1、Heart Failure,Xiaojuan Bai,7 years program of China Medical University,Objective :1.Mastering clinical manifestation ,diagnosis and management of heart failure2.Grasping causes,pathophysiology of heart failure3.Understanding classification and investigation of heart failure,1.general concept1)causes
2、 of heart failure2)precipitating/aggravating factors3)pathophysiology4)type of heart failure2.chronic and acute heart failure 1)clinical manifestation2)investigation3)diagnosis and differential diagnosis4)management,Content,Heart failure is an imprecise term used to describe the state that develops
3、when the heart cannot maintain an adequate cardiac output or can do so only at the expense of an elevated filling pressure.,Definition,pulmonary congestion,systemic venous congestion ,tissue perfusion deficiency due tolow cardiac output .,Clinical Features,left ventricular end-diastolic pressure18mm
4、Hg, right ventricular end-diastolic pressure10mmHg,heart failure = cardiac insuffiency.,Hemodynamic Features,Causes of heart failure,1.Reduced ventricular contractility a. Cardiomyopathy, myocardial infarction. b. Metabolic dysfunction,2.ventricular overload a. pressure overload- hypertension , aort
5、ic stenosis, pulmonary hypertension, pulmonary valve stenosis.b. volume overload - mitral regurgitation, aortic regurgitation , atrial septal defect, ventricular sepals defect , hyperthyroidism, artery-venous fistula. c. ventricular inflow obstruction-hypertrophy , mitral stenosis, tricuspid stenosi
6、s, restrictive cardiomyopathy, constrictive pericarditis .endocardial fibrosis and other disorders that cause a stiff myocardium.,Precipitating / aggravating factors,myocardial ischemia or infarctioninfection arrhythmiapulmonary embolismexertionpregnancy and parturitionanemia intravenous fluid overl
7、oad, electrolytedisturbance, acid-base imbalance,Pathophysiology,1. Frank-Starlings Law of the heart a. The cardiac output is a function of the preload, the afterload, and myocardial contractility.b.Preload: the volume and pressure of blood in the ventricle at the end of diastole.c. Afterload :the a
8、rterial resistance.,2. RAAS in Heart Failure,2. RAAS in Heart Failure,3.myocardium impaired and remodeling,initial myocardium impaired ventricular overload myocardium infarction inflammation,disease progress heart failure complication death,chamber enlargement myocardial hypertrophy embryo gene phen
9、otype extracellular matrix change,secondary conduct factor sympathetic nervous system RAAS endothelins TNF- ,IL-6 mechanical stress oxidative stress,4.Diastolic heart failureHeart failure may develop as a result of poor ventricular filling and high filling pressure caused by abnormal ventricular rel
10、axation,sarcoplasmic reticulum intake Ca2+free Ca2+ in myocyte degrade slowly b. In CHD with obvious ischemia ,before contractility dysfunction, have occurred relaxation dysfunctionc. In hypertrophy and hypertrophic cardiomyopathy, left ventricular end-diastolic filling pressure pulmonary hypertensi
11、on ,pulmonary congestion diastolic heart failure,relaxation dysfunction,Type of heart failure Heart failure can be described or classified in several ways.,1. Acute and chronic heart failure 2. Left ,right and biventricular heart failure 3. High and low output heart failure 4. Diastolic and systolic
12、 dysfunction 5.Asymptomatic and congestive heart failure,Low output heart failure:Clinical manifestation of abnormal peripheral circulation:vasoconstriction in system , cold, pale, extremities cyanosis,in the late period,output per minute decrease and lead to difference of pulse pressure decrease, t
13、he above manifestationoccur in the majority of CHF.High output heart failure:Extremities warm,flush, difference of pulse pressure increase, seen in hyperthyroidism,anemia,pregnancy,Systolic dysfunction Heart failure may develop as a result of impaired myocardial contraction .Diastolic dysfunctionHea
14、rt failure can also be due to poor ventricular filling pressure caused by abnormal ventricular relaxation ,which is commonly found in patients with left ventricular hypertrophy, hypertension and ischemic heart disease.,1 Chronic heart failure Definitionsame meaning as congestive heart failure,clinic
15、al manifestation 1.left ventricular heart failure mainly manifested with pulmonary congestion and reduction of cardiac output A symptom 1.dyspnea 1)breathlessness 2) paroxysmal nocturnal dyspnea:often with wheeze sound in both lung cardiogenic asthma,3)Orthopnea: in decubitus,blood volume flow to he
16、art increase elevated enddiastolic filling pressure pulmonary venous and capillary pressure increase interstitial pulmonary edema pulmonary compliance decrease respiratory resistance 4)acute pulmonary edema,2. cough and hemoptysispink-tinged or brownish sputum3. fatigue on exertion 4. urinary system
17、 symptomin early period ,nocturia increasein later period, oliguria,B. Sign 1.general sign dyspnea after activity,also cyanosis, jaundice , difference of pulse pressure decrease, SBp decrease, rapid heart rate , peripheral vasoconstriction ,extremities cyanosis, cold, sinus tachycardia.,2.Heart sign
18、diffuse and laterally displaced apical impulsegallop in early diastolic period , accentuated p2 systolic murmur at cardiac apexpulses alternans occur when left ventricular ejective impedance increase3.Lung signmoist rales in the base of lung CHF patients occur pleural fluid,2.Right ventricular Failu
19、resystemic circulation congestion Symptom1)gastrointestinal tract symptom:anorexia, distention ,nausea ,vomiting ,constipation 2)kidney symptomkidney congestion renal function decrease 3)hepatic region pain: congestion , cardiac cirrhosis 4)dyspnea,Sign 1.heart signheart dilatewhen right heart failu
20、re is obvious,strong impulseoccur in the systolic period at the left sternal border, obvious beat occur infraxiphoiddiastolic galloprelative tricupid incompetence 2.hepatic cervical reflux 3.congestive liver and tenderness occur before edemaAcute : jaundice , ALT increaseLong term: cardiac cirrhosis
21、,4.edemaoccur after cervical filling and liver large, is typical sign of right heart failure. at first occur in foot, ankle , anterior tibia.In the early period,edema occur in the morning, worsein the evening ,disappear after sleeping.In the late time,systemic , symmetric, pitting edema If complicat
22、ed with malnutrition or hepatic dysfunction , face edema occur, prognosis is poor.5.pleural fluid and ascites,3.biventricular heart failure have clinical manifestation of left and right heart failure.,Conditions with normal systolic function and decreased diastolic function include:(1) systemic arte
23、rial hypertension(2) myocarditis(3) hyretrophic cardiomyopathy(4) congestive cardiomyopathy,In the setting of left ventricular dysfunction, which of following neurohormonal factors would be activated?(1)Norepinephrine(2)Endothelin(3)Arginie vasopreein(4)Endothelial-derived relaxing factor,Investigat
24、ion1.routine examination blood, urine, renal function, electrolyte, liver function2.ECGa.no specific findings .b.Abnormalities may provide etiological clue(ventricular hypertrophy,AMI,bundle branch block)c.V1ptf-0.03mm/s left atrial overload,3.Echocardiography:evaluating LV as well as other chamber
25、dimensions, ejection fraction, and wall motion abnormality. a.M:obtained directing a stationary ultrasonography beam at some portion of the heart. b.Two-dimensional Echo (2-DE):provides spatially correct images of heart and has become the dominant echocardiographic modality c.Doppler Echo:using ultr
26、asonography to record the flow of blood within the cardiovascular system.,4.X ray a evaluation of chamber enlargement b pulmonary venous congestionKerley B lines:reflect chronic elevation of left atrial pressure and represent chronic thickening of the interlobular septa from edema.venous blood redis
27、tribution to the upper lobes. C pulmonary venous pressure25-30mmHg(3.3-4KPa) interstitial edema occur.,Invasive homodynamic monitoring,Diagnosis and differential diagnosisClinical diagnosis include :etiology(basic cause and induce cause), pathoanatomy, pathophysiology,heart rhythm cardiac function,N
28、YHA classification no activity limit , daily activity dont lead to inertia, dyspnea, palpitation. slight activity limit , no symptom at rest ,daily activity lead to inertia, dyspnea, palpitation or angina pectoris. obvious activity limit , no symptom at rest , daily activity lead to inertia, dyspnea
29、, palpitation or angina pectoris. cannot do any activity , have symptom at rest.,Forrester classification,Killip classification, no heart failure symptom, no moist rales, PCWP may elevate slight to moderate heart failure, 50%lung field moist rales, may occur lung edema cardiac shock, Bp90mmHg, oligu
30、ria 20ml/h, skin cold, cyanosis, tachypnea, rapid pulseV cardiogenic shock and pulmonary edema,Differential diagnosis1. Left heart failurePulmonary ,cardiogenic dyspnea 2. Right heart failureconstrictive pericarditisrenal edema hepatic cirrhosis,Management of heart failure 1.Etiologic treatmentbasic
31、 cause , precipitating causes.2.Reduction of ventricular overload a.rest and sedative agent b.salt-intake control normal adult intake 3-6g salt per day0 heart failure : 2g salt/per day 0heart failure : 1g salt/per day 0heart failure : 0.4g salt/per day,c.water intake controlmay not limit water intak
32、e strictly, intake water 1.5-2.0L per dayin severe heart failure, water retention, seral albumin decrease, dilutive hyponatremia, not only limit salt intake ,but also control water intake,d.diuretics,Reasonable application of diuretics1. strictly following indication 2. combined medicationK-sparing
33、diuretics is contradicted in renal dysfunction 3. intermissional therapy 4. Pay attention to water and electrolyte disturbance,Differential of deficit sodium and diluted hyponatremia deficit sodium hyponatremia occurred after using many diuretics. feature: postohypotension, oliguria, high urine grav
34、ity, should intake salt diluted hyponatremiaalso called refractory heart failure ,hyponatremia of high blood volume ,should limit water-intake,e.Vasodilator drugs Indication 1.Left end-diastolic filling pressure18mmHg, pulmonary congestion 2.clinical manifestation of peripheral circulatory perfusion
35、 deficiency CI2.2L/min.m2 3.valve insufficiency, ventricular septal defect pulmonary hypertension,valve regurgitation with cardiac dysfunctionIf blood volume deficiency ,should fluid replacement at first,then use vasodilator drugs.,ACE-I ContradictionSevere renal dysfunction, renal artery stenosis,
36、obvious mitral and aortic stenosisAmerican and European guideline : that all heart failure patients including asymptomatic failure, except patients that have contradiction or cannot tolerate ACE-I, should use ACE-I, and for the long term therapy.,3.increase cardiac output a.Digitalis Pharmacologyinc
37、rease myocardial contractile forceInhibit Na+-K+ ATPase Na+ -Ca2+change intracellular Ca2+ increase contractility increaseincrease cardiac output Renal flow increase SAS activity decrease peripheral vasodilate peripheral resistance decrease,RAAS activity decrease Reduction of water and salt retentio
38、n due to aldosterone decrease Prolong atrioventricular conductionHighly effective in the treatment of atrial fibrillation in addition to slowing ventricular response ,it may convent the rhythm to normal sinus mechanism.,Use carefullyHypertrophic cardiomyopathy Mitral stenosis with sinus rhythm Peric
39、ardium constriction Pulmonary heart disease High degree AVB AMI in 24h,Digitalis toxicityInduce causeHypokalemiaHypomagnemiaHypercalcemiaAcid intoxicationHypoxiaRenal dysfunction Severe myocardial lesionHypothyroidism,Clinical manifestation of digitalis Systemic toxic effects:Gastrointestinal tract
40、symptom:nausea, vomiting , anorexia, diarrhea, confusion,amblyopia Cardiac symptom:arrhythmia Prolonged PR interval and AV conduction. Increase the automaticity of Purkinje fibers and enhance reentry ,resulting in extrasystoles, ventricular fibrillation.,TreatmentStopping using digitalisUse potassiu
41、m,magnesium if serum K is low.Rapid arrhythmia : lidocarine or diphenine sodium,1-4mg/min usually dont cardioversionSlowly arrhythmia atropine0.5-1mg.,b. Other inotropic agent1.-adrenocepter agonists Dopamine 1-5ug/Kg.min activate dopamine receptor ,renal flow increase10ug/Kg.min activate -receptor,
42、 vasoconstrictDobutamine 2-7.5ug/Kg.min,2.Phosphodiesterase inhibitorInhibit cAMP degrade increase intracellular cAMP Ca2+ increase cardiac contraction increaseAmrinone Milrione,3.Aldosterone antagonistProtect aldosterone escape.,4.-adrenocepter antagonistsRecent clinic trials have shown ,when given
43、 in very small doses under carefully monitored conditions , they can increase ejection fraction, improve symptoms and reduce the frequency of hospitalization in patient with chronic heart failure. Relieve toxiation of catecholamine. On the base of using ACE-I, diuretics , digitalis, using bloker. Gi
44、ven in very small incremental dosesBisoprool 1.25mg metoprolol 6.25mg,5.diastolic heart failure treatment treat primary diseaserelax myocardiumrevert myocardial hypertrophydecrease preloadcontrol tachycardiacalcium channel blocker,and blocker can be useful.,6.Refractory heart failure1)Have the etiol
45、ogy and precipitating causes been established?2)Are drug dose optimal?3)Is the patient adhering to an adequate low-salt diet?4)Need another cardiac transplantation.,7.Acute pulmonary edema Emergency treatment 1)position:Dont keep patient in a supine position 2)Maintain oxygenation:high concentration
46、s of O2 should be given by mask or nasal cannula. 3)Morphine sulfate 3 - 5mg IV or 5- 10mg IM can reduce agitation,reduce transient arterial and venous dilation, decrease the respiratory rate, slow the heart rate,and reduce respiratory and cardiac work.,4)Intravenous administration of a rapidly acti
47、g diuretic , eg.(furosemide 40mg IV) can be initiate a prompt diuresis in 15 to 20 min. 5)Rotating tourniquets are effective with Bp cuff applied to 3 limbs, inflated midway between diastolic and systolic pressure,deflated and rotated 10 to 20 min. 6)Vasodilator drugs 7)Digitalis 8)Aminophylline 9)o
48、thers,Pathophysiologic consequences of a myocardial infarction include:(1)increased systolic load due to the akinetic segment (2)decreased ejection fraction that approximates the amount of muscle loss. (3)hypertrophy of noninfarcted myocardium. (4)decreased end-diastoic volume,Supportive evidence th
49、at left-sided failure is present includes all the following EXCEPT: A.abnormally elevated filling pressures as detected by right heart catheterization B.a cardiac index of 3.5 liters/min/m2 C.a reduction in maximum oxygen consumption determined noninvasively by exercise D.the presence of pulmonary rales on physical examination E.low left ventricular ejection fraction at rest on echocardiography,
