However, the greater resistance (afterload) againstwhich the heart must pump, reduces the ejectionfraction and the perfusion of the tissue.The reduced perfusion of the kidneys activatesthe renin-angiotensin system(RAS), leading to reninsecretion and subsequent elevated plasmaangiotensin II and aldosterone levelsangiotensin II causes peripheral vasoconstrictionand aldosterone increases sodium retention, leadingto increased water retention, oedema, and anincreased preload
However, the greater resistance (afterload) against which the heart must pump, reduces the ejection fraction and the perfusion of the tissue. The reduced perfusion of the kidneys activates the renin-angiotensin system(RAS), leading to renin secretion and subsequent elevated plasma angiotensin II and aldosterone levels. angiotensin II causes peripheral vasoconstriction and aldosterone increases sodium retention, leading to increased water retention, oedema, and an increased preload
Intrinsic cardiac compensation:The increased cardiac preload leads toincomplete emptying of the ventricles andincrease in end-diastolic pressureThe heart eventually fails, owing tothemassiveincrease in myocardialenergyrequirements
Intrinsic cardiac compensation: The increased cardiac preload leads to incomplete emptying of the ventricles and increase in end-diastolic pressure. The heart eventually fails, owing to the massive increase in myocardial energy requirements
pathophysiology of heart failureCardiacdysfunctionContractiondiastoleloutput !β,RIvasoconstrictionneurohormoneRAStCAafterloadfconstrictionSodiumMyocardiumhypertrand waterophyReconstitutionVesselthickening,BloodreconstitutionvolumepreloadVein blood
Myocardiumhypertr ophy Reconstitution Cardiac dysfunction Contraction diastole output neurohormone 1R RAS CA constriction Sodium and water Blood volume Vein blood vasoconstriction afterload Vesselthickening, reconstitution preload pathophysiology of heart failure
pathophysiology of heart failureCardiacInotropic agentsdysfunctionImprovediastoleContractiondiastoleoutputBRblockerβ,RIvasoconstrictionneurohormoneRASTCAconstrictionafterloaddiureticsACEISodiumreduceMyocardiumhypertrand waterafterloadophyReconstititionVesselthickening,Bloodreconstitutionvolumepreload tACEIDeduct preloadVein blood
reduce afterload Cardiac dysfunction Contraction diastole output neurohormone 1R RAS CA constriction Myocardiumhypertr ophy Reconstitution Sodium and water Blood volume Vein blood vasoconstriction afterload Vesselthickening, reconstitution preload ACEI Improve diastole Inotropic agents R blocker diuretics Deduct preload pathophysiology of heart failure ACEI
Therapeutic strategies in CHF1. Chronic heart failure is typically managed byreduction inphysical activity.2. Low dietary intake of sodium (<1.5g every day)3. Treatment with vasodilators, diuretics andinotropicagents
Therapeutic strategies in CHF 1. Chronic heart failure is typically managed by reduction in physical activity. 2. Low dietary intake of sodium (<1.5g every day) 3. Treatment with vasodilators, diuretics and inotropic agents