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Heart Failure

Heart Failure. & Starling’s Law. “The inability of the heart to supply adequate blood flow and therefore oxygen delivery to peripheral tissues and organs ” Warwick Cardiology Society. http://www.cvphysiology.com/Heart%20Failure/HF002.htm. Learning Objectives 1.

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Heart Failure

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  1. Heart Failure & Starling’s Law “The inability of the heart to supply adequate blood flow and therefore oxygen delivery to peripheral tissues and organs” Warwick Cardiology Society http://www.cvphysiology.com/Heart%20Failure/HF002.htm

  2. Learning Objectives 1 • Understand how the pumping activity of the heart is affectedby changes in venous return and total peripheral resistance

  3. Quick review on Starling’s Law • Relation of venous return (and hence preload) to stroke volume (due to force generation) • Stretch  Sarcomere lengthening  ↑ force generated  ↑ SV • Length-tension and force-velocity relationships • Note other non-Starling relationship (Trop C-calcium sensitivity due to increased sarcomere length) • Not just one Starling curve – curve depends on ionotropy/afterload state • High afterload/decreased ionotropy Curve shifted down and R-wards • Low afterload/increased ionotropy Shifts curve up and leftwards

  4. Learning Objectives 2 • Explain the pathophysiology of heart failure • Describe the clinical characteristics of the principal types of heart failure, and the circumstances which lead to its development • Identify targets for drug action for the manipulation of cardiac output • Describe the principlesinvolved in the general managementof heart failure, and the categories of drugsused in its therapy.

  5. Principle types of heart failure & Circumstances for development • Pathophysiology • Clinical characteristics • Principles of management • Categories of drugs and their targets

  6. HF types

  7. Pathophysiology • Causes: • Intrinsic – e.g. dilated and hypertrophic cardiomyopathies • Extrinsic – uncontrolled HTN, ↑SV, hormonal (e.g. Hyperthyroidism), Pregnancy, Drugs (alcohol, cocaine)

  8. ‘HEART FAILED’ • H – Hypertension • E – Endocarditis/environment (e.g. heat wave) • A – Anaemia • R – Rheumatic Heart Disease and other valvular disease • T - Thyrotoxicosis • F – Failure to take medications • A – Arrhythmia • I – Infection/Ischaemia/Infarction • L – Lung problems (PE, pneumonia, COPD) • E – Endocrine (Phaeochromocytoma, hyperaldosteronism) • D – Dietary indiscretions

  9. Pathophysiology cont… • Cardiac dysfunction  changes to: • Vascular function • Systolic and Diastolic • Neurohumoral status • Vasoconstriction via: • Sympathetics • R-A system • ADH • ANP • Increases preload and afterload  aggravate HF • Blood volume • ↓ renal perfusion • Sympathetic adrenergic • RAAS • ADH • Relate to Venous pressure & oedema Purpose: Maintain cardiac output + Arterial Blood Pressure Some of these compensatory changes can worsen cardiac function

  10. Clinical Characteristics

  11. Others: • Ascites • Pleural effusion (excess fluid between 2 pleural layers) • Cardiac dilatation (increased ventricular end-diastolic volume) or hypertrophy (increased end-systolic ventricular pressure) • AF

  12. Management Principles • Aim: • Improve QOL via symptomatic relief • Prevent hospital admission and reduce length of stay of any admissions • How: • Non-pharmacological • Pharmacological

  13. Non-pharmacological • Lifestyle advice: • Smoking cessation • Low salt diet • Safe alcohol use • Weight loss for BMI >30 • Exercise regimes • Secondary prevention for CAD • Once only pneumococcal vaccination and annual Influenza vaccination

  14. Categories of drugs & targets • Beta Blockers (-lols) • ACEi or ARBs (-prils, -sartans) • Digoxin • Aldosterone antagonists/K+ sparing diuretics (Spironolactone, Eplerenone) • Loop diuretics (Furosemide/Bumetanide) • Stop/avoid aggravating drugs (nSAIDs, Calcium antagonists, steroids, glitazones) • Carvedilol, Bisoprolol, Metoprolol targets the SNS via B1 receptor and dampens activity • Lisinopril, Ramipril target ACE and downregulates activity • Candesartan, Losartan, Valsartan target AT Receptor and downregulates activity • Digoxin targets Na+/K+ pump in cardiomyocytes to indirectly increase intracellular calcium • Aldosterone antagonists target MR to decrease aldosterone binding • Loop diuretics target the loop of Henle to cause increased diuresis

  15. RAAS

  16. Investigations • CXR (HERB-B) • Heart enlargement • Pleural Effusion • Re-distribution (alveolar oedema) • KerleyB-Lines • Bronchiolar-alveolar cuffing • ECG • Likely abnormal • Bloods • Anaemia, thyrotoxicosis etc, BNP (re: V distension – hence 1st line test) • ECHO • Underlying anatomical problems (cardiomyopathy, valves, pericardial effusion) • MRI Bilateral effusions oedematous

  17. References • http://www.cvphysiology.com/Heart%20Failure/HF002.htm • Last year’s lecture by Dr Banerjee • Wikipedia (I know…naughty) • USMLE 2012 • Toronto Notes 2012 Remember, a common cause of RHF is LHF!

  18. Questions?

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