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Don’t Forget لا تنسوا أقصانا

Don’t Forget لا تنسوا أقصانا. Refractory Heart Failure. Prof. A. ABU-HASHEM (M.D. Cardiology) Zagazig, Egypt. “In these hearts …… their reserve force lost and with it the power of meeting the demands in maintaining the circulation during severe exertion”……. (Osler, 1892).

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Don’t Forget لا تنسوا أقصانا

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  1. Don’t Forget لا تنسوا أقصانا

  2. Refractory Heart Failure Prof.A. ABU-HASHEM(M.D. Cardiology)Zagazig, Egypt

  3. “In these hearts …… their reserve force lost and with it the power of meeting the demands in maintaining the circulation during severe exertion”……. (Osler, 1892).

  4. “ A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with requirements of the metabolizing tissues” (Braunlwald, 1986).

  5. Most cases of CHF respond favorably to pharmaco and non-pharmaco therapies. • Some do not improve or suffered from rapid recurrence despite optimal therapy and have symptoms at rest or minimal exertion, can not perform daily activities, frequently suffering from anasarca and cachexia and require repeated hospitalization; Refractory HF.

  6. EPIDEMIOLOGY • CHF is major cause of mortality and morbidity especially among elderly and is considered a serious health problem. • 4-7 million is USA have CHF. • 400,000 new cases every year. • CHF is the 1ry cause of death in 40,000 / year. • CHF is the most frequent cause of hospitalization in medicare population.

  7. EPIDEMIOLOGY • RHF accounts for 5% of symptomatic HF. • Incidence of RHF increases with age and is more in males. • Risk of death in mild CHF is 5-10% annually. • This increases much in RHF up to 50%.

  8. EPIDEMIOLOGY The burden associated with RHF is expected to increase due to : • Ageing of the population. • Increase numbers of elderly with CAD and HPN. • Improved diagnosis e.g echo.

  9. ETIOLOGY • Ischemic (extensive CAD, multiple MI). • Non-ischemic CM (younger, some with family history). • Hypertension. • Valvular. • Viral myocarditis.

  10. Precipitating (Aggravating) Factors. • Cardiac : arrhythmias, M.I. • Non cardiac : anemia, pul.embolism, infections, other illness. • Treatment-related: poor compliance, NSAID, steroids, B.B.

  11. Chamber dilatation Wall stress Vent-Dysfunction Toxic effects (Apoptosis, myocyte loss)  HR, Arrhythmia Neuro-hormones Renal Vasoconstriction H2o and Na retention Vasoconstriction (afterload) The vicious circle of pathophysiology

  12. Changes is the biology and volume of myocytes and non-myoctes components of the myocardium Changes in geometry ( from prolate ellipse to more spherical shape), volume and architexture Vent. Remodeling • Impairment of skeletal muscle metabolism. •  TNF… muscle atrophy. • Resulting in cachexia, and exercise intolerance More functional deterioration

  13. Symptoms of RHF • Dyspnea III or IV . • Orthopnea,PND,exertional and nocturnal dry cough. • Fatigue, weakness. • Dizzy spells or palpitations due to frequent tachyarrhythmias . • Fluid retentions, LL edema, ascites….

  14. Physical exam. • Increased JVP with prominent V-wave. • Generalized anasarca. • Cardiac dilatation, galloping and murmurs. • Fine lung crepitations. • Tender hepatomegaly.

  15. Functional evaluation • NYHA classification (insensitive, subjective) • Six-minute walk (<305 met. in 6 min.  bad prognosis). • Peak maximal oxygen utilization (MVO2 < 10 ml/kg/min in high risk pt.). • Exercise testing: modified Bruce or Naughton protocols (reduced speeds and slow increments). • Metabolic equivalents and work capacity (METs) are reduced.

  16. Diagnostic investigations • Confirm the clinical diagnosis. • Identify an underlying causes. • Identify precipitating factors. • Guide therapy. • Determine prognosis.

  17. ECG • Nonspecific ST- T changes. • Chambers enlargement. • Old MI. • BBB and other conduction defects. • Tachyarrhythmias: AF, A fl, VPCs, VT….

  18. Chest x-ray • Upper lobe congestion. • Interstitial edema. • Kerley’s A and B lines. • Pleural effusions.

  19. Echo Doppler • Dimensions, volumes, wall thickness. • Function: EF, FS, diastolic dysfunction. • Valvular structure and function. • Pressures: m PAP, RVSP. • Spont. echo contrast, masses, thrombi. • Pericardial diseases.

  20. TEE • Inadequate TTE. • Suspected IE. • Prosthetic valve function • LAA thrombi.

  21. Echo (cont.) • DSE: at low dose for detection of viable myocardium. • Myocardial tissue contrast: to detect ischemia and viability.

  22. Radionuclide scintigraphy • Non diagnostic echo study • RV functions • Viable myocardium • PET is more sensitive than Thallium- 201 study.

  23. Cardiac magnetic resonance • The most accurate for volumes, thickness and masses. • Detection of myocardial necrosis, perfusion and function. • Quantitative biochemical information: myocardial energetics.

  24. Other tests • Routine laboratory:  ESR, anemia,  serum iron, thrombocytopenia. • Electrolyte: Na+, k+, Mg++ . • Liver and kidney function tests. • Thyroid function.

  25. Other tests • Viral study (serum or myocardial biopsy). • Serum ANP or urinary proatrial natriuretic peptide (N-ANP) or (N-BNP). • Spirometry and respiratory function tests in selected cases.

  26. Invasive tests • Usually not required, but may be needed to elucidate the cause of RHF. • Coronary angiography. • Hemodynamic monitoring. • Endomyocardial biopsy.

  27. Diagnostic criteria of RHF Major : • Resting LVEF < 30%. • NYHA III or IV. • Peak VO2<14ml/kg/min on symptom limited testing (4-5 METs).

  28. Diagnostic criteria of RHF Minor : • No or minimal response after at least 3m of full standard therapy (ACEI,digoxin, diuretics) . • Serum Na < 130 mq./L. in pt. not treated with ACEIs. • Plasma norepinephrine > 900 pg/ml. Contributing : • More than one hospitalization for worsening HF in the past 6 ms. • Cardiac cachexia.

  29. Management of RHF Prevention of RHF • The basic aims of prevention are to : • Limit myocardial damage. • Modulate and reduce neuroendocrine activation. • This includes : • Treatment of risk factors (smoking/ lipids/ HPN…). • Revascularization for cases with significant reversible ischemia.

  30. Management of RHF • Life style modification • Diet : small meals, less fat, high fiber diet. • Limited dietary sodium  2 gm/day. • Reduced fluid intake. • Avoidance of traveling to high altitude, very hot or humid places. Short air flights are preferred to other means of transport.

  31. Non pharmacological therapy • Exercise and rehabilitation : • Regular physical activity is recommended according to the patient’s condition. • Walking or cycling for 10-30 min/day 3-7d/w. • Moderate – intensity resistance training improves strength, endurance, HR variability, and forearm blood flow.

  32. Non pharmacological therapy • Rest: • Necessary in severe RHF. • Passive mobilization and respiratory exercise are advised. • Education of the patient and relatives about disease condition, life style modification,drug side effects.

  33. Specific pharmacological therapy Diuretics • Loop diuretics, thiazides and potassium sparing. • RALES mortality study : (low dose spironolactone + ACEIs + loop diuretics) markedly and progressively improved survival in RHF irrespective of etiology.

  34. Treatment of diuretics resistance : • Fluid restriction. • Change the route (oral to i.v.) and timing (single multiple & continuous infusion) • Combination therapy (Furosemide . HCZ)

  35. Furosemide + HSS • High dose Furosemide (i.v. infusion for 500-1000 mg) plus hypertonic saline solution (150 ml 1.4-4.6% NaCl) bid in 30 min for 6-12 days. • Improved clinical and hemodynamic parameters, reduced hospitalization, and maintained the obtained results over time in comparison with the use of high dose Furosemide as bolus.

  36. ACEIs • Start with small doses with gradual increments. • Regular check up of renal function and K+. • Significantly improved survival and reduce hospitalization. • Many trials (SOLVD, SAVE, PROMISE, PROVED,…)

  37. ACEIs • Dry cough, hypotension,  K+, renal insufficiency are side effects. • ARBS: are the best substitute in the presence of side effects (CHARM study). • Combination therapy remains to be defined (ON TARGET).

  38. Vasodilators • Isosorbide dinitrate and hydralazine in combination in V-HeFT trial yield significant survival benefit in comparison to placebo and prazocin.

  39. Digitalis • Routine for CHF and AF. • In SR : debates regarding its beneficial effects vs toxic effects( DIG trial). • Smaller doses, in elderly, renal or hepatic insufficiency. • Serum digoxin levels and electrolyte check up.

  40. Inotropes • Dobutamine, Dopamine and Milrinone. • The routine use in RHF is not recommended. • Best indicated in: acute HF, bridge to definitive treat. (revascularization or transplantation) or palliation in end stage RHF.

  41. Inotropes • Combination of B-blockers and phosphodiesterase inhibitors (milrinone and enoximone) seems to be beneficial, with less side effects.

  42. B- Blockers • HF is associated with enhanced adrenergic activity with its direct and indirect toxic myocardial effects. • B-B is indicated in mild-moderate HF pretreated with standard therapy. • CAPRICORN study using Carvedilol and MERIT heart failure trial using Metoprolol, showed reduction in total mortality by 34% and SCD by 41%.

  43. B- Blockers • However, symptomatic benefit may be delayed and initial worsening may occur. • It is an important issue in decision making about starting B.B in severely symptomatic cases.

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