* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Congestive Heart Failure
Remote ischemic conditioning wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Electrocardiography wikipedia , lookup
Rheumatic fever wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Coronary artery disease wikipedia , lookup
Mitral insufficiency wikipedia , lookup
Lutembacher's syndrome wikipedia , lookup
Artificial heart valve wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Jatene procedure wikipedia , lookup
Heart failure wikipedia , lookup
Cardiac surgery wikipedia , lookup
Quantium Medical Cardiac Output wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Heart arrhythmia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Prepared By Dr.Mustafa Alshehabat 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) 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. 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……………… Pathophysiological Changes in HF Ventricular Dilatation. Myocyte Hypertrophy. Salt and Water Retention. Sympathetic Stimulation. Peripheral Vasoconstriction. 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. Classification of heart failure No limitation. Normal physical exercise doesn’t 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. I. 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 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 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. 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. Edema Bilateral lower extremity edema Hypertension Hypertrophic Cardiomyopathy Compensatory Mechanisms Increased Heart Rate Sympathetic = Norepinephrine Dilation Frank Starling = Contractility Neurohormonal Redistribution of Blood to the Brain Low Output Increased Preload Increased Afterload Increased Salt Flow Vasoconstriction Norepinephrine Renal Blood Renin Angiotension I Angiotension II Aldosterone Infiltration of Interstitial Space Normal Micro-anatomy Micro-anatomy with fluid movement. Acute Pulmonar y Edema a true lifethreatening emergency Treatment Selected patients • Prevention. Control of risk factors • Life style All • 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 Treatment Objectives Survival Morbidity Exercise capacity Quality of life Neurohormonal changes Progression of CHF Symptoms (Cost) Treatment Pharmacologic Therapy • Diuretics • ACE inhibitors • Beta Blockers • Digitalis • Spironolactone • Other Diuretics • Essential to control symptoms secondary to fluid retention • Prevent progression from HT to HF • Spironolactone improves survival • New research in progress 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 Medulla Inhibit exchange of Cl-Na-K in the thick segment of the ascending loop of Henle Loop of Henle Collecting tubule Diuretics. Indications 1.Symptomatic HF, with fluid retention • Edema • Dyspnea • Lung Rales • Jugular distension • Hepatomegaly • Pulmonary edema (Xray) AHA / ACC HF guidelines 2001 ESC HF guidelines 2001 Loop Diuretics / Thiazides. Practical Use • Start with variable dose. Titrate to achieve dry weight • Monitor serum K+ at “frequent intervals” • Reduce dose when fluid retention is controlled • Teach the patient when, how to change dose • Combine to overcome “resistance” • Do not use alone 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 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 ACE-i. Mechanism of Action VASOCONSTRICTION VASODILATATION ALDOSTERONE PROSTAGLANDINS Kininogen VASOPRESSIN SYMPATHETIC tPA Kallikrein Angiotensinogen RENIN Angiotensin I A.C.E. ANGIOTENSIN II Inhibitor BRADYKININ Kininase II Inactive Fragments ACE-I. Clinical Effects • Improve symptoms • Reduce remodelling / progression • Reduce hospitalization • Improve survival 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 ACE-I. Adverse Effects • Hypotension (1st dose effect) • Worsening renal function • Hyperkalemia • Cough • Angioedema • Rash, ageusia, neutropenia, … 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 ß-Adrenergic Blockers Mechanism of action • Density of ß1 receptors • Inhibit cardiotoxicity of catecholamines • Neurohormonal activation • HR • Antiischemic • Antihypertensive • Antiarrhythmic • Antioxidant, Antiproliferative ß-Adrenergic Blockers Clinical Effects • Improve symptoms (only long term) • Reduce remodelling / progression • Reduce hospitalization • Reduce sudden death • Improve survival ß-Adrenergic Blockers Indications • Symptomatic heart failure • Asymptomatic ventricular dysfunction - LVEF < 35 - 40 % • After AMI AHA / ACC HF guidelines 2001 ESC HF guidelines 2001 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 Digitalis Na-K ATPase Na+ K+ Na-Ca Exchange Na+ Myofilaments K+ Na+ Ca++ Ca++ CONTRACTILITY Digitalis. Mechanism of Action Blocks Na+ / K+ ATPase => Ca+ + • Inotropic effect • Natriuresis • Neurohormonal control - Plasma Noradrenaline Peripheral nervous system activity RAAS activity Vagal tone - Normalizes arterial baroreceptors NEJM 1988;318:358 Digitalis. Clinical Effects • Improve symptoms • Modest reduction in hospitalization • Does not improve survival Digitalis. Indications • When no adequate response to ACE-i + diuretics + beta-blockers AHA / ACC Guidelines 2001 • In combination with ACE-i + diuretics if persisting symptoms ESC Guidelines 2001 • AF, to slow AV conduction Dose 0.125 to 0.250 mg / day Aldosterone Inhibitors Spironolactone ALDOSTERONE - Competitive antagonist of the aldosterone receptor (myocardium, arterial walls, kidney) • Retention Na+ • Retention H2O • Excretion K+ • Excretion Mg2+ • Collagen Edema deposition Fibrosis Arrhythmias - myocardium - vessels Spironolactone. Practical use • Do not use if hyperkalemia, renal insuf. • Monitor serum K+ at “frequent intervals” • Start ACE-i first • Start with 25 mg / 24h • If K+ >5.5 mmol/L, reduce to 25 mg / 48h • If K+ is low or stable consider 50 mg / day New studies in progress Angiotensin II Receptor Blockers (ARB) RENIN Angiotensin I Angiotensinogen ACE Other pathways ANGIOTENSIN II AT1 Receptor Blockers AT1 Vasoconstriction RECEPTORS Proliferative Action AT2 Vasodilatation Antiproliferative Action NITRATES HEMODYNAMIC EFFECTS 1- VENOUS VASODILATATION Pulmonary congestion Preload Ventricular size Vent. Wall stress MVO2 2- Coronary vasodilatation Myocardial perfusion 3- Arterial vasodilatation Afterload 4- Others • Cardiac output • Blood pressure 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) 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 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 ? HEART FAILURE MODELS CONGESTIVE - Digoxin, Diurétics HEMODYNAMIC - Vasodilators NEUROHUMORAL - ACE inhibitors, - Blockers, Spironolactone IMMUNOLOGICAL - Cytokine inhibitors THANK YOU