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HEMODYNAMICS OF AS
Aortic Stenosis
• Etiology based on location– Supravalvular– Subvalvular-– Valvular
Congenital Bicuspid Rheumatic Senile degenerative
Pathophysiology
Pressure gradient across the aortic valve increases exponentially (not linearly) with decreasing aortic valve area
Pathophysiology
• Increase in afterload
• Progressive hypertrophy-Concentric hypertrophy-- II sarcomeres
• Decrease in systemic and coronary flow
Compensatory Mechanisms
• Adaptive and maladaptive • Progressive worsening of left ventricular
outflow obstruction leads to hypertrophy• Compensatory hypertrophy required to
maintain wall stress (afterload)• Augmented preload with increased atrial kick
preserve LV systolic function
Subendocardial ischemia
• Perivascular fibrosis- ECM ellaboration• Large diameter myocytes impairing O2 diffusion• Hgh LVEDP- dec cor diastolic perfusion pr• Inc O2 consumption from inc mass and wall stress• Epicardial CAD
• ↓ I EF:- 1) NL Contractility increased - Afterload “ mismatch” increased preload- noncompliant vent asynchronous uncoordinated contraction- wall stress
2) decreased contractility- multifactorial ↓ s upply to endocardium ↓ cor flow reserve cytoskeletal abnormalities diastolic dysfunction pathological LVH
• In mild AS, intracardiac pressures and CO - normal • As the valve becomes more stenotic- normal at rest, unable
to increase CO during exercise
• Progressive narrowing of the valve leads to decreased stroke volume and cardiac output even at rest
• In moderate to severe AS, patients may develop elevated filling pressures to compensate for the increase in LV end-diastolic pressure
• In a minority of patients LV systolic failure occurs- further elevation in intracardiac pressures
• the degree to which hypertrophy may go on is limited by the coronary blood flow
• The aortic obstruction imposes some limits on the perfusion pressure available for the coronary vessels, and also on the output available for them.
• Moreover, the increased systolic resistance to flow in the hypertrophied muscle cuts down on whatever coronary flow normally does occur in systole.
• As the obstruction progresses to a critical level, the high afterload “overwhelms” the left ventricle and systolic function begins to decrease.
• With continued severe afterload excess, myocyte degeneration and fibrosis occurs and produces irreversible left ventricular systolic dysfunction
Angina
• Progressive LV hypertrophy from aortic stenosis leads to increased myocardial oxygen needs– Hypertrophy may compress the coronary arteries– Reduced diastolic filling may result in classic
angina, even in the absence of coronary artery disease
• 35% presentation• 50% die in 5 years
Syncope• Cardiac output no longer increases with
exercise• A drop in systemic vascular resistance that
normally occurs with exertion may lead to hypotension and syncope
• Rest- arrythmias, av block
• 15% presentation• 50% die in 3 years
Heart Failure
• Changes in LV function may no longer be adequate to overcome the outflow obstruction– Hypertrophic remodeling leads to diastolic
dysfunction– Afterload excess results in decreased ejection
fraction – systolic dysfunction• 50% presentation• 50% die in 2 years
There may be a plateau or an anacrotic pulse or a late peaking and small volume pulse, pulsus parvus, and tardus The pulse pressure may be reducedIn supravalvular AS, the right brachial and carotid pulsations are of greater amplitude than the left-sided ones
• Mask severity High CO & elastic vesselsIncreased stiffness in elderlyARHTN
• Exaggerate severityLV Systloic dysfnMSHypovolemia
• In supravalvular AS- the right brachial pulse and the carotid may be stronger than the left brachial
• Coanda effect -properly directed jet , attach to a convex surface instead of moving in a straight line
• Obstruction in the supravalvular AS is such that the high-velocity jet is directed towards the right innominate artery
The apex beat is hyperdynamic and sustained due to associated left ventricular hypertrophy. A thrill in the aortic area indicates AS not severity
• INTENSITY NL- Pliable, thin valves –BAV without calcificationDec –thickened rigid valves , calcificationSevere -the stroke volume is ejected slowly and over a longer period and also
leads to poor distension of the aortic root--softer A2
• SPLITTING A2 moves into P2- 1) ↑ LV ejection 2) longer time for LV pr to drop below
aortic at end systole
SingleParadoxical splitt
S4
• Correlates wit large LV-AO gradient and abnormally elevated LVEDP
AEC• Localises and suggests etiology
• sudden cessation of opening motion of abnormal valve leaflets(doming)
• Lost with calcification and thickening
• High frequency- 40-80 msec after S1 – best heard at apex-constant
MURMUR• Crescendo –decrescendo – shape of the pr diff bet LV-Ao
• Site of max intensity and radiation-• Length of the murmur-severity - time to peak intensity- 2nd half• Frequency and pitch- rough ,grunting Harsh- mixed frequency at base – effect of jet to Ao high freq musical- vib fom leaflets with intact commissures , at apex
-Gallavardin murmur• Amplitude - generally louder –severe - nonspecific
SEVERITY
Classification of SeverityAortic Jet Velocity
(m/s)
Mean Gradient (mm Hg)
Aortic valve Area (cm2)
Normal < 2.5 =4(velocity)2
Bernoulli’s equation
3 – 4
Mild 2.5 – 2.9 < 25 1.5 – 2
Moderate 3 – 4 25 – 40 1 – 1.5
Severe > 4 > 40 < 1
• Doppler data– Peak instantaneous gradient over time
• Cath data– Peak to peak data
• However, calculated mean P Grd are comparable
AORTIC STENOSIS- (LV-AO)METHOD EASE OF USE DISADVANTAGE
PULLBACK +++++ LEAST ACCURATE
FEMORAL SHEATH +++++ PRESSURE AMPLIFICATION ILIAC ARTERY STENOSIS
DOUBLE ARTERIAL PUNCTURE
+++ EXTRA VASCULAR ACCESS RISK
PIG TAIL- DOUBLE LUMEN
+++ DAMPING
PIG TAIL + PRESSURE +++ EXPENSE
TRANSEPTAL ++ RISK
AVA
Pull back hemodynamics : Peak – peak gradient alignment mismatch Distortion of pulse - femoral artery peripheral pulse amplification catheter in LVOT central aorta - pressure recovery
Carballo’s sign
Pull back
LVSP = left ventricular systolic pressure; MGnet= transvalvular pressure gradient after pressure recovery MGvc = transvalvular pressure gradient at the venacontractaSAP= systolic aortic pressure SAPvc = systolic aortic pressure at the vena contracta; SV = stroke volumeSvi= stroke volume index ZVA= valvulo-arterial impedance.
Schematic representation of the flow and static pressure across the left ventricular (LV) outflow tract, aortic valve, and ascending aorta during systole
Doppler derived gradients- using CW doppler @ vena contractaCatheter derived gradients- downstream vena contracta- pressure recovery
GRADIENT DERIVED BY CATH IS LOWER THAN DOPPLER DERIVED GRADIENT
Pressure recovery- exaggerated in-Smaller aorta-Stiffer aorta-Hypertension
Hypertension may mask the severity of stenosis, anPresence of stenosis may affect the optimal treatment of hypertension Combination of AS and hypertension- “double-loads” th ventricle Total afterload = the valve obstruction + elevated SVR
stenosis severity Underestimated- “recovered”pressure, rather than vencontracta pressure, is rec
Stenotic valve area
Torricelli’s law• F = A X V A = F / V A = F / V Cc F- FlowA- Valve areaV- Velocity of flowCc- coefficient of contraction
Mitral Valve = constant 0.7 (later changed 0.85)Aortic valve: assumed to be 1
GORLIN FORMULA
Problems
• cardiac output Fick - oxygen consumption Thermodilution- low output state - significant TR• Duration of flow (SEP-DFP)• Alignment mismatch• Calibration errors
LOW OUTPUT LOWGRADIENT AS• Mean gradient < 40 in the setting of EF < 40 %
• Dobutamine
• Stoppage pnt- 40µ / kg / min - mean gradient > 40 mm hg -CO inc by 50 % -HR inc to < 140 / min - intolerable symptoms / side effects• True stenosis-mean gradient > 30 mm hg - AVA remains 1.2 cm2 / less
Aortic valve area (AVA) is calculated based on the principle that volume flow proximal to the valve equals volume flow through the narrowed orifice
• Continuity equation V/S bernoulli
Co-existing ARLV-dysfunction
Continuity equation V /S bernoulli
Simplification of the continuity equation is the Dimensionless ratio of outflow tract to aortic velocity: Velocity ratio= (VLVOT) / VAS
• Reflects the relative valve si ze compared with the area of the patient’s outflow track
• Particularly useful when images of outflow tract diameter are
suboptimal
• Ratio approaches 1 with a normal valve
• A ratio 0.25 indicates a valve area 25% of expected-severe stenosis
AVA MACS
N > 2cm2 N > 15 mm
< 0.75 cm2 < 8 mm
> 1 cm2 > 12 mm
gray area 8 – 12 mm
Maximal aortic cusp separation (MACS) Vertical distance between right CC and non CC during systole Stenotic AV → decreased MACS
M- mode
CATH
• 30% of patients with mild-to-moderate AS have clinical evidence of coronary disease; at pre-operative catheterization, significant coronary disease is present in about 50%
• LV systolic dysfunction is an uncommon consequence of AS =about 5% of patients
Survival among Patients with Severe Symptomatic Aortic Stenosis Who Underwent Valve Replacement and Similar Patients Who Declined to Undergo Surgery10
AS w/ low output/low gradient
