Management Of Chf


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Management Of Chf

  1. 1. Heart Failure <ul><li>Final common pathway for many cardiovascular diseases whose natural history results in symptomatic or asymptomatic left ventricular dysfunction </li></ul><ul><li>Cardinal manifestations of heart failure include dyspnea, fatigue and fluid retention </li></ul><ul><li>Risk of death is 5-10% annually in patients with mild symptoms and increases to as high as 30-40% annually in patients with advanced disease </li></ul>
  2. 2. Main causes <ul><li>Coronary artery disease </li></ul><ul><li>Hypertension </li></ul><ul><li>Valvular heart disease </li></ul><ul><li>Cardiomyopathy </li></ul><ul><li>Cor pulmonale </li></ul>
  3. 3. Compensatory changes in heart failure <ul><li>Activation of SNS </li></ul><ul><li>Activation of RAS </li></ul><ul><li>Increased heart rate </li></ul><ul><li>Release of ADH </li></ul><ul><li>Release of atrial natriuretic peptide </li></ul><ul><li>Chamber enlargement </li></ul><ul><li>Myocardial hypertrophy </li></ul>
  4. 4. NYHA Classification of heart failure <ul><li>Class I: No limitation of physical activity </li></ul><ul><li>Class II: Slight limitation of physical activity </li></ul><ul><li>Class III: Marked limitation of physical activity </li></ul><ul><li>Class IV: Unable to carry out physical activity without discomfort </li></ul>
  5. 5. New classification of heart failure <ul><li>Stage A: Asymptomatic with no heart damage but have risk factors for heart failure </li></ul><ul><li>Stage B: Asymptomatic but have signs of structural heart damage </li></ul><ul><li>Stage C: Have symptoms and heart damage </li></ul><ul><li>Stage D: Endstage disease </li></ul><ul><li>ACC/AHA guidelines, 2001 </li></ul>
  6. 6. Types of heart failure <ul><li>Diastolic dysfunction or diastolic heart failure </li></ul><ul><li>Systolic dysfunction or systolic heart failure </li></ul>
  7. 7. Factors aggravating heart failure <ul><li>Myocardial ischemia or infarct </li></ul><ul><li>Dietary sodium excess </li></ul><ul><li>Excess fluid intake </li></ul><ul><li>Medication noncompliance </li></ul><ul><li>Arrhythmias </li></ul><ul><li>Intercurrent illness (eg infection) </li></ul><ul><li>Conditions associated with increased metabolic demand (eg pregnancy, thyrotoxicosis, excessive physical activity) </li></ul><ul><li>Administration of drug with negative inotropic properties or fluid retaining properties (e. NSAIDs, corticosteroids) </li></ul><ul><li>Alcohol </li></ul>
  8. 8. Goals of treatment <ul><li>To improve symptoms and quality of life </li></ul><ul><li>To decrease likelihood of disease progression </li></ul><ul><li>To reduce the risk of death and need for hospitalisation </li></ul>
  9. 9. Approach to the Patient with Heart Failure <ul><li>Assessment of LV function (echocardiogram, radionuclide ventriculogram) </li></ul>EF < 40% Assessment of volume status Signs and symptoms of fluid retention No signs and symptoms of fluid retention Diuretic (titrate to euvolemic state) ACE Inhibitor  -blocker Digoxin
  10. 11. Effects of SNS Activation in Heart Failure <ul><li>Dysfunction/death of cardiac myocytes </li></ul><ul><li>Provokes myocardial ischemia </li></ul><ul><li>Provokes arrhythmias </li></ul><ul><li>Impairs cardiac performance </li></ul><ul><li>These effects are mediated via stimulation </li></ul><ul><li>of  and  1 receptors </li></ul><ul><li>Am J Hypertens 1998; 11: 23S-37S </li></ul>
  11. 13. Carvedilol in Heart Failure <ul><li>Effective receptor-blockade approach to heart failure </li></ul><ul><li>Negative inotropic effect counteracted by vasodilation </li></ul><ul><li>Provides anti-proliferative, anti-arrhythmic activity and inhibition of apoptosis </li></ul><ul><li>Prevents renin secretion </li></ul><ul><li>Drugs of Today 1998; 34 (Suppl B): 1-23. </li></ul>
  12. 14. US Multicenter Program Placebo Carvedilol % Risk (n=398) (n=696) Reduction All-cause 31 22 65% mortality (7.8%) (3.2%) Death due to progressive 13 5 heart failure (3.3%) (0.7%) Sudden death 15 12 (3.8%) (1.7%) Risk of hospitalization for 78 78 27% cardiovascular reasons (19.6%) (14.1%) Combined risk of 98 110 38% mortality & hospitalization (25%) (16%) NEJM 1996; 334:1349-1355
  13. 15. ANZ Multicentre Heart Failure Trial Placebo Carvedilol % Risk (n=208) (n=207) Reduction All-cause 26 20 24% mortality (12.5%) (10%) Risk of hospitalization for 84 64 28% cardiovascular reasons (40%) (31%) Combined risk of 97 74 29% mortality & hospitalization (47%) (36%) Lancet 1997; 349: 375-380.
  14. 16. Effect of carvedilol on progression of congestive heart failure All randomized patients Endpoint Placebo Carvedilol (n=134) (n=232) Primary endpoint 28 (21%) 25 (11%)* Death due to CHF 4 (3%) 0 (0%) Hospitalization due to worsening CHF 8 (6%) 9 (4%) Increase in CHF medication 16 (12%) 16 (7%) * Placebo vs. carvedilol, p = 0.008 Drugs of Today 1998; 34 (Suppl B): 1-23.
  15. 17. COPERNICUS: Effect on Mortality 35% Mortality (%) 22nd Congress of European Society of Cardiology, August 2000
  16. 18. COPERNICUS: Mortality reduction in special patient groups with carvedilol Mortality reduction (%) 22nd Congress of European Society of Cardiology, August 2000 EF<20%, hospitalised for heart failure in year prior to study entry EF < 15%, hospitalised 3 or more times during prior year for worsening heart failure
  17. 19. Carvedilol vs. Metoprolol Change in LVEF (%) from baseline Circulation 2000; 102: 546-551
  18. 20. Dosage guidelines for Carvedilol in heart failure <ul><li>Patient selection </li></ul><ul><li>Stable on background medications (diuretics, digoxin and/or ACE inhibitors) </li></ul><ul><li>Not in a fluid-overload state </li></ul><ul><li>Not hypotensive </li></ul><ul><li>Before dose increase </li></ul><ul><li>Evaluate for </li></ul><ul><li>Worsening heart failure </li></ul><ul><li>Vasodilation </li></ul><ul><li>Bradycardia </li></ul><ul><li>After each new dose initiation </li></ul><ul><li>Observe for signs of dizziness or light headedness for one hour </li></ul>3.125 mg bid 2 weeks Doubled every 2 weeks Max dose 25 mg bid (<85 kg); 50 mg bid (>85 kg)
  19. 21. Management of Complications <ul><li>Transient worsening of heart failure (e.g. increasing dyspnea, </li></ul><ul><li>decreasing exercise capacity) </li></ul><ul><li>Increase dose of diuretic and/or ACE inhibitor </li></ul><ul><li>If necessary, reduce carvedilol dose and/or prolong titration interval </li></ul><ul><li>Search for other possible causes (e.g. thyroid malfunction, infection, non-compliant drug intake, excessive liquid intake, etc.) </li></ul><ul><li>Vasodilatory Symptoms (dizziness, light headedness, </li></ul><ul><li>symptomatic hypotension) </li></ul><ul><li>Decrease diuretic dose and, if necessary, ACE inhibitor dose </li></ul><ul><li>If the cessation of both is not successful, reduce carvedilol dose and/or prolong titration interval </li></ul>
  20. 22. Management of Complications (Contd.) <ul><li>Bradycardia (Pulse rate below 55 beats/min) </li></ul><ul><li>Check and eventually reduce digitalis dose </li></ul><ul><li>If necessary, reduce carvedilol dose and/or prolong titration interval </li></ul><ul><li>Withdraw carvedilol only in the event that hemodynamics are affected </li></ul><ul><li>Symptoms of Bronchial obstruction </li></ul><ul><li>Search for other possible causes (e.g., concurrent infection, subacute pulmonary edema) </li></ul><ul><li>Reduce dose of, or withdraw, carvedilol only after possible causes for symptoms have been ruled out </li></ul>
  21. 23. The role of angiotensin II in the progression of heart failure Coronary artery disease Cardiac overload Cardiomyopathy Left ventricular dysfunction  Arterial blood pressure  Angiotensin II  Peripheral organ blood flow  Skeletal muscle blood flow Exercise intolerance  Renal blood flow Oedema Cardiac remodelling Renin release Aldosterone release Vasoconstriction Na+ and water retention Inotropy and hypertrophy of vascular and cardiac cells Left ventricular dilation & hypertrophy Pump failure
  22. 24. ACE Inhibitors: physiologic benefits <ul><li>Arteriovenous Vasodilatation </li></ul><ul><li> pulmonary arterial diastolic pressure </li></ul><ul><li> pulmonary capillary wedge pressure </li></ul><ul><li> left ventricular end-diastolic pressure </li></ul><ul><li> systemic vascular resistance </li></ul><ul><li> systemic blood pressure </li></ul><ul><li> maximal oxygen uptake (MVO 2 ) </li></ul>
  23. 25. ACE Inhibitors: physiologic benefits <ul><li> LV function and cardiac output </li></ul><ul><li> renal, coronary, cerebral blood flow </li></ul><ul><li>No change in heart rate or myocardial contractility </li></ul><ul><li>no neurohormonal activation </li></ul><ul><li>resultant diuresis and natriuresis </li></ul>
  24. 26. ACE Inhibitors: clinical benefits <ul><li>Increases exercise capacity </li></ul><ul><li>improves functional class </li></ul><ul><li>attenuation of LV remodeling post MI </li></ul><ul><li>decrease in the progression of chronic HF </li></ul><ul><li>decreased hospitalization </li></ul><ul><li>enhanced quality of life </li></ul><ul><li>improved survival </li></ul>
  25. 27. Asymptomatic Patients <ul><li>Enalapril </li></ul><ul><li>SOLVD Prevention Trial </li></ul><ul><li>EF<35%  HF progression,  hospitalization </li></ul><ul><li>Captopril </li></ul><ul><li>SAVE, GISSI-3, ISIS-4 Post MI, EF <40%  overall mortality,  re-infarction  hospitalization,  HF progression </li></ul>
  26. 28. Symptomatic Patients <ul><li>Hydralazine + Isosorbide dinitrate </li></ul><ul><li>VHeFT-I  mortality, improved functional class as compared with use of digoxin and diuretics VHeFT-II proved less effective than enalapril </li></ul>
  27. 29. Dosage of ACE inhibitors: ATLAS study <ul><li>Low-dose High-dose </li></ul><ul><li>(2.5-5 mg) (32.5-35mg) </li></ul><ul><li>Cardiovascular 44.9% 42.5% </li></ul><ul><li>mortality </li></ul><ul><li>All-cause mortality </li></ul><ul><li>+ hospitalisation for 83.8% 79.7% </li></ul><ul><li>cardiovascular reason </li></ul><ul><li>All-cause mortality + </li></ul><ul><li>hospitalisation for 60.4% 55.1% </li></ul><ul><li>heart failure </li></ul><ul><li>Circulation 1999;100:2312-18 </li></ul>
  28. 30. AIRE <ul><li>AIRE Study demonstrated efficacy of ramipril on mortality and morbidity in CHF post-MI NYHA class I-III patients </li></ul><ul><li>2006 patients enrolled in a double-blind,randomized, placebo-controlled study </li></ul><ul><li>27% reduction in the risk of death </li></ul><ul><li>23% decrease in progression to severe / resistant heart failure </li></ul>Lancet. 1993; 342:821-828
  29. 31. Guidelines to ACE Inhibitor Therapy <ul><li>Contraindications </li></ul><ul><ul><li>Renal artery stenosis </li></ul></ul><ul><ul><li>Renal insufficiency (relative) </li></ul></ul><ul><ul><li>Hyperkalemia </li></ul></ul><ul><ul><li>Arterial hypotension </li></ul></ul><ul><ul><li>Cough </li></ul></ul><ul><ul><li>Angioedema </li></ul></ul><ul><li>Alternatives </li></ul><ul><ul><li>Hydralazine + ISDN, AT-II inhibitor </li></ul></ul>
  30. 32. Guidelines to ACE Inhibitor Therapy <ul><li>All patients with symptomatic heart failure and those in functional class I with significantly reduced left ventricular function should be treated with an ACE inhibitor, unless contraindicated or not tolerated </li></ul><ul><li>ACE inhibitors should be continued indefinitely </li></ul><ul><li>It is important to titrate to the dosage regimen used in the clinical trials … in the absence of symptoms or adverse effects on end-organ perfusion </li></ul><ul><li>In very severe heart failure, hydralazine and nitrates added to ACE inhibitor therapy can further improve cardiac output </li></ul>
  31. 33. ACE Inhibitor Therapy in Heart Failure Patients (Ejection Fraction < 0.40) Systolic Blood Pressure <100 mmHg (or elevated creatinine) 100-139 mmHg (or recent intense diuresis) > 140 mmHg Lowest Dose, Short-Acting Usual Starting Dose, Long-or Short-Acting Intermediate Dose, Long- or Short-Acting Follow-Up Every 1-2 Weeks Stable BP and Creatinine Level Symptomatic Low BP or Rising Creatinine Level Residual Excess Fluid? Stop Diuretic and ACE Inhibitor Therapy Return to Baseline BP and Creatinine Level ? Increase ACE Inhibitor Dose; Follow-Up Every 1-2 Weeks Target Dose Resume ACE Inhibitor Titration Refer to specialist Stop ACE Inhibitor Therapy Y N Y N
  32. 34. Diuretics <ul><li>Indicated in patients with symptoms of heart failure who have evidence of fluid retention </li></ul><ul><li>Enhance response to other drugs in heart failure such as beta-blockers and ACE inhibitors </li></ul><ul><li>Therapy initiated with low doses followed by increments in dosage until urine output increases and weight decreases by 0.5-1kg daily </li></ul>
  33. 35. Digoxin <ul><li>Enhances LV function, normalizes baroreceptor-mediated reflexes and increases cardiac output at rest and during exercise </li></ul><ul><li>Recommended to improve clinical status of patients with heart failure due to LV dysfunction and should be used in conjunction with diuretics, ACE inhibitors and beta-blockers </li></ul><ul><li>Also recommended in patients with heart failure who have atrial fibrillation </li></ul><ul><li>Digoxin initiated and maintained at a dose of 0.25 mg daily </li></ul><ul><li>Adverse effects include cardiac arrhythmias, GI symptoms and neurological complaints (eg. visual disturbances, confusion) </li></ul>
  34. 36. Summary of drug treatment for CHF <ul><li>Asymptomatic Mild to moderate Moderate </li></ul><ul><li>LV dysfunction CHF to severe CHF </li></ul><ul><li>ACE inhibitor Digoxin Digoxin </li></ul><ul><li>Beta blocker Diuretics Diuretics </li></ul><ul><li>ACE inhibitor ACE inhibitor </li></ul><ul><li>Beta blocker Beta blocker </li></ul><ul><li>Spironolactone </li></ul>