highlights hemodynamic in cath lab in patients of aortic stenosis and hocm

1. Hemodynamics in cath lab:
Aortic stenosis & HOCM
RAHUL ARORA

2. 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.

3. 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

4. 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

5. 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

7. 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obstruction when the catheter is withdrawn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

8. Artifacts can result when a
multiple-side-hole pigtail catheter
is incompletely advanced into the
LV chamber

9. 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

10. A. The tracings demonstrating the significant time delay for
the pressure waveform to reach the RFA.
B. Realignment using tracing paper.

11. 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.

12. Supra Valvular AS
Valvular AS
Sub valvular AS
Aorta pull back tracing- level of
stenosis

13. Hakki formula
Heart rate x SEP or DFP x constant ≈1
Calculation of stenotic valve area

15. Mean GD
Automated computerized analysis

16. 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.

17. 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

18. # 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

21. 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:

22. 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

23. 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.

24. 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

26. 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

27. 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

29. 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

30. THANK
YOU

31. • 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.

32. 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

34. 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

35. 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)

36. 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 Sec
cm3 /sec