Heart Failure

“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

• 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