cardiac dimensions were normalized to body surface area (BSA). ITBV index (ITBVI) was calculated as follows: qf-ITBVI = PTT x qf-cardiac output (CO)/60 x BSA.12 Furthermore, ITBVI was estimated from the contrast intensity vs time curves using a nonlinear mixed effect modeling (NONMEM) approach. The NONMEM program (version V, level 1.1; GloboMax LLC; Hanover, MD) with the first-order conditional estimation and interaction analysis procedure was used. The structural model of the lung used was a "tank in series" model. This type of model is suitable for describing intravascular peaks and has been used previously to describe the lung kinetics of the intravascular marker indocyanine green in man.13 Systemic vascular resistance index was calculated as mean arterial pressure/qf-cardiac index (CI).

Statistical Analysis
The reproducibility of PTT measurements and the agreement between the two methods for estimation of ITBVI were assessed according to Bland and Altman.14 An unpaired, two-tailed Student t test was used to compare the two groups. A linear regression analysis was performed to relate LVEDV index (LVEDVI) and cine-SVI to qf-ITBVI and cine-SVI to LVEDVI; p < 0.05 was considered to indicate statistically significant difference. Data are presented as mean ± SD.

Results

There were no differences between the groups regarding age, height, or weight (Table 1 ). The emphysema patients had the typical functional features of severe pulmonary emphysema: severe obstruction to expiratory airflow and considerable hyperinflation (Table 1).


View this table:
[in this window]
[in a new window]

  		Table 1.. Patient Characteristics and Lung Function Data*

 
Cardiac Volumes and Function by Cine MR
LVEDVI (p = 0.002), LV SV index (LVSVI) [p = 0.0001], RV end-diastolic volume index (RVEDVI) [p = 0.0042], RV SV index (RVSVI) [p = 0.0001], LV ejection fraction (p = 0.0006), and right ventricular ejection fraction (p = 0.0067) were significantly lower in the emphysema group (Fig 1; Table 2 ). In contrast, LV end-systolic volume index, RV end-systolic volume index, LV wall mass index, and septal curvature did not differ between the two groups. RV wall thickness was < 3 mm in all patients. There was a close correlation between RVSVI and LVSVI (r = 0.96, p < 0.001) and between RVEDVI and LVEDVI (r = 0.83, p < 0.001). The relationships between LVEDVI and cine-SV index (SVI) [Fig 6] and between RVEDVI and RVSVI were highly correlated (r = 0.79 and 0.82, respectively; p < 0.0001 for both).


View this table:
[in this window]
[in a new window]

  		Table 2.. Cardiac Function With Cine Image Acquisition*

 
Quantification of Aortic Flow Using MR Phase Velocity Mapping
SVI (p = 0.0001) and CI (p = 0.019) were significantly lower in the emphysema group (Table 3 ). Heart rate (p = 0.0006) and systemic vascular resistance index (p = 0.032) were significantly higher in the emphysema group (3,110 ± 719 dyne·s/cm5/m2 vs 2,392 ± 566 dyne·s/cm5/m2).


View this table:
[in this window]
[in a new window]

  		Table 3.. Quantification of Aortic Flow by MR Phase Velocity Mapping*

 
Contrast-Enhanced, Time-Resolved, Two-Dimensional MR Angiography of the Heart and Lungs
There was a good reproducibility for estimation of PTT with a bias of – 0.32 s, SD of the differences of 0.77 s, an error (double SD divided by the mean of the repeated measurements) of 21.9%, and limits of agreement from – 1.87 to 1.23 s (Table 4 ). There was no difference in mean PTT between the two groups. The NONMEM-calculated ITBVI showed good agreement with qf-ITBVI with a bias of 0.01, SD of the differences of 0.03 L/m2, an error of 16%, and limits of agreement from – 0.05 to 0.05 L/m2 (Fig 3).


View this table:
[in this window]
[in a new window]

  		Table 4.. PTT and ITBVI*

 
qf-ITBVI and NONMEM-ITBVI were both significantly lower (p = 0.001 and p = 0.001, respectively) in patients with emphysema compared to healthy volunteers (Fig 4). Both LVEDVI (r = 0.83, p < 0.001; Fig 5) and cine-SVI (r = 0.82, p < 0.001) correlated closely to qf-ITBVI.

Discussion

The main findings of this study were that cardiac performance was compromised in patients with severe pulmonary emphysema, as demonstrated by a lower SVI, when compared to control subjects matched for gender, age, and BSA. Although we have not proven a cause-effect relationship, the close relationship between ITBVI and LVEDVI and between LVEDVI and SVI (Fig 5, 6) strongly suggest that a low preload, caused by intrathoracic hypovolemia, contributes to the impaired LV performance seen in patients with severe emphysema. Furthermore, our data confirm the results from our previous study4 of anesthetized patients with severe emphysema studied with transesophageal two-dimensional Doppler echocardiography before and after lung volume reduction surgery. In that study, the emphysema group had a lower LV performance as demonstrated by a lower SVI and CI, associated with a lower baseline LV preload, as indicated by a lower LV end-diastolic area index and mitral Doppler flow indexes of impaired LV filling when compared to anesthetized nonemphysematous patients.4

A decreased ITBV compromising cardiac performance has, to our knowledge, not previously been demonstrated in patients with severe emphysema. Intrathoracic hypovolemia in patients with severe emphysema could be explained by the well-known dynamic hyperinflation and hence the generation of PEEPi seen in these patients.3151617 Tschernko et al3 showed that minimal PEEPi levels range from 5 to 7.5 cm H2O in patients with severe emphysema316 In the present study, we did not measure PEEPi or intrathoracic pressure, which is a major limitation of this study. However, our patients’ characteristics and lung function data were similar to those described by Tschernko et al.3 It would therefore seem reasonable that PEEPi levels were high also in the present study. In patients with normal lung function and in volunteers, positive pressure respiration with positive end-expiratory pressure depletes the intrathoracic vascular bed and the heart, decreasing both pulmonary vascular and RV and LV end-diastolic volumes.18192021222324 Furthermore, positive end-expiratory pressure induces changes in the mitral Doppler-derived indexes indicative of impaired LV filling.192425 One could speculate that the PEEPi-induced decrease in ITBV is caused by a decreased compliance of the pulmonary vascular bed in emphysema due to the hyperinflated lungs, which may redistribute blood to the periphery.

A reduction in ITBV could alternatively be explained by a diminution of the pulmonary vascular bed and a decreased pulmonary blood volume as a consequence of the disease, since all patients had severe emphysema. However, our suggestion that high PEEPi levels are of importance to explain the decreased ITBV in severe emphysema is supported by our findings that lung volume reduction surgery improves LV performance in emphysematous patients.4 This improvement is accompanied by an increase in LV end-diastolic area index and mitral Doppler flow indexes of improved LV filling.4 Lung volume reduction surgery is associated with an alleviation of PEEPi,231617 which thus could normalize a low ITBV, as well as low RV and LV end-diastolic blood volumes in these patients.

The lower RV and LV preload in patients with emphysema could be caused by external compression (pulmonary tamponade) from the hyperinflated lungs increasing end-diastolic stiffness. However, we have previously shown that the LV end-diastolic pressure-area relationship is not different from that seen in nonemphysematous patients, indicating that the hyperinflated lungs do not increase LV end-diastolic stiffness in patients with severe emphysema.4 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 previously,2627 and by us in the present study. A third explanation for the low LVEDV in these patients could be a leftward shift of the interventricular septum, causing an underfilling of the LV, as has been shown in patients with primary pulmonary hypertension,28 and also in some patients with emphysema.26 This mechanism is less likely since the configuration of the interventricular septum did not differ between the groups. Furthermore, none of the patients in the present study had severe pulmonary hypertension (systolic PA pressure > 55 mm Hg), as evaluated by Doppler echocardiography, and none had RV hypertrophy.

Indirect evidence that the left ventricle of emphysema patients is hypovolemic in diastole is our recent study29 on patients with severe emphysema in which LV dimensions and performance were evaluated using transesophageal two-dimensional echocardiography and PA thermodilution catheter before and during central blood volume expansion by passive leg elevation. LV filling pressures and LV end-diastolic areas increased by 20 to 30% and 12 to 16%, respectively, which in turn caused a twofold- to threefold-greater increase in SV for a certain increase in preload, and a greater increase in LV area ejection fraction in patients with emphysema compared to control subjects. Thus, the left ventricle operates on a steeper portion of the Frank-Starling relationship in emphysema patients and thus has a less than optimal diastolic stretch of the myocardial sarcomeres at baseline. This could explain the lower LV and RV ejection fractions in the emphysema patients compared to control subjects in the present study.

We measured PTT by subtracting the times of peak AO and PA signal intensities30 rather than by subtracting the first moment of the curves to achieve mean transit time, which, by definition, is used for calculation of ITBV.12 However, it has been shown that PTT is an excellent approximate of mean transit time, PTT being < 4% higher than mean transit time.31 The utility of the PTT approach is supported by the NONMEM modeling analysis, which gave very similar results. The transit time of an indicator is proportional to its volume of distribution (ITBV) and inversely proportional to flow (CO), according to fundamental principles of tracer kinetics.32 In our study, PTT was not significantly different from control because the low CO, which would have increased PTT, was accompanied by a decreased ITBV, which will decrease PTT. In other words, the time for oxygen uptake is maintained in emphysema patients, in spite of the low CO, because of the low ITBV.

In all MRI procedures, errors may occur due to motion artifacts. Patients in the emphysema group were thus less likely to hold their breath during expiration for 25 to 30 s. In spite of this, contrast-enhanced, time-resolved, two-dimensional MR angiography provided PTT measurements with a high reproducibility in the present study. In addition, in our control group, PTT was 7.5 ± 1.6 s, which is comparable to 7.2 ± 1.2 s as shown by Shors et al30 in their control subjects.

In conclusion, we have shown that intrathoracic hypovolemia may explain why cardiac performance is impaired in patients with emphysema. Low SVs in these patients were associated with low LV and RV end-diastolic volumes and low ITBVs. These findings might have clinical implications in the perioperative hemodynamic management of these patients with respect to IV fluid therapy and to the hemodynamic response to positive pressure ventilation.

Footnotes

Abbreviations: AO = ascending aorta; BSA = body surface area; CI = cardiac index; CO = cardiac output; ITBV = intrathoracic blood volume; ITBVI = intrathoracic blood volume index; LV = left ventricular; LVEDV = left ventricular end-diastolic volume; LVEDVI = left ventricular end-diastolic volume index; LVSVI = left ventricular stroke volume index; MR = magnetic resonance; NONMEM = nonlinear mixed effect modeling; PA = pulmonary artery; PEEPi = intrinsic positive end-expiratory pressure; PTT = peak transit time; qf = quantitative aortic flow; ROI = regions of interest; RV = right ventricular; RVEDVI = right ventricular end-diastolic volume index; RVSVI = right ventricular stroke volume index; SV = stroke volume; SVI = stroke volume index

This study was supported by the Swedish Medical Research Council, No. 13156 and the Medical Faculty of Gothenburg.

No financial or other potential conflicts of interest exist for any of the authors.

Received for publication September 11, 2006. Accepted for publication December 10, 2006.

References

  1. Okubadejo, AA, Jones, PW, Wedzicha, JA (1996) Quality of life in patients with chronic obstructive pulmonary disease and severe hypoxaemia. Thorax 51,44-47[Abstract]
  2. Sciurba, FC, Rogers, RM, Keenan, RJ, et al Improvement in pulmonary function and elastic recoil after lung-reduction surgery for diffuse emphysema. N Engl J Med 1996;334,1095-1099[Abstract/Free Full Text]
  3. Tschernko, EM, Gruber, EM, Jaksch, P, et al Ventilatory mechanics and gas exchange during exercise before and after lung volume reduction surgery. Am J Respir Crit Care Med 1998;158,1424-1431[Abstract/Free Full Text]
  4. Jorgensen, K, Houltz, E, Westfelt, U, et al Effects of lung volume reduction surgery on left ventricular diastolic filling and dimensions in patients with severe emphysema. Chest 2003;124,1863-1870[CrossRef][ISI][Medline]
  5. Tyberg, JV, Grant, DA, Kingma, I, et al Effects of positive intrathoracic pressure on pulmonary and systemic hemodynamics. Respir Physiol 2000;119,171-179[CrossRef][ISI][Medline]
  6. World Medical Association declaration of Helsinki.. Recommendations guiding physicians in biomedical research involving human subjects. JAMA 1997;277,925-926[CrossRef][ISI][Medline]
  7. The American Society for Transplant Physicians (ASTP)/American Thoracic Society(ATS)/European Respiratory Society(ERS)/International Society for Heart and Lung Transplantation(ISHLT).. International guidelines for the selection of lung transplant candidates. Am J Respir Crit Care Med 1998;158,335-339[ISI][Medline]
  8. Pennell, DJ Ventricular volume and mass by CMR. J Cardiovasc Magn Reson 2002;4,507-513[CrossRef][ISI][Medline]
  9. Rajappan, K, Bellenger, NG, Anderson, L, et al The role of cardiovascular magnetic resonance in heart failure. Eur J Heart Fail 2000;2,241-252[CrossRef][ISI][Medline]
  10. Sievers, B, Kirchberg, S, Bakan, A, et al Impact of papillary muscles in ventricular volume and ejection fraction assessment by cardiovascular magnetic resonance. J Cardiovasc Magn Reson 2004;6,9-16[CrossRef][ISI][Medline]
  11. Roeleveld, RJ, Marcus, JT, Faes, TJ, et al Interventricular septal configuration at MR imaging and pulmonary arterial pressure in pulmonary hypertension. Radiology 2005;234,710-717[Abstract/Free Full Text]
  12. Zierler, KL Circulation times and the theory of indicator-dilution methods for determining blood flow and volume. Handbook of physiology 1962,585-615 American Physiological Society, distributed by Williams & Wilkins. Bethesda, MD:
  13. Upton, RN, Ludbrook, G A physiologically based, recirculatory model of the kinetics and dynamics of propofol in man. Anesthesiology 2005;103,344-352[CrossRef][ISI][Medline]
  14. Bland, JM, Altman, DG Statistical methods for assessing agreement between two methods of clinical measurement. Lancet 1986;1,307-310[CrossRef][ISI][Medline]
  15. Marchand, E, Gayan-Ramirez, G, De Leyn, P, et al Physiological basis of improvement after lung volume reduction surgery for severe emphysema: where are we? Eur Respir J 1999;13,686-696[Abstract]
  16. Tschernko, EM, Kritzinger, M, Gruber, EM, et al Lung volume reduction surgery: preoperative functional predictors for postoperative outcome. Anesth Analg 1999;88,28-33[Abstract/Free Full Text]
  17. Tschernko, EM, Wisser, W, Wanke, T, et al Changes in ventilatory mechanics and diaphragmatic function after lung volume reduction surgery in patients with COPD. Thorax 1997;52,545-550[Abstract]
  18. Brienza, N, Dambrosio, M, Cinnella, G, et al Effects of PEEP on intrathoracic and extrathoracic blood volumes evaluated with the COLD system in patients with acute respiratory failure: preliminary study [in Italian]. Minerva Anesthesiol 1996;62,235-242
  19. Huemer, G, Kolev, N, Kurz, A, et al Influence of positive end-expiratory pressure on right and left ventricular performance assessed by Doppler two-dimensional echocardiography. Chest 1994;106,67-73[ISI][Medline]
  20. Koolen, JJ, Visser, CA, Wever, E, et al Transesophageal two-dimensional echocardiographic evaluation of biventricular dimension and function during positive end-expiratory pressure ventilation after coronary artery bypass grafting. Am J Cardiol 1987;59,1047-1051[CrossRef][ISI][Medline]
  21. Mitaka, C, Nagura, T, Sakanishi, N, et al Two-dimensional echocardiographic evaluation of inferior vena cava, right ventricle, and left ventricle during positive-pressure ventilation with varying levels of positive end-expiratory pressure. Crit Care Med 1989;17,205-210[ISI][Medline]
  22. Peters, J, Hecker, B, Neuser, D, et al Regional blood volume distribution during positive and negative airway pressure breathing in supine humans. J Appl Physiol 1993;75,1740-1747[Abstract/Free Full Text]
  23. Terai, C, Uenishi, M, Sugimoto, H, et al Transesophageal echocardiographic dimensional analysis of four cardiac chambers during positive end-expiratory pressure. Anesthesiology 1985;63,640-646[ISI][Medline]
  24. Yamada, T, Takeda, J, Satoh, M, et al Effect of positive end-expiratory pressure on left and right ventricular diastolic filling assessed by transoesophageal Doppler echocardiography. Anaesth Intensive Care 1999;27,341-345[ISI][Medline]
  25. Meijburg, HW, Visser, CA, Wesenhagen, H, et al Transesophageal pulsed-Doppler echocardiographic evaluation of transmitral and pulmonary venous flow during ventilation with positive end-expiratory pressure. J Cardiothorac Vasc Anesth 1994;8,386-391[CrossRef][Medline]
  26. Vonk Noordegraaf, A, Marcus, JT, Roseboom, B, et al The effect of right ventricular hypertrophy on left ventricular ejection fraction in pulmonary emphysema. Chest 1997;112,640-645[ISI][Medline]
  27. Vonk-Noordegraaf, A, Marcus, JT, Holverda, S, et al Early changes of cardiac structure and function in COPD patients with mild hypoxemia. Chest 2005;127,1898-1903[CrossRef][ISI][Medline]
  28. Gan, CT, Lankhaar, JW, Marcus, JT, et al Impaired left ventricular filling due to right to left ventricular interaction in patients with pulmonary arterial hypertension. Am J Physiol Heart Circ Physiol 2006;290,H1528-H1533[Abstract/Free Full Text]
  29. Jorgensen K, Houltz E, Westfelt U, et al. Left ventricular performance and dimensions in patients with severe emphysema. Anesth Analg 2007 (in press)
  30. Shors, SM, Cotts, WG, Pavlovic-Surjancev, B, et al Heart failure: evaluation of cardiopulmonary transit times with time-resolved MR angiography. Radiology 2003;229,743-748[Abstract/Free Full Text]
  31. Slutsky, RA, Carey, PH, Bhargava, V, et al A comparison of peak-to-peak pulmonary transit time determined by digital intravenous angiography with standard dye-dilution techniques in anesthetized dogs. Invest Radiol 1982;17,362-366[ISI][Medline]
  32. Peters, AM Fundamentals of tracer kinetics for radiologists. Br J Radiol 1998;71,1116-1129[Abstract]




This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Article Archive
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via ISI Web of Science (1)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Jörgensen, K.
Right arrow Articles by Ricksten, S.-E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Jörgensen, K.
Right arrow Articles by Ricksten, S.-E.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS