Heart Failure Flashcards
Aetiology
Left sided
- HTN (most common)
- IHD
- valve disease
- cardiomyopathy
- myocarditis
Right sided
- lung disease > pulm HTN > cor pulmonale
- right sided cardiomyopathy (arrhythmogenic RV dysphasia (rare))
Congestive or biventricular failure
- RV failure due to pulmonary HTN and pulmonary fluid overload due to LV failure
NYHA classification
I - no effect in normal daily activity
II - slight limitation in physical activity but able to walk 100m on flat. Lethargy, dyspnoea, palpitations
III - marked limitation of physical activity (I.e. walking around house). Comfortable at rest
IV - Symptoms at rest. Discomfort with any minimal exertion
Classifications
Left vs right Systolic vs diastolic Different aetiologies Acute vs chronic NYHA
Symptoms
Pump failure
- fatigue
- asthenia
- weight loss (cardiac cachexia due to high circulating interleukin levels)
Congestion
- breathlessness, orthopnoea, PND, ankle swelling
Signs
Tachycardia Raised JVP Displaced apex RV heave 3rd HS or gallop rhythm Fine bibasal creps Sacral or ankle oedema
Investigations
- ECG - abnormal in >90% of cases
- CXR
- Echo
- angio
- exercise testing/ cardiopulmonary exercise testing if considering transplant
- myocardial viability testing to consider revascularisation to rescue ‘hibernating’ ischaemic myocardium. Thallium-scanning vs cardiac MRI vs stress echo vs PET
Management
- Firstly find and correct (if possible) underlying aetiology
- diuretics for congestive sx
- ACE-I and beta-blockers improve sx and prognosis in all grades of failure
- spironolactone (aldosterone receptor inhibitor) - improves prognosis in NYHA III/IV despite optimal use of above.
- epleronone has similar effects as spiro post-MI with fewer SE’s
- graded, aerobic exercise improves sx and prognosis with all grades
- Biventricular pacing
- digoxin can improve sx (by a whole functional class) but doesn’t effect prognosis
- transplant. 1st year mortality 15% but 5% per year thereafter. Median survival 8 years
Neurohormonal changes with chronic CCF
Low cardiac output causes reduced glomerular filtration, this causes a reduction in the quantity of sodium reaching distal convoluted tubules. Sensed by juxtaglomerular apparatus leading to release of renin.
Renin converts angiotensinogen into angiotensin 1 which is then converted to angiotensin 2 (by ACE). A2 increases afterload by causing vasoconstriction as well as salt and water retention, worsening congestive symptoms.
Acute response to reduced cardiac output is activation of sympathetic nervous system. When output remains reduced there is chronic high levels of adrenaline and NA. This causes vasoconstriction, salt and water retention, and tachycardia (increasing oxygen demand)
What are the indications for bivwntricular pacing?
Those with NYHA III/IV despite at least 1 month optimal medical management and widened QRS (>120ms) should be considered. This can improve symptoms and prognosis