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Prepared By Dr.Mustafa Alshehabat Slide 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) Slide 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. Slide 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 Slide 5 Pathophysiological Changes in HF Ventricular Dilatation. Myocyte Hypertrophy. Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction. Slide 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. Slide 7 Classification of heart failure I. No limitation. Normal physical exercise doesnt cause fatigue, dyspnea or palpitations. II. Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnea or palpitations. III. Marked limitation. Comfortable at rest but gentle physical activity produces marked symptoms of HF. IV. Symptoms of HF occur at rest and are exacerbated by any physical activity. Slide 8 Kussmauls 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 Slide 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.sternumcardiacheartsystole The normal apex beat can be palpated in the precordium left 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.palpatedprecordiumdextrocardia Slide 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.pulmonary hypertensionBeta-blockers 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).Left bundle branch block 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 abnorm al S4 is heard in people with conditions that increase resistance to ventricular filling, such as a weak left ventricle. Slide 11 Edema Bilateral lower extremity edema Slide 12 Hypertension Hypertrophic Cardiomyopathy Slide 13 Compensatory Mechanisms Increased Heart Rate Sympathetic = Norepinephrine Dilation Frank Starling = Contractility Neurohormonal Redistribution of Blood to the Brain Slide 14 Low Output Increased Preload Increased AfterloadNorepinephrine Increased SaltVasoconstrictionRenal Blood Flow Renin Angiotension I Angiotension II Aldosterone Slide 15 Infiltration of Interstitial Space l Normal Micro-anatomy l Micro-anatomy with fluid movement. Slide 16 Acute Pulmonar y Edema a true life- threatening emergency Slide 17 Slide 18 Treatment Prevention. Control of risk factors Prevention. Control of risk factors Life style Life style Treat etiologic cause / aggravating factors Treat etiologic cause / aggravating factors Drug therapy Drug therapy Personal care. Team work Personal care. Team work Revascularization if ischemia causes HF Revascularization if ischemia causes HF ICD (Implantable Cardiac Defibrillator) ICD (Implantable Cardiac Defibrillator) Ventricular resyncronization Ventricular resyncronization Ventricular assist devices Ventricular assist devices Heart transplant Heart transplant Artificial heart Artificial heart Neoangiogenesis, Gene therapy Neoangiogenesis, Gene therapy All Selected patients Slide 19 Treatment Objectives Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms(Cost) Slide 20 Treatment Pharmacologic Therapy Treatment Pharmacologic Therapy Diuretics ACE inhibitors Beta Blockers Digitalis Spironolactone Other Diuretics ACE inhibitors Beta Blockers Digitalis Spironolactone Other Slide 21 Diuretics Essential to control symptoms Essential to control symptoms secondary to fluid retention Prevent progression from HT to HF Prevent progression from HT to HF Spironolactone improves survival Spironolactone improves survival New research in progress New research in progress Slide 22 Cortex Medulla Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle Thiazides Inhibit active exchange of Cl-Na in the cortical diluting segment of the ascending loop of Henle K-sparing Inhibit reabsorption of Na in the distal convoluted and collecting tubule 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 Loop diuretics Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Loop of Henle Collecting tubule Diuretics Slide 23 Diuretics. Indications 1.Symptomatic HF, with fluid retention Edema Edema Dyspnea Dyspnea Lung Rales Lung Rales Jugular distension Jugular distension Hepatomegaly Hepatomegaly Pulmonary edema (Xray) Pulmonary edema (Xray) AHA / ACC HF guidelines 2001 ESC HF guidelines 2001 Slide 24 Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weightStart with variable dose. Titrate to achieve dry weight Monitor serum K + at frequent intervalsMonitor serum K + at frequent intervals Reduce dose when fluid retention is controlledReduce dose when fluid retention is controlled Teach the patient when, how to change doseTeach the patient when, how to change dose Combine to overcome resistanceCombine to overcome resistance Do not use aloneDo not use alone Slide 25 Loop diuretics. Dose (mg) InitialMaximum InitialMaximum 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 Slide 26 Thiazides, Loop Diuretics. Adverse Effects K +, Mg + (15 - 60%) (sudden death ???) K +, Mg + (15 - 60%) (sudden death ???) Na + Na + Stimulation of neurohormonal activity Stimulation of neurohormonal activity Hyperuricemia (15 - 40%) Hyperuricemia (15 - 40%) Hypotension. Ototoxicity. Gastrointestinal. Alkalosis. Metabolic 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 Slide 27 VASOCONSTRICTION VASODILATATION Kininogen Kallikrein Inactive Fragments Angiotensinogen Angiotensin I RENIN Kininase II Inhibitor ALDOSTERONE SYMPATHETIC VASOPRESSIN PROSTAGLANDINS tPA ANGIOTENSIN II BRADYKININ ACE-i. Mechanism of Action A.C.E. Slide 28 ACE-I. Clinical Effects Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival Improve symptoms Reduce remodelling / progression Reduce hospitalization Improve survival Slide 29 Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % Selected high risk subgroups Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % Selected high risk subgroups ACE-i. Indications AHA / ACC HF guidelines 2001 ESC HF guidelines 2001 Slide 30 ACE-I. Adverse Effects Hypotension (1st dose effect) Hypotension (1st dose effect) Worsening renal function Worsening renal function Hyperkalemia Hyperkalemia Cough Cough Angioedema Angioedema Rash, ageusia, neutropenia, Rash, ageusia, neutropenia, Slide 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 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 Slide 32 -Adrenergic Blockers Mechanism of action -Adrenergic Blockers Mechanism of action Density of 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HR Antiischemic Antihypertensive Antiarrhythmic Antioxidant, Antiproliferative Density of 1 receptors Inhibit cardiotoxicity of catecholamines Neurohormonal activation HR Antiischemic Antihypertensive Antiarrhythmic Antioxidant, Antiproliferative Slide 33 -Adrenergic Blockers Clinical Effects -Adrenergic Blockers Clinical Effects Improve symptoms (only long term) Reduce remodelling / progression Reduce hospitalization Reduce sudden death Improve survival Improve symptoms (only long term) Reduce remodelling / progression Reduce hospitalization Reduce sudden death Improve survival Slide 34 Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % After AMI Symptomatic heart failure Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % After AMI AHA / ACC HF guidelines 2001 ESC HF guidelines 2001 -Adrenergic Blockers Indications Slide 35 Hypotension Hypotension Fluid retention / worsening heart failure Fluid retention / worsening heart failure Fatigue Fatigue Bradycardia / heart block Bradycardia / heart block -Adrenergic Blockers Adverse Effects Review treatment (+/-diuretics, other drugs) Review treatment (+/-diuretics, other drugs) Reduce dose Reduce dose Consider cardiac pacing Consider cardiac pacing Discontinue beta blocker only in severe cases Discontinue beta blocker only in severe cases Slide 36 Na + K+K+ K+K+ K+K+ K+K+ Ca ++ Na-K ATPase Na-Ca Exchange Myofilaments Digitalis CONTRACTILITY - Slide 37 Digitalis. Mechanism of Action Blocks Na + / K + ATPase => Ca + + Inotropic effect Inotropic effect Natriuresis Natriuresis Neurohormonal control Neurohormonal control - Plasma Noradrenaline - Peripheral nervous system activity - RAAS activity - Vagal tone - Normalizes arterial baroreceptors NEJM 1988;318:358 Slide 38 Digitalis. Clinical Effects Improve symptoms Modest reduction in hospitalization Does not improve survival Improve symptoms Modest reduction in hospitalization Does not improve survival Slide 39 Digitalis. Indications When no adequate response to When no adequate response to ACE-i + diuretics + beta-blockers ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001 AHA / ACC Guidelines 2001 In combination with ACE-i + diuretics In combination with ACE-i + diuretics if persisting symptoms if persisting symptoms ESC Guidelines 2001 ESC Guidelines 2001 AF, to slow AV conduction AF, to slow AV conduction Dose 0.125 to 0.250 mg / day Slide 40 ALDOSTERONE Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Retention Na + Retention H 2 O Excretion K + Excretion Mg 2+ Collagen depositionFibrosis - myocardium - myocardium - vessels - vessels Spironolactone Edema Arrhythmias Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) Aldosterone Inhibitors - Slide 41 Spironolactone. Practical use Do not use if hyperkalemia, renal insuf.Do not use if hyperkalemia, renal insuf. Monitor serum K + at frequent intervalsMonitor serum K + at frequent intervals Start ACE-i firstStart ACE-i first Start with 25 mg / 24hStart with 25 mg / 24h If K + >5.5 mmol/L, reduce to 25 mg / 48hIf K + >5.5 mmol/L, reduce to 25 mg / 48h If K + is low or stable consider 50 mg / dayIf K + is low or stable consider 50 mg / day New studies in progress New studies in progress Slide 42 RENIN Angiotensinogen Angiotensin I ANGIOTENSIN II Angiotensin I ANGIOTENSIN II ACE Other pathways Vasoconstriction Proliferative Action Proliferative Action Vasodilatation Antiproliferative Action Antiproliferative Action AT1 AT2 AT1 Receptor Blockers AT1 Receptor Blockers RECEPTORS Angiotensin II Receptor Blockers (ARB) Slide 43 1- VENOUS VASODILATATION Preload 2- Coronary vasodilatation Myocardial perfusion 3- Arterial vasodilatation Afterload 4- Others 1- VENOUS VASODILATATION Preload 2- Coronary vasodilatation Myocardial perfusion 3- Arterial vasodilatation Afterload 4- Others Pulmonary congestion Ventricular size Vent. Wall stress MVO 2 NITRATES HEMODYNAMIC EFFECTS Cardiac output Blood pressure Slide 44 Nitrates. Clinical Use CHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspnea In acute CHF and pulmonary edema:NTG sl / iv Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency) CHF with myocardial ischemia Orthopnea and paroxysmal nocturnal dyspnea In acute CHF and pulmonary edema:NTG sl / iv Nitrates + Hydralazine in intolerance to ACE-I (hypotension, renal insufficiency) Slide 45 Heart Transplant. Indications Refractory cardiogenic shock Refractory cardiogenic shock Peak VO2 < 10 ml / kg / min Peak VO2 < 10 ml / kg / min Severe symptoms of ischemia not amenable to revascularization Severe symptoms of ischemia not amenable to revascularization Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Recurrent symptomatic ventricular arrhythmias refractory to all therapeutic modalities Contraindications: age, severe comorbidity Slide 46 Heart Failure and Myocardial Ischemia Coronary HD is the cause of 2/3 of HF Coronary HD is the cause of 2/3 of HF Segmental wall motion abnormalities are not specific if ischemia Segmental wall motion abnormalities are not specific if ischemia Angina coronary angio and revascularization Angina coronary angio and revascularization No angina No angina Search for ischemia and viability in all ? Search for ischemia and viability in all ? Coronary angiography in all ? Coronary angiography in all ? Slide 47 HEART FAILURE MODELS CONGESTIVE - Digoxin, Diurtics HEMODYNAMIC - Vasodilators NEUROHUMORAL - ACE inhibitors, - Blockers, Spironolactone IMMUNOLOGICAL - Cytokine inhibitors Slide 48 THANK YOU