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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.
slide5
Principle types of heart failure & Circumstances for development
  • Pathophysiology
  • Clinical characteristics
  • Principles of management
  • Categories of drugs and their targets
pathophysiology
Pathophysiology
  • Causes:
    • Intrinsic – e.g. dilated and hypertrophic cardiomyopathies
    • Extrinsic – uncontrolled HTN, ↑SV, hormonal (e.g. Hyperthyroidism), Pregnancy, Drugs (alcohol, cocaine)
heart failed
‘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
pathophysiology cont
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

slide13
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
management principles
Management Principles
  • 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
  • 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
  • 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
investigations
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

references
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!

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