1. Heart Failure

2. Clinical syndrome that develops when the heart cannot maintain adequate output, or can do so only at the expense of elevated ventricular filling pressure.

3. Heart Failure  Results from any structural or functional abnormality that impairs the ability of the ventricle to eject blood (Systolic Heart Failure) or to fill with blood (Diastolic Heart Failure).

4. The prevalence of heart failure rises with age Almost all forms of heart disease can lead to heart failure.

5. Mechanisms of heart failure  Reduced ventricular contractility CAD (segmental dysfunction) ‘cardiomyopathy(global dysfunction) o Ventricular outflow obstruction Hypertension, aortic stenosis (left heart failure) Pulmonary hypertension, pulmonary stenosis (right heart failure).  Ventricular inflow obstruction Mitral stenosis, tricuspid stenosis  Ventricular volume overload Ventricular septal defect.  Arrhythmia Atrial fibrillation,Tachycardia cardiomyopathy Complete heart block Bradycardia.  Diastolic dysfunction Constrictive pericarditis, Restrictive cardiomyopathy Cardiac tamponade.

6. Pathophysiology  Cardiac output is determined by preload (the volume and pressure of blood in the ventricles at the end of diastole) afterload (the volume and pressure of blood in the ventricles during systole) and myocardial contractility. Fall in cardiac output. activates counter regulatory neurohumoral mechanisms, renin–angiotensin–aldosterone system leads to vasoconstriction, sodium and water retention, and sympathetic nervous system activation. Activation of the sympathetic nervous system may initially sustain cardiac output through increased myocardial contractility (inotropy)and heart rate (chronotropy). Prolonged sympathetic stimulation also causes negative effects, including cardiac myocyte apoptosis, hypertrophy and focal myocardial necrosis. Sympathetic stimulation also causes peripheral vasoconstriction and arrhythmias.

7. The Vicious Cycle of Congestive Heart Failure Decreased Blood Pressure and Decreased Renal perfusion Stimulates the Release of renin, Which allows conversion of Angiotensin to Angiotensin II. Angiotensin II stimulates Aldosterone secretion which causes retention of Na+ and Water, increasing filling pressure LV Dysfunction causes Decreased cardiac output

8. Types of Heart Failure -Left, right and biventricular heart failure. -Diastolic and systolic dysfunction. -High-output failure. -Acute and chronic heart failure.

9. Causes of Low-Output Heart Failure chronic  Systolic Dysfunction  Coronary Artery Disease  Idiopathic dilated cardiomyopathy (DCM)  Hypertension  Valvular Heart Disease  Diastolic Dysfunction  Hypertension  Coronary artery disease  Hypertrophic obstructive cardiomyopathy (HCM)  Restrictive cardiomyopathy

10. Factors that may precipitate or aggravate heart failure in pre-existing heart disease  Myocardial ischaemia or infarction  Intercurrent illness, e.g. infection  Arrhythmia, e.g. atrial fibrillation  Inappropriate reduction of therapy  Administration of a drug with negative inotropic (β- blocker)or fluid-retaining properties (NSAIDs, corticosteroids)  Pulmonary embolism  Conditions associated with increased metabolic demand, e.g. pregnancy, thyrotoxicosis, anaemia  IV fluid overload, e.g. post-operative IV infusion

11. Clinical Presentation of HeartFailure(Acute)  Sudden onset of dyspnoea that rapidly progresses to acute respiratory distress, orthopnoea and cough.  The patient appears agitated, pale and clammy. The peripheries are cool to the touch and the pulse is rapid. The BP is usually high, The jugular venous pressure (JVP) is usually elevated.  Auscultation A ‘gallop’ rhythm, with a third heart sound, is heard. A new systolic murmur may signify acute mitral regurgitation or ventricular septal rupture. crepitations at the lung bases, or throughout the lungs if pulmonary oedema is severe.

12. Clinical Presentation of Heart Failure(Chronic)  Due to excess fluid accumulation: Dyspnea (most sensitive symptom Orthopnea, Paroxysmal Nocturnal Dyspnea (PND) Edema Hepatic congestion Ascites  Due to reduction in cardiac output: Fatigue (especially with exertion) Weakness Poor renal perfusion leads to oliguria and uraemia Chronic heart failure is sometimes associated with marked weight loss (cardiac cachexia).

13. Physical Examination in Heart Failure  Dyspniac  Cool, pale, cyanotic extremities Have sinus tachycardia, diaphoresis and peripheral vasoconstriction  Displaced Apex  S3 gallop Low sensitivity, but highly specific  Crackles or decreased breath sounds at bases (effusions) on lung exam  Elevated jugular venous pressure  Lower extremity edema  Ascites  Hepatomegaly  Splenomegaly

14. Complications  Renal failure  Hypokalaemia  Hyperkalaemia  Hyponatraemia  Impaired liver function  Thromboembolism  Atrial and ventricular arrhythmias

15. Lab Analysis in Heart Failure  CBC Since anemia can exacerbate heart failure  Serum electrolytes and creatinine before starting high dose diuretics  Fasting Blood glucose To evaluate for possible diabetes mellitus  Thyroid function tests Since thyrotoxicosis can result in A. Fib, and hypothyroidism can results in HF.  Iron studies To screen for hereditary hemochromatosis as cause of heart failure.  ANA To evaluate for possible lupus  Viral studies If viral mycocarditis suspected  BNP brain natriuretic pepetide

16. Chest X-ray in Heart Failure  Cardiomegaly  Cephalization of the pulmonary vessels  Kerley B-lines  Pleural effusions

17. Cardiomegaly

18. Pulmonary vessel congestion

19. Pulmonary Edema due to Heart Failure

20. Kerley B lines

21. Cardiac Testing in Heart Failure  Electrocardiogram: May show specific cause of heart failure: Ischemic heart disease Dilated cardiomyopathy: first degree AV block, LBBB, Left anterior fascicular block  Echocardiogram: Left ventricular ejection fraction Structural/valvular abnormalities

22. Further Cardiac Testing in Heart Failure  Exercise Testing Should be part of initial evaluation of all patients with CHF.  Coronary arteriography Should be performed in patients presenting with heart failure who have angina or significant ischemia. Endomyocardial biopsy Not frequently used Really only useful in cases such as viral-induced cardiomyopathy

23. Management of acute HF  acute medical emergency:  Sit the patient up to reduce pulmonary Congestion.  Give oxygen (high-flow, high-concentration).  IV diuretics (lasix)  Continuous monitoring of cardiac rhythm, BP.  Administer nitrates, such as IV glyceryl trinitrate until clinical improvement occurs or systolic BP falls.  Intravenous opiates must be used sparingly in distressed patients.  If these measures prove ineffective, inotropic agents may be required to augment cardiac output, particularly in hypotensive patients ( Dopamine).

24. Management of chronic heart failure  General measures  Drug therapy  Device therapy  Cardiac transplant

25. General measures  Education  Diet  Good general nutrition and weight reduction for the obese  Avoidance of high-salt foods and added salt.  Alcohol  Smoking cessation  Exercise  Regular moderate aerobic exercise within limits of symptoms  Vaccination  Consider influenza and pneumococcal vaccination  Treatment of the underlying cause of heart failure (CAD)

26. Drug therapy 1. ACE inhibitor (or ARB if not tolerated) 2. Beta blockers 3. Potassium sparing diuretics 4. Hydralazine, Nitrate 5. Loop diuretics 6. Digoxin

27. Diuretics  Loop diuretics  Furosemide, buteminide  diuretics produce an increase in urinary sodium and water excretion, leading to reduction in blood and plasma volume  Potassium-sparing diuretics  Spironolactone, eplerenone  Help enhance diuresis  Maintain potassium  Shown to improve survival in CHF

28. ACE Inhibitor  Improve survival in patients with all severities of heart failure.  Begin therapy low and titrate up as possible:  Enalapril – 2.5 mg po BID  Captopril – 6.25 mg po TID  Lisinopril – 5 mg po Q Daily  If cannot tolerate, may try ARB

29. Beta Blocker therapy  Certain Beta blockers (carvedilol, metoprolol, bisoprolol) can increase ejection fraction, improve symptoms, reduce the frequency of hospitalisation and reduce mortality.  Contraindicated: Heart rate <60 bpm Symptomatic bradycardia Signs of peripheral hypoperfusion COPD, asthma PR interval > 0.24 sec, 2 nd or 3 rd degree block

30. Hydralazine plus Nitrates  Dosing: Hydralazine Started at 25 mg po TID, titrated up to 100 mg po TID Isosorbide dinitrate Started at 40 mg po TID/QID  Decreased mortality, lower rates of hospitalization, and improvement in quality of life.

31. Other medication in Heart Failure  Digoxin can be used to provide rate control in patients with heart failure and atrial fibrillation. In patients with severe heart failure, digoxin reduces the likelihood of hospitalisation for heart failure,  Statin therapy is recommended in CHF for the secondary prevention of cardiovascular disease.  Some studies have shown a possible benefit specifically in HF with statin therapy

32. Meds to AVOID in heart failure  NSAIDS Can cause worsening of preexisting HF  Thiazolidinediones Include rosiglitazone (Avandia), and pioglitazone (Actos) Cause fluid retention that can exacerbate HF  Metformin People with HF who take it are at increased risk of potentially lethal lactic acidosis

33. Implantable Cardioverter-Defibrillators for HF( ICD) -CRT  Sustained ventricular tachycardia is associated with sudden cardiac death in HF.  About one-third of mortality in HF is due to sudden cardiac death.  Patients with ischemic or nonischemic cardiomyopathy, NYHA class II to III HF, and LVEF ≤ 35% have a significant survival benefit from an implantable cardioverter- defibrillator (ICD) for the primary prevention of SCD.

34. Cardiac-Resynchronization-Therapy

35. Management of Refractory Heart Failure  Inotropic drugs: Dobutamine, dopamine, milrinone, nitroprusside, nitroglycerin  Mechanical circulatory support: Intraaortic balloon pump Left ventricular assist device (LVAD)  Cardiac Transplantation