CHRONIC CONGESTIVE HEART FAILURE American Heart Association in collaboration with

1. CHRONIC CONGESTIVE HEART FAILURE American Heart Association in collaboration with Sociedad Española de Cardiologia June, 1999

2. Committee on Post Graduate Education, Council on Clinical Cardiology, American Heart Association Developed in collaboration with the Sociedad Española de Cardiologia Prepared by: Ann F. Bolger, MD José Lopez Sendón, MD The content of these slides is current as of June, 1999. Future revisions will be posted on the American Heart Association website (www.americanheart.org).

3. DEFINITION “The situation when the heart is incapable of maintaining a cardiac output adequate to accommodate metabolic requirements and the venous return." E. Braunwald

4. Chronic Congestive Heart Failure EVOLUTION OF CLINICAL STAGES NORMAL No symptoms Normal exercise Normal LV fxn Asymptomatic LV Dysfunction Compensated CHF No symptoms Normal exercise Abnormal LV fxn Decompensated CHF No symptoms Exercise Abnormal LV fxn Symptoms Exercise Abnormal LV fxn Refractory CHF Symptoms not controlled with treatment

5. - Synergistic LV contraction - LV wall integrity - Valvular competence DETERMINANTS OF VENTRICULAR FUNCTION CONTRACTILITY PRELOAD AFTERLOAD STROKE VOLUME HEART RATE CARDIAC OUTPUT

6. TREATMENT OBJECTIVES Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms

7. TREATMENT PHARMACOLOGIC THERAPY DIURETICS INOTROPES VASODILATORS NEUROHORMONAL ANTAGONISTS OTHERS (Anticoagulants, antiarrhythmics, etc)

8. DIURETICS Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle Cortex K-sparing Inhibit reabsorption of Na in the distal convoluted and collecting tubule Loop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Medulla Loop of Henle Collecting tubule

9. DIURETIC EFFECTS • Volume and preload • Improve symptoms of congestion • No direct effect on CO, but • excessive preload reduction may • Neurohormonal activation • Levels of NA, Ang II and PRA • Exception: with spironolactone

10. THIAZIDESMECHANISM OF ACTION Excrete 5 - 10% of filtered Na+ Elimination of K Inhibit carbonic anhydrase: increase elimination of HCO3 Excretion of uric acid, Ca and Mg No dose - effect relationship

11. LOOP DIURETICSMECHANISM OF ACTION • Excrete 15 - 20% of filtered Na+ • Elimination of K+, Ca+ and Mg++ • Resistance of afferent arterioles • -Cortical flow and GFR • - Release renal PGs • - NSAIDs may antagonize diuresis

12. Eliminate < 5% of filtered Na+ Inhibit exchange of Na+ for K+ or H+ Spironolactone = competitive antagonist for the aldosterone receptor Amiloride and triamterene block Na+ channels controlled by aldosterone K-SPARING DIURETICSMECHANISM OF ACTION

13. DIURETICSADVERSE REACTIONSThiazide and Loop Diuretics • Changes in electrolytes: • Volume • Na+, K+, Ca++, Mg++ • metabolic alkalosis • Metabolic changes: • glycemia, uremia, gout • LDL-C and TG • Cutaneous allergic reactions

14. DIURETICSADVERSE REACTIONS Thiazide and Loop Diuretics • Idiosyncratic effects: • Blood dyscrasia, cholestatic jaundice and acute pancreatitis • Gastrointestinal effects • Genitourinary effects: • Impotence and menstrual cramps • Deafness, nephrotoxicity • (Loop diuretics)

15. DIURETICSADVERSE REACTIONS K-SPARING DIURETICS • Changes in electrolytes: • Na+, K+, acidosis • Musculoskeletal: • Cramps, weakness • Cutaneous allergic reactions : • Rash, pruritis

16. American Heart Association in collaboration with Sociedad Española de Cardiologia CHRONIC CONGESTIVE HEART FAILURE The content of these slides is current as of June, 1999. Future revisions will be posted on the American Heart Association website (www.americanheart.org)

17. Medical Nutrition Therapy • Energy: Moderate 1.3-1.5 x BEE • Severe 1.6-1.8 x BEE • Protein (variable) 1.0-1.5 • Na+ Restriction • Fluid Restriction (inpatient) • Small Frequent Meals • Nutrient dense foods/bevs • Easy to chew foods