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Compensatory Mechanisms in Heart failure

Compensatory Mechanisms in Heart failure. Dr. Riaz Motara School of Medicine Dept of Cardiology Baragwanath Hospital. Objectives. The Frank Starling Effect Neurohormonal response Beneficial effects Detrimental effects Hypertrophy Concentric Eccentric. The Frank-Starling Effect.

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Compensatory Mechanisms in Heart failure

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  1. Compensatory Mechanisms in Heart failure Dr. Riaz Motara School of Medicine Dept of Cardiology Baragwanath Hospital

  2. Objectives • The Frank Starling Effect • Neurohormonal response • Beneficial effects • Detrimental effects • Hypertrophy • Concentric • Eccentric

  3. The Frank-Starling Effect • “ Energy of contraction is proportional to the initial length of the muscle fibre”. • For the heart, the length of the muscle fibres ie. preload is proportional to the end-diastolic volume. • The relation between ventricular stroke volume and end-diastolic volume is called the Frank-Starling curve.

  4. The Frank-Starling Effect • Left ventricular stroke volume determined by • Preload (venous return + end diastolic volume) • Contractility (force per given end diastolic volume) 3. Afterload (aortic impedence and wall stress)

  5. The Frank-Starling Effect

  6. The Frank-Starling Effect in Heart failure

  7. Neurohormonal Adaptations • The principle systems involved in the response to heart failure are the : • Sympathetic nervous system • Renin-angiotensin system • Atrial natriuretic peptide • Cytokine systems • Nitric oxide

  8. Sympathetic Nervous System • One of the 1st responses to a decrease in cardiac output is activation of the SNS, resulting in both increased release and decreased uptake of norepinephrine at adrenergic nerve endings. • This results in augmentation of ventricular contractility and heart rate which maintains cardiac output, particularly during exercise. With progressive worsening of ventricular function, these mechanisms are no longer sufficient.

  9. Sympathetic Nervous System • Increased sympathetic activity also leads to systemic and pulmonary vasoconstriction, which initially contribute to the maintenance of blood pressure by increasing ventricular preload. • Renal vasoconstiction at the efferent arteriole, increases the filtration fraction that allows GFR to be maintained despite a fall in renal blood flow. • Both NE and angiotensin II stimulate proximal tubular sodium reabsorption, which contributes to sodium retention characteristic of heart failure.

  10. Sympathetic Nervous System • Down regulation of beta-1 receptors • Normal density of beta-2 receptors • Beta-2 receptor stimulation associated with increased propensity for ventricular fibrillation.

  11. The Renin-Angiotensin System

  12. The Renin-Angiotensin System

  13. Atrial Natriuretic Peptide

  14. Nitric Oxide • CHF associated with endothelial dysfunction. • Decreased NO synthesis • Decreased flow-dependent dilation

  15. Cytokines • Heart failure characterised by increased circulating levels of pro-inflammatory cytokines • TNF-alpha, IL-6, IL-2 and IL-1 beta • Chemokines • Cotransport inhibitory factor • Cyclooxygenase-2 • Metalloproteinases

  16. Cytokines • Toxic to myocardium • Promotes the generation of ROS • Increased myocyte loss/apoptosis • Promotes ventricular fibrosis and dilatation • Leads to ventricular dysfunction • Prognostic importance

  17. Hypertrophy • Increased synthesis of mitochondria • Increased myofibrillar mass • Activation of embryonic cardiac growth factors • Concentric hypertrophy • Pressure overload • Eccentric hypertrophy • Volume overload

  18. Frank-Starling Effect Preload Contractility Afterload Hypertrophy Concentric eccentric Neurohormonal adaptation SNS RAS ANP Cytokines NO Summary

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