1. HEMODYNAMICS OF AS

2. Aortic Stenosis Etiology based on location Supravalvular Subvalvular-
Congenital
Bicuspid
Rheumatic
Senile degenerative

3. Pathophysiology
Pressure gradient across the aortic valve increases exponentially (not linearly) with decreasing aortic valve area

6. Pathophysiology Increase in afterload
Progressive hypertrophy-Concentric hypertrophy-- II sarcomeres
Decrease in systemic and coronary flow

8. 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

9. 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

11. increased - Afterload “ mismatch” increased preload- noncompliant vent
↓ 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

17. 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

20. 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

26. 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

27. 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

28. 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

30. 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 reduced
In supravalvular AS, the right brachial and carotid pulsations are of greater amplitude than the left-sided ones

31. Mask severity
High CO & elastic vessels
Increased stiffness in elderly AR
HTN
Exaggerate severity
LV Systloic dysfn MS
Hypovolemia

32. Timing and amplitude of the carotid pulse –severity
When the upstroke is delayed due to significant aortic stenosis, the rise is slow and sustained”
In normals, most of the stroke volume is ejected during the first third of systole
In aortic stenosis, this rapid ejection cannot occur- takes all of systole to eject the same volume.
decreased mass or volume ejected per unit time leads to a considerable decrease - ejection momentum despite increased velocity of ejection
In addition, the increased velocity of flow caused by the significant pressure gradient between the left ventricle and the aorta caused by the stenosis produces a Venturi effect on the lateral walls of the aorta.
This has the effect of significantly reducing the net pressure rise in the aorta

33. 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

34. The apex beat is hyperdynamic and sustained due to associated left ventricular hypertrophy. A thrill in the aortic area indicates AS not severity

35. INTENSITY
NL- Pliable, thin valves –BAV without calcification
Dec –thickened rigid valves , calcification
Severe -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
Single
Paradoxical splitt

37. S4
Correlates wit large LV-AO gradient and abnormally elevated LVEDP

38. AEC Localises and suggests etiology
sudden cessation of opening motion of abnormal valve leaflets(doming)
Lost with calcification and thickening
High frequency msec after S1 – best heard at apex-constant

39. Aortic ejection sounds and clicks, when present, are usually heard over the left sterna border and the apex.
However, when caused by aortic root aneurysm they may be louder at the second and third right intercostal space at the sternal border

41. 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

42. SEVERITY

43. Classification of Severity
Aortic 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
25 – 40
1 – 1.5
Severe
> 4
> 40
< 1

45. However, calculated mean P Grd are comparable
Doppler data
Peak instantaneous gradient over time
Cath data
Peak to peak data
However, calculated mean P Grd are comparable

46. 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

47. 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

48. AO & peripheral aorta (femoral sheath) showing peripheral amplification of 20 mmHg

50. Pull back

53. pulse pressure will increase after a PVC (negative Brockenbrough sign)
Brockenbrough sign post PVC compensatory pause causes increased filling, and increased preload. Frank-Starling law causes post PVC increased LV contraction with characteristically increased gradient
pulse pressure will increase after a PVC inAS(negative Brockenbrough sign)

56. LVSP = left ventricular systolic pressure;
Schematic representation of the flow and static pressure across the left ventricular (LV) outflow tract, aortic valve, and ascending aorta during systole
LVSP = left ventricular systolic pressure;
MGnet= transvalvular pressure gradient after pressure recovery
MGvc = transvalvular pressure gradient at the venacontracta
SAP= systolic aortic pressure
SAPvc = systolic aortic pressure at the vena contracta;
SV = stroke volume
Svi= stroke volume index
ZVA= valvulo-arterial impedance.

57. Downstream from the orifice, the flow stream expands and decelerates with a corresponding decrease in kinetic and increase in potential energy, a phenomenon called “pressure recovery”
Thus, the net P between the LV and the mid-ascending aorta is lower than the pressure drop immediately adjacent to the valve
Doppler measures velocity at the narrowest orifice, thus Doppler Ps are higher than the net P .
The clinical impact of pressure recovery usually is small but can be significant with mild stenosis and a small aortic root or with a doming congenitally stenotic valve

58. PRESSURE RECOVERY Fluid energy= pressure energy+ kinetic energy
Narrowed orifice (vena contracta) highest velocity
Downstream - flow stream expands
Deccleration (decreased velocity- kinetic)
Conversion kinetic – pressure
(pressure recovery)

59. Doppler derived gradients- using CW doppler @ vena contracta
Catheter 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

60. Hypertension may mask the severity of stenosis, an Presence 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

61. Stenotic valve area Torricelli’s law F = A X V A = F / V A = F / V Cc
F- Flow
A- Valve area
V- Velocity of flow
Cc- coefficient of contraction

64. Mitral Valve = constant 0.7 (later changed 0.85)
Aortic valve: assumed to be 1

65. GORLIN FORMULA Empirical constant includes
Conversion of cms H2o to units of pressure
Contraction co-efficient
Velocity co-efficient
Difference-
valve area calculated-
and valve area at surgery

66. GORLIN FORMULA Problems cardiac output Fick - oxygen consumption
Thermodilution- low output state
- significant TR
Duration of flow (SEP-DFP)
Alignment mismatch
Calibration errors

68. 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

70. Aortic valve area (AVA) is calculated based on the principle that volume flow proximal to the valve equals volume flow through the narrowed orifice

71. Continuity equation V/S bernoulli
Co-existing AR
LV-dysfunction

72. 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

73. M- mode Maximal aortic cusp separation (MACS)
Vertical distance between right CC and non CC during systole
Stenotic AV → decreased MACS

74. M- mode
Maximal aortic cusp separation (MACS)
Vertical distance between right CC and non CC during systole
Stenotic AV → decreased MACS
AVA
MACS
N > 2cm2
N > 15 mm
< cm2
< 8 mm
> 1 cm2
> 12 mm
gray area
8 – 12 mm

83. CATH

85. 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%

86. LV systolic dysfunction is an uncommon consequence of AS =about 5% of patients

87. Survival among Patients with Severe Symptomatic Aortic Stenosis Who Underwent Valve Replacement and Similar Patients Who Declined to Undergo Surgery10

89. AS w/ low output/low gradient