New 2018 Edition The muscle manual contains evidence based, easily accessible information on topics including musculoskeletal anatomy, anatomical variation, kinesiology, muscle testing, palpation, osteology, biomechanics, trigger point referral patterns, nerve and vessel pathways, differential diagnosis, massage and soft tissue techniques and much more. Used as a required text for many colleges and universities, this text is a valuable study guide for students, therapists and doctors preparing for board exams, oral practical exams, objective structured clinical examinations (OSCE) and many other licensure examinations. This text bridges the gap between classroom education and practical clinical application.
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ISBN: 978-0-9732742-2-6 Pages: 465 pages References: 360. The quick reference evidence informed Muscle Manual is designed as a quick reference guide for health care students, therapist, practitioners, doctors & instructors, and as a companion to the,.
This text bridges the gap between classroom education and practical clinical application. It contains current, easily accessible information on topics including musculoskeletal anatomy, anatomical variation, kinesiology, muscle testing, palpation, osteology, biomechanics, trigger point referral patterns, peripheral neurology, differential diagnosis, treatment techniques and much more. Video content available via. In addition, this text is a valuable study guide for students, therapists and doctors preparing for board exams, oral practical exams, objective structured clinical examinations (OSCE) and many other licensure examinations. 480 pages with over 2000 Illustrations & Images.
Free Web-based Video, Image & Testing Resources. Multidisciplinary Peer Reviewed (DC, DO, MD, ND, PhD, PT, RMT, RN). Pocket-Sized, Portable, Concise Presentation. A Must-Have for Classroom & General Practice 465 pages, Coil Bound Size: 16cm (6″) x 23cm (9″) x 2.5cm (1″) Weight: 650g (1lb 7oz) ISBN: 978-0-9732742-2-6. Abductor Pollicis Longus. 270 Adductor Longus & Brevis.
334 Adductor Magnus. 338 Anconeus. 265 Articularis Genu. 332 Auricularis.
55 Biceps Brachii. 220 Biceps Femoris. 344 Brachialis. 222 Brachioradialis.
256 Buccinator. 64 Central Hand Muscles. 282 Coracobrachialis.
218 Corrugator Supercilii. 59 Cross Syndrome. 441 Deltoid. 202 Depressor Anguli Oris. 66 Depressor Labii Inferioris. 66 Depressor Septi Nasi. 58 Diaphragm.
150 Exercise prescription. 442 Erector Spinae Group. 140, 178 Extensor Carpi Radialis B.
260 Extensor Carpi Radialis L. 258 Extensor Carpi Ulnaris. 266 Extensor Digiti Minimi.
264 Extensor Digitorum Longus. 362 Extensor Digitorum. 262 Extensor Hallucis Longus. 364 Extensor Indicis. 276 Extensor Pollicis B. 272 External Oblique. 170 Eye Muscles.
76 Fascia. 40 Fibularis Brevis. 370 Fibularis Longus. 368 Fibularis Tertius. 366 Flexor Carpi Radialis. 242 Flexor Carpi Ulnaris. 246 Flexor Digitorum Longus.
382 Flexor Dig. 250 Flexor Dig. 248 Flexor Hallucis Longus. 384 Flexor Pollicis Longus.
252 Foot Muscles. 387 Gastrocnemius. 372 Gluteus Maximus. 302 Gluteus Medius. 304 Gluteus Minimus. 306 Gracilis. 336 Hand Muscles.
286 Hypothenar Muscles. 280 Iliacus. 318 Infraspinatus. 206 Intercostal Muscles.
148 Internal Abdominal Oblique. 172 Lateral Pterygoid. 70 Latissimus Dorsi.
134 Levator Anguli Oris. 61 Levator Labii Sup. 60 Levator Palpebrae Sup.
57 Levator Scapulae. 92 Ligaments Ankle. 350 Elbow. 191 Finger. 81 Sacroiliac. 156 Shoulder.
191 Spine. 118 Wrist. 229 Longus Capitis. 106 Longus Cervicis (colli).
107 Massage. 421 Contract Relax. 441 Contraindications. 423 Effleurage. 424 Frictions.
433 Heat vs Cold. 448 IASTM.
436 Myofascial Release. 434 Petrissage. 426 Kneading.
427 Muscle Comp. & Wring 428 Picking-up & Skin Roll 429 Pin & Stretch. 438 PNF/MET. 440 Shaking, Jostling & Rocking 432 Stretching Techniques.
439 Stroking. 425 Tapotement. 430 Trigger Point Therapy.
435 Vibrations. 431 Masseter. 69 Medial Pterygoid. 71 Mentalis. 67 Multifidi. 180 Muscle Testing. 36 Nerves.
393 Cranial Nerves. 410 Femoral. 408 Median.
403 Musculocut. 402 Obturator. 408 Radial Nerve. 401 Sciatic. 406 Ulnar nerve. 404 Obturator Externus/internus 313 Omohyoid. 104 Orbicularis Oculi.
56 Orbicularis Oris. 65 Pain cycle. 454 Palpation. Iv, 121 Palmaris Longus. 244 Pectineus. 332 Pectoralis Major.
216 Pectoralis Minor. 130 Pharynx & Soft Palate. 72 Piriformis.
308 Plantaris. 376 Platysma. 54 Popliteus. 378 Pronator Quadratus.
254 Pronator Teres. 240 Psoas Major & Minor. 316 Quadratus Femoris. 314 Quadratus Lumborum. 176 Rectus Abdominis.
168 Rectus Capitis Ant. 105 Rectus Femoris.
324 Rhomboid Major & Minor. 136 Risorius. 61 Rotatores. 183 Sartorius. 322 Scalenes. 110 Semimembranosus.
342 Semispinalis. 144 Semitendinosus. 340 Serratus Anterior. 214 Serratus Posterior Sup. 138 Soleus. 374 Splenius Capitis & Cerv.
94 Squat & rise. 184 Sternocleidomastoid (SCM). 98 Subclavius. 129 Suboccipital Muscles. 96 Subscapularis. 210 Superior & Inf. 310 Supinator.
268 Suprahyoid Muscles. 100 Supraspinatus. 204 Temporalis. 68 Temporoparietalis.
67 Tensor Fasciae Latae. 320 Teres Major. 212 Teres Minor. 208 Thenar Muscles. 278 Tibialis Anterior. 360 Tibialis Posterior. 380 Tongue.
74 Transversospinalis Group. 144 Transversus Abdominis.
174 Trapezius (mid. 132 Trapezius (upper fibers). 90 Triceps Brachii.
224 Vastus Intermedius. 328 Vastus Lateralis. 326 Vastus Medialis. 330 Vascular supply. 393 Visceral referrals.
458 Zygomaticus Major/Minor. portocontentbox align='center' animationtype='bounce' This edition is now discontinued, but is still available as an.
Please check out the 2nd edition textbook: /portocontentbox The Spinal Manual is the among best integrated physical medicine guides available for students, clinicians & instructors; topics included - regional anatomy, orthopedic and special tests, history, signs and symptoms, physical exam, muscle testing, posture & gait, diagnostic imaging, multidisciplinary management, patient follow-up, prognosis, rehab exercises, and clinical exam forms and patient handouts –. With coil binding the book is easy to use in both the classroom and clinical practice.
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124 Vessels, 76 Nerves (peripheral & cranial). Origins, Insertions, Actions. Blood & Nerve supply. Palpation, Kinesiology.
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This text contains concise, easily accessible information on topics including anatomy, kinesiology, soft tissue release, MET, PIR/PNF, IASTM, functional rehab., joint mobilization & manipulation, acupuncture, electrotherapies (MENS, TENS, US, laser, IFC), athletic taping, nutrition and much more. This text is a valuable study guide for students, practitioners and doctors preparing for National Board Exams, State/Province Board Exams, Clinical Skills Examinations and many other standardized licensure examinations. Over 1500 Illustrations & Images, 1000s of references. Online Video, Image & Text Resources. Multidisciplinary Peer Reviewed (DC, DO, MD, ND, PhD, PT, RMT, RN). Clear Presentation & Logical Format Saves Time - Perfect for Board Exam Review.
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Methods and Results Forty-one HF patients of New York Heart Association (NYHA) class: Group A=class I/II (n=26) and Group B=class III/IV (n=15) and an equal number matched controls (CTL) were recruited. Participants underwent echocardiography (ECHO), spirometry, and posterioanterior and lateral chest radiographic evaluation (RAD) for volumetric estimation of the total thoracic cavity (TTC), diaphragm, heart, and lungs. ANOVA demonstrated no difference between groups for TTC volume (p=0.63). RAD cardiac volumes (% TTC volume) were significantly different among all groups (p. INTRODUCTION Chronic heart failure (HF) is associated with mild to moderate changes in pulmonary function, including restrictive and obstructive changes as well as a reduction in lung diffusing capacity (DLCO) -. Although heart failure induced causes of altered lung function remain unclear, they have been attributed to respiratory muscle weakness, pulmonary hypertension, changes in lung fluid balance, and chronic neurohumoral changes -.
Because the lungs and heart both reside in a common enclosure (chest wall) and the cardiac muscle is less compliant than the lungs another potential contributor to the changes in pulmonary function in HF relates to progressive cardiac enlargement within the thoracic cavity. Such changes in cardiac volume would be expected to result in primarily restrictive lung changes manifested as reductions in total lung volume and vital capacity. In addition, it may be expected that a relationship also exists between cardiac volume and maximal expiratory airflows as well as the DLCO. As cardiac filling pressures increase and pulmonary congestion progressively develops, blood flow may back up into the bronchial circulation and influence airway caliber resulting in airflow limitations. Further, the reduction in DLCO with disease severity is likely related to lung fluid imbalance and chronic changes at the alveolar-capillary membrane. Epidemiological studies have shown a link between pulmonary function and mortality, particularly related to cardiovascular events -.
Although the causal link between lung function and cardiac mortality remains unclear, it may be associated with the progressive changes in cardiac size. Studies have implied a marginal link between cardiac size and lung function in HF, -; however, these studies are limited by echocardiographic measurement of left ventricular mass as opposed to total heart size and one-dimensional estimates of the cardio-thoracic relationship. Importantly, these studies may have inadequately represented the importance of changes in total cardiac size on lung function in relation to the constraints imposed by the thoracic cavity. The focus of this study was to examine the relationship between radiographically determined cardiac volume and maximal lung volumes, maximal expiratory airflows, and DLCO in patients with long standing, but stable HF. Further, we sought to determine if a commonly obtained echocardiographic measure of cardiac size in this population might be as predictive of lung function changes.
We hypothesized that increased competition for intrathoracic space caused by changes in cardiac volume associated with chronic HF contributes to changes observed in pulmonary function and the commonly derived echocardiographic measures of cardiac dimension would inadequately predict these changes. Population Characteristics Forty-one HF patients were recruited from the Mayo Clinic Heart Failure Service and the Cardiovascular Health Clinic (a preventive and rehabilitative center) over the period of 2000 to 2004.
Patients included those with a history of ischemic or dilated cardiomyopathy, stable HF symptoms (3 months), duration of HF symptoms 1 year, left ventricular ejection fraction (EF) ≤35%, body mass index (BMI) 50%), without history of hypertension, lung disease or coronary artery disease (CAD). 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 HIPAA guidelines. Control Group A Group B p-value N (% Female) 41 (39) 26 (54) 15 (40) 0.39 Age (yr) 57.8 ± 13.1 56.6 ± 12.6 55.4 ± 12.7 0.81 Height (cm) 171.0 ± 9.4 170.6 ± 9.4 173.2 ± 10.6 0.68 Weight (kg) 75.1 ± 13.6 81.0 ± 15.1 87.2 ± 14.0. 0.02 BMI (kg/m 2) 25.5 ± 3.0 27.9 ± 4.8 29.2 ± 5.6. 0.01 BSA (m 2) 1.87 ± 0.21 1.93 ± 0.21 2.01 ± 0.18 0.08 Smoking History (pack yrs) 3.02 ± 7.07 2.90 ± 6.26 2.33 ± 4.48 0.94 Exercise History (min/week) 187.6 ± 168.7 62.9 ± 87.8. 56.0 ± 60.3.
Radiographic Volumetric Evaluation The PA and LAT radiographic views were used to make volumetric estimations of the total thoracic cavity (TTC), diaphragm, cardiac, and lungs (TLC R) based on the assumptions of a partial ellipsoid as initially described by Barnhard and colleagues and later by Glenn and Greene as well as others -. This methodology has been shown to be valid and reliable,. Details of this technique from our laboratory, in a companion cohort of HF and matched controls, are published elsewhere. Briefly, the inner most edge of the intra-thoracic cavity and outer most edge of the cardiac silhouette on both radiographic views were manually traced on a digitizing tablet (AccuGrid A43BL, Numonics Corp, Montgomeryville, Pennsylvania) with data exported to a digitizing software program (Didger 3, Golden Software Inc, Golden, Colorado) on a personal computer for offline analysis. Coordinate data were used to make linear measurements for the volumetric computation. The volumetric measures for total thoracic cavity volume (TTCV), cardiac volume (CV), and the total radiographic lung volume (TLC R) were calculated as follow: TTCV=(1/4 π).D 1.D 2.D 3 where D n represents width, depth and height of the PA and LAT views, CV=(1/6π).D 1.D 2.D 3 where D n represents diameters of the atrium and ventricles in the PA and LAT views and TLC=TTCV=(CV+DV+PBV+PTV) where DV represents diaphragm volume, PBV pulmonary blood volume and PTV, parenchymal tissue volume (for details see reference ). Echocardiographic Evaluation Doppler and 2D echocardiographic measurements were performed according to the recommendations of the American Society of Echocardiography.
Left atrial (LA) dimension, left ventricular (LV) mass, LV internal dimension during systole and diastole (LVIDs and LVIDd, respectively), interventricular septal thickness (IVST), LV posterior wall thickness and left atrial end-diastolic dimension were measured. Left ventricular mass was calculated using the formula of Troy and colleagues.
Left ventricular mass index was calculated as left ventricular mass divided by body surface area. The LV ejection fraction (EF%) was calculated using the modified Simpson’s rule. Transmitral inflow velocity was obtained from a 2-dimensional apical window with the pulsed wave Doppler function facilitating the calculation of maximal early flow velocity (E), maximal late flow velocity (A), the ratio of maximal early to late flow velocity (E/A), and deceleration time of the early diastolic filling. Pulmonary Function Evaluation Participants underwent spirometry evaluation including, forced vital capacity (FVC) and assessment of maximal expiratory airflows including forced expiratory volume in one second (FEV 1), mean forced expiratory flow between 25% and 75% of the FVC (FEF 25-75) and maximal FEF (FEF max). Participants also underwent assessment of the diffusing capacity of the lung for carbon monoxide (DLCO) and measurement of alveolar volume (TLC VA) using the single breath method.
Spirometry and DLCO measures were collected in accordance with the American Thoracic Society (ATS) standards,. Statistical Analysis Statistical analysis and graphic presentation were accomplished using SPSS (v 12.0, Chicago, IL) and Graphpad Prism (v 4.0, San Diego, CA). One-way analysis of variance (ANOVA) was used to test means across the groups with Bonferonni post-hoc analysis where appropriate. Unpaired t-tests were used to compare the control and the entire CHF group.
Partial correlations were calculated between radiographic measures and measures of HF severity adjusting for age, height, weight, body surface area, smoking history, and systolic and diastolic blood pressure. Standardized beta coefficients were calculated from linear regression. Fischer’s exact test was used to test for differences in categorical variables. Statistical significance was set at p. Population Characteristics The clinical characteristics of each study group are reported in. Notable differences include a lower body mass index for the control group compared to Group B (p.
Radiographic Evaluation The radiographic volumetric measurements are reported in. There were no differences between the groups for TTC volume (p=0.63).
The groups differed significantly in blood and parenchymal tissue, cardiac, and lung volumes expressed in absolute terms (p. Control Group A Group B p-value Absolute Volumetric Estimations Total Thoracic Volume (cm 3) 8445.0 ± 1496.8 8070.8 ± 1716. 6 8252.0 ± 1493.5 0.63 Blood and Tissue Volume (cm 3) 937.6± 134.2 997.5± 160.9 1049.4 ± 121.2. 0.03 Diaphragm Volume (cm 3) 942.6 ± 295.2 936.3± 331.4 1161.3 ± 493.2 0.09 Cardiac Volume (cm 3) 608.6 ± 156.7 978.7 ± 350.7.
1337.5 ± 384.0. † 0.001 Lung Volume (cm 3) 5956.3 ± 1197.2 5158.5 ± 1422.4 4703.8 ± 1361.3. 0.003 Percent of Total Thoracic Cavity Volume Blood and Tissue (%) 11.3 ± 2.1 12.8 ± 3.4 13.1 ± 2.6. 0.03 Diaphragm (%) 11.1 ± 2.7 11.8± 4.0 13.9 ± 5.1.
0.04 Cardiac (%) 7.3 ± 1.7 12.3 ± 4.4. 16.8 ± 6.0. †. Echocardiographic Evaluation The results of the primary structural echocardiographic evaluation are also shown in. The LV mass was greater in both HF groups compared to the CTL group (p.
Pulmonary Function Evaluation The results of the pulmonary function evaluation are detailed in. The HF group demonstrated primarily restrictive changes compared to the CTL group, noted by the reduction in the% predicted FVC, and FEV 1 with a comparable FEV 1/FVC ratio. Group A demonstrated a reduced FEF 25-75 compared to the CTL group (p. Control Group A Group B p-value FVC (L) 4.24 ± 1.05 3.43 ± 1.03. 3.44 ± 1.42. 0.003%Pred 105.9 ± 13.1 85.2 ± 16.8. 78.9 ± 21.9.
Comparison of Radiographic and Echocardiographic Measures of Cardiac Size in Predicting Lung Volumes and Restrictive Pulmonary Changes details the partial correlation coefficients between the TLC R, TLC VA, and DLCO and the radiographically and echocardiographically determined cardiac size. This analysis highlights the negative relationship between lung volume and cardiac size, although the echocardiographically determined measures of cardiac size did not correlate with the% predicted TLC VA. There also was a significant relationship between DLCO and left atrial dimension and the absolute cardiac volume. The relationship with the absolute cardiac volume however was no longer significant but rather demonstrated a trend after correcting for TTC volume. Partial Correlation p-value Standardized Beta Coefficient t-statistic p-value TLC R LA Dimension (mm) -0.52.
indicates radiographic measures. Outlines the relationship between FVC, FEV 1, and FEF 25-75 and radiographically and echocardiographically determined cardiac size. The partial correlation coefficient suggests a close relationship between both the radiographically determined cardiac volume and FVC. There was also a close correlation between the echocardiographically determined LV Mass and LV Mass Index and FVC. There were no significant relationships between radiographically and echocardiographically determined cardiac dimensions and FEF 25-75. The partial correlation analysis demonstrated a minor trend towards a significant relationship between FEF 25-75 and left atrial dimension although there were no other significant relationships.
Partial Correlation p-value Standardized Beta Coefficient t-statistic p-value FVC LA Dimension (mm) -0.42 0.005 -0.30 -2.11 0.04 LV Mass Index (g/m 2) -0.31 0.05 0.95 2.46 0.02 Cardiac Volume (cm 3).0.40 0.008 0.92 3.59. Correlation between the percent of the TTC volume that is taken up by the heart and the radiographically determined TLC.
Correlation between the percent of the TTC volume that is taken up by the heart and the spirometrically determined percent predicted FVC. Correlation between the TTC volume that is taken up by the heart and the TLC measured as the percent predicted alveolar volume. Correlation between the percent of the TTC volume that is taken up by the heart and the spirometrically determined percent predicted FEV 1. Primary Findings Chronic heart failure often results in restrictive and to a lesser degree obstructive changes in pulmonary function. Heart failure also is associated with gas exchange abnormalities including reductions in DLCO. Reasons for these changes in lung function are likely multifactorial, particularly during times of decompensation.
However, in stable, well managed HF patients who are not morbidly obese and who have a limited smoking history, increased cardiac volume may play an important role in reducing maximal lung volumes and to a lesser extent maximal airflows. It is possible that the association observed between lung function and cardiovascular mortality in large epidemiological studies, including those associated with the Cardiovascular Health Study and Framingham Heart Study, may be partially due to this link with cardiac size, which is also associated with severity of heart failure.
The findings of the present study suggest that although newer echocardiographic derived measures of cardiac dimensions appear to be associated with lung function, these measures are less predictive than radiographically determined cardiac volume. The reasons for the more predictive nature of the radiographic estimation of cardiac size may be due to the incorporation of the entire cardiac mass as opposed to individual chamber assessment as well as the normalization of the heart and lung estimations for the total thoracic volume.
Results of Epidemiological Studies in Relation to Pulmonary Function In a prospective follow-up of approximately 2,500 individuals over 5 years, Beaty and colleagues demonstrated that pulmonary function impairment is a significant risk factor for short- and long-term morbidity and mortality, despite adjustment for potential confounding factors such as age, gender, and smoking status. These authors suggest that impairment of pulmonary function not only contributes to morbidity and mortality independently but also does so through its pathogenic contribution to several non-respiratory diseases. This relationship also has been documented in patients at risk for myocardial infarction and sudden death, those with obstructive airway disease, and those with lung cancer.
Thus it is apparent that pulmonary limitations, including those of a restrictive nature, not only act as a marker of underlying disease but also significantly elevate an individuals risk for morbidity and mortality independently. Pulmonary Function Changes in Chronic Heart Failure A number of studies have examined the baseline changes in pulmonary function in patients with CHF. These include relatively minimal change compared to age and height predicted measures, primarily restrictive abnormalities, obstructive changes, and combined restrictive and obstructive alterations.
It is apparent that disorders of the heart frequently contribute detrimentally to the pulmonary system. Although the specific mechanisms causing altered lung function in HF are not entirely clear, these changes have been ascribed to respiratory muscle weakness, chronic pulmonary congestion and hypertension, changes in lung fluid balance, as well as neurohumoral changes -. However, because the pulmonary and cardiac systems are hemodynamically and mechanically linked, it would be expected that progressive increases in cardiac volume within a closed thoracic cavity may contribute to the pulmonary function abnormalities in HF patients. One would expect such changes in cardiac size to result in primarily restrictive lung changes manifested as reductions in TLC as well as VC. Influence of Heart Size on Restrictive and Obstructive Pulmonary Function Changes Cardiac enlargement, commonly seen in HF, leads to reductions in intrathoracic space and limits the ability of the lungs to fill adequately.
This could potentially reduce the effectiveness of the elastic recoil component of exhalation due to insufficient stretch of the lungs and result in reduced maximal expiratory flows,. The inability of the lungs to fill due to a mechanical limitation of space would be represented by primarily restrictive changes exhibited as reduced TLC, FVC, and FEV 1. As such, the present study demonstrated significantly reduced TLC in HF patients, measured either as the radiographically estimated volume and reported as a percent of the total thoracic cavity or total alveolar volume from single breath gas dilution. Also, our results suggest that both TLC measures were closely related to the radiographically determined absolute cardiac size and the cardiac size in relation to the thoracic cavity. Similar to the findings of Ulrik and colleagues who demonstrated no relationship between LV end-diastolic volume and indices of pulmonary function, the results of this study do not demonstrate a significant relationship with TLC and the echocardiographically determined measures of cardiac size. In support of the relationship between cardiac size and restrictive alterations of pulmonary function, we noted significantly reduced FVC and FEV 1in the HF patients as compared to the control group. Further, as is typical of a restrictive pattern of pulmonary dysfunction, both the FVC and FEV 1 were reduced proportionately resulting in a normal FEV 1/FVC ratio.
When examining the reduction of FVC and FEV 1 in relation to the radiographically and echocardiographically determined cardiac size it was apparent that the strongest predictor of reduced FVC and FEV 1 was the radiographically determined cardiac size reported as a percentage of the total thoracic cavity volume. These results are consistent with a previous study by Hosenpud and colleagues who have shown a significant relationship between the difference in heart size before and after transplantation and the change in FVC as well as significant proportional improvements in FVC and FEV 1 associated with cardiac transplantation, in HF patients. However, this relationship described by Hosenpud et al. Could also have been related to factors other than cardiac size, such as reduced lung congestion and lower pulmonary vascular pressures. The relationship with lung function would also be influenced by factors such as the size of the donor heart relative to the previous heart size and the general size of the thoracic cavity.
The present study focused on the impact of cardiac size alone and controlled for the size of the thoracic cavity. In addition, the potential for bias related to the size of the post-transplant heart or post-transplant changes in hemodynamic status is minimized by evaluating hemodynamically stable and optimally managed patients. With this, there was relatively little difference between the three groups with regard to LV filling pressures. Although there was a significant difference in the early mitral inflow velocity (E-wave) between Group B and the control participants these results do not account for the differences in heart size or relationships between heart size and pulmonary function as seen between the two heart failure groups. These results would suggest that the cardiac volume, as opposed to LV filling pressure, plays a larger role in the reduction of pulmonary function in this population. Further, in contrast to previous reports, the present study also demonstrates the relationship between heart size and maximal airflows and DLCO. The present study uses a more comprehensive radiographic volumetric assessment of cardiac size and compares this to the more commonly reported echocardiographic measure of LV mass.
The echocardiographic LA dimension, LV mass and LV mass index also showed a significant correlation (albeit less than the total radiographically determined cardiac size) with the reductions in FVC and FEV 1, supporting the relationship between heart size and lung volumes. The results of this study also demonstrate that the percent predicted mean forced expiratory flow during the mid portion of the FVC (FEF 25-75) as well as the DLCO were significantly reduced in our HF patients as compared to the control group. The relatively similar reduction in FEF 25-75 compared to the reduction in FEV 1 suggests a pure restrictive breathing pattern, with no evidence of significant airway involvement. This is consistent with previous findings from our group in which we found minimal obstructive changes in a stable, non-smoking HF population. Importantly the forced expiratory airflows were not apparently related to cardiac size measured either by radiographic or echocardiographic methods. In contrast, the radiographically determined cardiac size and echocardiographically determined LA diameter were related to the DLCO. Agostoni and colleagues have shown that the cardiothoracic index is an independent predictor of DLCO; however when corrected for alveolar volume these relationships were lost or greatly reduced.
Thus, elevated cardiac size likely plays a role in the reduced DLCO by a direct mechanical compression of the lung resulting in reduced alveolar volume and overall TLC with subsequent limitation of membrane diffusion capacity. Conversely, It has also been suggested that an acute reduction in cardiac size by transplantation results in either no change or significant reduction in DLCO, however, these findings have been attributed to significant pulmonary vascular structural changes associated with disease severity. Potential Limitations A potential limitation of this study is the relationship between total body weight and pulmonary function. It is well known that obesity can result in similar pulmonary function changes as those observed in this study.
The HF patients in this study were significantly heavier than the control group. In an effort to control for this difference, as well as other potentially confounding factors, the regression analyses were adjusted for age, height, weight, body surface area, systolic blood pressure, and diastolic blood pressure. Thus, the results presented demonstrate relationships which are independent of these potentially confounding influences. Clinical Implications It is clear that the HF associated changes in cardiac size within a closed thoracic cavity pose significant constraints on the lungs and result in reductions in lung volumes and contributes to the overall restrictive breathing pattern often reported in heart failure patients. In addition, the cardiomegaly associated changes in lung function may contribute to the inspiratory load, result in low lung volume breathing, limit the encroachment on the inspiratory reserve volume during times of increased ventilatory demand, and contribute to symptoms of dyspnea.