congestive heart failure definition


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CONGESTIVE HEART FAILURE DEFINITION 1920's - " organ physiology " paradigm - interplay between the abnormal heart and the circulation. The focus on circulatory abnormalities 1960's - " cell biochemistry " paradigm - depressed contractility and impaired relaxation - PowerPoint PPT Presentation


  • CONGESTIVE HEART FAILUREDEFINITION1920's - "organ physiology" paradigm - interplay between the abnormal heart and the circulation. The focus on circulatory abnormalities 1960's - "cell biochemistry" paradigm - depressed contractility and impaired relaxation1980's - "gene expression" paradigm - molecular alterations in the myocardial cells Heart failure is a clinical syndrome in which impaired cardiac pumping decreases ejection and impedes venous return. These haemodynamic abnormalities are generally complicated by depressed myocardial contractility and relaxation, which reflect biochemical and biophysical disorders in the myocardial cells. This latter, in turn, are due to partly to molecular abnormalities that not only impair the heart's performance, but also acceletrate the deterioration of the myocardium and hastens myocardial cell death.PATHOPHYSIOLOGY OF HEART FAILUREHeart failure can develop:a.) Acutely resulting from acute myocardial infarction secondary to an infectious or infiltrating process (virus, bacterial, rotozoal)b.) Chronically (over months or years) as the end-stage of different heart diseases. This low output failure can result from:a.) decrease in myocardial contractile reserve, due to: myocardial infarction cardiomyopathy increased afterload (eg. hypertension)b.) valvular disease (eg. aortic stenosis or mitral regurgitation)c.) prolonged rhythm disturbances (eg. ventricular tachycardia)

  • The primary signs and symptoms of all types of CHF include: tachycardia decreased exercise tolerance shortness of breath peripheral and pulmonary edema cardiomegalyCardinal feature: cardiac output (CO falls short of what is required for normal tissue perfusionReason: decrease in cardiac contractilityLow output failure: responds to positive inotropic drugsHigh output failure: the demands of the body are so great that even increased CO is insufficient (eg. hyperthyreodism, beri-beri, anaemia, arteriovenous shunt). Respond poorly to positive inotropic drugs.Haemodynamics of heart failureForward or inotropic failure - reduced ejection into the aorta and pulmonary artery Backward or lusitropic failure - inadequate emptying of the venous reservoirs

  • SITE OF FAILUREBACKWARD FAILUREFORWARD FAILURERight heart failureIncreased systemicReduced ejection intovenous pressurepulmonary arteryLeft heart failureIncreased pulmonaryReduced ejection into the avenous pressureaortaBecause blood flows in a circle, none of these occurs in pure form. In "Forward failure" - when the ventricle empties poorly, the filling is reducedIn "Backward failure" - when filling is reduced, the stroke volume is reducedIn right ventricular failure: the increase in systemic venous pressure and decreased ejection of blood into the pulmonary artery reduce the output of the left ventricle

    In left ventricular failure: increased pulmonary venous pressure impedes the blood out of the lungs increases pulmonary capillary pressure. This is transmitted across the pulmonary circulation and results in increased pulmonary arterial pressure which can impair right ventricular ejection.

  • Signs and symptoms of heart failureThe clinical picture in heart failure consists of: signs (the objective manifestations of depressed cardiac performance), symptoms (abnormalities perceived by the patient).Left heart failure: is a "forward failure" - reduced ejection, "backward failure" - rise in pulmonary capillary pressure.Systemic reflex activation: vasoconstriction increased blood pressure (to maintain perfusion of vital organs; ie. heart, brain)Despite the increased sympathetic tone perfusion decreases to the skeletal muscle: fatigue and skeletal muscle myopathy to the kidneys: oliguria, sodium and water retention to the tissues: cyanosis Because of the backward failure pulmonary congestion impaired respiration Dyspnea (difficulty breathing) due to arterial hypoxia, and decreased lung compliance (excess fluid transudates from the pulmonary capillaries) depth and rate of breathing increase). Typical in supine position. Mild HF: dyspnea occurs only during heavy exerciseSevere HF: dyspnea is present at rest (bubbling noises during respiration)End-stage HF: fluid fills the bronchial system; pulmonary edema Right heart failure: is a backward failure rather than a forward failure. The central venous pressure is over the maximum. Edema (liver, kidneys, spleen, GIT, skin, genitalies) Cyanosis

  • Cardiomegaly - one of the major signs of heart failure. Initially due to the operation of the Frank-Starling relationship Remodelling of the ventricular wall is a complex processPressure overload (hypertension, aortic stenosis `inward' hypertrophy, reduced ventricular cavity (concentric hypertropy)Volume overload (aortic regurgitation) the ventricle dilates (eccentric hypertrophy)Grading of severity of heart failure according to the New York Heart Association (NYHA)NYHA I. Signs of heart failure appears only heavy exertion and disappear after its discontinuationNYHA II.On normal workload signs of CHF appears in the evening but disappear after night restNYHA III. At rest minimal signs of CHF causing no complains but marked signs of CHF on walking, which are not fully relieved by night rest.NYHA IV. Signs of CHF even at bed rest.

  • Compensatory mechanisms in heart failureExtrinsic reflex mechanisms for compensation: Sympathetic nervous system (SNS)Renin-angiotensin-aldosterone hormonal response.Increased sympathetic outflow: tachycardia, increased contractility, increased vascular tone (venous tone) increased ventricular filling pressure dilatation of the heart increased fiber stretchIncreased aldosterone secretion: sodium and water retention increased blood volume edema.

  • Developed tensionPCWP (Hgmm)normalfailingVelocity ofcontractionLOADnormalfailingIntrinsic compensatory mechanism: myocardial hypertrophy Increased muscle mass (to maintain cardiac performance) Hypoxic myocardium Decreased oxygen supply to the myocardium

    12Depressed contractility in heart failure reflected either as a reduced peak tension development (1) or depressed force-velocity curve (2)

  • Pathophysiology of cardiac performanceCardiac performance depends on at least 4 primary function:A: PRELOAD (LVEDP, LVEDV, reflected as central venous pressure) Preload refers to the diatolic loading conditions of the heart;- Left ventricle: left atrial pressure (or pulmonary capillary wedge pressure = PCWP)- Right ventricle: right atrial pressure for the right ventricle. These are the "filling pressures"Left ventricular function curve: (SV or SW against the filling pressure)

    The ascending limb (bellow 15 mmHg) represents the classic Frank-Starling relation. Beyond approximately 15 mmHg, there is a plateau of performance. Preload greater than 20-25 mmHg result in pulmonary congestion.

  • The Frank-Starling low of the heart describes the property of cardiac muscle to increase its contractility as the length of the myocardial fiber (stretch) is increased.To accomplish this increase in stretch, more blood must be returned to the heart by:a.) Increased sympathetic tone causing vasoconstriction decreased venous blood storage (pooling) increased end-diastolic volume (or filling pressure) and CO.b.) Redistribution of blood from viscera to heartc.) Fluid or sodium retention due to decreased renal perfusion, and renin-angiotensin-aldosterone activation. This increases volume of blood returned to the heart and also may cause edema.REDUCTION OF PRELOAD: DIURETICSB: AFTERLOAD: is the resistance against which the heart must pump blood. Systemic vascular resistance is frequently increased in CHF (increased sympathetic outflow and circulating catecholamines). This may speed failure.REDUCTION OF AFTERLOAD: ARTERIAL VASODILATORSC: CONTRACTILITY: is the vigor of contraction of heart muscle. In CHF the primarily defect: reduction in the intrinsic contractility (dP/dt)INCREASE IN CONTRACTILITY: POSITIVE INOTROPIC DRUGS.D: HEART RATE: is the major determinant of cardiac output (CO)- When CO decreases HR increases (beta-adrenoreceptor activation)- Consequences:- diastole shortens - myocardial perfusion worsens- hypoxia

  • CARDIAC HYPERTROPHYThe most important intrinsic compensatory mechanisms. Complex biochemnical biophysical mechanisms in the background.a.) Energetics in the failing heartImbalance betwen energy production and energy utilization.Cause: is the overload itself Result: "state of energy starvation" (increased energy utilization and decreased high energy phosphate production).b.) Structural changes in the chronically overloaded heartFailing heart is not equal with a normal enlarged heart (sportmens heart)Architectural changes:Pressure overload - the walls of the heart thickenVolume overload - dilated heartChronic heart failure: hyperthrophied heart: myocyte necrosis (fibroblast poliferation) muscle is replaced by connective tissue the heart begins to dilate wall tension incerases propensity for arrhythmias c.) Altered blood supply Imbalance between the capillary density and muscle mass (increased intercapillary distance) Decreased coronary reserve (underperfused subendocardium) Subendocardial necrosis

  • d.) Altered proportion of mitochondria and myofibrils Imbalance between myofibrils and mitochondria (more energy-consuming myofibrils must be supplied with ATP by relatively fewer mitochondria) Exacerbated energy starvation NOTE:a.) Many of these sings and symptoms of CHF are a direct result of these compensatory mechanisms.b.) Despite all attempts to compensate, the cardiac function deteriorateVITIOUS CYCLE occur, and CO cannot be maintained without medical interventionArrhythmogenic mechanisms in the hyperthropied heart Enlargement and fibrosis of the atria and ven