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

http://www.mdconsult.com/das/article/body/281414523-4/jorg=clinics&source=&sp=10394337&sid=0/N/121864/I3.fig

• 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