Aortic stenosis
| Headline | |
|---|---|
| Etiology | Valvular AS: most commonly calcific; bicuspid valve, rheumatic, congenital (Williams syndrome). Mild = “aortic sclerosis” |
| Epidemiology | |
| Clinical presentation | Dyspnoea, angina, palpitation, cardiogenic syncope Murmur: ejection systolic murmur radiating to carotids, loudest on expiration (sit up, breathe out) Heart sounds: soft S2 Apex beat: heaving, non-displaced Pulse: slow-rising pulse, narrow pulse pressure |
| Pathogenesis | - LV needs to generate more force to overcome the narrow valve - → LV failure; LV hypertrophy - ↓ LV end diastolic pressure = ↓ coronary perfusion pressure - critical AS → pulmonary hypertension |
| Diagnostic investigations | Echo - 'moderate' = aortic valve index <0.7 (as a proportion to body surface area); critical = aortic valve index <0.5 |
| Management | Valve replacement/TAVI - Referral if severe (aortic valve area <0.6), EF<55%, ↑ BNP or exertional symptoms Avoid nitrates See below for the sick AS patient |
critical care considerations
These patients have a fixed cardiac output
- avoid AF and tachycardia
- ↑ time for blood to squeeze through a tight valve = need to compensate for diastolic failure
- AF = worse diastolic filling
- keep well-filled
- decreasing systemic vascular resistance won't change afterload - as the restriction is at the aortic valve
- preserve contractility - avoid beta blockers, CCBs
- in particular be cautious with anaesthetics e.g. propofol!