Cardiovascular System >
Heart Failure (HF)

“A Syndrome where the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressure”

Classifications
  • Systolic HF – LV has reduced ability to pump
  • Diastolic HF – LV has difficulty relaxing, so has difficulty filling → CO falls.
  • Heart failure with reduced ejection fraction (HFREF)
  • Heart failure with moderately reduced ejection fraction (HMREF)
  • Heart failure with preserved ejection fraction (HFPEF)
  • Left-sided vs Right-sided (not often just RHF, LHF leads to RHF)
  • High output vs Low output
  • Acute vs Chronic
Risk Factors & Aetiology
  • Ischaemic heart disease
  • Hypertensive heart disease
  • Diabetic microvascular disease
  • HIV, Myocarditis, Idiopathic
  • Valvular heart disease
  • Cor pulmonale
  • Cardiomyopathy
  • Toxins
Pathophysiology
  • Compensation – to increase HR or SV & therefore CO
    • Frank-Starling mechanism – Impaired cardiac function causes accumulation of venous blood & therefore raised filling pressure (preload) which consequently increases CO
  • Neuro-hormonal activation
    1. Increased sympathetic outflow – activated by baroceptor reflex & Ang II
      • ↑ HR & force of contraction (β1) → increases CO
      • Vasoconstriction (α1) → increases afterload which increases SV
      • Renal stimulation (β1) → activation of RAAS
      • HF: increased myocardial work, myocardial remodelling & further cell death
    2. Activation of RAAS – renin release from SNS & ↓ RBF → ↑ Ang II & aldosterone
      • ↑ salt & water retention → increase CVP / preload which increases SV
      • Vasoconstriction → increases afterload which increases SV
      • Activation of SNS → vicious circle in HF
      • HF: increased myocardial work, hypertrophy & fibrosis
    3. Release of ADH → stimulated by ↓ BP & RAAS
      • ↑ salt & water retention → ↑ CVP / preload → ↑ SV
      • HF: increased myocardial work
  • Decompensation – CO only maintained by ever-increasing CVP & HR causing myocardial damage
    • The heart has to work harder leading to energy deficit → dysfunction of ATP dependent transporters → Ca2+ overload → arrhythmias → sudden death
    • Oxidative stress/cytokines – promote further damage/cell death
    • Myocardial remodelling – heart changes in size, shape, structure or function from direct effects of Ang II, aldosterone and NA through SNS and RAAS activation
      • Myocardial dilatation → reduces cardiac efficiency as has to contract harder to develop the same pressure (caused by ↑ LVEDP) → La Place’s law
      • Myocardial hypertrophy → ventricle less compliant which impedes filling
Clinical Presentation
  • Symptoms:
    • Worsening breathlessness
    • Decreased exercise capacity
    • Inability to lie flat / needs to sleep in chair
    • Cough
    • Leg swelling
    • Tiredness/lack of energy
  • Signs:
    • Inspection – look tired, overweight, breathless, swollen legs
    • CVS – blood pressure, HR, regular pulse? JVP? Added heart sound S3, pitting oedema
    • RESP – pleural effusion, inspiratory crackles
  • Cardinal symptoms:
    • Orthopnoea – Breathlessness on lying flat due to increased pulmonary venous pressures
    • Paroxysmal nocturnal dyspnoea – Acute pulmonary oedema bought on by lying flat. Need to open window
Investigations
  • Examination
    • Low BP, heart sounds? Lungs – crackles. Raised JVP = RHF
  • Bloods
    • BNP (released in response to ventricular stretch – good for ruling out HF)
    • Kidney function?
    • Liver function – low protein level?
    • Anaemia?
    • Thyroid function?
  • Imaging
    • Chest X-Ray (not conclusive):
      • A – Alveoli oedema/ distension – bat wing opacities
      • B – Kerley B lines 
      • C – Cardiomegaly
      • D – Dilated upper lobe vessels
      • E – Pleural effusions
    • Echocardiogram:
      • Size, systolic/diastolic function, valves, infarction?
  • Special
    • ECG
      • Sinus tachycardia, AF, LBBB
    • Coronary angiography
Management
  • Aim:
    • Reduce symptoms to improve QoL, lengthen survival & slow cardiac deterioration
  • Conservative:
    • Restricting the intake of salt & water
    • Lose weight
    • Exercise
    • Stop smoking
    • Reduce alcohol intake
  • Medical:
    • Diuretic (Loop/thiazide) – Furosemide, Bendroflumethiazide
    • ACE inhibitor / Ang II Receptor Antagonist – Ramipril, Candesartan
    • β-blocker – Bisoprolol
    • Aldosterone antagonist – Spironolactone
    • Others – Digoxin, Ivabradine, nitrates
  • Surgical:
    • Re-vascularisation by bypass surgery
    • Cardiac Transplant
    • Left ventricular assist device
    • Total artificial heart
Complications
  • Cardiovascular:
    • Cardiac arrest
    • Valve abnormalities
    • Stroke
  • Non-Cardiovascular:
    • Renal Failure
    • Hepatic Dysfunction
    • Venous Stasis
    • Depression

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