1 / 34

COPD and heart failure

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.

lucien
Télécharger la présentation

COPD and heart failure

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. COPD and heart failure Jelena Ostojić, MD, University hospital “Sestre milosrdnice”, Department of Internal medicine, Zagreb, Croatia

  2. 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.

  3. 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

  4. Patients mainly die of nonrespiratory diseases. • Cardiovascular diseases: 25% • Cancer (lung cancer): 20-33% • Respiratory diseases (respiratory failure during exacerbations): 4-35%

  5. 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

  6. Low grade systemic inflammation • COPD: inverse ratio between FEV1 and circulating CRP • Coronary atherosclerosis, ischaemic CMP • FEV1 is as good predictor of cardiovascular mortality as serum cholesterol Hole DJ. BMJ 1996;313:711-5

  7. Prevalence of COPD in patients with HF

  8. Prevalence of COPD in patients with HF • Prevalence of COPD is greater in: more recent studies • Greater awareness? • Ageing population? • Up to one third of patients labelled with COPD do not fulfill GOLD criteria

  9. Prevalence of COPD in patients with HF • Among 219 patients discharged from tertiary US centre with both HF and COPD: • 82% recieved echocardiography • 36% pulmonary function testing Damarla M, Celli BR. Respir Care 2006;51:1120-1124

  10. Prevalence of COPD in patients with HF • COPD strongly predicts hospitalisation rate and duration and non-cardiovascular mortality • 5-year mortality as high as 69% (58% in patients without COPD) • Respiratory infections associated with cardiac decompensations in 10-16% admissions Nieminen MS. Eur Heart J 2006;27:2725-2736

  11. Prevalence of heart failure in COPD patients • 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

  12. Typical clinical features: dyspneain COPD. High energy demands on respiration • High pressure output of inspiratory muscles during resting breathing • High oxygen cost • Inspiratory flow resistance increased • Static hyperinflation (loss of elastic recoil) • High minute ventilation • Dynamic hyperinflation (expiratory flow limitation)

  13. Dyspnea in COPD: hyperinflation • Smaller zone of apposition • Decrease in the curvature of the diaphragm • Increased elastic recoil of the thoracic cage • Worsening of the length-tension relationship

  14. Dyspnea in COPD: respiratory pressure generation • Inspiratory muscles adapted to hyperinflation (shortening of diaphragmatic sarcomeres, decrease in number) • Parallel reductions in maximal inspiratory and expiratory pressures: generalised muscle weakness • Electrolyte disturbancies • Blood gas abnormalities • Cardiac decompensation • Weight loss with muscle waisting • Steroid myopathy

  15. Dyspnea in COPD: malnutrition • 20% of stable patients, 70% patients requiering mechanical ventilation: weight loss, muscle waisting • Decrease in muscle mass despite normal BMI • Inspiratory muscle stength decreased about 30% • Decrease in type IIb fibers (fatigue sensitive) • Relative increase in type I and IIa fibers (fatigue resistent) • Decrease in total muscle force output

  16. Dyspnea in COPD: malnutrition TNF-α • Decrease in muscle anabolism • Increase in muscle catabolism • NF-κB, ubiquitin-proteasome pathway • Insulin resistance • Decrease in thyreoid hormones • Increase in glucagon, cortisol, corticosterone, occasionaly catecholamines • Inhibition of contractility

  17. Dyspnea in COPD: steroid myopathy • 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

  18. Dyspnea in acute respiratory failure • Inspiratory effort equally divided in offsetting • 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

  19. Dyspnea in chronic heart failure elevated pLA increased lung stiffness postcapillary reversible pulmonary hypertension bronchial congestion compensatory vascular remodelling

  20. Dyspnea in chronic heart failure • Low cardiac output • Inspiratory muscle weakness • Fewer type II fibers (2.0 times more force than type I fibers) • Reduced cross-sectional area of rib cage muscles and diaphragm • Decreased regional blood flow • Structural abnormalities of diaphragmatic fibers (idiopathic dilated CMP) • Hyperpnea predisposes hyperinflation • Decreased static lung compliance • Increased respiratory work • Atrophy of limb muscle fibers

  21. Diagnostic pitfalls: radiology • 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

  22. Diagnostic pitfalls: echocardiography, CMR • Inadequate visualisation related to air trapping (10-50%) • High cost of comprehnsive echo-Doppler cardiac examination • Limited examination? • Cardiac magnetic resonance imaging

  23. Diagnostic pitfalls: natriuretic peptides • Prognostic information • Monitoring therapy • Screning for subclinical disease • Up to 50% patients with LV disfunction • High negative predictive value for ruling out HF

  24. Diagnostic pitfalls: natriuretic peptides • atrial natriuretic peptide, ANP • stored in granules • released with minor triggers (eg. exercise) • B-type natriuretic peptide, BNP • minimal storage • released in bursts biologically active BNP volume expansion, pressure overload pre-proBNP proBNP wall stress NTproBNP

  25. Diagnostic pitfalls: natriuretic peptides • BNP: half-life of 20 min • NTproBNP: half-life of 1-2hr • Increased levels with age, in women • ARDS, right HF: elevation within the gray zone • Acute coronary syndrome:elevated BNP in the absence of concomitant HF • Sepsis

  26. Evaluation of HF during COPD exacerbation BNP (pg/ml) <100 100-500 >500 HF unlikely R or moderate L HF overt L HF ACE inhibition, diuretics 2D Doppler echocardiography

  27. Safety of drug cocktails: ACE inhibitors • 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

  28. Safety of drug cocktails: beta-blockers B1B • 20-fold higher affinity for B1R than B2R • Lose selectivity at the high end of dose ranging • Patients with mild to severe COPD: free of adverse respiratory effects, FEV1 unchanged • Do not attenuate B2R agonist-induced bronchodilatation Nonselective BB with alpha blockade • Attenuate B2R agonist-induced bronchodilatation • Data regarding carvedilol in COPD? Camsari A.Heart vessels 2003;18:188-92

  29. Safety of drug cocktails: concomittant use of BB with inhaled beta-agonists • B2B agonists increase risk for CHF decompensation and all-cause mortality in CHF • 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

  30. Safety of drug cocktails: beta-blockers • Selective B1B should not be withheld in patients with moderate-to-severe COPD • Real life: less than 10% of patients with COPD recieve BB

More Related