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Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Conclusion
This muscle fiber atrophy is associated with significant reductions in tissue force generation, thus limiting resting tonality and potentially contributing the upward crescent shape of the diaphragm. Another potential contributor to the increased diaphragm volume includes ascites. Mutoh and col-leagues have shown, using a piglet model, a 40% reduction in TLC as a result of increased abdominal volume through a surgically implanted water-filled balloon. Although this relationship has yet to be fully examined in humans, the majority of the heart failure patients in the present study were clinically stable and did not have apparent ascites or otherwise significant abdominal distension.
Importantly, a potential limitation to this study is the use of a single equation to estimate pulmonary blood and parenchymal tissue volumes in control subjects and patients with chronic heart failure. Understandably, the use of a single prediction equation may have a tendency to slightly underestimate actual volumes in this population. Until recently, pulmonary fluid accumulation was thought to be a chronic process occurring as a result of cardiac contractile insufficiency leading to elevated left atrial pressure, increased pulmonary venous pressure, and concomitant distension of the pulmonary vasculature, coupled with generalized central and peripheral fluid accumulation and retention. buy birth control pills online
Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Discussion
These authors also suggest that, due to the increase in cardiac size, diffusion capacity of the lung suffers adversely, primarily as a consequence of a reduction in membrane diffusion as opposed to pulmonary capillary blood volume. Although moderate but significant correlations were observed between the cardiothoracic index and various components of pulmonary function, these findings may be underestimated for a number of reasons.
For instance, these authors only examined these relationships based on a one-dimensional measure of the thorax and heart. Also, they did not report data on the pulmonary thoracic index or other radio-graphically determined lung measurements. Thus, it is difficult to extrapolate these findings to true cardiac or lung volumes in relation to the volume of the thoracic cavity. The present investigation sought to expand this previous work and to gain a better understanding of the actual changes in cardiac volume in patients with stable chronic heart failure according to disease severity. In addition, we determined the impact that changes in cardiac volume have on lung volume using a three-dimensional volumetric analysis. Our results show a close association between the increase in cardiac volume and the loss of lung volume within a closed thoracic cavity, consistent with the restrictive pulmonary function pattern typically observed in heart failure patients. read
Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Results
The relationship between NYHA class and absolute lung volume and percentage of TTCV that is taken up by the lung is shown in Figure 3, top, A, and bottom, B, respectively. These data suggest a clear relationship between increasing NYHA class and elevated cardiac volume and reduction in lung volume. Figure 4 demonstrates the close correlation (r = — 0.81, p < 0.001) between elevated cardiac size and reduction in lung volume within the entire population separated by groups. In this study, we found the following in patients with heart failure compared to control participants: (1) marked increases in cardiac size reaching twice that of healthy age- and gender-matched control participants; (2) a clear relationship between the severity of heart failure and increase in cardiac size; (3) and a negative correlation between the percentage of TTC occupied by lung and the percentage of TTC occupied by the heart. add comment
Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Statistical Analysis
Statistical analysis and graphic presentation were accomplished using statistical software (Prism version 4.0; Graphpad; San Diego, CA). One-way analysis of variance was used to test for differences in means among the groups, and unpaired t test was used to compare the means of the participant characteristics and radiographic variables between the control and chronic heart failure groups and between chronic heart failure groups. Pearson correlation coefficients were calculated between radiographic measures and measures of heart failure severity. Fisher Exact Test was used to examine the difference in medication usage and other categorical variables between groups. Statistical significance was set at p < 0.05 for all analyses. Data are presented as mean ± SD or number and percentage of the group, as appropriate.
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Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Population Characteristics
The TTC volume (TTCV) was determined as follows: (1) the posteroanterior and lateral view-digitized tracings were divided vertically into five sections, with the upper two sections equally divided into 2.75-cm segments, and the third and fourth sections equally divided between the most superior border of the diaphragm and lower border of the second section; (2) the fifth section included the region from the dome of the diaphragm to the insertion of the diaphragm with the rib cage; (3) and the volume of each elliptical cylindroid was calculated using the following formula:
TTCV = (1/4то) X Dx X D2 X D3
where D1 is the width across the posteroanterior view, D2 is the depth from the lateral view, and D3 is the height of the posteroanterior view. Total thoracic volume was defined as the sum of each of the individual segment volumes (Fig 1). in detail
Total cardiac volume was calculated using the following formula:
cardiac volume = (1/6to) X Dj X D2 X D3
where D1 is the long diameter measured by establishing the longest line from the junction of the superior venous pedicle with the right atrium to the apex of the left ventricle from the posteroanterior view of the cardiac silhouette, D2 is the transverse diameter defined as the sum of two perpendicular lines extended from D1 to the furthest points of the left and right ventricular borders, and D3 is the depth of the cardiac silhouette defined as the longest diameter on the lateral view approximately perpendicular to D1 (Fig 1).
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Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure: Population Characteristics
This retrospective analysis utilized data from 44 chronic heart failure patients from the database of the Mayo Clinic Heart Failure Service or the Cardiovascular Health Clinic (a preventive and rehabilitative center) from 2000 to 2004 (Table 1). Inclusion criteria included patients with a history of ischemic or dilated cardiomyopathy, stable heart failure symptoms (> 3 months), duration of heart failure symptoms > 1 year, left ventricular EF < 35%, body mass index (BMI) < 35 kg/m2, and nonsmokers with a smoking history < 10 pack-years. Patients were treated with standard optimized medications for heart failure at the time of the study. An equal number of control participants were recruited via advertisement from the surrounding area and were matched with the heart failure group for age, gender, and height. Control participants had normal cardiac function (EF > 50%) and were without history of hypertension, lung disease, or coronary artery disease. All participants gave written informed consent after being provided a description of study requirements. The study protocol was approved by the Mayo Clinic Institutional Review Board; all procedures followed institutional and Health Insurance Portability and Accountability Act guidelines.
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Competition for Intrathoracic Space Reduces Lung Capacity in Patients With Chronic Heart Failure
Chronic heart failure is a progressive disease resulting in severe morbidity and mortality. Interestingly, certain resting measures of cardiac function (ie, ejection fraction [EF]) correlate poorly with exercise tolerance, and thus it is clear that chronic heart failure becomes a systemic disorder, influencing a number of organ systems that may contribute to activity intolerance. Because the pulmonary system lies in series with the heart, accepts nearly all of the cardiac output, and is exposed to similar intratho-racic pressure changes, it would be expected that changes in cardiac structure and function may have adverse consequences on the pulmonary system. Most studies suggest mild-to-moderate changes in the pulmonary system with chronic heart failure, including both restrictive and obstructive changes as well as a reduction in lung diffusing capacity. Causes for changes in lung function remain unclear but have been thought to be related to respiratory muscle weakness, chronic pulmonary hypertension, and changes in lung fluid balance. Another possible contributor to the changes in pulmonary function relates to the progressive cardiac enlargement within a closed thoracic cavity. Such changes in cardiac volume would result in primarily restrictive lung changes manifested as reductions in total lung volume as well as vital capacity.” review