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Unformatted text preview: MD Seminar
Pulmonary manifestation of
Dr. Gaurav Prakash
April 8,2006 Pulmonary circulation.
Low pressure & high flow system
Range mean Pulm art pressure
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.
1. Mitral valve diseases
-pericardial restriction. Starling principle and interstitial fluid
micro-vascular filtration and lymph flow. α Capillary pressure
micro. Pulmonary venous hypertension
Fluid in interstitial space
Peri-bronchial and peri-vascular spaces
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
animals) (Broaddus VC, J appl Physiol.)
Physiol.) Resorption into blood vessels
expectoration Histo-pathologic change in PVH
PVH→ excess interstitial edema →organized and form
Medial hypertrophy of muscular pulmonary arteries.
Muscularisation of smaller branches → narrowing.
Sustained hypertension---- stimulates growth factor release
Sustained hypertension---e.g. fibronectin ,tenascin – C + release of endogenous serine
Serine elastase breaks internal elastic lamina.
Now growth factors directly stimulate muscular layer of
B.vessels. 3 Pulmonary capillary stress failure
changes in blood gas barrier
Pulmonary venous hypertension ↓
Disruption of endothelial and alveolar
epithelial layer ↓
Thickening of basement membrane
( pars dense)
Changes in gene expression for extra-cellular matrix protein.
extra- Pulmonary hemodynamics
pressure = flow x resistance
Resistance = pressure / flow.
Pulmonary venous resistance (PVR)
Measured in “wood units”
Which is “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
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.
Early in course recurrent pulmonary
edema Over next few years Less severe episodes.
Ongoing remodeling Old cases Infrequent pul.edema
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
IV Acute pulmonary edema.
Only one case report: reduction in all volumes
( 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
not increase (unlike ILD).
REASON: simultaneously existing resp muscle
dysfunction in CHF. 7 Pulmonary function abnormality
respiratory muscle weakness.
Meyer etal (circulation ,2001)
Max insp pressure (MIP)—diaphragm— alt test SNIFF
Max. exp.pressure (MEP)—Truncal muscle—
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
functional changes in muscle cells.
e.g. atrophy of type 1 muscle fibers. 8 Pulmonary function abnormality
DLCO = overall alveolar capillary conductance
--------------------------------------------------------PULMONARY RESISTANCE TO GAS TANSFER: 1/ DLC0 = 1 / DM + 1 / VC
DM= membrane diffusive conductance.
VC= red cell conductance ( pulmonary capillary volume)
red Pulmonary function abnormality
DLCO NYHA III NYHA IV 80 72 71 68 35 61 77 129 87 (%CONTROL)
(%CONTROL) 9 Role of angiotensis system
ACE -converts angiotensin
bradykinin. 2 weeks of enalapril therapy (Guazzi etal circulation,1997) CHF patient
96% DLCO Change Only sys HTN, no
No change blocked by asprin
no effect from ARB
MECHANISM : ACE gene polymorphism
(DD,ID,II) DD genotype -- higher ACE levels, low DLCO, FEV1, VO2. PULMONARY SYMPTOMS OF HEART
↑ respiratory resistance ( upto 80%) on lying supine, which was reversed on
sitting up. Normal
SITTING CHF SUPINE SITTING SUPINE Breathlessn 0
(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 )
FEV1 / FVC ratio studied.
Rise from 66% to 71% after treatment of acute LVF.
overall pattern is restrictive
(1)FEV1/FVC = 80%
Increased methacholine responsiveness
blocked by methoxamine ( alpha agonist) inference: mucosal vessel dilation , generalized mucosal
swelling. PULMONARY SYMPTOMS OF HEART
DISEASES: poor exercise tolerance.
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
(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.
(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
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 OSA- 11%
OSA- Effect of hypoxia on heart.
increased sympathetic stimulation. 12 Unusual manifestations.
Hemosidrosis from microvascular hemorrhage.
(may be visible as small nodules on CxR.)
OSSIFIC NODULES : consist of lamellated bone
that forms with in alveoli...........(irregular
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.
– 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:
– 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
– Predictor of adverse outcome in CHF pts.
(Maisel etal, NEJM,2002)
etal, 16 ...
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This note was uploaded on 12/03/2011 for the course MEDICINE 350 taught by Professor Dr.aslam during the Winter '07 term at Medical College.
- Winter '07