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CARDIAC FAILURE DEFINITION It is a complex syndrome, that can result from any structural or functional cardiac disorder. A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body or physiological circulation.  It is commonly termed congestive h...

CARDIAC FAILURE DEFINITION It is a complex syndrome, that can result from any structural or functional cardiac disorder. A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body or physiological circulation.  It is commonly termed congestive heart failure (CHF/ccf) since symptoms of increase venous pressure are often prominent  Types of Heart failure PREVALENCE   The incidence is 2-4 % (35-64 years) 10% > 65 yrs.  Prognosis is still bad, upto 50% deaths in 5 years  It accounts 5% of admissions in medical wards  Cost of Mx !! > 1 Billion $ / year (UK stats) Underlying causes of systolic heart failure include the following: • Coronary artery disease Diabetes mellitus Hypertension • Valvular heart disease (stenosis or regurgitant lesions) • Arrhythmia (supraventricular or ventricular) • Idiopathic cardiomyopathy • Infections and Underlying causes of diastolic heart failure include the following: Coronary artery disease Diabetes mellitus Hypertension Valvular heart disease (aortic stenosis) Hypertrophic cardiomyopathy Restrictive cardiomyopathy (amyloidosis, sarcoidosis) Constrictive pericarditis Underlying causes of right heart failure include the following: LV failure Coronary artery disease (ischemia) Pulmonary hypertension Chronic pulmonary disease Pulmonary valve stenosis Pulmonary embolism Neuromuscular disease Causes of acute heart failure include the following: Acute valvular (mitral or aortic) regurgitation Myocardial infarction (MI) Myocardit is Arrhythmi a Drugs (eg, cocaine, calcium channel blockers, or causes of high-output heart failure include the following: Anemia Hyperthyroidism Beriberi heart disease Paget disease of bone Albright syndrome (fibrous dysplasia) Multiple myeloma Pregnancy Glomerulonephri tis Polycythemia vera Carcinoid syndrome Common Causes of ccf  CAD is the most common cause (35-40%)  Dilated cardiomyopathy (30-34 %)  Hypertension (15-20%) PATHOPHYSIOLOGY  Neurohormonal changes  Hemodynamic changes  Cellular changes-myocyte  The Frank-Starling mechanism afterloa d Preloa d SYMPTOMS     Leg swelling Shortness of breath Orthopnea paroxysmal nocturnal dyspnea Low cardiac output symptoms Abdominal symptoms: PHYSICAL SIGNS  Leg edema  Increased Jugular Venous Pressure  Displaced and sustained apical impulses  Third S3 – low pitched sound that is heard rapid filling of ventricle  Fourth heart Sound (S4)     - - Usually at the end of diastole Exact mechanism is not known Could be due to contraction of atrium against stiff ventricle during PHYSICAL SIGNS contd….     Pale, cold sweaty skin Hepatomegaly Inspiratory crackles (Rales) Ascitis Framingham Criteria for Diagnosis of of (Heart Heart Failure Failurediagnosis requires 1 . Criteria: Major or more criteria positive) Acute pulmonary edema Cardiomegaly Hepatojugular reflex Neck vein distention Paroxysmal nocturnal Dyspnea or Orthopnea Pulmonary rales Third Heart Sound (S3 Gallup Rhythm) Criteria: Minor (Heart Failure diagnosis requires 2 or more criteria positive) Ankle edema Dyspnea on exertion Hepatomegaly Nocturnal cough Pleural Effusion Tachycardia (Heart Rate >120 beats per minute) Differential Diagnosis  Pericardial diseases  Liver diseases  Nephrotic syndrome/chronic renal failure  Protein losing enteropathy LABORATORY FINDINGS Complete blood count (CBC), which may indicate anemia or infection as potential causes of heart failure Urinalysis (UA), which may reveal proteinuria, which is associated with cardiovascular disease Serum electrolyte levels, which may be abnormal owing to causes such as fluid retention or renal dysfunction Blood urea nitrogen (BUN) and creatinine levels, which may indicate decreased renal blood flow Fasting blood glucose levels, because elevated levels indicate a significantly increased risk for heart failure (diabetic and nondiabetic patients) LABORATORY FINDINGS Liver function tests (LFTs), which may show elevated liver enzyme levels and indicate liver dysfunction due to heart failure B-type natriuretic peptide (BNP) and N-terminal pro-Btype (NT-proBNP) natriuretic peptide levels, which are increased in heart failure; these measurements are closely correlated with the NYHA heart failure classification ELECTROCARDIOGRAM  Old MI or recent MI/ ischaemia  Arrhythmia  Left Bundle Branch Block Chest X-ray  Size and shape of heart  Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema)  Pleural effusion ECHOCARDIOGRAM  Function of both ventricles  Wall motion abnormality that may signify Coronary Artery Disease  Valvular abnormality  Intra-cardiac shunts  Ejection Fraction Cardiac Catheterization  Is indicated when CAD  valvular  If heart transplant is indicated heart is suspected • Treatment  Treatment of cardiac failure  Treatment of underlying cause Diet and Activity  Salt restriction  Fluid restriction  Daily weight (tailor therapy)  Gradual exertion programs afterloa d Preloa d Treatment of cardiac Failure Diuretic Therapy   The most effective symptomatic relief Mild symptoms  HCTZ  Chlorthalidone  Metolazone Block Na reabsorbtion in loop of henle and distal convoluted tubules-furosemide  Thiazides are ineffective with GFR < 30/min  Diuretics (cont.)  Side Effects  Pre-renal azotemia  Skin rashes  Neutropenia  Thrombocytopen ia  Hyperglycemia  ↑ Uric Acid K+ Sparing Agents  Triamterene & amiloride – acts tubules to ↓ K secretion  on distal Spironolactone (Aldosterone inhibitor) recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin- aldosterone system with subsequent effect on myocardial remodeling and Inhibitors of renin-angiotensinaldosterone system  Renin-angiotensin-aldosterone is activation early in the course of heart failure role system in the and plays an important progression of the syndrome   Angiotensin inhibitors converting enzyme Side effects of ACE inhibitors  Angioedema  Hypotension  Renal insuffiency  Rash Angiotensin II receptor blockers  Has comparable effect to ACE Inhibitors  Can be used in certain conditions when ACE Inhibitors are contraindicated (angioneurotic edema, cough)  Eg losrtan., telmisartan  The Digitalis Glycosides (Digoxin, Digitoxin) role of digitalishas declined because of safety  somewh at concern Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant: Reduction in hospitalization Reduction in symptoms of HF Digitalis (cont.) Mechanism of Action +ve inotropic effect by -↑ Na-Ca exchange   Vagotonic effect  Arrhythmogenic effect Digitalis Toxicity  Narrow therapeutic to toxic ratio  Non cardiac manifestations Anorexia, Nausea, vomiting, Headache, Altered Digitalis Toxicity  Cardiac manifestations  Sinus bradycardia and arrest  A/V block (usually 2nd degree)  Atrial tachycardia with A/V Block  Development of junctional rhythm in patients with a fib  PVC’s, VT/ V fib (bi-directional VT) β Blockers  Has been traditionally contraindicated in pts with CHF  Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV function  In addition to improved LV function multiple studies show improved survival  The only contraindication decompensated CHF is severe Vasodilators  Reduction of afterload by arteriolar vasodilatation (Ca channel blockers/ace) reduce LVEDP, O2 consumption,improve myocardial perfusion,  stroke volume and COP  Reduction of preload By venous dilation ( Nitrate) ↓ the venous return  ↓ the load on both ventricles. Usually the maximum benefit is achieved by using agents with both action.  Positive inotropic agents  These are the drugs that improve myocardial contractility (β adrenergic agonists, dopaminergic agents, phosphodiesterase inhibitors), dopamine, dobutamine, milrinone, amrinone  Several studies showed ↑ mortality oral with inotropic agents  So the only use for them now is in acute sittings as cardiogenic shock TREATMENT  Correction of reversible causes  Ischemia  Valvular heart disease  Thyrotoxicosis and other high output status  Shunts  Arrhythmia  Atrial fibrillation, Atrial flutter,  Medications  Ca channel blockers, Antiarrhythmics Anticoagulation (coumadine)  Atrial fibrillation  H/o embolic episodes  Left ventricular apical thrombus Antiarrhythmics  Most common cause of SCD in these patients is ventricular tachyarrhythmia  Patients with h/o sustained VT or SCD → ICD implant New Methods  Implantable ventricular assist devices  Biventricular pacing (only in patient with LBBB &  Artificial Heart CHF) Cardiac Transplant  It has become more widely used since the advances in immunosuppressive treatment  Survival rate  1 year 80% - 90%  5 years 70% Prognosis  Annual mortality rate depends on patients symptoms and LV function  5% in patients with mild symptoms and mild ↓ in LV function  30% to 50% in patient with advances LV dysfunction and severe symptoms  40% – 50% of death is due to SCD THANK YOU