pulm_HD - MD Seminar Pulmonary manifestation of cardiac...

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Unformatted text preview: MD Seminar Pulmonary manifestation of cardiac diseases. cardiac Dr. Gaurav Prakash April 8,2006 Pulmonary circulation. Low pressure & high flow system Range mean Pulm art pressure (mmhg) mmhg) 25/10 15 P.Capillary pressure 6- 9 7 P. Venous pressure 1- 4 2 P. vascular resistance (PVR) 1- 4 3 P. Blood flow (L/min) 4- 6 5 1 Causes Main way by which heart influence lung is by increasing pulmonary venous pressures. Main causes: 1. Mitral valve diseases 2. CHF -IHD -cardiomyopathy -myocarditis -pericardial restriction. Starling principle and interstitial fluid dynamics dynamics micro-vascular filtration and lymph flow. α Capillary pressure micro. Pulmonary venous hypertension ↓ Fluid in interstitial space ↓ Alveolar septae ↓ Peri-bronchial and peri-vascular spaces Periperi↓ Via lymphatics to systemic veins (safety valve) in heart failure, systemic venous pressures are elevated This impair with proper lymphatic drainage. This 2 Safety factors Extremely low permeability of alveolar epithelium. Active Na+ transport by alveolar epithelial cell. Perimicrovascular and peribronchial interstitial compliance Pleural spaces ( 25% of pulm edema fluid in experimental 25% animals) (Broaddus VC, J appl Physiol.) Physiol.) Resorption into blood vessels expectoration Histo-pathologic change in PVH PVH→ excess interstitial edema →organized and form hyaline material. Medial hypertrophy of muscular pulmonary arteries. Muscularisation of smaller branches → narrowing. MECHANISM Sustained hypertension---- stimulates growth factor release Sustained hypertension---e.g. fibronectin ,tenascin – C + release of endogenous serine e.g. elstase. elstase. Serine elastase breaks internal elastic lamina. Serine Now growth factors directly stimulate muscular layer of Now B.vessels. 3 Pulmonary capillary stress failure changes in blood gas barrier changes Pulmonary venous hypertension ↓ Disruption of endothelial and alveolar epithelial layer ↓ Thickening of basement membrane ( pars dense) pars ↓ Alveolar fibrosis. MECHANISM: Changes in gene expression for extra-cellular matrix protein. extra- Pulmonary hemodynamics Poiseuille equation pressure = flow x resistance OR Resistance = pressure / flow. Pulmonary venous resistance (PVR) Measured in “wood units” units” Which is “mmhg/ l/min” mmhg/ l/min” In normal adults PVR = 1 wood unit. 4 Pulmonary hemodynamics Butler etal (J Am coll Card,1999) Controls CHF 35 13.7 At Rest 12 24 At exersice 30 38 PVR ( woods unit) At rest Resistance = pressure / flow. 1.0 1.9 At max exersice. exersice. 0.6 2.0 O2 uptake (ml/min/kg) PA pressure (mmhg) (mmhg) Fall in PVR was not seen in patient of CHF. Inference : in CHF recruitment of reserve cap beds is not possible because of elevated resistance in pulm circulation. Sustained PHT : effect Gibbs etal ( J Am Col Card,1990) Studied level of pulm pressure in day to day activities. Peak tredmill pressure 100% Climbing stairs 90 % Walking at level ground 73% Lying supine 63% 63% Inference : these episodic rises in pressures; causes ongoing pulmonary vascular changes in otherwise compensated heart failure. 5 Natural history of PVH Prototype : severe Mitral stenosis. stenosis. Early in course recurrent pulmonary edema Over next few years Less severe episodes. Ongoing remodeling Old cases Infrequent pul.edema pul.edema Severe PAH Cor pulmonale Pulmonary complication of PVH 6 Pulmonary function abnormality Changes in lung volume. CHF / MS (Am J Respir Crit Care,2000) as disease progressed NYHA I TLC↓ TLC ERV↓ ERV RV↑ RV FRC→ FRC IV IV Acute pulmonary edema. no studies. no Only one case report: reduction in all volumes Only ( Br Heart J,1951) Pulmonary function abnormality change in lung compliance alveolar destruction and fibrosis produced by PVH. ↓ Reduction in lung compliance. ↓ Results in low TLC and VC NOTE: Despite fibrosis; lung recoil pressures do NOTE: not increase (unlike ILD). REASON: simultaneously existing resp muscle REASON: dysfunction in CHF. 7 Pulmonary function abnormality respiratory muscle weakness. Meyer etal (circulation ,2001) Max insp pressure (MIP)—diaphragm— alt test SNIFF (MIP)— diaphragm— Max. exp.pressure (MEP)—Truncal muscle— (MEP)— muscle— COUGH 2yr prospective study of CHF pt. Non surviver ( n=57) MIP 60% control Survivor ( n=187) MIP 77%control Pulmonary function abnormality respiratory muscle weakness. McPortland Hughes Hammond VC % pred 93 86 60 MEP %control 100 80 49 MIP % control 81 76 40 MIP is sensitive indicator of 1 year survival. PATHOGENESIS : structural , biochemical and structural functional changes in muscle cells. e.g. atrophy of type 1 muscle fibers. 8 Pulmonary function abnormality diffusion capacity DLCO = overall alveolar capillary conductance overall --------------------------------------------------------PULMONARY RESISTANCE TO GAS TANSFER: 1/ DLC0 = 1 / DM + 1 / VC DLC0 DM DM= membrane diffusive conductance. membrane VC= red cell conductance ( pulmonary capillary volume) red Pulmonary function abnormality diffusion capacity NYHA II DLCO NYHA III NYHA IV 80 72 71 68 35 61 77 129 87 (%CONTROL) (%CONTROL) DM (%CONTROL) (%CONTROL) VC (%CONTROL) 9 Role of angiotensis system ACE -converts angiotensin -inactivate bradykinin. bradykinin. 2 weeks of enalapril therapy (Guazzi etal circulation,1997) CHF patient 84% 96% 96% DLCO Change Only sys HTN, no CHF No change blocked by asprin no effect from ARB MECHANISM : ACE gene polymorphism ACE (DD,ID,II) DD genotype -- higher ACE levels, low DLCO, FEV1, VO2. PULMONARY SYMPTOMS OF HEART DISEASE: Orthopnea DISEASE Elevated diaphragm. ↑ respiratory resistance ( upto 80%) on lying supine, which was reversed on sitting up. Normal SITTING CHF SUPINE SITTING SUPINE Breathlessn 0 ess (VAS) (VAS) 0 2.2 3.9 VC (L) 4.5 4.4 2.6 2.4 FRC (L) 3.7 3.05 3.3 3.1 97 76 66 FEV1(%pred) 103 10 PULMONARY SYMPTOMS OF HEART DISEASE : wheeze DISEASE ACUTE LVF: -geometric narrowing of airways -increased vagal tone -- bronchoconstriction (arch int med ) Light &George Light (arch FEV1 / FVC ratio studied. FEV1 Rise from 66% to 71% after treatment of acute LVF. Rise CHF: overall pattern is restrictive (1)FEV1/FVC = 80% (2)TLC reduced. Increased methacholine responsiveness blocked by methoxamine ( alpha agonist) inference: mucosal vessel dilation , generalized mucosal swelling. PULMONARY SYMPTOMS OF HEART DISEASES: poor exercise tolerance. DISEASES AT REST : -low O2 ( Increasing with clinical severity of CHF) -no change in PaCO2. -rise in lactate levels ( low pH) AT EXERCISE: - low PaO2 ( unrelated to clinical severity ) - low PCO2 levels - earlier and higher rise in lactate levels. Cause : (1) no recruitment of blood flow at apex during exercise (2) regional VA/ Q mismatch. (Wasserman etal, circulation,1997) etal, 11 Interesting observation REGIONAL VARIATION IN VENTILATION SERIES OF 180 pts of CHF with cardiomegaly. cardiomegaly. (Alexander etal, BMJ,1989) (Alexander etal, Ventilation checked by Krypton 81m gas OBSERVATION 1 : reduction in left lower lobe ventilation in supine posture which improved on turning prone. OBSERVATION 2 : CHF pt with large LV avoid sleeping on left side. (Wiener etal Am Rev Respir Dis,1990) Sleep disorders in CHF Cheyne stokes resp-central sleep apnea ( CSR-CSA) respCSR• frequently observed in severe CHF. • more in CHF with large LV & high PCWP. • PATHOGENESIS: respiratory control instability that is PATHOGENESIS: caused by fluctuation of CO2 levels. Incidence in CHF: of CSA - 40 % of of OSA- 11% OSA- Effect of hypoxia on heart. Increased afterload increased sympathetic stimulation. 12 Unusual manifestations. Hemosidrosis from microvascular hemorrhage. (may be visible as small nodules on CxR.) CxR.) OSSIFIC NODULES : consist of lamellated bone that forms with in alveoli...........(irregular shapes) increased interstitial markings---- pulmonary markings---fibrosis. Lung disease or heart disease. Not uncommon diagnostic dilemma in EMOPD. Over all accuracy of clinical evaluation=70%. (Mulrow CD etal, J Gen Int Med). etal, on CxR extra shadows of coexisting lung disease may obscure pulmonary edema. Atypical pulmonary edema. 13 Atypical pumonary edema. 59/F, hypertensive, MR, resp failure. Atypical pumonary edema. 60/M, CAD , progressive dyspnea 14 Lung disease or heart disease. CT scan may help: characteristic finding in CHF. characteristic – Septal thickening – ground glass opacities. – Peri-bronchovascular interstitial thickening. Peri– Pleural effusion. – cardiomegaly Lung disease or heart disease. Pleural effusion: etio ?? CHF or lung dis. Indication for thoraco-centesis only if: – fever – unilateral effusion – B/L but sig. discrepancy in two side. 15 Lung disease or heart disease Role of B-type natriuretic peptide ( BNP) in emergency departments. – 80 to 90 % diagnostic accuracy – 96% negative predictive value at level <50 pg/ml. – Predictor of adverse outcome in CHF pts. (Maisel etal, NEJM,2002) etal, 16 ...
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