Fonction diastolique Pressions de remplissage Dysfonction

Fonction diastolique
Pressions de remplissage
Dysfonction diastolique
Alain Combes
Service de Réanimation
Institut de Cardiologie
Hôpital Pitié-Salpêtrière, AP-HP, Paris
Université Pierre et Marie Curie, Paris 6
www.reamedpitie.com
Background
For patients > 65 years old,
CHF is the most common diagnosis
at discharge from hospital
| The population is aging
|
z In
the early 1900s,
• ~ 4% population was > 65
z 2010:
1/3 population > 65
Background
Among the elderly, cardiovascular
disease is the MOST common cause
of mortality and morbidity
| In the US, 5 M people have CHF
|
z Half
caused by diastolic
dysfunction
z With preserved LV function
Fact #1
|
|
Everyone and their mother over the age of
40-50 has E/A reversal, during resting 2D
echo.
The actual incidence is ~25-30% in
individuals > 45 y
z Over the past 10 years, incidence of
Diastolic CHF has increased.
• 70 y.o pts’ incidence of CHF:
• SHF = DHF
• 80 y.o pts’ incidence of CHF: DHF > SHF
Fact #2
Diastolic dysfunction ≠ Diastolic CHF
| Diastolic dysfunction characterizes
abnormal relaxation of the LV,
|
z An
|
echo finding…
Diastolic CHF describes a clinical
syndrome of CHF in patient
z With
preserved LV function
Causes of Diastolic dysfunction
Æ Heart Failure
Hypertension
| Hypertension
| Hypertension
| Hypertension
| Hypertension
| Hypertension
| Hypertension
|
Other Causes of
Diastolic Heart Failure
Plan…
1.
2.
3.
4.
5.
6.
7.
8.
9.
Brief Review of diastolic physiology
MV inflow patterns
IVRT – Isovolumic Relaxation Time
DT – Deceleration Time
Velocity of propagation
Tissue Doppler of the MV annulus
E/E’
Atrial Fibrillation and Sinus Tachycardia
Diseases of the Pericardium
Déterminants du VES
|
Pré-charge
|
Fonction POMPE ventriculaire
|
z
Performance systolique
z
Performance diastolique
Post-charge
Définition de la précharge du cœur
|
Ensemble des facteurs qui contribuent à
créer la contrainte = stress
z
Qui s’exerce sur la paroi ventriculaire en
télédiastole
z
Juste avant la phase de contraction
isovolumique
Pré-charge et Loi de Laplace
|
|
|
Pré-charge = contrainte σ en fin de
diastole
σ = P x r /2h, dynes/cm²
La précharge VG est donc:
z
z
|
Proportionnelle à la pression qui règne
dans la cavité et au rayon du ventricule
Inversement proportionnelle à l’épaisseur
de la paroi
Donc pression et volume (ou diamètres)
télé-diastoliques sont des approximations
de la précharge
Déterminants de la pré-charge
|
Retour veineux, qui dépend
z
Volume sanguin circulant, Volémie
• Apports/pertes liquidiens, fonction rénale…
|
z
Résistance/compliance du réseau veineux capacitif
(rôle du système nerveux autonome)
z
Pressions intra-thoracique et intra-abdominale
z
Débit cardiaque (circuit fermé)
Compliance du ventricule Dt et du péricarde
z
Performance diastolique de la pompe cardiaque
Performance systolique
|
|
|
= Contractilité, état inotrope du myocarde:
z Propriété inhérente du myocarde à se contracter
z Génération d’une force augmentant vitesse et
amplitude du raccourcissement des fibres
myocardiques
z Indépendamment des conditions de charge (pré et
post charge ventriculaire) et de la fréquence
cardiaque
Augmentée par l’effort, les catécholamines endogènes ou
pharmacologiques, les digitaliques…
Indices pour évaluer l’état inotrope:
z dP/dt, FE VG, Travail systolique VG…
z Élastance en fin de systole +++
Courbes P/V ventriculaires
A-B: Systole
C-D: Diastole
end-diastole
Pré-Charge
Élastance en fin de systole
Effet inotrope et courbes P/V
Ees +
Effet inotrope positif
Ees -
Effet inotrope négatif
Performance diastolique
|
= État lusitrope du myocarde:
z Diastole cardiologique:
• relaxation isovolumique + remplissage ventricule
z
z
|
|
|
Au niveau moléculaire, capacité à faire baisser la
concentration de Ca++ intracellulaire
Phosphorylation de protéines du SR, phospholamban
en particulier, qui augmente la vitesse de
réabsorption Ca
Varie le plus souvent parallèlement à l’état inotrope
du myocarde
Influence compliance péricarde + thorax
Un des déterminants de la pré-charge ventriculaire
Normal Diastolic function
|
Occupies about 2/3 of cardiac cycle
z Takes
|
longer than systole
Active process
z Requires
|
energy
Abnormalities of diastolic function
z ALWAYS
precede those of systolic
function
z Ex: Acute MI
Effet lusitrope et courbes P/V
Effet lusitrope positif
Effet lusitrope négatif
Systolic vs. Diastolic Failure
Normal Diastolic function
1. Isovolumic
Relaxation
2. Early rapid
diastolic filling
phase
3. Diastasis
4. Late diastolic
filling due to atrial
contraction
Quinones, ASE Review 2007
Normal Diastolic function
|
|
|
|
When LV pressure
becomes less than LA
pressure, MV opens
Rapid early diastolic
filling begins
Driving force is
predominantly elastic
recoil and normal
relaxation
~80% LV filling during
this phase
Normal Diastolic function
|
|
|
As a result of rapid
filling, LV pressure
rapidly equilibrates with
and may exceed LA
pressure
Results in deceleration
of MV inflow
Late diastolic filling is
from atrial contraction
z It’s ~ 20% LV filling
MV Inflow Patterns
MV Inflow Patterns
MV inflow Patterns
5 stages – Normal and Stages I – IV
diastolic dysfunction
| Stage I – Impaired relaxation
| Stage II – Pseudo-normal
| Stage III – Restrictive Filling,
reversible
| Stage IV – Restrictive Filling,
irreversible
|
MV PW inflow patterns
MV inflow pattern limitations
Advantages
Disadvantages
IVRT and DT
IVRT – Isovolumic relaxation time
|
|
Time interval
between aortic
valve closure and
mitral valve
opening
Usually obtained
from Apical view
with Doppler
sample between
AV and MV
|
|
Normal = 70–90 ms
It will lengthen with
impaired LV
relaxation and
decrease with
increase in LV filling
pressures
E Deceleration time
|
DT - Peak of the E
wave – time
interval for the E
wave velocity to
reach 0
E Deceleration time
|
|
Nl = 160 – 220 ms
Deceleration time increases
z
|
Conversely, if there is a decrease in LV
compliance or a significant increase in LA
pressure
z
z
|
If there is abnormal relaxation
Æ DT decreases
Pathologic – suggests elevated filling pressures
The LV can also relax vigorously from
tremendous elastic recoil such as young healthy
people (short DT but normal)
IVRT + DT: Strengths and
Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
Velocity of
mitral flow
Propagation
(color M-mode of MV inflow)
Velocity of propagation of mitral
inflow
|
Normally, there is an
intraventricular
pressure gradient
z
|
|
Apical < Base
This gradient
decreases with a
decrease in myocardial
relaxation
Color M mode displays
color coded mean
velocities from the
annulus to the apex
over time.
Velocity of propagation of mitral
inflow
|
|
|
|
|
|
|
Color flow baseline
needs to be shifted to
lower the nyquist limit.
The central highest
velocity jet should be
blue.
Trace the slope of the
first aliasing line.
> 50 cm/s normal
< 50 cm/s abnormal
Load dependent
Hard to do accurately
Velocity of propagation of mitral
inflow
|
Vp has been used to estimate filling
pressures (PCWP)
1.
2.
3.
|
E/Vp > 1.5 Æ PCWP > 15 mmHg
PCWP = 4.5 [1000/(2 x IVRT) + Vp] – 9
PCWP = (5.27 x E/Vp) + 4.6
Falsely high in
z
z
Restrictive Cardiomyopathy and
Hypertrophic cardiomyopathy
MV inflow propagation velocity:
Strengths and Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
LA Volume
LA Volume Index
|
|
|
EASY TO DO!!
The new echo GOLD
STANDARD for LA
size
Correlates much
better with the true
gold standard which
is MRI.
|
|
Has been called the
HbAIC of cardiac
disease. Robust marker
of clinical outcomes
WHAT DO YOU NEED:
z BSA (remember, it’s
an index)
z A4C and A2C traced
LA’s
z Shortest length
LA volume
|
|
|
Divide the LA volume by
BSA!!
A-L method is used most
commonly (we don’
don’t like calculus)
22 +/- 6 ml/m²
(normal)
z
z
z
28-34 - mild
34-40 - moderate
>40 - severe
LA volume: Strengths and
Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
Pulmonary
Vein Profile
Pulmonary
venous flow
Pulmonary venous flow
|
|
|
Normally 4 different waves seen – S1/S2/D/A
Normal S – dominance
Young people can have a D dom normally
Pulmonary Vein Profile
|
|
PVs1 – early in systole
and relates to atrial
relaxation. A decrease
in LA pressure
promotes forward flow.
PVs2 – mid systole.
Represents the
increase in pulmonary
venous pressure and
decrease in LAP due to
MV annulus descent
z
|
Normally the S2>S1
Distinction only
identifiable in about
30% people, normally
Pulmonary Vein Profile
|
|
PVd – occurs after
opening of the MV and
in conjunction with
decrease in LA
pressure
Pva – increase with
atrial contraction.
z
z
May result in a flow
reversal into the PV
Depends upon
•
•
•
LV diastolic pressure
LA compliance
HR
PV profiles in diastolic
dysfunction
Duration and speed of PVa increase if impaired compliance
Pulmonary Vein flow: Strengths
and Weaknesses
Strengths
Weaknesses
Lester et al, JACC 2008; 51; 679 - 689
Tissue Doppler
Tissue Doppler
Measuring tissue velocity and NOT
blood flow
| Speed of tissue is ~ 1/10 of arterial
blood.
|
z
z
z
|
Arterial blood velocity ~ 150 cm/s
Venous Blood velocity ~ 10 cm/s
Myocardial Tissue velocity ~ 1 – 20 cm/s
Speed expressed in cm/s
Tissue Doppler – What we
change on echo Machines
|
Doppler instruments are altered to
reject the high velocity of blood
|
Requires a high frame rate
|
DECREASE GAIN!
|
Lower aliasing velocities
QUESTION
WHAT ARE THE 3 profiles
seen on Tissue Doppler?
Tissue Doppler
|
3 velocity profiles are seen –
z
|
S’ – systolic velocity of the MV annulus.
z
z
|
Normally should be > 6 cm/s
Can perform segmental or regional functional assessment
E’ – Early Diastolic velocity
z
z
z
|
Systolic (S’), Early Diastolic (E’) and late diastolic (A’)
2 sites are typically measured – medial and lateral – Normal
Range…
E’m – > 10 cm/s
E’l > 15 cm/s
A’ - Late diastolic velocity.
z
z
z
z
Atrial contraction
Correlates with LA function
Increases in early diastolic dysfunction
decreases with LA dysfunction (later diastolic dysfunction)
TDI - applications
Beyond E’ and E/E’, mostly in
research…
| Evaluation of Thick Walls
|
z
z
|
LVH, HCM, Infiltrative CM, Restrictive CM,
& Athlete's Heart
Normal TDI and strain vs abnormal TDI
and strain
Viability Assessment akinetic vs scar
z
Relates to Tissue velocity gradients
Tissue Doppler :
Normal Profiles
Medial
> 10 cm/s
Lateral
> 15 cm/s
Tissue Doppler
|
|
|
E’ velocity is essential for classifying the
diastolic filling pattern and estimating
filling pressures
Helpful to differentiate myocardial disease
from pericardial disease
Normally E’ increases with an increase in
the transmitral gradient
z
|
Exertion or increase preload
In Diastolic Dysfunction
z
It’s low & doesn’t increase as much with
exertion or inc. preload
Tissue Doppler
|
E’ decreases with aging
z
|
Partially Load independent!
z
|
|
Precedes even E/A reversal
Reproducible
One of the earliest markers for diastolic
dysfunction
Correlates with filling pressures, especially
when used as a ratio
z E/E’
Tissue Doppler
STRENGTHS
1. Can be obtained in
most patients
2. Early marker of
diastolic dysfunction
3. Not influenced by
changes in heart rate
4. Primarily load
independent in
disease states
WEAKNESSES
1. Influenced by local
changes in wall motion
(infarction)
2. Not accurate in
significant MV disease
- M Annular Calcification
- M Valve Regurgitation
Information derived from
Tissue Doppler
|
E/E’ can estimate PCWP
z
z
z
|
>15 Æ wedge > 20
< 8 – normal
8 - 15 ??
E/E’ has been validated
in clinical studies as a
marker of elevated
PCWP (> 15)
|
|
Elevated E/E’ is
predictive of poor
outcomes in MI
Significantly
decreased E’
associated with higher
mortality
E/E’ is a robust clinical marker
|
What the ratio
means?
z
z
z
Nagueh et al, JACC 1997; 30: 1527 - 1533
> 15 Æ elevated
filling pressures
< 8 Æ Nl
8 – 15 Æ ???
Assessment of Diastolic filling in
A-fib and Sinus Tachycardia
|
|
A fibrillation:
z No A wave from Mv inflow and blunted
PVs wave
z DT time measurement is tricky, variable
z Can use E/E’
z Can use DT of the PVd wave
Sinus Tachycardia
z E and A waves may fuse
z Use E/E’
Let’s Review
Normal MV inflow
E/A = 0.9-1.5
| IVRT 70-90 ms
| DT = 160-220 ms
| Vp > 50 cm/s
| LAVi < 28 ml/m²
| S – dominant PV
pattern
| E/E’ <8
|
Stage I
IVRT > 90 ms
| DT > 240 ms
| E/A < 0.9
| LAVI>28 ml/m²
| E/E’<10
| Vp < 50 cm/s
| S – dominant
PV pattern
|
Stage II
|
|
|
Looks the same
like normal –
hence the name
“pseudonormal”
Many of the
parameters are
the same as
Normal LV inflow
PV – S blunting or
D dominant PV
How do I differentiate between
Stage II and normal?
| Valsalva
– shouldn’t change normal but pseudonormal
should look like Stage I. Also Stage III should look like stage I
should look like Stage I. Also Stage III should look like stage I
| E’
(Tissue Doppler) – Normal is normal.
Lower velocities with diastolic dysfunction (E’m <10, E’l < 15).
Lower velocities with diastolic dysfunction (E’m <10, E’l < 15).
| Left
atrial volume – With elevated filling
pressures, the left atrium will remodel and enlarge (LA Volume
pressures, the left atrium will remodel and enlarge (LA Volume
Index > 28 ml / m2)
| Velocity
of propagation (normal) or < 50 cm/s (abnormal)
(normal) or < 50 cm/s (abnormal)
|D
> 50 cm/s
– dominant pulmonary veins
The 4 Phased Valsalva Maneuver
Nishimura et al. Mayo clinic proceedings. 2004;79: 577-578.
PHASES
| I - AO pressure
increases (increase in IT
pres.)
| II – AO and PP decrease
because dec. in preload.
Reflex tachycardia.
| III – AO pressure
decreases more in
response to release of IT
pressure
| IV – recovery period.
Preload, AO, PP +
increase.
Stage II
Valsalva
ÎÎÎ
Stage III – Restrictive, reversible
IVRT < 70 ms
| DT < 160 ms
| E/A > 2:1
| E’ < 5cm/s
| Vp < 50 cm/s
| LAVI > 35 ml/m²
| D>>S (PV Pattern)
| PVAr >35 cm/s
|
Stage III – Restrictive,
reversible
Valsalva
ÎÎÎ
Stage IV – restrictive irreversible
|
|
|
|
|
|
|
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IVRT < 70ms
DT < 130ms
E/A > 2.5
E’ < 5 cm/s
Vp < 50 cm/s
LAVI > 40 ml/m²
No valsalva
change
D>>S (PV pattern)
PVar > A
Differential diagnosis:
Pericardial constriction
Causes of pericardial
constriction
Prior Cardiac surgery
| Idiopathic
| Pericarditis
| Prior Radiation
| Collagen Vascular
| Infection (TB)
|
Constrictive Pericarditis
|
|
|
|
|
Everything we’ve spoken about for
diastolic dysfunction DOES NOT
APPLY HERE
Not uncommon
Escapes clinical and echo detection
Pericardial Thickness may be normal
in 1/5th of cases
Calcification of the pericardium may
only occur in ~ 20% pts on CXR
Constrictive Pericarditis – some
Echo findings
Thickened pericardium (~ 80%)
| Abnormal ventricular septal motion
| Flattening of the posterior wall
during diastole
| Respirophasic variation of
Ventricular cavity size
| Dilated IVC
|
Echo criteria to diagnose
Pericardial Constriction
|
Dissociation between intrathoracic
and intra-pericardial pressures
z Normally
|
they’re related
Exaggerated ventricular
interdependence
z i.e.
the filling of one, significantly
impacts the filling of the other
Doppler Findings in Constrictive
Pericarditis
Respiratory variation of >25% in mitral E velocity
Doppler Findings in
Constrictive Pericarditis
|
Increased regurgitation flow with expiration in the
hepatic vein
Other features of constriction
|
Tissue doppler that is > 7 cm/s (annulus
paradoxus)
z
z
|
PW MV inflow that looks like restrictive
filling pattern Æ
z
|
Unless the myocardium is involved, myocardial
relaxation is intact
Septal annular velocities are normal or even
increased (not close to the pericardium like the
lateral annulus)
E/A > 1.5 and DT < 160 ms
E/E’ is inversely proportional to the PCWP
z
As opposed to myocardial diseases
Prognosis
|
|
Steady rise in prevalence of CHF with
preserved LV function
By the 7th decade, incidence of diastolic CHF =
z
|
By the 8th decade, incidence of diastolic CHF >
z
|
Incidence of systolic CHF
Systolic CHF
The survival of patients with the clinical
syndrome of heart failure is similar in those
with preserved versus those with a reduced LV
ejection fraction
Treatment
Treatment
En réa…
OAP « Flash »
Montrer films et images Doppler
OAP flash
|
2 situations :
z
Évènement aigu sur dysfonction
diastolique
z
Poussée HTA +++
Ischémie myocardique
Tachycardie / trouble du rythme…
z
Évolution de l’IC chronique
z
z
OAP Flash en pratique
|
Chez le patient ambulatoire :
• Signes d'insuffisance cardiaque congestive
• Dyspnée aigue souvent mal tolérée
• HTA +++
• Fonction VG normale, IM sur Echo
|
Dans la période périopératoire :
• Réduction de la capacité d'adaptation face
aux variations de volémie
• Variations du rythme cardiaque mal
tolérées
TTT de OAP flash
|
Oxygénothérapie
z
|
Nitrés
z
|
|
|
En bolus pour contrôler l’HTA
Morphiniques possibles
TTT étiologique
z
|
+/- CPAP, VNI, intubation
HTA / ischémie / tachycardie : AC/FA
Diurétiques, pas toujours…
PAS DE DOBUTAMINE
Conclusion
|
|
|
|
|
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Diastolic Dysfunction and Diastolic HF
z Frequent entities in the clinical practice
z Particularly in hypertensive population
Diagnosis of diastolic HF if
z Signs of HF and
z Normal EF (50% or more)
BUT should be confirmed by a Doppler examination
Diastolic HF associated to 4X increase mortality
Treatment of diastolic HF partially empirical
z ACE inhibitors
z Angiotensin-inhibitors
z β-blockers
Prevention of diastolic HF
z Better control of blood pressure
Implications réa
| Impact VM sur stade 2
| Vm = Valsalva
|