Mechanisms of heart failure • Definition of heart failure s a complex clinical syndrome that can result from impairs the ability of the ventricle to eject blood nifestations of heart failure are dyspnoea and fati t exercise tolerance) and fluid retention to pulmonary and peripheral oedema). ties impair the functional capacity and quality of dividuals. us recommendations for the management of chronic heart failur HF - AJC Jan 21,1999 vol 83(2A) - Packer M et al
Mechanisms of heart failure. Definition of heart failure. Heart failure is a complex clinical syndrome that can result from any cardiac disorder that impairs the ability of the ventricle to eject blood. The cardinal manifestations of heart failure are dyspnoea and fatigue - PowerPoint PPT Presentation
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Mechanisms of heart failure• Definition of heart failure
Heart failure is a complex clinical syndrome that can result from any cardiac disorder that impairs the ability of the ventricle to eject blood. The cardinal manifestations of heart failure are dyspnoea and fatigue(which may limit exercise tolerance) and fluid retention (Which may lead to pulmonary and peripheral oedema). Both abnormalities impair the functional capacity and quality of life of affected individuals.
Consensus recommendations for the management of chronic heart failureACTION HF - AJC Jan 21,1999 vol 83(2A) - Packer M et al
Definition of heart failure"Heart failure occurs when an abnormality of cardiac function causesthe heart to fail to pump blood at a rate required by the metabolizingtissues or when the heart can do so only with an elevated filling pressure. The heart's inability to pump a sufficient amount of blood to meet theneeds of the body tissues may be due to insufficient or defective cardiacfilling and/or impaired contraction and emptying.Compensatory mechanisms increase blood volume and raise cardiac filling pressures, heart rate, and cardiac muscle mass to maintain the heart's pumping function and cause redistribution of blood flow”.
National Heart, Lung and Blood Institute
Mechanisms of heart failure
• Reduced volume of blood delivered to the systemic arterial bed.
• One or both ventricles has elevated filling pressures.
• Result: Retention of sodium and water in the intravascular and intersititial compartments.
• Dyspnoea and oedema
Symptoms of heart failure• Dyspnoea - breathlessness - Increased awareness of respiration
or difficulty in breathing .• If due to cardiac causes it is usually due to left ventricular failure
and pulmonary congestion.– Pulm. capillary Hypertension
• Restrictive ventilatory defect -VC and TV reduced• Lungs are stiffer -increased work of breathing• Air trapping - earlier closure of dependent airways• Airways resistance increased - congestion of peripheral airways.• V/Q mismatch - hypoxaemia• Increased ventilatory drive
•Primary abnormality of the heart muscle - Cardiomyopathies/myocarditis•Coronary atherosclerosis - Ishaemia and infarction of the muscle•Longstanding excessive haemodynamic burden i.e valvular abnormality causing myocardial damage
Systolic dysfunction with a depressed LV ejection fraction (usually <40%)Generally accompanied by an increase in left ventricular end-diastolic and end systolic volumes
Pathophysiological mechanisms that causes raised filling pressures and/ poor tissue
• An increased cardiac load– Cardiac output = Stroke vol x heart rate
– Pre-load Contractility Afterload
• Preload: Tension of the myocardial fibers at the end of diastole (degree of stretch): Venous filling pressure.
• Afterload: Myocardial wall tension developed during systolic ejection: LV: resistance of aortic valve, peripheral vascular resistance and elasticity of major blood vessels. Laplace: T= PR/2xwall thickness. Ventricular wall tension is increased by ventricular dilatation, incr. intra-ventricular pressure or reduction in wall thickness
• Afterload: – Systemic and pulmonary resistance– Physical characteristics of the vessel walls– The volume of blood that is ejected.Increase in after load decreases CO with an increase in end-diastolic
volume which in turn increases afterload (Laplace)• Examples (LV)
or reduction in wall thickness: see Laplace – conditions that cause volume overload – I.e Aortic and mitral regurgitation, dilated cardiomyopathies etc
Mechanisms of load induced effects on cardiac performance
Myocardial remodelling in heart failure:•Geometric remodelling•Change in myocardial gene expression
•Contractile proteiens (Myosin heavy chains), Na-K-ATPase, Ca-ATPase,Beta 1 adrenoreceptors
•Abnormal calcium homeostasis•Prolongation of the calcium current in association with prolongation of contraction and relaxation (Decr. Sarcolemmm Ca-ATPase activty etc.)
•Apoptosis.•Programmed cell death – initiated cytokines, free radicals etc.
Mechanisms of load induced effects on cardiac performance
Myocardial remodelling in heart failure:Geometric remodelling:Ventricular hypertrophy - compensatory mechanism of increased load:Increase in size of cells, mitochondria, myofibrils,interstitial collagenStimulus for hypertrophy:•Pressure overload:
•Systolic wall stress increases•Parallel replication of myofibrils:•Thickening of myocytes: •Concentric hypertrophy
•Volume overload:•Diastolic wall stress increases•Sarcomeres replicates in series•Elongation of myocytes•Ventricular dilatation / eccentric hypertrophy
The High Output States
• Low out-put failure (commonest)– Impaired peripheral circulation with systemic vasoconstriction and
shunting of blood to the vital organs– Cold, pale / cyanotic extremities.– Pulse pressure may narrow
• High output failure: Heart is required to pump abnormally large quantities of blood to deliver the required quota of oxygen to metabolizing tissues– Reduced vascular resistance, increased vascular capacitance and blood
volume– Extremities are warm and flushed, pulse pressure may be wide– Arterial-mixed venous oxygen difference normal or reduced due to
delivery of large amounts of arterial blood to non-metabolizing tissues.
• Mitral regurgitation: LA dilates and pressure rises (compliance), LV dilates (vol. overload - proportion of CO regurgitated) – CO increases. LV dysfunction: Pulm. venous congestion due to mitral regurgitation and LV failure.
• Aortic stenosis: Obstruction to LV outflow, LV hypertrophy (concentric – pressure overload), relative LV ischaemia, LV dysfunction: LV end-diastolic pressures and LA pressures rise, pulm. congestion.
• Aortic regurgitation: Proportion of LV EF regurgitated, LV Dilates (volume overload) and CO increases. Diastolic pressure declines and