hemodynamic in cath lab: aortic stenosis and hocm
TRANSCRIPT
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Hemodynamics in cath lab: Aortic stenosis & HOCM
RAHUL ARORA
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INTRODUCTION• stenotic lesions start in anatomic LVOT extend upto the descending
portion of aortic arch.
• obstruction
• valvular,
• subvalvular
• Fixed
• dynamic
• supravalvular.
• impose increased afterload on LV and if severe and untreated lead
to hypertrophy, eventual dilation and failure of LV.
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Role of cardiac catheterization in AS
What information can be obtained in AS ?
• measurement of pressure gradient
• level of stenosis
• analysis of the pressure waveforms
• estimation of valve area
• measurement of cardiac output
Discrepancy between echo findings and patient symptoms
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Methods of measuring a transvalvular gradient in AS
1. retrograde approach
• AO catheter retrograde above AO valve, LV retrograde with pressure wire or pigtail.
• LV retrograde with pigtail, AO pressure from side arm of long sheath or femoral sheath.
• LV and AO retrograde with dual lumen pigtail
• LV retrograde with pigtail and ‘‘pullback’’ pressure from LV to AO
2. antegrade approach
• LV via transseptal, AO catheter retrograde above AO valve
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CAVEAT: both measurement at same time with direct measurement of aortic pressure is best
means of assessment.
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
TRANSEPTAL ++ RISK
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Carabello Sign
rise in arterial blood pressure during left heart catheter pullback in
patients with severe aortic stenosis
Mechanism : related to partial obstruction of an already narrowed
aortic orifice by the retrograde catheter & relief of this
obstruction when the catheter is withdrawn
AVA<0.6cm2
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Artifacts can result when a
multiple-side-hole pigtail catheter
is incompletely advanced into the
LV chamber
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Simultaneous measurement of aortic and FA pressure demonstrating
peripheral amplification
Peripheral amplification
# increase in peak systolic pressure and pulse pressure in peripheral
arteries as compared to the central aorta
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A. The tracings demonstrating the significant time delay for
the pressure waveform to reach the RFA.
B. Realignment using tracing paper.
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THREE INVASIVE MEASUREMENTS
Mean gradient
• represents the area under the LV-Ao
pressure curve
• corresponds to echo mean gradient
Peak to peak gradient
• no true physiological meaning
• difference between maximum aortic
and max LV pressures
Peak instantaneous gradient
• maximum difference between LV &
aorta during systole.
• corresponds to maximum
instantaneous gradient by echo.
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Supra Valvular AS
Valvular AS
Sub valvular AS
Aorta pull back tracing- level of
stenosis
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Hakki formula
Heart rate x SEP or DFP x constant ≈1
Calculation of stenotic valve area
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Mean GD
Automated computerized analysis
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Low-Flow, Low-Gradient Aortic Stenosis
With Normal and Depressed LVEF
# Decreased EF (<40%) - Low Flow –Low Gradient AS
# Normal EF ( ≥ 50%) - Paradoxical Low Flow –Low Gradient AS
⇊ in gradient ➨ ⇊ in trans-valvular flow.
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Low-flow, Low-Gradient severe AS with decreased LVEF
# valve area <1 cm2
# mean aortic valve gradient < 40 mm Hg
# ejection fraction <40%
# pseudo aortic stenosis ➨ medications that increase cardiac output
will usually increase the calculated AVA
# Intravenous dobutamine - 5 μg/kg/min ➔➔ 20 μg/kg/min
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# true severe aortic stenosis
(1) a mean aortic valve gradient greater than 30 mm Hg
(2) an aortic valve area ≤ 1.2 cm2
Effects of dobutamine infusion in patients with and without valvular AS
# Pseudo severe As
Peak stress
- MG < 30 mm Hg
- EOA >1.0-1.2 cm2
- ab. in EOA> 0.3 cm2
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Paradoxical Low flow –low Gradient Severe AS:
- indexed AVA < 0.6 cm2/m2
- Gradient < 40 mmHg
- EF > 50%
- Stroke volume index (SVi) : < 35 mL/m2
Paradoxical Low flow –low Gradient Severe AS:
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Physiopathology : paradoxical LF- AS despite preserved EF
Pronounced concentric LV remodelling and smaller LV cavity size
≈ restrictive physiology
# Decrease in SV is due to deficient ventricular filling
# smaller LV cavity size
# deficient ventricular emptying
# Intrinsic myocardial dysfunction causing EF lower than expected (50-60%)
# Prevalence increases with
- older age
- female gender
- concomitant systemic HTN
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ROLE OF CARDIAC CATHERIZATION IN TAVR
• pre TAVR evaluation
• to measure the gradient.
• for evaluation in case of
discrepancy between echo
and clinical symptoms.
• for evaluation of low flow
low gradient aortic
stenosis.
• post TAVR
• to measure the success of
procedure by measuring
residual stenosis.
• to look for complications in
form of aortic regurgitation.
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Hypertrophic cardiomyopathy
dynamic intraventricular pressure gradient
may/ may not have systolic pressure gradient at rest
gradient - provoked with : Valsalva maneuver
: extra systole
: systemic vasodilator (amyl nitrate)
: inotropic stimulation
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HOCM : SPIKE-AND- DOME CONFIGURATION OF PULSE WAVE
dynamic outflow obstruction ➨
characteristic arterial pressure
waveform “spike-and-dome
configuration
• early spike ➨ rapid lv ejection by
the hypercontractile myocardium
• pressure dip & doming ➨ reflect
the dynamic outflow obstruction
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Valsalva maneuver : produces a marked increase in the gradient
: change in the FA pressure waveform to a spike-and-
dome configuration.
LV and FA pressure tracings in HCM
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Brokenbrough-Braunwald-Morrow sign
Post PVC potentiation in HOCM
PVC ➨⇈in intracavitary gradient ➨⇈ed contractility (⇈ed Ca2+)
# Post PVC beat is associated with a reduction in aortic systolic
pressure and pulse pressure ≈ B-B-M sign
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THANK
YOU
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• NO OBSTRUCTION AT ONSET OF VENTRICULAR EJECTION.
• BRISK, INITIAL UPSTROKE- PEAK SYSTOLIC PRESSURE.
• OBSTRUCTION PROGRESSIVELY DURING SYSTOLE AS THE CONTRACTILE
FORCE OF THE LV BUILDS.
• WHEN OBSTRUCTION REACHES A MAXIMUM ,AORTIC PRESSURE DROPS.
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MECHANISM
• NORMALLY AFTER A PVC, COMPENSATORY PAUSE
• DIASTOLIC FILLING TIME & DIASTOLIC VOLUME
• INCREASED STRETCH
• SV AND CONTRACTILITY (FRANK STARLING LAW)
• ARTERIAL SYSTOLIC PRESSURE TO RISE
• IN HCM PARADOXICAL DECREASE IN SV DUE INCREASED CONTRACTILITY CALCIUM LEADING
TO DECREASED ORIFICE SIZE AND INCREASED GRADIENT
• DIMINISHED PULSE PRESSURE
• REDUCED SV CAUSED BY INCREASED DYNAMIC OBSTRUCTION
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1. Torricelli's law:
flow across a round orifice F = AV CC
F = flow rate A = orifice area
V = velocity of flow CC = coefficient of orifice contraction
GORLIN FORMULA:
2. relates pressure gradient and velocity of flow - Torricelli's law
V = velocity of flow
Cv = coefficient of velocity - correcting for energy loss as pressure energy is converted to
kinetic or velocity energy
h = pressure gradient in cm H2O
g = gravitational constant (980 cm/sec2) for converting cm H2O to units of pressure
A = F
VCC
Calculation of stenotic valve area
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C = empirical constant accounting for CV and CC
h = mm Hg (rather than cm H2O)
GORLIN FORMULA:
C - empirical constant ( 0.85 for mitral valve, 1.0 for Aortic valve)
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Flow (F) = is the total cardiac output expressed in terms of the seconds
per minute during which there is actually forward flow across the valve.
F= CO (ml or cm3/min)
SEP (sec/min) x HR
cm3 x min
Min x Seccm3 /sec