Cardio - Aortic Stenosis Flashcards
describe the symptoms associated with AS and explain why these occur
Pts may be asymptomatic for many yrs but may still be susceptible to sudden events. Symptoms often occur on exertion.
- angina (increased LV pressure to force blood into aorta causes concentric LV hypertrophy and thus increased O2 demand)
- syncope on exertion (CO unable to increase enough to accomodate fall in TPR causing hypotension)
- dyspnoea (due to HF)
what type of murmur would you hear in a pt with AS? where?
- systolic crescendo-decrescendo ejection murmur
- in aortic area, radiates to carotids
- +/- ejection clic (esp. with bicuspid valves)
- +/- 4th heart sound in severe AS due to LVH
describe the pulse and BP in a pt with AS
Pulse:
- sinus rhythm, increased HR
- slow-rising (anacrotic), weak/low volume pulse (pulsus parvus et tardus)
BP:
- decreased BP
- narrow pulse pressure on BP measurement
What would you feel on palpation of a pt with AS?
- apex beat: non-displaced, pressure-loaded, sustained
- aortic thrill (rare)
describe 3 causes for AS.
- Age-related calcification: due to mechanical stress. RFs: smoking, HTN, hyperlipidaemia, DM
- Congenital biscupid valve: increased stress on 2 leaflets causes increased risk of calcification at an earlier age
- Chronic rheumatic fever (more common in developing countries): inflammation results in fibrosis and commissural fusion
describe 3 pathological effects of AS``
- increased LV pressure (to force blood into aorta)… concentric LV hypertrophy… increased O2 demand… angina
- decreased CO/LHF… syncope on exertion
- RBC sheer stress… microangiopathic haemolytic anaemia… haemoglobinuria
Which investigations would you perform on a pt with suspected AS?
- Bedside tests
i. Urine dipstick: may show haematuria
ii. ECG: rule out MI, may show evidence of LVH or LV strain - Imaging
iii. Echocardiography: key Dx tool - confirms presence of AS, assesses degree of valve calcification, LV function and wall thickness, detects presence of other associated valve disease or aortic pathology and provides prognostic info. TOE should be considered when TTE is of insufficient quality.
iv. Multislice CT: important Dx tool for evaluation of aortic root, calcium distribution, number of leaflets, ascending aorta and peripheral artery pathology and dimensions before undertaking TAVI - Other
v. Exercise testing: contra-indicated in symptomatic pts with AS but recommended in physically active asymptomatic pts for unmasking Sx - monitor for presence of Sx, changes in BP and/or ECG
vi. Natriuretic peptides: predict prognosis in normal and low-flow severe AS, and may be useful in asymptomatic pts
vii. Cardiac catheterisation: to measure pressures across the valve to assess disease severity and need for intervention
Describe the conservative management for a pt with mild-moderate AS.
- avoid heavy exertion
- modification of atherosclerotic risk factors, e.g. HTN treatment (carefully titrated to avoid hypotension)
- maintenance of sinus rhythm is important - use of anti-arrhythmic drugs as indicated
In younger pts with no sig. calcification, monitor every 2-3 yrs. In presence of significant calcification, re-evaluate yearly.
Describe the management of severe symptomatic AS. What are the different options?
Requires early surgical intervention as no medical therapy for AS is able to improve outcome.
- Surgical aortic valve replacement - definitive therapy. Operative mortality is 1-3% (<70 yrs) and 4-8% (selected older adults).
- balloon valvuloplast - only used to treat adults unsuitable for surgery or palliatively in paeds until child is old enough for surgery. Re-stenosis and clinical deterioration occur within 6-12 mths in most pts.
- transcatheter aortic valve implantation (TAVI) - recent dev. providing method of AVR without risks of surgical AVR. Balloon valvuloplasty is performed, followed by insertion of specialised valve device. Used in pts unsuitable for surgery, with 60-80% 1 yr survival and significant improvement of health status and QoL.
describe 4 complications of AS.
- congestive HF: eventually leads to decompensation with raised end-diastolic pressure, pulmonary hypertension and CHF
- infective endocarditis: damaged valves are susceptible
- systemic embolism: emboli may be produced in calcified AS, resulting in stroke, acute limb ischaemia, etc.
- sudden cardiac death: occurs in <0.2 pts/yr
What is the prognosis of untreated severe AS in asymptomatic pts? in symptomatic pts?
What is the prognosis after successful AVR?
- Asymptomatic pts: 20-50% event-free survival at 2 yrs. Sudden cardiac death is truly rare.
- Symptomatic pts: v. poor prognosis with 15-50% survival at 5 yrs and sudden cardiac death being a frequent cause of death.
- After AVR, symptoms and QoL generally greatly improved, with long-term survival close to age-matched general pop. in older pts. (but lower survival in younger pts)
what is Heyde’s syndrome?
Massive GI bleeding due to angiodysplasia - disruption of pentamer structure of von Willebrand factor as it crosses severely stenotic aortic valve, causing increased tendency to bleed from angiodysplasia
