Aortic Stenosis
Gems / Priorities1 / 14
- classification is MEAN pressure gradient
- main problem = FIXED STROKE VOLUME due to LVH
- priorities = optimal LV filling
- HD goals
- Maintain myocardial O2 delivery
Definition / diagnostic criteria2 / 14
- Aortic valve stenosis
- Obstruction of blood flow across the AV
Classification3 / 14
Severity | MPG mmHg | AVA cm2 | PVel m/sec | Ca Score |
---|---|---|---|---|
Critical | > 80 | < 0.5 | ||
Severe | 40 - 80 | 0.5 - 1.0 | > 4 | 2065 (M) / 1275 (F) |
Moderate | 20 - 40 | 1.1 - 1.5 | 3 - 4 | |
Mild | < 20 | 1.5 - 2.5 | 2.5 - 3 | |
Normal | 2.6 - 3.5 | < 2.5 |
- MPG = mean peak gradient
- severe > 40 mmHg
- critical > 80 mmHg
- AVA = aortic valve area
- severe < 1.0 cm2
- critical < 0.5 cm2
- Indexed AVA cm2/m2
- severe < 0.6 cm2/m2
- Pvel = peak velocity
Epidemiology4 / 14
- Overview
- most common VHD in Europe/USA
- Incidence
- 2-7% of 65+
- Prevalence
- Gender
- males 4x
Prognosis / Complications5 / 14
- often latent period of 30 years
- progression = recent change
- ⬆30/7 mortality 2.1% (cf 1.0%)
- ⬆risk MACE
- high-risk surgery
- severe + symptomatic
- coexisting MR (mod/sev)
- pre-existing CAD
- ⬆risk MACE
- acquired vWF
- degradation of vWF across aortic valve
- high shear forces ⮕ structural changes
- result = platelet dysfunction
Aetiology / Causes / Risk Factors6 / 14
- Calcific (degenerative) = 80% (most common)
- degenerative condition = inflammation and progressive calcification, limiting movement of AV
- RF: elderly (65+), HChol, HT, smoking, DM
- Calcific Bicuspid valve (congenital)
- frequency 1-2%
- most common congenital abnormality of the heart
- RF: male
- There can be MIXED disease in bicuspid AV
- abnormal valve -> ⬆turbulent flow -> ⬆fibrosis + calcification
- Rheumatic heart disease
-
autoimmune condition, following Streptococcal (Group A) infection
-
molecular mimicry -> inflammation
-
tissues affected: heart, joints, CNS
-
less common now
-
NB. concomitant mitral valve disease
-
Rare
-
Metabolic, eg. Fabry's disease (lysosomal storage disease)
Pathophysiology7 / 14
-
end result of inflammatory process
-
endothelial damage
- mechanical stress
- lipid accumulation
- fibrosis
-
leaflet thickening
-
leaflet calcification
-
AS
-
⬆AL on LV
-
⬆wall tension required
-
⬆pressure gradient, ⬆wall tension
- ⬆difference between LV and Aortic root to maintain SV
- turbulent flow = ejection systolic murmur
-
1: latent phase
- abnormal valve, LVOTO
-
2: compensatory phase
- LVH to overcome LVOTO and maintain EF
- ⬆CMRO2, ⬇supply, diastolic dysfunction
-
3: Decompensation
- ⬆LVH, ⬇EF
- pulmonary oedema, MR
-
4: Symptomatic phase
- narrower valve = ⬇AVA = ⬆kinetic energy, but ⬇pressure
- result = ⬇perfusion pressure of coronary As
- Dyspnoea, Exertional syncope, Angina
-
initial = systolic failure / dysfunction
- LV unable to maintain SV (normal proportion of EDV) = ⬇EF%
- compensation
- concentric LVH
- ⬆INO = sustained apex beat
- cost
- ⬇ventricular compliance = diastolic failure
- ⬆MVO2 (⬆myocardial tissue)
-
later
- ⬆LVEDP ⮕ ⬇coronary BQ, ⬆myocardial ischaemia (subendocardial)
-
late = LV systolic failure
- ⬇INO, LV dilatation ⮕ ⬇⬇CO = acute decompensation
-
both lead to CCF, with SOB and bibasal crackles
-
NB. Pressure-volume loop for AS
- loop is shifted up and right
Symptoms / History8 / 14
-
Classic triad = DEA
- dyspnoea 50% = 1st symptom
- exertional syncope = 35%
- angina 15%
-
symptomatic
- ⬇ability to adjust to myocardial demand
- exhausation of compensatory mechanisms
- prone to EXERTIONAL symptoms (SOB, syncope)
-
angina
- ⬇coronary BQ
- ⬆O2 demand (LVH, ⬆myocardial mass)
- may not have CAD = a MISMATCH between supply and demand
- CAD 50%
-
dyspnoea
-
multifactorial
-
LVH / diastolic dysfunction, ⬆LVEDP
-
syncope
-
inadequate CO
-
⬇SV with ⬆HR
-
vasoD with exercise
-
epistaxis/bruising
Signs / Examination9 / 14
Main
- ESM radiating to carotids
- sustained apex beat / heaving apex
- slow rising pulse
- "parvus et tardus" carotid pulse
- parvus = small volume
- tardus = delayed
- narrow pulse pressure
- ⬆DBP (⬆EDV), eg. 130/110
- may radiate to apex = Gallavardin phenomenon
- but doesn't radiate to left axilla (MR does)
- thrill = palpable murmur
- severe AS
Others
- Soft S2 (soft A2)
- marker of severity
- Aortic component of S2 quieter as valve leaflets fail to oppose forcefully
- S3
- S4 (4th heart sound)
- atria contracting against stiff, hypertrophied ventricles
- Reversed splitting
Investigations10 / 14
- Echo = TTE/TOE
- valve = peak flow, AVA, AR
- consequences = LV, LA, MV, post-stenotic aortic dilatation
- ECG
- LVH
- LV strain (severe)
- LA deviation
- Left heart catheter study
- retrograde catheterisation of aortic valve = assess PG
- Cardiac MRI
- assess consequences of stenosis
- CXR
- Cardiomegaly
- LVF
- calcification
Management11 / 14
- no medical management
- valve replacement
- percutanous = TAVI = transcatheter AV implantation
- minimally invasive
- for patients not suitable for open procedure
- open = AVR
- for severe AS / symptomatic
- percutanous = TAVI = transcatheter AV implantation
- valvotomy
- percutaneous balloon aortic valvuloplasty (BAV)
- TAVI
- newer generation = allow percutaneous valve insertion = valve-in-valve = Inspiris
- if future restenosis
- open valvotomy
- coronary angiogram
- determine if CABG required at same time
Anaesthetic considerations12 / 14
- Pre-op
- severe
- asymptomatic
- reasonable to proceed to surgery
- appropriate intraop and postop monitoring ***
- asymptomatic
- severe
- Intra-op
- 1:preload
- avoid hypovolaemia ⮕ ⬇CO
- must have adequate SV
- "full"
- guided by CO monitoring
- 2:rate
- aim rate 50-60
- avoid tachycardia ⮕ ⬇⬇LV filling ⮕ ⬇CO
- ⬇time for coronary filling
- ⬆MRO2 and ischaemia
- avoid bradyC = limit of SV = APO
- LV has fixed SV (⬇compliance) = unable to ⬆filling with ⬇HR
- 3:rhythm
- maintain SINUS rhythm
- atrial contraction contributes 40% filling in stiff hypertrophied LV ⮕ ⬇CO
- avoid arrhythmias ⮕ ⬇LV filling
- cardioversion if HDI with arrhythmia
- 4:contractility
- already hyper-contractile
- do not give negative inotropes (BB, CBB)
- 5:afterload
- maintain AL for coronary perfusion *** = "tight"
- coronary A perfusion is dependent on aortic root pressure
- prevent vasoD / venoD
- avoid ⬇SVR / ⬇DBP ⮕ ⬇coronary BQ
- ⬇SVR does NOT ⬇AL (AS is fixed)
- ⬆DBP required for CPP because of ⬆LVEDP
- caution with neuraxial blockade
- maintain AL for coronary perfusion *** = "tight"
- decompensation
- VASOPRESSORS are key intervention (not inotropes)
- 1:preload
- Post-op
Common questions / related topics13 / 14
- classification of AS severity (AVA, TVPG)
- NYHA classification of perioperative risk: should surgery be cancelled?
- treatment: when is surgery indicated?
- options of anaesthesia (non-cardiac surgery)
- antibiotic prophylaxis
- central neuraxial blockade and AS
- haemodynamic goals during non-cardiac surgery (and how to achieve)
- role for invasive monitoring
- problems with PA caths?
- cardiac arrest: priorities?
- ventricular Pressure/Volume relationship in AS
Links / References14 / 14
https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-15/Aortic-valve-stenosis-evaluation-and-management-of-patients-with-discordant-grading
Final FRCA In A Box
https://derangedphysiology.com/main/required-reading/cardiothoracic-intensive-care/Chapter%202.1.3/aortic-stenosis
https://www.escardio.org/Journals/E-Journal-of-Cardiology-Practice/Volume-18/physical-examination-in-aortic-valve-disease-do-we-still-need-it-in-the-modern