Congestive Heart Failure,

1. Congestive Heart Failure, Prepared By Dr.Mustafa Alshehabat

2. Terminology • Heart Failure:The inability of the heart to maintain an output adequate to maintain the metabolic demands of the body. • Pulmonary Edema:An abnormal accumulation of fluid in the lungs. • CHF with Acute Pulmonary Edema:Pulmonary Edema due to Heart Failure (Cardiogenic Pulmonary Edema)

3. What is HF Complex syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to function as a pump to support a physiological circulation.

4. Pathophysiology • Main Causes of Heart Failure: • Ischemic Heart Disease (35-40%) • Cardiomyopathy(dilated) (30-34%) • Hypertension (15-20%) • Other Causes: • Valvular Heart Disease. • Congenital Heart Disease. • Alcohol and Drugs. • Arrhythmias………………

5. Pathophysiological Changes in HF • Ventricular Dilatation. • Myocyte Hypertrophy. • Salt and Water Retention. • Sympathetic Stimulation. • Peripheral Vasoconstriction.

6. Signs & Symptoms Symptoms: • Exertional Dyspnoea • Orthopnia • Paraxysmal Nocturnal Dyspnoea Signs: • Cardiomegaly • Elevated Jugular Venous Pressure • Tachycardia • Hypotension • Bi-basal crackles • Pleural effusion • Ankle Edema • Ascites • Tender hepatomegaly.

7. Classification of heart failure • No limitation. Normal physical exercise doesn’t cause fatigue, dyspnea or palpitations. • Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnea or palpitations. • Marked limitation. Comfortable at rest but gentle physical activity produces marked symptoms of HF. • Symptoms of HF occur at rest and are exacerbated by any physical activity.

8. Kussmaul’s Sign This is a rise in the JVP seen with inspiration. It is the opposite of what is seen in normal people and this reflects the inability of the heart to compensate for a modest increase in venous return. This sign is classically seen in constrictive pericarditis in association with a raised JVP. This condition was originally described in tuberculous pericarditis and is rarely seen. Kussmauls sign is also seen in right ventricular infarction, right heart failure, tricuspid stenosis, and restrictive cardiomyopathy. It is not seen in acute cardiac tamponade- although it may be seen if tamponade occurs with a degree of constricive pericardiditis

9. PMI • The apex beat, also called the point of maximum impulse (PMI), is the furthermost point outwards (laterally) and downwards (inferiorly) from the sternum at which the cardiac impulse can be felt. The cardiac impulse is the result of the heart rotating, moving forward and striking against the chest wall during systole. • The normal apex beat can be palpated in the precordiumleft 5th intercostal space, at the point of intersection with the left midclavicular line. In children the apex beat occurs in the fourth rib interspace medial to the nipple. The apex beat may also be found at abnormal locations; in many cases of dextrocardia, the apex beat may be felt on the right side. Lateral and/or inferior displacement of the apex beat usually indicates enlargement of the heart.

10. Heart Sounds •  S1 • The first heart sound - S1 - is in time with the pulse in your carotid artery in your neck. The sound of the tricuspid valve closing may be louder in patients with pulmonary hypertension due to increased pressure beyond the valve. Non-heart-related factors such as obesity, muscularity, emphysema, and fluid around the heart can reduce both S1 and S2.     The position of the valves when the ventricles contract can have a big effect on the first heart sound. If the valves are wide open when the ventricule contracts, a loud S1 is heard. This can occur with anemia, fever or hyperthyroid.     When the valves are partly closed when the ventricule contracts, S1 is faint. Beta-blockers produce a fainter S1. Structural changes in the heart valves can also affect S1. Fibrosis and calcification of the mitral valve may reduce S1, while stenosis of the mitral valve may cause a louder S1. • S2 • The second heart sound marks the beginning of diastole - the heart's relaxation phase - when the ventricles fill with blood. In children and teenagers, S2 may be more pronounced. Right ventricular ejection time is slightly longer than left ventricular ejection time. As a result, the pulmonic valve closes a little later than the aortic valve.     Higher closing pressures occur in patients with chronic high blood pressure, pulmonary hypertension, or during exercise or excitement. This results in a louder A2 (the closing sound of the aortic valve).     On the other hand, low blood pressure reduces the sound. The second heart sound may be "split" in patients with right bundle branch block, which results in delayed pulmonic valve closing. Left bundle branch block may cause aortic valve closing (A2) to be slower than pulmonic valve closing (P2). • S3 • During diastole there are 2 sounds of ventricular filling: The first is from the atrial walls and the second is from the contraction of the atriums. The third heart sound is caused by vibration of the ventricular walls, resulting from the first rapid filling so it is heard just after S2. The third heart sound is low in frequency and intensity. An S3 is commonly heard in children and young adults. In older adults and the elderly with heart disease, an S3 often means heart failure. • S4 • The fourth heart sound occurs during the second phase of ventricular filling: when the atriums contract just before S1. As with S3, the fourth heart sound is thought to be caused by the vibration of valves, supporting structures, and the ventricular walls. An abnormal S4 is heard in people with conditions that increase resistance to ventricular filling, such as a weak left ventricle.

11. Edema Bilateral lower extremity edema

12. Hypertension • Hypertrophic Cardiomyopathy

13. Compensatory Mechanisms • Increased Heart Rate • Sympathetic = Norepinephrine • Dilation • Frank Starling = Contractility • Neurohormonal • Redistribution of Blood to the Brain

14. CHF Vicious Cycle Low Output Increased Preload Increased Afterload Norepinephrine Increased Salt Vasoconstriction Renal Blood Flow Renin Angiotension I Angiotension II Aldosterone

15. Infiltration of Interstitial Space • Normal Micro-anatomy • Micro-anatomy with fluid movement.

16. Acute Pulmonary Edema a true life- threatening emergency

18. Treatment • Prevention. Control of risk factors • Life style • Treat etiologic cause / aggravating factors • Drug therapy • Personal care. Team work • Revascularization if ischemia causes HF • ICD (Implantable Cardiac Defibrillator) • Ventricular resyncronization • Ventricular assist devices • Heart transplant • Artificial heart • Neoangiogenesis, Gene therapy All Selected patients

19. Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms Treatment Objectives (Cost)

20. Treatment Pharmacologic Therapy • Diuretics • ACE inhibitors • Beta Blockers • Digitalis • Spironolactone • Other

21. Diuretics •Essential to control symptoms secondary to fluid retention • Prevent progression from HT to HF • Spironolactone improves survival • New research in progress

22. 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

23. Diuretics. Indications • 1. Symptomatic HF, with fluid retention • Edema • Dyspnea • LungRales • Jugulardistension • Hepatomegaly • Pulmonary edema (Xray) AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

24. LoopDiuretics / Thiazides. Practical Use • Startwith variable dose. Titratetoachievedryweight • Monitor serum K+ at “frequentintervals” • Reduce dosewhen fluid retentioniscontrolled • Teachthepatientwhen, howtochangedose • Combine toovercome “resistance” • Do not use alone

25. Loop diuretics. Dose (mg) Initial Maximum Bumetanide 0.5 to 1.0 / 12-24h 10 / day Furosemide 20 to 40 / 12-24h 400 / day Torsemide 10 to 20 / 12-24h 200 / day AHA / ACC HF guidelines 2001

26. Thiazides, Loop Diuretics. Adverse Effects • K+, Mg+ (15 - 60%) (sudden death ???) • Na+ • Stimulation of neurohormonal activity • Hyperuricemia (15 - 40%) • Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic Sharpe N. Heart failure. Martin Dunitz 2000;43 Kubo SH , et al. Am J Cardiol 1987;60:1322 MRFIT, JAMA 1982;248:1465 Pool Wilson. Heart failure. Churchill Livinston 1997;635

27. ACE-i. Mechanism of Action VASOCONSTRICTION VASODILATATION ALDOSTERONE PROSTAGLANDINS VASOPRESSIN tPA Kininogen SYMPATHETIC Kallikrein Angiotensinogen RENIN BRADYKININ Angiotensin I A.C.E. Kininase II Inhibitor ANGIOTENSIN II Inactive Fragments

28. ACE-I. Clinical Effects • Improve symptoms • Reduce remodelling / progression • Reduce hospitalization • Improve survival

29. ACE-i. Indications • Symptomatic heart failure • Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % • Selected high risk subgroups AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

30. ACE-I. Adverse Effects • Hypotension (1st dose effect) • Worsening renal function • Hyperkalemia • Cough • Angioedema • Rash, ageusia, neutropenia, …

31. ACE-I. Contraindications • Intolerance (angioedema, anuric renal fail.) • Bilateral renal artery stenosis • Pregnancy • Renal insufficiency (creatinine > 3 mg/dl) • Hyperkalemia (> 5,5 mmol/l) • Severe hypotension

32. ß-Adrenergic Blockers Mechanism of action • Density of ß1 receptors • Inhibit cardiotoxicity of catecholamines • Neurohormonal activation • HR • Antiischemic • Antihypertensive • Antiarrhythmic • Antioxidant, Antiproliferative

33. ß-Adrenergic Blockers Clinical Effects • Improve symptoms (only long term) • Reduce remodelling / progression • Reduce hospitalization • Reduce sudden death • Improve survival

34. ß-Adrenergic Blockers Indications • Symptomatic heart failure • Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % • After AMI AHA / ACC HF guidelines 2001 ESC HF guidelines 2001

35. ß-Adrenergic Blockers Adverse Effects • Hypotension • Fluid retention / worsening heart failure • Fatigue • Bradycardia / heart block • Review treatment (+/-diuretics, other drugs) • Reduce dose • Consider cardiac pacing • Discontinue beta blocker only in severe cases

36. Digitalis - Na-K ATPase Na-Ca Exchange Na+ K+ Na+ Ca++ Ca++ Myofilaments K+ Na+ CONTRACTILITY

37. - Plasma Noradrenaline - Peripheral nervous system activity - RAAS activity - Vagal tone - Normalizes arterial baroreceptors Digitalis. Mechanism of Action Blocks Na+ / K+ATPase => Ca+ + • Inotropic effect • Natriuresis • Neurohormonal control NEJM 1988;318:358

38. Digitalis. Clinical Effects • Improve symptoms • Modest reduction in hospitalization • Does not improve survival

39. Digitalis. Indications • When no adequate response to ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001 • In combinationwith ACE-i + diuretics ifpersistingsymptoms ESC Guidelines 2001 • AF, toslow AV conduction Dose 0.125 to 0.250 mg / day

40. Aldosterone Inhibitors ALDOSTERONE Spironolactone - Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) • Retention Na+ • Retention H2O • Excretion K+ • Excretion Mg2+ • Collagen • deposition • Fibrosis • - myocardium • - vessels Edema Arrhythmias

41. Spironolactone. Practical use • Do not use ifhyperkalemia, renal insuf. • Monitor serum K+ at “frequentintervals” • Start ACE-i first • Startwith 25 mg / 24h • If K+ >5.5 mmol/L, reduce to 25 mg / 48h • If K+isloworstableconsider 50 mg / day • New studies in progress

42. Angiotensin II Receptor Blockers (ARB) RENIN Angiotensin IANGIOTENSIN II Angiotensinogen ACE Other pathways AT1 Receptor Blockers RECEPTORS AT1 AT2 Vasoconstriction Proliferative Action Vasodilatation Antiproliferative Action

43. • Cardiac output• Blood pressure NITRATESHEMODYNAMIC EFFECTS 1- VENOUS VASODILATATION Preload2- Coronary vasodilatation Myocardialperfusion 3- Arterial vasodilatation Afterload 4- Others Pulmonary congestionVentricular sizeVent. Wall stressMVO2

44. Nitrates. Clinical Use • CHF with myocardial ischemia • Orthopnea and paroxysmal nocturnal dyspnea • In acute CHF and pulmonary edema:NTGsl / iv • Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency)

45. Heart Transplant. Indications • Refractory cardiogenic shock • Peak VO2 < 10 ml / kg / min • Severe symptoms of ischemia not amenable to revascularization • Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity

46. Heart Failure and Myocardial Ischemia • Coronary HD is the cause of 2/3 of HF • Segmental wall motion abnormalities are not specific if ischemia • Angina coronary angio and revascularization • No angina • Search for ischemia and viability in all ? • Coronary angiography in all ?

47. HEART FAILURE MODELS CONGESTIVE- Digoxin, Diurétics HEMODYNAMIC - Vasodilators NEUROHUMORAL - ACE inhibitors, - Blockers, Spironolactone IMMUNOLOGICAL - Cytokine inhibitors

48. THANK YOU