Transcript HEMODYNAMICS OF DIASTOLIC HEART FAILURE DR VIVEK PILLAI, SENIOR RESIDENT IN CARDIOLOGY, MCH- KOZHIKODE 59 slides DEFINITION. As per the consensus document by the European Working Group HFnlEF.

HEMODYNAMICS OF DIASTOLIC
HEART FAILURE
DR VIVEK PILLAI,
SENIOR RESIDENT IN CARDIOLOGY,
MCH- KOZHIKODE
59 slides
DEFINITION.
As per the consensus document by the European Working
Group HFnlEF is defined as
-1) signs and symptoms of congestive heart failure.
-2)LVEF > 50% and a non dilated LV(<97 ml 3).
-3)Evidence of elevated LV filling pressures.
The last criterion is fulfilled in three ways-a)invasive hemodynamics with PCWP> 12 mm Hg or
LVEDP > 16 mm Hg.
- b)unequivocal echo evidence of elevated filling pressureE/e’ > 15.
-c) equivocal echo evidence(E/e’ > 8 but < 15 and a positive
BNP(NT-BNP> 220pg/ml or BNP > 200 pg/ml).
Factors influencing diastolic filling.
RV – LV
Interaction
Hemodynamic basis of symptoms and
signs.
-Exertional dyspnea-frequently an early event in diastolic
Hf- caused by pulmonary congestion.
- Elevated LV filling pressures→ transmission into
LA→transmitted into pulm. Vasc bed→pulm.
Congestion and dyspnea.
- later on this mechanism operates in the recumbent
position and at rest-giving rise to orthopnea.
- Stiff ventricle may give rise to an S4 on auscultation.
Diastolic heart failure- a continuum.
NORMAL DIASTOLE
-Diastole- means to send apart.
What constitutes normal diastolic function?-Normal
diastolic function allows the ventricle to fill
adequately during rest and exercise, without an
abnormal increase in diastolic pressures.
Best defined as the time period beginning at the
end of ventricular ejection( closure of semilunar
valves) and extending to closure of the AV valves.
Phases of diastole
• 1) isovolumic relaxation
phase.
• 2)rapid filling phase.7080% filling.
• 3)slow filling phase(
diastasis)- 5% of LV filling.
• 4) atrial filling phase-1525%.
• Early diastolic filling is driven by the LA-LV
pressure gradient.
• LA-LV pressure gradient depends on a number
of factorsa)rate of relaxation of the LV.
b)LV diastolic stiffness.
c)LV elastic recoil.
d) LV contractile state.
e)LA pressures.
f) ventricular interaction.
g)pericardial constraint.
h) LA stiffness.
i) pulmonary vein properties.
j)mitral orifice area.
LV RELAXATION.
• Is an active , energy dependent process,begins
during the ejection phase of systole ,
continues into the isovolumic relaxation and
rapid filling phase.
• Enhanced LV relaxation thus ↑es the LA-LV
pressure gradient, without ↑ing LA pressures,
and enhanced filling during exercise without
the need for elevated LA pressures.
INVASIVE MEASUREMENT OF
RELAXATION.
• The time constant of relaxation(ᵼ) describes
the rate of LV pressure decay during
isovolumic relaxation.
• Measurement of tau requires high fidelity
manometer tipped LV catheters.
• Weiss equation
– P=P0*e-t/τ(P0 is the LV pressure at end ejection.)
– τ=-(1/slope of Ln LVP Vs time)
– Normal <40 ms
– Relaxation is complete by 3.5 tau
– Larger value of tau-more impaired relaxation
• A simpler method to determine tauᵼ= IVRT/ln( syst.pressure)-ln( LA pressure).
tau is preload independent but afterload
dependent.
limitation- the isovolumic LV pressure decay is
not a simple exponential decay.
Actually LV pressure falls faster during the latter
part of isovolumic relaxation.
NON INVASIVE ASSESMENT OF
RELAXATION.
• By means of doppler echo.
• The transmitral flow velocity vs time profile is
affected by impaired relaxation in a variable
manner.
a)relaxation impaired but LA pressures not
elevated : slower LV pressure decay and higher
LV minimum pressure assoc with impaired
relaxation will ↓ the early diastolic LA-LV
pressure gradient.
E/A ratio.
• Healthy young individuals , most diastolic
filling occurs in early diastole.
• E/A ratio is > 1.
• In impaired relaxation, early diastolic filling
↓es progressively, and a vigorous atrial
contraction (‘ atrial kick occurs”)
Doppler profile of impaired relaxation.
• E vel- will be reduced.
• Duration of early diastolic filling will be
prolonged- E dec time.
• Reduced LA emptying during early diastole
↑es atrial preload, and the velocity of filling
with atrial contraction (Avel)↑es while the E/A
ratio decreases.
Deceleration time
• DT is prolonged in impaired
relaxation.
• Longer time required for
equilibration of LA and LV
pressures.
• Normal value is 193+_ 23
msecs.
• However when prolonged
this index fails to
distinguish b/w normal and
pseudonormal ratio.
PULMONARY VENOUS
PATTERN.
-provides a window
towards assesment of
diastolic function.
-normally consists of 3
waveforms,
a)systolic forward flow,b)
diastolic forward flow c)
atrial flow reversal.
Systolic forward flow is
due to
1) atrial relaxation.
2) mitral annulus
descent towards cardiac
apex with vent systole.
3) Biphasic in 37%
individuals.
Biphasicitya) s1 is due to atrial relaxation→ lowers LA
pressure→pulm venous return into LA →↑ LA
volume.
• b) second peak s2 in mid to late systole is
provided by an additional increase in LA volume
as the mitral annulus descends towards card.
Apex in vent systole.
• Pulm venous systolic forward flow is closely
related to LA pressure.
• When LA pressure is elevated systolic filling from
pulm veins is reduced.
• Diastolic forward flowoccurs in diastole when there is an open
conduit b/w the pulm veins,LA ,open mitral
valve and the LV.
reflects LV filling.
normally diastolic flow is slightly less than
systolic forward flow velocity.
• Atrial flow reversal- refers to the retrograde flow back into the pulm
veins, secondary to atrial contraction.
- with atria contraction, blood is not only ejected
into LV but also backward into pulm. Veins.
-the magnitude and duration of atrial flow reversal
is determined by transmitral and atriovenous
pressure gradients, which are influenced by LA syst.
Fn, LA and LV compliance.
Pseudonormalisation.
• Transition from impaired relaxation to restrictive
physiology.
• Transmitral inflow may resemble a normal profile.
• Result of decreased LV compliance alongwith a
moderate increase in LA pressure.
• Higher driving pressure across the mitral valve.
• If there is also a ↓ in the compliance of the ventricle,
ventricular pressure rises rapidly in early diastole and
the previously lengthened dec. time is shortened.
USE OF THE VALSALVA MANEUVER
• How does it help in unmasking diastolic
dysfunction?
-reduces the elevated LA pressure on performing
the maneuver.
-suspend breathing at the end of normal
inspiration and then to strain down without
breathing at expiration.
- An adequate valsalva maneuver is defined as a
10% redn in maximal E velocity from the baseline.
TRANSMITRAL DOPPLER
FLOW PATTERNS
A)
B)
C)
NORMAL E/A RATIO OF
PSEUDONORMALISATION.
UNMASKING OF DIASTOLIC
DYSFUNCTION USING THE
VALSALVA MANEUVER.
ADVANCED DIASTOLIC
DYSFUNCTION.
Use of pulmonary venous flow profile.
• Pts with a pseudonormal filling pattern have an
elevated LVEDP which can be identified by
a)increase in flow reversal into the pulm. Veins
with atrial contraction and/or
b) shortening of duration of the mitral A wave
compared with pulmonary venous AR duration
with atrial contraction.
Disadvantagesdifficulty in obtaining a pulm venous profile.
ILLUSTRATION-SYMPTOM
FREE SUBJECT WITH NORMAL
2D ECHO.
Mitral inflow doppler show s E
velocity .8m/sec. and A velocity of .6
m/sec.
DT was normal at 200 msec..
Difficult to differentiate b/w normal
and pseudonormal here.
Pulm venous dopplerPredominant systolic forward flow.6m/sec.
Diastolic forward flow is .4 m/sec.
Pulm venous atrial flow reversal
velocity is < .4 m/sec and duration is
lesser than duration of A wave.
Use of color M-mode prop velocity
• This modality allows acquisition of information about
velocity, time and space along the entire line of the Mmode cursor.
• Accurately assess the transmitral propagation flow velocity
from the mitral annulus across the cavity of the LV.
• Appears to be preload independent- hence may be useful
in identification of pts with pseudonormal inflow.
• Normal prop . Velocity-.84+-.11 m/s.
• Abnormal relaxation results in significant slowing of this
velocity.
• Pseudonormalisation can be identified when flow
propagation velocity is < .50 m/s.
Method of obtaining Color
M- mode flow
propagation velocity
- 4 chamber view.
- M-mode cursor placed as
parallel as possible to flow
direction.
- Temporally performed in
early diastole,coincident
with the E wave.
- -shift the color baseline to
a new nyquist limit, an
aliasing border ( blue to
red)- Then a tangent is drawn
from the mitral valve to a
point 4 cm distal.,
representing the early
diastolic flow propagation
velocity.
Restrictive physiology
• Relaxation is still impaired in these individuals but it is now
masked by a marked ↑ in LA pressure.
• Crossover b/w LA and LV pressure is not delayed.
• Mitral valve opening occurs earlier than normal.
• ↑ed LA pressure increases transmitral gradient, in early
diastole - ↑ peak E wave.
• Early opening of mitral valve – shortening of IVRT.
• Rapid equalisation of pressures and hence dec. time is
shortened.
• Because of high LVEDP-little or no filling occurs with atrial
contraction- blunted A wave.
• Thus E/A ratio is > 2.
The pulm. venous trace in restrictive
filling.
• Increase in diastolic forward flow(D) wave and
a ↓ in systolic forward flow( S) wave.
• Due to
a) rapid vent. Filling in diastole due to
elevated LA pressure and ↓ LV compliance.
b)it follows that there must be ↑ filling of the
atrium via pulm veins in diastole.
c)with most of the atrial filling in diastole ,
there is a decrease in syst. Filling.
• ↑ed flow reversal into pulm veins during
atrial contraction( AR velocity).
• Duration of flow reversal is longer than that
of the mitral A wave.
• This phenomenon can be explained by ↑ed
LVEDP.
• Diastolic MR and TR may be present in pts
with restrictive physiology.
• Indicative of markedly elevated vent.diastolic
pressure that>> LA pressure→reversal of flow
through diastole.
• Restrictive filling is associated with greater
filling pressures , more symptoms and a
worsened prognosis.
Doppler tissue imaging in diast. Fn
assessment.
• Tissue doppler imaging records systolic and
diastolic velocities in the myocardium and the
corners of the mitral annulus.
• For the purpose of diastolic function
assesment, the tissue doppler mitral annulus
velocity is of prime importance.
Method
• Apical 4 chamber view.
• Sample volume placed on the annulus near
mitral valve insertion.
• Both septal and medial sites should be
recorded.
• Because of high signal amplitude, spectral gain
should be lowered.
• High sweep speed b/w 50- 100 cm/sec.
• Most useful measurement is peak annular
velocity in early diastole-e’.
• E’ velocity depends primarily on LV relaxation.
• When diastolic function is abnormal e’ is
relatively independent of preload.
• However when diastolic function is normal, e’
↑es with higher filling pressure.
• Usually combined with E to obtain the familiar
E/e’ ratio.
• E’ should be measured from both septal and
lateral locations.
• Most pts lateral e’ will be higher than septal
e’s and thus E/e’ will be lower if the lateral
position is used for e’.
• Septal e’< 8 cm/s and/or lateral e’ < 10cm/s
suggest diastolic dysfunction.
E/e’ ratio.
• E velocity obtained from the transmitral flow pattern
and e’ from TDI of the lateral mitral annulus.
• Rough hemodynamic correlation.
• Correlation is better in pts with depressed EF but
reasonable in pts with normal EF.
• E/e’< 8- normal filling pressures.
• E/e’ > 15- correlates with a PCWP > 12 mmHg.
• Many pts fall in the intermediate zone where the E/e’
ratio is >8 and <15 ,such pts cannot be determined to
have diast dysfunction by this method alone.
Difficulties.
• Not reliable in pts with prosthetic mitral
valves, annular rings and significant annular
calcification.
• Or In regional wall motion abnormalities.
LV diastolic stiffness.
• Stiffness or elastance is defined as the
relationship between the change in stress and
the resulting strain.
• Elastance of the LV varies over the cardiac
cycle (time-varying elastance.
• End-systolic and end-diastolic elastance are
defined by the changes in systolic or diastolic
pressure associated with a change in ESV or
EDV.
EDPVR
EDPVR-end diastolic pressure vol.
relationship
• Why EDPVR?-evaluates the passive diastolic ventricular
properties unlike tau which is for active vent.
relaxation.
• Only way to truly demonstrate that HFnlEF pts have
abnormalities of passive diastolic properties is to
demonstrate an upward shift of the pressure
vol.curve.
• Also by characterising EDPVR it is possible to
demonstrate that not only is the LVEDP elevated ,but
the ventricles have ↓ capacitance( ↓ filling volume at
any given filling pressure).
In the absence of an upward shift
LVEDP may be increased simply
because of ↑ preload vol., without
any change in diastolic properties.
STIFFNESS-( beta)
Slope of the pressure vol. relationship
Depends on filling pressures.
Increase in vent. Pressures leads to
increase in calculated stiffness.
STIFFNESS ASSESSMENT BY DOPPLER
ECHO.
• If there is doppler evidence of increased filling
pressures, and LV dimension or volume is
normal, then ↑ stiffness is inferred.
• Furthermore, if the deceleration time of the early
diastolic transmitral flow velocity profile is short,
despite evidence of impaired relaxation (reduced
e’), rapid equalization of LV and LA pressures
during early diastolic filling and increased LV
diastolic stiffness are inferred.
ATRIAL DYSFUNCTION IN DIASTOLIC
HEART FAILURE.
• Mean LA pressure- the resistance to filling that
pulm venous system faces.
• Early on in diast.Hf the LA systolic fn compensates
for reduced filling→ atrial failure ensues.
• Hemodynamic trace of LA pressure waveformlarge v waves( in the absence of MR)→reflects
↓LA compliance.
• ↓ LA compliance may play a role in dev. Of Pulm
HT in HFnlEF.
• ↓LA syst fn necessitates higher LA mean
pressures for augmenting early diastolic filling.
LEFT ATRIAL VOLUME
• An increase in LA size is the morphological
expression of chronic diastolic dysfunction.
• Chamber vol. should be obtained from 4-c and 2c views.
• LA area should be measured at end systole, when
volume is largest.
• Minnesota based popn study( n=2042)
characterised LAVindexed –
23+-6 ml/ m2( normal).
25+-8ml/m2(grade 1 diastolic dysn).
31+_8 ml/ m2( grd 2 diast. Dysfn).
48+-12 ml/ m2( grd ¾ diast. Dysfn.)
EMERGING CONCEPTS OF
DIASTOLIC DYSFUNCTION
• Not isolated from systole.
tan et al
• In HFnlEF there are
combined systolic and
diastolic abnormalitiesinvolving ventr. Twist and
deformn( strain) which lead
to↓ vent, suction,delayed
untwisting and impaired
early diast. Fillingoperative in exercise when
diastole shortens.
• In diastolic HF-↑ in LV diastolic pressure→↑
in LA pressure and pulm venous pressuresigns and symptoms of pulm venous
congestion.
• Postcapillary pulm HTN may precipitate Right
heart failure.
• LV stroke vol. and card. Output may decline
due to ↓ EDV ( preload).
• Chronic elevation of pulm venous pressure
may be assoc. with ↑ PVR.
SUMMARY
REFERENCES
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1) Braunwald’s heart disease- 9th edition.
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4) Manual of cardiovascular medicine-4th edition.- Griffin.
5) Diastolic dysfunction and left atrial volume- a population based
study.Pritchett,Mahoney et al- JACC. 2005;45(1):87-92.
6)Diastolic heart failure –review,Mandinov et al. Cardiovascular Research 45 (2000)
813–825.
7) Current Perspectives on Cardiac Function in Patients With Diastolic Heart
Failure- Wang and Nagueh, Circulation. 2009;119:1146-1157.
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echocardiography
• Thank you!