Aortic Stenosis (and Valve Replacement) Flashcards
(42 cards)
What is the diagnosis?
A 78-year-old man presents to his primary care physician with 2 months of progressive shortness of breath on exertion. He first recognised having to catch his breath while gardening and is now unable to walk up the stairs in his house without stopping. Previously he was healthy and active. On physical examination there is a loud systolic murmur at the right upper sternal border radiating to the carotid vessels.
Aortic stenosis
Describe the aortic stenosis murmur.
Crescendo decrescendo systolic murmur - flow during systole is slowest at the very start and end and fastest in the middle
Ejection systolic murmur
Heaving apex beat
Slow rising pulse and narrow pulse pressure
Also:
- soft/absent S2
- S4
- thrill
- duration of murmur
- left ventricular hypertrophy or failure
Typically grade _>_3/6
How common is AS?
MOST COMMON valvular disease in the US/EU
Second most common cause of cardiac surgery
10% of those >80yrs affected
Preceded by aortic sclerosis - 25% of _>_65yrs have aortic sclerosis
Define aortic sclerosis.
Aortic valve thickening without flow limitation
What are the risk factors for AS?
Age >60
Congenital bicuspid valve
Rheumatic heart disease
CKD
Other:
- High LDL
- Hyperlipoproteinaemia
- HTN
What causes aortic stenosis?
- Senile calcification - most common (80% - older patients >65yo)
- Congenital bicuspid valve (~20% - younger patients <65yo)
Other:
- William’s syndrome (supravalvular aortic stenosis)
- Rheumatic fever
- Subvalvular: HOCM
What is the pathophysiology of aortic stenosis?
- Calcification is no longer thought to be due to age “wear and tear”
- But thought to be an active process whereby valvular endocardium is damaged due to abnormal flow or other trigger
- Damage causes atherosclerosis → fibrosis and calcium deposition
- This causes limit to aortic leaflet mobility and eventually stenosis
In rheumatic disease the process is autoimmune inflammatory
What investigations would you do for aortic stenosis?
Main investigations:
*Echo + Doppler* - diagnostic. Will show elevated pressure gradient across the aortic valve
ECG - abnormal in 90% with AS. LVH and absent Q waves. Often also conduction problems e.g. LBBB or complete AV block (due to septal calcification),
CXR - to assess for pulmonary congestion or other lung pathology
Other:
CT angiography for concomitant coronary heart disease. Normal CT also for measuring aortic valve calcium score.
Cardiac catheterisation - more direct measure of the elevated aortic pressure gradient
What are the symptoms of aortic stenosis?
Symptoms:
- Exertional syncope/presyncope, angina, dyspnoea = SAD
- Fatigue
- HF symptoms: paroxysmal nocturnal dyspnea (PND), orthopnoea, oedema.
Signs:
- Slow rising pulse (carotid parvus et tardus)
- ESM*, S4, S2 diminished and single (due to decreased mobility of aortic valve leaflets)
- Signs of heart failure
Is aortic stenosis a systolic or diastolic murmur?
Systolic
How can you distinguish aortic stenosis murmur from other systolic murmurs? Where is it best heard?
- Best heard in aortic area
- Radiates to carotids
- Louder during squatting
- Quieter in Valsalva and handgrip
How do you manage aortic stenosis?
Asymptomatic:
- observe
- OR consider surgery if valvular gradient >40mmHg or LV systolic dysfunction
Symptomatic:
Valve replacement
Medical:
- HTN (ACEi/ARB)
- statins
- aspirin/clopidogrel post-TAVI
What are the valve replacement options in AS?
Access types: surgical or percutaneous
- Surgical AVR (SAVR) = young, low/medium operative risk patients.
- Transcatheter AVR (TAVR) = for patients with a high operative risk. Older patients
-
Balloon valvuloplasty = inserting balloon to open up the valve
- may be used in children with no aortic valve calcification
- in adults limited to patients with critical aortic stenosis who are not fit for valve replacement - does not improve mortality but improves symptoms
Valve types: mechanical or tissue
- Mechanical - best for younger patients, last whole life but need lifelong warfarin
- Tissue/Bioprosthetic - bovine/porcine. Last 15-20yrs , lifelong anticoagulation not necessary.
What are the complications of untreated AS?
Symptom onset indicates poor prognosis - average survival of only 2-5yrs without valve replacement
Acute heart failure -due to afterload burden
Sudden cardiac death due to ventricular arrhythmia
What are the complications of AS treatment?
After any open heart surgery there will be poor LV function
Infection of prosthetic valve
Thrombosis secondary to mechanical valve
Re-stenosis
What is the prognosis with AVR?
SAVR - <70yrs old have 1.3% risk of death from surgery, 99% life expectancy at 5yrs and 85% at 10yrs
TAVR- 20% absolute reduction in mortality at 1yr, 30% alive at 3yrs compared to 5% on standard therapy
Rarely, what bleeding disorder may patients with AS acquire?
von Willebrand deficiency - due to turbulent flow across a stenotic valve. Will present with epistaxis and bruising.
What common HTN medications should not be used in AS?
- NITRATES - can reduce afterload quickly so cause hypotension. Do not use in AS.
Which of these are signs of aortic stenosis?(4)
- Angina
- Sinus tachycardia
- Dizziness
- Ejection systolic murmur radiating to the carotids
- Narrow pulse pressure
Angina, dizziness, ESM radiating to carotids, narrow pulse pressure
Aortic stenosis – can present with angina, dyspnoea, dizziness and faints. Signs – slow rising pulse, narrow pulse pressure, heaving undisplaced apex, aortic thrill, ejection systolic murmur heard at the left sternal edge and radiating to the carotids. Aortic sclerosis is senile degeneration of the valve. There is an ejection systolic murmur, no carotid radiation and a normal pulse.
What happens during S1?
S1 - closing of the mitral and tricuspid valves (AV valves)
What happens during S2? When might you get a physiological splitting of S2?
S2 - closing of the aortic and pulmonary valves (semilunar valves)
Normal, physiologic splitting of S2: inspiration lowers intrathoracic pressure, increasing the compliance of the pulmonary vascular bed,–> increased right heart filling –> RV systole is lengthened, causing the pulmonic valve to close after the aortic valve, resulting in splitting of the second sound at 3LICS or 4LICS.
.
What are S3 and S4?
gallop rhythm heart sounds
When might you get paradoxical, peristent or wide splitting of S2?
Paradoxical splitting: results from delayed onset or prolongation of left ventricular systole e.g. in prolonged LV emptying, aortic stenosis, LBBB– eliminated on inspiration
Persistent splitting: results from delayed onset or prolongation of right ventricular systole, or shortened duration of left
- Widened split S2 – prolong PV emptying – pulmonay stenosis, RBBB
- Fixed Split S2 – ASD
S1: Normal wide splitting S1 – RBBB, LV pacing, ectopic beats
What causes S3?
- Caused by early diastole
- Associated with rapid ventricular filling e.g. HF (the ventricles and chordae are stiff and weak so they reach their limit much faster than normal)
- Can be normal in children, young adults and pregnant women because the heart functions so well that the ventricles easily allow rapid filling.
“Kentucky”
- heard 0.1sec after second heart sound
- like rapid ventricular filling causing chordae tendinae to pull their full length and twang like guitair strings
