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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

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
Learning Objectives 1

  • Understand how the pumping activity of the heart is affectedby changes in venous return and total peripheral resistance


Q uick review on starling s l aw
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


Learning objectives 2
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.



Hf types
HF types development


Pathophysiology
Pathophysiology development

  • Causes:

    • Intrinsic – e.g. dilated and hypertrophic cardiomyopathies

    • Extrinsic – uncontrolled HTN, ↑SV, hormonal (e.g. Hyperthyroidism), Pregnancy, Drugs (alcohol, cocaine)


Heart failed
‘HEART FAILED’ development

  • 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


Pathophysiology cont
Pathophysiology developmentcont…

  • 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



  • Others: development

    • Ascites

    • Pleural effusion (excess fluid between 2 pleural layers)

    • Cardiac dilatation (increased ventricular end-diastolic volume) or hypertrophy (increased end-systolic ventricular pressure)

    • AF


Management principles
Management Principles development

  • Aim:

    • Improve QOL via symptomatic relief

    • Prevent hospital admission and reduce length of stay of any admissions

  • How:

    • Non-pharmacological

    • Pharmacological


Non pharmacological
Non-pharmacological development

  • 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


Categories of drugs targets
Categories of drugs & targets development

  • 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


RAAS development


Investigations
Investigations development

  • 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


    References
    References development

    • 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!


    Questions
    Questions? development


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