Hemodynamics in cath lab: Aortic stenosis & HOCM

RAHUL ARORA

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.

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

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

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

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obstruction when the catheter is withdrawn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

Artifacts can result when a

multiple-side-hole pigtail catheter

is incompletely advanced into the

LV chamber

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

A. The tracings demonstrating the significant time delay for

the pressure waveform to reach the RFA.

B. Realignment using tracing paper.

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.

Supra Valvular AS

Valvular AS

Sub valvular AS

Aorta pull back tracing- level of

stenosis

Hakki formula

Heart rate x SEP or DFP x constant ≈1

Calculation of stenotic valve area

Mean GD

Automated computerized analysis

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.

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

# 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

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:

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

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.

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

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

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

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

THANK

YOU

• 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.

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

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

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)

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