heart failure英文课件

心力衰竭双语教学英文课件杭州师范大学医学院附属医院薛树仁教授HEART FAILUREProf.Shu-Ren Xue MD FESC FACCdate posted: March, 2008Definition of heart failure Clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject bloodDirect Causes1-Myocardial abnormalities (CHD!) 2-Hemodynamic overload3-Ventricular filling abnormalities 4-Ventricular dyssynergy5-Changes in cardiac rhythmAggravating Factors•Pregnancy •Arrhythmias (AF)•Infections •Thromboembolism •Hyper/hypothyroidi sm •Endocarditis •Obesity •Hypertension •Physical activity •Dietary excessPathophysiologyHF is summarized best asan imbalance in Starling forcesimbalance in the degree of end-diastolic fiber stretch proportional to the systolic mechanical work expended in an ensuing contraction. Characterized as a malfunction between the mechanisms that keep the interstitium and alveoli dryopposing forces that are responsible for fluid transfer to the interstitium.Heart Rate = Cardiac Output Heart Failure:Determinants of CardiacOutputStrokeVolumePreload AfterloadContractility xPatterns of ventricular hypertrophyHeart failure associated with aortic valvular lesions (A)Initial / Ongoing Evaluation •Identify heart disease•Assess functional capacity (NYHA, 6 min walk, …)•Assess volume status: (edema, rales, jugular, hepatomegaly, body weight)•Lab assessment: routine: electrolytes, renal funct. Repeat ECHO, RX only if significantchanges in functional status•Assess prognosisThe New York HeartAssociation's functional classification of CHF . Class I describes a patient who is not limited with normal physical activity bysymptoms.Class II occurs when ordinary physical activity results in fatigue, dyspnea, orother symptoms.Class III is characterized by a marked limitation in normal physical activity. Class IV is defined by symptoms at rest or with any physical activityEpidemiologyIn US: More than 3 million people have CHF, 400,000 new patients present yearly. Prevalence of CHF is 1-2% of the general population.Approximately 30-40% of patients with CHF are hospitalized every year.The 5-year mortality rate after diagnosis was as 60% in men and 45% in women.SYMPTOMSAnxiety、Dyspnea at rest、Dyspnea on exertion .Orthopnea and paroxysmal nocturnal dyspnea (PND).Cough productive of pink, frothy sputum.Edema.Nonspecific Weakness、Lightheadedness、Abdominal pain、Malaise、Wheezing、Nausea.The varied faces of heart failurePhysical SIGN peripheraledema,jugularvenousdistention, tachycardia Tachypnea,.Hypertension、Pulsus alternansSkin may be diaphoretic or cold,gray, and cyanotic.Wheezing rales.Apicalimpulse displaced laterally. auscultation may reveal aortic or mitral valvular abnormalities,S3or S4.Lower extremity edemaDiagnosisImaging StudiesHeart failure associated with mitral regurgitation (B)Lab Studies:1. atrial natriuretic peptide（ANP）and brainnatriuretic peptide（BNP））arginine vasopression, AVPendothelinIncreased creatinine, hyperbilirubinemia, and dilutional hyponatremia are observed in severe cases.elevated alanine aminotransferase (ALT) aspartate aminotransferase (AST) suggestive of a congestive hepatopathy. Cardiac enzymes and other serum markers for ischemia or infarction.Arterial blood gas (ABG) in evaluationof hypoxemia, ventilation/perfusion (V/Q) mismatch, hypercapnia, and acidosis. proteinuria are observed in early and mild-to-moderate disease.DIFFERENTIALS：Acute Respiratory Distress Syndrome，Altitude Illness -Pulmonary Syndromes ，Chronic Obstructive Pulmonary Disease and Hyperventilation SyndromeMyopathies，Pericarditis and Cardiac TamponadeBacterial Pneumonia, Immunocompromised Pneumothorax, Iatrogenic, Spontaneous andHeart disease No symptoms HF Risk Factors No Heart disease No symptoms Asymptomatic LV dysfunction Refractory HF symptoms Prior or current HF SymptomsStages in the evolution of Heart Failure A BCDAHA / ACC HF guidelines 2001Heart disease (any)Hypertension Diabetes, Hyperchol.Family Hx Cardiotoxins AsymptomaticLV dysfunctionSystolic / Diastolic Marked symptomsat rest despitemax. therapy Dyspnea, Fatigue Reduced exercise tolerance Stages in the Evolution of Heart Failure Clinical Characteristics AB CDAHA / ACC HF guidelines 2001ACE-i βblockersTreat risk factors Avoid toxics ACE-i in selected p.In selected patientsPalliative therapyMech. Assist deviceHeart Transplant ACE-iβblockersDiuretics / Digitalis Stages in the Evolution of Heart Failure Treatment AB CDAHA / ACC HF guidelines 20018070605040302054-60>6050403020100Post MI n=196<3031-3536-4546-53CardiacMortality%LVEFBrodie B. et alAm J Cardiol 1992;69:1113PrognosisTreatment ObjectivesSurvivalMorbidityExercise capacityQuality of lifeNeurohormonal changesProgression of CHFSymptoms(Cost)Treatment•Prevention. Control of risk factors •Life style •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 All S e l e c t e d p a t i e n t sTreatment Pharmacologic Therapy•Diuretics•ACE inhibitors•Beta Blockers•Digitalis•Spironolactone•OtherDiuretics•Essential to control symptoms secondary to fluid retention •Prevent progression from HT to HF • Spironolactone improves survival • New research in progressCortex MedullaThiazidesInhibit active exchange of Cl-Nain the cortical diluting segment of the ascending loop of HenleK-sparingInhibit reabsorption of Na in the distal convoluted and collecting tubuleLoop diureticsInhibit exchange of Cl-Na-K in the thick segment of the ascendingloop of HenleLoop of HenleCollecting tubule DiureticsDiuretics. Indications1.Symptomatic HF, with fluid retention•Edema•Dyspnea•Lung Rales•Jugular distension•Hepatomegaly•Pulmonary edema (Xray)AHA / ACC HF guidelines 2001ESC HF guidelines 2001Loop Diuretics / Thiazides. Practical Use Start with variable dose. Titrate to achieve dry weightMonitor serum K+at “frequent intervals”Reduce dose when fluid retention is controlled Teach the patient when, how to change doseCombine to overcome “resistance”Do not use aloneLoop diuretics. Dose (mg)Initial Maximum Bumetanide0.5 to 1.0 / 12-24h 10 / day Furosemide20 to 40 / 12-24h 400 / day Torsemide10 to 20 / 12-24h 200 / dayAHA / ACC HF guidelines 2001Thiazides, Loop Diuretics. Adverse Effects •K+, Mg+(15 -60%) (sudden death ???)•Na+• Stimulation of neurohormonal activity•Hyperuricemia (15 -40%)•Hypotension. Ototoxicity. Gastrointestinal.Alkalosis. MetabolicSharpe N. Heart failure. Martin Dunitz 2000;43Kubo SH , et al. Am J Cardiol 1987;60:1322MRFIT, JAMA 1982;248:1465Pool Wilson. Heart failure. Churchill Livinston 1997;635Diuretic ResistanceNeurohormonal activationRebound Na+uptake after volume lossHypertrophy of distal nephronReduced tubular secretion (renal failure, NSAIDs) Decreased renal perfusion (low output)Altered absortion of diureticNoncompliance with drugsBrater NEJM 1998;339:387Kramer et al. Am J Med 1999;106:90Managing Resistance to Diuretics •Restrict Na+/H 2O intake (Monitor Natremia)•Increase dose (individual dose, frequency, i.v.)• Combine: furosemide + thiazide / spiro / metolazone •Dopamine (increase cardiac output)•Reduce dose of ACE-i•UltrafiltrationMotwani et al Circulation 1992;86:439VASOCONSTRICTIONVASODILATATIONKininogen KallikreinInactive FragmentsAngiotensinogenAngiotensin IRENINKininase IIInhibitorALDOSTERONE SYMPATHETICVASOPRESSINPROSTAGLANDINS tPAANGIOTENSIN IIBRADYKININACE-i. Mechanism of ActionA.C.E.ACE-I. Clinical Effects•Improve symptoms•Reduce remodelling / progression •Reduce hospitalization•Improve survivalPlaceboEnalapril12111098765Probabiility of DeathMonths0.10.800.20.30.70.40.50.6p< 0.001p< 0.002CONSENSUSN Engl J Med 1987;316:14294321ACE-i50403020100Months0612p = 0.0036%Mortality241830364248Enalapriln=1285Placebon=1284SOLVD (Treatment)N Engl J M 1991;325:293n = 2589CHF-NYHA II-III -EF < 35ACE-iMortality,%4SAVEN Engl J Med 1992;327:669Years3020100123PlaceboCaptopriln=1115n=1116p=0.019² -19%n = 22313 -16 days post AMI EF < 4012.5 ---150 mg / dayAsymptomatic ventriculardysfunction post MIACE-i。