Transcript COPD and heart failure - Združenje pnevmologov Slovenije

COPD and heart failure
Jelena Ostojić, MD,
University hospital “Sestre milosrdnice”, Department of
Internal medicine, Zagreb, Croatia
COPD: definition
Preventable and treatable disease with some significant
extrapulmonary effects that may contribute to the
severity in individual patients.
Its pulmonary component is caracterised by airflow
limitation that is not fully reversible. The airflow
limitation is usually progressive and associated with
an abnormal inflammatory response of the lung to
noxious particles or gases.
COPD: epidemiology
•
Fourth commonest cause of death
•
By year 2020. will be ranked third
and fifth of the worldwide burden of
disease
•
Rising prevalence among women
Patients mainly die of nonrespiratory
diseases.

Cardiovascular diseases: 25%

Cancer (lung cancer): 20-33%

Respiratory diseases (respiratory failure during
exacerbations): 4-35%
Ignored combination

Prevalence of COPD ranges from 20-32% in
CHF

Risk ratio of developing CHF is 4.5 in COPD

Tobacco use
Global epidemics
Almost half of people aged 65 yrs or more: at least 3 chronic
medical conditions


Rutten FH. Am Heart J 2002;143:412-7, O’Connor CM.J Card Fail 2005;11:200-5,
Gustaffson F. Eur Heart J 2004;25:129-35
Low grade systemic inflammation
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COPD: inverse ratio between FEV1 and circulating CRP
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Coronary atherosclerosis, ischaemic CMP
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FEV1 is as good predictor of cardiovascular mortality as
serum cholesterol
Hole DJ. BMJ 1996;313:711-5
Prevalence of COPD in patients with
HF
reference
Prevalence (%)
country
Data collection
n
population
Data source
Bangdiwala
15
USA, Canada
1988-1989
6273
HF
hospitalisation
SOLVD
Registry
Auerbach
19
USA
1989-1994
1298
HF
hospitalisation
SUPPORT
Study
Vaccarino
27
USA
1994-1995
2445
HF
hospitalisation
Conneticut
Peer Review
Org
Gambassi
19
USA
1992-1996
86 094
outpatient
SAGE Database
Baker
25
USA
1991-1997
23 505
HF
hospitalisation
Cleveland
Health Quality
Choice
Program
Kosiborod
33
USA
1992-1999
3 957 520
HF
hospitalisation
Medicare
Havranek
33
USA
1993-1999
34 587
HF
hospitalisation
National Heart
Failure Project
Kamalesh
52
USA
1999-2000
495
outpatient
Indianapolis
Veterans
Affairs Medical
Centre
Lee
21
Canada
1999-2001
2624
HF
hospitalisation
EFFECT study
Brown
12
Scotland
1995
27 477
HF
hospitalisation
Scottish
Morbidity
Record
Gustaffson
22
Denmark
1993-1996
5491
HF
hospitalisation
DIAMOND-CHF
Registry
Prevalence of COPD in patients with
HF
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Prevalence of COPD is greater in: more recent
studies


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Greater awareness?
Ageing population?
Up to one third of patients labelled with COPD do
not fulfill GOLD criteria
Prevalence of COPD in patients with
HF
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Among 219 patients discharged from tertiary US
centre with both HF and COPD:
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82% recieved echocardiography

36% pulmonary function testing
Damarla M, Celli BR. Respir Care 2006;51:1120-1124
Prevalence of COPD in patients with
HF

COPD strongly predicts hospitalisation rate and
duration and non-cardiovascular mortality
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5-year mortality as high as 69% (58% in patients
without COPD)
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Respiratory infections associated with cardiac
decompensations in 10-16% admissions
Nieminen MS. Eur Heart J 2006;27:2725-2736
Prevalence of heart failure in COPD
patients
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
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Cigarette smoking is associated with 50% increased
risk of HF
Prevalence of unrecognised HF in COPD patients
presenting to the ED with acute dyspnea: 20.9%
Unrecognized HF: cause of AECOPD or weaning
difficulties in COPD
McCollough PA. Acad Emerg Med 2003;10:198-204
Typical clinical features: dyspnea
in COPD. High energy demands on respiration

High pressure output of inspiratory muscles
during resting breathing
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High oxygen cost
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Inspiratory flow resistance increased
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Static hyperinflation (loss of elastic recoil)
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High minute ventilation
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Dynamic hyperinflation (expiratory flow limitation)
Dyspnea in COPD: hyperinflation
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Smaller zone of apposition
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Decrease in the curvature of the diaphragm
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Increased elastic recoil of the thoracic cage
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Worsening of the length-tension relationship
Dyspnea in COPD:
respiratory pressure generation

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Inspiratory muscles adapted to hyperinflation
(shortening of diaphragmatic sarcomeres, decrease in
number)
Parallel reductions in maximal inspiratory and
expiratory pressures: generalised muscle weakness

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Electrolyte disturbancies
Blood gas abnormalities
Cardiac decompensation
Weight loss with muscle waisting
Steroid myopathy
Dyspnea in COPD:
malnutrition
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20% of stable patients, 70% patients requiering
mechanical ventilation: weight loss, muscle waisting
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Decrease in muscle mass despite normal BMI
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Inspiratory muscle stength decreased about 30%
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Decrease in type IIb fibers (fatigue sensitive)
Relative increase in type I and IIa fibers (fatigue
resistent)
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Decrease in total muscle force output
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Dyspnea in COPD:
malnutrition
TNF-α
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Decrease in muscle anabolism
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Increase in muscle catabolism
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


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NF-κB, ubiquitin-proteasome pathway
Insulin resistance
Decrease in thyreoid hormones
Increase in glucagon, cortisol, corticosterone, occasionaly
catecholamines
Inhibition of contractility
Dyspnea in COPD:
steroid myopathy


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Mainly type IIb fibers
Minimum dose that causes steroid myopathy is not
known
It takes 2-3 months to recover
Nava S. Eur Respir J 2002;20:497-499
Dyspnea in acute respiratory failure
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Inspiratory effort equally divided in offsetting



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Intrinsic PEEP
Elastic recoil
Inspiratory resistance
Abnormal mechanics (bronchoconstriction, bronchial edema,
pulmonary edema, lung inflammation)
Rapid shallow breathing aggravates abnormalities in lung
elastance, intrinsic PEEP, CO2 clearance

Expiratory muscle recruitment increases intrinsic PEEP
and breathing effort

Increased CO2 production, deadspace ventilation, elevated
respiratory drive
Dyspnea in chronic heart failure
elevated pLA
increased lung stiffness
postcapillary reversible
pulmonary hypertension
bronchial congestion
compensatory vascular
remodelling
Dyspnea in chronic heart failure

Low cardiac output
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Inspiratory muscle weakness
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Fewer type II fibers (2.0 times more force than type I fibers)
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Reduced cross-sectional area of rib cage muscles and diaphragm
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Decreased regional blood flow
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Structural abnormalities of diaphragmatic fibers (idiopathic dilated
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Hyperpnea predisposes hyperinflation
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Decreased static lung compliance
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Increased respiratory work
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Atrophy of limb muscle fibers
CMP)
Diagnostic pitfalls: radiology

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Chest hyperinflation reduces cardiothoracic ratio
Pulmonary vascular remodelling and radiolucent
lung fields mask typical alveolar shadowing in
pulmonary oedema
Asymetric, regional and reticular patterns of
pulmonary oedema
Vascular bed loss with upper lobe venous
diversion mimics HF
Diagnostic pitfalls: echocardiography,
CMR

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Inadequate visualisation related to air trapping (1050%)
High cost of comprehnsive echo-Doppler cardiac
examination
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Limited examination?
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Cardiac magnetic resonance imaging
Diagnostic pitfalls: natriuretic peptides
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Prognostic information
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Monitoring therapy
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Screning for subclinical disease
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Up to 50% patients with LV disfunction
High negative predictive value for ruling out HF
Diagnostic pitfalls: natriuretic peptides
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atrial natriuretic peptide, ANP


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stored in granules
released with minor triggers (eg. exercise)
B-type natriuretic peptide, BNP


minimal storage
released in bursts
volume expansion,
pressure overload
biologically active
BNP
pre-proBNP
proBNP
wall stress
NTproBNP
Diagnostic pitfalls: natriuretic peptides
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BNP: half-life of 20 min
NTproBNP: half-life of 1-2hr
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Increased levels with age, in women
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ARDS, right HF:
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Acute coronary syndrome: elevated BNP in the absence
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Sepsis
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of concomitant HF
elevation within the gray zone
Evaluation of HF during COPD
exacerbation
BNP (pg/ml)
<100
HF unlikely
100-500
R or moderate L
HF
>500
overt L HF
ACE inhibition, diuretics
2D Doppler echocardiography
Safety of drug cocktails: ACE
inhibitors
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Cornerstone of treatment in CHF
May prevent SM atrophy and improve respiratory
muscle strength
No increased risk of cough and bronchospasm
Anker SD.Lancet 2003;361:1077-83.
Packard A. Ann Pharmacother 2002;36:1058-67
Safety of drug cocktails: beta-blockers
B1B
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20-fold higher affinity for B1R than B2R
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Lose selectivity at the high end of dose ranging
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Patients with mild to severe COPD: free of adverse respiratory
effects, FEV1 unchanged
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Do not attenuate B2R agonist-induced bronchodilatation
Nonselective BB with alpha blockade
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Attenuate B2R agonist-induced bronchodilatation
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Data regarding carvedilol in COPD?
Camsari A.Heart vessels 2003;18:188-92
Safety of drug cocktails: concomittant
use of BB with inhaled beta-agonists
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B2B agonists increase risk for CHF decompensation
and all-cause mortality in CHF
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Combination with nonselective BB: beneficial?

Both selective and nonselective BB with alpha
blockade are to be avoided during COPD
exacerbation due to the insufficient safety data
Au DH. Chest 2003;123:1964-9
Safety of drug cocktails: beta-blockers
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Selective B1B should not be withheld in
patients with moderate-to-severe COPD
Real life: less than 10% of patients with
COPD recieve BB