HEART FAILURE IN TROPICAL MEDICINEE.pptx

HEART FAILURE

1. HEART FAILURE PROFESSOR B.C. ANISIUBA

2. OUTLINE 1. INTRODUCTION 2. AETIOLOGY 3. PATHOPHYSIOLOGY 4. CLINICAL SYNDROMES OF HEART FAILURE 5. CLASSIFICATION OF HEART FAILURE 6. INVESTIGATIONS 7. TREATMENT

3. OUTLINE (continued) 9. TREATMENT

4. 1. INTRODUCTION Traditionally, heart failure is described as a condition in which the heart is unable to generate enough cardiac output to meet the varying needs of the body in the presence of normal filling pressures. It is a syndrome comprising symptoms and signs of pulmonary and systemic congestion caused by varying aetiologies . It about 1% of the population above 60 years. The prognosis is worse than that of many cancers: 50% of people with severe heart failure die within one year of diagnosis. A new universal definition of heart failure is now available:

5. 1. INTRODUCTION

6. 2. AETIOLOGY A. Underlying Diseases Causing Heart failure Common causes of heart failure in our environment include: Hypertension, Valvular heart diseases, Diabetes mellitus, Cardiomyopathies, Peripartum heart failure, Toxic damage from alcohol and recreational/therapeutic drugs, congenital heart diseases, ischaemic heart disease and infections (endocarditis)

7. 2. AETIOLOGY B. Precipitating Factors for Heart Failure These are conditions that can make a patient with heart disease develop heart failure for the first time or cause decompensation in a previously stable patient: Non-adherence to medications, inappropriate reduction in the intensity of treatment, uncontrolled hypertension, arrhythmias, development of another heart disease, concomitant systemic infection, pulmonary embolization, intense prolonged physical exercise or emotional crisis, severe climate change such as intense cold, concomitant use of cardiac depressant drugs, and high output states such as anaemia and thyrotoxicosis.

8. 3. PATHOPHYSIOLOGY The aetiologic factors mentioned above induce cardiac stress. They force the heart to work harder in order to maintain normal cardiac output. The cardiac stress can be direct ( ischaemia , infection, arrhythmias and congenital cardiac defects} Indirect stress include vascular pathology (such as hypertension, resistance to cardiac output:HOCM , reduced venous return), volume imbalances, and restrictive defects (pericardial constriction/tamponade)

9. 3. PATHOPHYSIOLOGY In the presence of these aetiologic factors which reduce cardiac output, compensatory mechanisms occur to maintain cardiac output: A. Neurohumoral mechanisms B. Ventricular dilatation C. Ventricular hypertrophy

10. 3. PATHOPHYSIOLOGY A. Neurohumoral Mechanisms This is mainly the activation of the adrenergic nervous system and the renin-angiotensin system. Adrenergic activation increases cardiac output by increasing the heart rate and the force of myocardial contractility. The side effect of adrenergic activation is increased oxygen consumption which can worsen cardiac ischaemia in some patients. It can also trigger ventricular arrhythmias which can lead to sudden death

11. 3. PATHOPHYSIOLOGY A. Neurohumoral Mechanisms ( contd ) Activation of the renin-angiotensin system increases blood volume by sodium and water retention leading to increase in blood volume and cardiac output. It also augment contractility by sympathetic nervous system stimulation. RAS activation however can lead to cardiac damage through myocardial fibrosis, and oxidative stress with resultant inflammation

12. 3. PATHOPHYSIOLOGY B. VENTRICULAR DILATATION Ventricular dilatation is one of the most important compensatory mechanisms by which a filing heart attempts to maintain the cardiac output. The stroke volume is enhanced when the end-diastolic fibre length is increased. This is called the Frank-Starling principle which states that “ The energy of contraction, however measured is a function of the length of the muscle fibre ”

13. 3. PATHOPHYSIOLOGY B. VENTRICULAR DILATATION (contd.): FRANK-STARLING PRINCIPLE

14. 3. PATHOPHYSIOLOGY The augmentation of cardiac output through chamber dilatation has a limit. Beyond a certain fibre length, the curve flattens because the interaction between actin and myosin myofilaments are compromised

15. 3. PATHOPHYSIOLOGY 3. VENTRICULAR HYPERTROPHY Ventricular hypertrophy is the compensatory mechanism seen in conditions of chronic volume and pressure overload. According to Laplace law, myocardial thickening limits the stress which the heart must generate to empty itself. Hypertrophy may be eccentric or concentric.

16. 3. PATHOPHYSIOLOGY 3. VENTRICULAR HYPERTROPHY (contd.) Concentric Hypertrophy Diseases such as hypertension and aortic stenosis generate pressure overload leading to increased systolic tension which causes sarcomere replication in parallel. The result is wall thickening at the expense of chamber size (concentric hypertrophy)

17. 3. PATHOPHYSIOLOGY 3. VENTRICULAR HYPERTROPHY (contd .) E ccentric Hypertrophy Diseases that cause volume overload such as ventricular septal defect, mitral and aortic regurgitation give rise to increased end-diastolic dimension and increased diastolic wall tension. They stimulate sarcomere replication in series and the result is chamber enlargement in addition to wall thickening: eccentric hypertrophy’

18. 3. PATHOPHYSIOLOGY 3. VENTRICULAR HYPERTROPHY (contd.) Eccentric and concentric hypertrophy allow the failing heart to meet the metabolic needs of the body using less oxygen. On the other hand, ventricular hypertrophy leads to chamber stiffness and impaired relaxation which can worsen cardiac function. It also leads to reduced coronary reserve which is also deleterious

19. 4. CLINICAL SYNDROMES OF HEART FAILURE Clinically, it is convenient to divide heart failure into left and right heart failure but practically, it is difficult for one side of the heart to fail in isolation. Clinical syndromes of heart failure include: Left heart failure Right heart failure Bi-ventricular failure

20. 4. CLINICAL SYNDROMES OF HEART FAILURE A. Left Heart Failure Some causes of left heart failure are: hypertension, mitral and aortic valve disease, cardiomyopathies and ischaemic heart disease. Symptoms include: exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, cough, haemoptysis , Cheyne -Stokes respiration, and non-specific symptoms such as restlessness, fatigue, confusion, mood disturbances and insomnia. Physical signs: tachycardia, displaced and heaving apex beat, left ventricular S3 or S4, functional mitral regurgitation, and bi-basal crepitations in the lung fields

21. 4. CLINICAL SYNDROMES OF HEART FAILURE B. Right Heart Failure Causes include: chronic lung disease ( cor pulmonale ), pulmonary embolism, left to right shunts, tricuspid valve disease, and pulmonary valve disease Symptoms: upper abdominal pain, anorexia, easy fullness, leg and abdominal swelling, fatigue, unexplained weight gain, nocturnal sweating, nocturia and extreme weakness. Signs: elevated jugular venous pulsation, tender smooth hepatomegaly, dependent pitting oedema , ascites, and pleural effusion.

22. 4. CLINICAL SYNDROMES OF HEART FAILURE C. Bi-Ventricular Failure Preferably used to describe a condition where the right heart has failed as a result of left heart failure. Clinical features are the combination of the 2 syndromes

23. 5. STAGING OF HEART FAILURE

24. 6. INVESTIGATIONS 1. Full B lood Count 2. Serum Electrolytes, Urea and Creatinine 3. Liver Function Tests 4. Urinalysis 5. Biomarkers: Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide (BNP), and their N-terminal fragments (NT-ANP and NT-BNP) 6. Chest X-ray (cardiomegaly, pulmonary plethora, upper lobe diversion, pleural effusion, Kerley B lines, hilar congestion (batwing appearance)

25. 6. INVESTIGATIONS 7. Electrocrdiogram : sinus tachycardia, supraventricular and ventricular ectopic beats, bundle branch block, left ventricular hypertrophy with strain. 8. Echocardiogram: detects chamber dilatation, reduced or normal ejection fraction, diastolic dysfunction, and specific features of different cardiovascular diseases. 9. Computed Tomographic Imaging: useful in pulmonary embolism 10. Magnetic Resonance Imaging: assesses myocardial viability. 11. Coronary Angiography: for ischaemic heart disease

26. CHEST X-RAY

27. ELECTROCARDIOGRAM

28. ECHOCARDIOGRAM

29. 7. TREATMENT OF HEART FAILURE A. GENERAL MEASURES Moderate physical activity as tolerated Restriction of sodium intake to 2-3gm daily Restriction of fluid intake to less than 2 litres daily if hyponatraemia is present

30. 7. TREATMENT OF HEART FAILURE B. PHARMACOLOGIC THERAPY Relief of Congestion/Low Cardiac Output Symptoms Inotropes: Digoxin, Dobutamine , Amrinone / Milrinone Diuretics: Loop diuretics ( Frusemide , Torsemide , Bumetanide) :Thiazide diuretics (HCTZ, Indapamide , Metolazone ) : Potassium-sparing ( Spironolactone,Triamterene ) Beta blockers: Metoprolol, Bisoprolol < Carvedilol

31. 7. TREATMENT OF HEART FAILURE B. PHARMACOLOGIC THERAPY Arrest/Reversal of Disease Progression ACEIs/ARBs Beta blockers Aldosterone antagonists: Spironolactone Prevention/Treatment of Complications Anticoagulants Anti-arrhythmic agents

32. 7. TREATMENT OF HEART FAILURE C. DEVICE THERAPY IN HEART FAILURE Implantable Cardioverter Defibrillator (ICD) Cardiac Resynchronisation Therapy (CRT)

33. 7. TREATMENT OF HEART FAILURE: SURGICAL MANAGEMENT

34. 7. TREATMENT OF HEART FAILURE ACUTE PULMONARY OEDEMA