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
- 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
- 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
- Release of ADH → stimulated by ↓ BP & RAAS
- ↑ salt & water retention → ↑ CVP / preload → ↑ SV
- HF: increased myocardial work
- Increased sympathetic outflow – activated by baroceptor reflex & Ang II
- 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?
- Chest X-Ray (not conclusive):
- Special
- ECG
- Sinus tachycardia, AF, LBBB
- Coronary angiography
- ECG
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