CONGESTIVE HEART FAILURE

1. CONGESTIVE HEART FAILURE MA. LENY ALDA G. JUSAYAN, MD

2. HEART FAILURE • Inability of the heart to pump an adequate amount of blood to the body’s needs • CONGESTIVE HEART FAILURE – refers to the state in which abnormal circulatory congestion exists a result of heart failure

4. CAUSES OF HEART FAILURE: • Final common pathway of many kinds of heart diseases • Ischemic, alcoholic, restrictive, hypertrophic • Optimal treatment requires identification of primary & secondary factors leading to CHF • HELPFUL RESULT of dilatation: increases cardiac output • HARMFUL RESULT of dilation: more wall tension, more oxygen is needed to produce any given stroke volume

5. CLASSIFICATION: • SYSTOLIC DYSFUNCTION: • Inadequate force is generated to eject blood normally • Reduce cardiac output, ejection fraction (< 45%) • Typical of acute heart failure • Secondary to AMI • Responsive to inotropics

6. CLASSIFICATION: • DIASTOLIC DYSFUNCTION • Inadequate relaxation to permit normal filling • Hypertrophy and stiffening of myocardium • Cardiac output may be reduced • Ejection fraction is normal • Do not respond optimally to inotropic agents

7. CLASSIFICATION: • HIGH OUTPUT FAILURE • Increase demand of the body with insufficient cardiac output • Hyperthyroidism, beri-beri, anemia, AV shunts • Treatment is correction of underlying cause

8. CLASSIFICATION: • ACUTE HEART FAILURE • Sudden development of a large myocardial infarction or rupture of a cardiac valve in a patient who previously was entirely well, usually predominant systolic dysfunction

9. CLASSIFICATION: • CHRONIC HEART FAILURE • Typically observed in patients with dilated cardiomyopathy or multivalvular heart diseases that develops or progresses slowly

11. PRECIPITATING CAUSES OF HEART FAILURE: • Infection • Anemia • Thyrotoxicosis & pregnancy • Arrythmias • Rheumatic, viral & other forms of myocarditis • Infective endocarditis • Systemic hypertension • Myocardial infarction • Physical, dietary, fluid, environmental & emotional excesses • Pulmonary embolism

13. PULMONARY CONGESTION & RESPIRATORY SYMPTOMS: • Result of dilatation & increasing left ventricular end diastolic pressure, left atrial pressure & capillary pressures • Results to pulmonary vascular congestion & symptoms associated with cough with blood tinged sputum

15. Cont. • EDEMA OF THE BRONCHIAL MUCOSA • Increases resistance to airflow producing respiratory distress similar to asthma (cardiac asthma)

16. Cont: • DYSPNEA • Results from reflexes initiated by vascular distention • Increased rigidity of lungs & impaired gas exchange resulting from interstitial edema • Accumulation of fluid in ALVEOLARS SACS (pulmonary edema)

17. Cont. TACHYCARDIA • An early compensatory response mediated by increased sympathetic tone EDEMA • compensatory response mediated by the renin angiotensin aldosterone system & by increased sympathetic outflow CARDIOMEGALY • a compensatory structural response

18. SYMPTOMS: • Due to inadequate perfusion of peripheral tissues (fatigue, dyspnea) • Elevated intracardiac filling pressures (orthopnea, PND, peripheral edema)

19. PHYSICAL EXAM: • Jugular venous distention • S3 • Rales • Pleural effusion • Edema • Hepatomegaly • Ascites

21. “All the signs of CHF are the consequences of inadequate force of contraction"

22. PATHOPHYSIOLOGY: • STARLING’S LAW “Within limits, the force of ventricular contraction is a function of the end-diastolic length of the cardiac muscle, which in turn is closely related to the ventricular end-diastolic volume.”

23. PATHOPHYSIOLOGY: • Heart failure results in DEPRESSION of the ventricular function curve • COMPENSATION in the form of stretching of myocardial fibers results • Stretching leads to cardiac dilatation which occurs when the left ventricle fails to eject its normal end diastolic volume

25. CARDIAC FAILURE  VENOUS PRESSURE  CARDIAC OUTPUT  SYMPATHETIC ACTIVITY  BLOOD PRESSURE  RENAL BLOOD FLOW  RENIN ANGIOTENSIN II  ALDOSTERONE  CAPILLARY FILTRATION  SODIUM RETENTION EDEMA

26. NEUROHUMORAL ACTIVATION DURING MYOCARDIAL FAILURE MYOCARDIAL FAILURE  CARDIAC OUTPUT  BLOOD PRESSURE/TISSUE PERFUSION ACTIVATION OF ADRENERGIC SYSTEM ARTERIOLAR CONSTRICTION INCREASED SYSTEMIC VASCULAR RESISTANCE INCREASED RESISTANCE TO EJECTION

27. COMPENSATORY RESPONSES DURING HEART FAILURE:  CARDIAC OUTPUT  CAROTID SINUS FIRING  RENAL BLOOD FLOW  SYMPATHETIC DISCHARGE  RENIN RELEASE  FORCE  RATE  PRELOAD  AFTERLOAD REMODELING • CARDIAC OUTPUT (VIA COMPENSATION)

28. Pathophysiology of Cardiac Performance

29. CLINICAL MANAGEMENT OF CONGESTIVE HEART FAILURE • OBJECTIVES: • Increase cardiac contractility • Decrease preload ( left ventricular pressure) • Decrease afterload (systemic vascular resistance) • Normalize heart rate and rhythm

30. Approaches:Reduce workload of heart • 1.Limit activity level reduce weight control hypertension • 2. Restrict sodium (low salt diet)3. Give diuretics (removal of retained salt and water)4. Give angiotensin-converting enzyme inhibitors(decreases afterload and retained salt and water)5. Give digitalis (positive inotropic effect on depressed heart)6. Give vasodilators (decreases preload & afterload)

31. DRUGS USED TO TREAT CONGESTIVE HEART DISEASE: • VASODILATORS • Reduce the preload (through venodilatation), or reduction in afterload (through arteriolar dilatation) or both • Decrease the load of the myocardium

32. DIURETIC AGENTS: • Reduce salt & water retention, thereby reducing ventricular preload INOTROPIC AGENTS: • Increase the strength of contraction of cardiac muscles

33. DRUGS USED TO TREAT CONGESTIVE HEART FAILURE VASODILATORS INOTROPIC AGENTS • CAPTOPRIL • ENALAPRIL • FOSINOPRIL • LISINOPRIL • QUINAPRIL • HYDRALAZINE • ISOSORBIDE • MINOXIDIL • SODIUM NIITROPRUSSIDE -DIGOXIN -DIGITOXIN -DOBUTAMINE -AMRINONE -MILRINONE DIURETICS -BUMETANIDE -FUROSEMIDE -HYDROCHLOROTHIAZIDE -METALAZONE

34. BASIC PHARMACOLOGY OF DRUGS USED IN CONGESIVE HEART FAILURE: DIGITALIS PHARMACOKINETICS: DIGOXIN DIGITOXIN • LIPID SOLUBILITY MEDIUM HIGH • ORAL AVAILABILITY 75% >90% • HALF-LIFE 40 HRS 168 HRS • PLASMA PROTEIN BINDING 20-40 HRS >90 HRS • PERCENTAGE METABOLIZED <20 >80 • VOLUME OF DISTRIBUTION 6.3 L/KG 0.6 L/KG

35. PHARMACOKINETICS: -T1/2 is long (40 hrs)-Therapeutic plasma concentration: 0.5-2 ng/ml-Toxic plasma concentration: >2 ng/ml *digitalis must be present in the body in certain "saturating" amount before any effect on congestive failure is noted this is achieved by giving a large initial dose in a process called "digitalization" -after intial dosages, digitalis is given in "maintenance" amounts sufficient to replace that which is excreted to avoid exceeding therapeutic range during digitalization:- the loading dose should be adjusted according to the health of the patient- slow digitalization (over 1 week) is the safest technique- plasma digoxin levels should be monitored

36. METABOLISM & EXCRETION: • Digoxin – not extensively metabolized, 2/3 excreted unchanged in the kidneys • Digitoxin – metabolized in the liver and excreted into the gut via the bile

38. MECHANISM OF ACTION: • Inhibit the monovalent cation transport enzyme coupled Na+, K+ ATPase & increased intracellular Na+ content  increases intracellular Ca2+ through a Na+ - Ca2+ exchange carrier mechanism. • Increased myocardial uptake of Ca2+ augments Ca2+ release to the myofilaments during excitation  invokes a positive inotropic response

40. MECHANISM OF ACTION: • Produce alterations in the electrical properties of both contractile cells and the specialized automatic cells, leading to increased automaticity & ectopic impulse activity • Prolong the effective refractory period of the AV node  slow ventricular rate in atrial flutter & fibrillation

41. PROPERTIES OF CARDIAC GLYCOSIDES:

42. EFFECTS IN HEART FAILURE: • Stimulates myocardial contractility • Improves ventricular emptying • Increase cardiac output • Augments ejection fraction • Promotes diuresis • Reduces elevated diastolic pressure & volume & end –systolic volume • Reduces symptoms resulting from pulmonary vascular congestion & elevated systemic venous pressure

44. DIGITALIS INTOXICATION: • Serious & potentially fatal complication • Anorexia, nausea & vomiting = earliest signs of digitalis intoxication • Arrythmias: ventricular premature beats, bigeminy, ventricular & atrial tachycardia w/ variable AV block • Chronic digitalis intoxication = exacerbations of heart failure, weight loss, cachexia, neuralgias, gynecomastia, yellow vision, delirium

45. TREATMENT OF DIGITALIS INTOXICATION: • Tachyarrythmias: withdrawal of the drug, treatment with beta blocker or lidocaine • Hypokalemia: potassium administration by the oral route

46. OTHER POSITIVE INOTROPIC DRUGS USED IN HEART FAILURE: • BIPYRIDINES • Amrinone & Milrinone • Parenteral forms only • Half-life: 2-3 hrs • 10-40% excreted in the urine • MOA: increase inward calcium influx in the heart during action potential & inhibits phosphodiesterase • ADVERSE EFFECTS: nausea, vomiting, thrombocytopenia, liver enzyme changes

47. BETA ADRENOCEPTOR STIMULANTS: • DOBUTAMINE • Increases cardiac output • Decrease in ventricular filling pressure • Given parenterally • CONTRAINDICATIONS: pheochromocytoma, tachyarrythmias • ADVERSE EFFECTS: precipitation or exacerbation of arrythmia

50. DRUGS WITHOUT POSITIVE INOTROPIC EFFECTS USED IN HEART FAILURE: • DIURETICS • Reduce salt & water retention  reduce ventricular preload • Reduction in venous pressure  reduction of edema & its symptoms, reduction of cardiac size  improved efficiency of pump function