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15 Left Ventricular Diastolic Function
201
Diastolic Function Assessment
The gold standard for assessing diastolic function
is the time constant (τ) of LV pressure decline
during diastole. However, the measurement of τ
requires an invasive pulmonary artery catheter. In
a routine clinical setting, echocardiography with
the Doppler technique is commonly used to
assess diastolic function. The key variables currently recommended for the assessment of LV
diastolic dysfunction include (1) Mitral inow
velocity pattern, (2) Mitral annular septal and lateral velocity, (3) Tricuspid regurgitation peak
velocity, and (4) Left atrium volume index
(Fig.15.2).
Mitral Inow Velocity Pattern
Mitral inow velocity is measured using the
pulse wave Doppler (PWD) in the apical fourchamber view. The sample volume (1–3mm) is
Fig. 15.2 Stages of diastolic dysfunction based on various echocardiographic parameters
202
R. Sato and S. Dugar
placed at the mitral leaet tip. Color ow can be
used to guide the appropriate site for the placement of sample volume. Optimization of gain
and lter settings is imperative to get a suitable
waveform. The mitral inow velocity pattern
represents the peak velocity of blood ow from
LA to LV determined by the LA-LV pressure
gradient during early and late diastolic lling.
Early diastolic lling velocity (E wave) is driven
by the rate of LV relaxation and left-sided preload, while late diastolic lling velocity (A
wave) is driven by LA contraction and LV lling
pressure. In. addition to peak E and A velocity
and ratio of E/A, deceleration time (DT) of E
wave and isovolumic relaxation time (IVRT)
can also be used to assess diastolic function.
More recently, LV global longitudinal diastolic
strain rate (SR) during isovolumic relaxation
and early diastole has been reported to have a
signicant association with the time constant of
LV relaxation. E/SR has been reported as a tool
to estimate LV lling pressures. These novel
parameters need to be validated in the ICU setting [10].
Normal Pattern (Grade 0)
The robust LV relaxation during early diastole
draws a large portion of blood from LA into LV
resulting in a large “E wave.” The contribution of
atrial kick to LV lling is relatively small generating a smaller “A wave” expressed in an E/A
ratio≥1.0.
LV Relaxation Abnormality Pattern (Grade 1)
As either the rate or the vigor of LV relaxation
gets impaired, the reduction in LV pressure during early diastolic dysfunction declines, diminishing the LA-LV pressure gradient. The
resultant “E wave” is attenuated. IVRT and DT
get elongated due to prolonged relaxation. In
addition, since more blood will remain in LA,
the amount of blood entering LV from LA during atrial kick augments “A wave.” The E/A
ratio in these cases will be <0.8. It is worth noting that elderly individuals can have this pattern without myocardial pathology as a part of
the aging process.
Pseudonormalization Pattern (Grade 2)
When LV compliance is impaired in addition to
relaxation, LVEDP increases.
The increase in LA afterload in the setting of
normal LA pressure attenuates the LV-LA gradient reducing blood ow from LA.The compensatory mechanism to maintain cardiac output
leads to an increase in LA pressure to overcome
the increase in afterload. The elevated LA pressure resets the LA-LV gradient, albeit at higher
lling pressures restoring the large “E wave” and
smaller “A wave,” hence this pattern is called
“pseudo-normal.” As LV compliance is impaired,
LV lling pressure rises quickly during early diastolic lling leading to early equalization of
LV-LA pressure. This is observed in the echocardiographic waveform shortening of DT in comparison to the normal pattern. Thus, the pattern of
relaxation and compliance abnormality as
described using the E/A ratio is >0.8.
Restrictive Pattern (Grade 3)
Further impairment of LV compliance leads to a
further increase in LA pressure and augmentation
of E wave. The LV diastolic pressure in poorly
compliant increases exponentially in early diastolic lling with minimal blood ow from LA to
LV with atrial contraction demonstrated with further shortening of DT and attenuated A wave
with E/A≥2.
Mitral inow velocity pattern has limitations.
It is age-dependent. Also, the U-shaped relation
with LV diastolic function as described above
makes it difcult to differentiate normal diastolic
function from pseudonormalization pattern.
Therefore, the American Society of
Echocardiography (ASE) recommends using the
E/A ratio in conjunction with myocardial relaxation parameters [10].
Mitral Annular Motion Velocity
Mitral annular myocardial velocity is measured
in apical four-chamber view using tissue Doppler
imaging (TDI). The use of TDI differs instead of
the standard Doppler eliminates the high pass lter and uses low gain amplication to exclude
Estimated L
=+
′
E
e
4
15 Left Ventricular Diastolic Function
203
blood ow and measure myocardial tissue velocity. The sample volume of pulsed wave (PW)
Doppler is placed on the septal and lateral mitral
annulus at the level of the insertion of the mitral
leaets. These parameters measure the peak
velocity of the longitudinal displacement of the
septal and lateral LV basal wall as it relaxes and
lls in diastole. The sample volume of PW should
be adjusted to 5–10mm to elucidate the complete
excursion of the mitral annulus. In routine Apical
four-chamber view, the recording displays movement toward the probe in systole and away from
the probe during diastole. Systolic wave (s′) presents as a positive wave, followed by early diastolic wave (e′) and atrial systolic wave (a′),
which present as negative waves. The Early diastolic annular velocity has been referenced as Ea,
Em, E′, or e′, whereas late diastolic velocity is
referred to as Aa, Am, A′, or a′. Measurements
should ideally be taken from both the septal and
lateral annulus, and then averaged to improve
accuracy and reproducibility. These regional
measurements of e′ at annulus are used as a surrogate for global LV relaxation. Hence, localized
abnormalities affecting annulus motion such as
mitral annular diseases or basal regional wall
motion abnormalities will limit its utility in
assessing diastolic dysfunction. A visual assessment of global myocardial activity may aid if
these regional measurements can be utilized as
representative of the global myocardial relaxation (Videos 15.1 and 15.2).
In patients with diastolic dysfunction, the
intensity of relaxation gets progressively
impaired and is displayed as attenuated e′ velocity. In the diastolic dysfunction denition, the
cutoffs for impaired relaxation are <7cm/s for
septal and <10 cm/s for ateral e′. Since the E
wave reects the early diastolic mitral inow
velocity, which is determined by LV lling pressure and the strength of LV relaxation measured
as e′, the ratio of E and e′ can be used as an indicator of LV lling pressure. In general, E/e′>14,
which corresponds to an LAP of 18 is considered
elevated.
eft Atrial Pressure LAP
()
Left Atrial Volume Index (LAVI)
The impaired LV relaxation and LV compliance
increase LA afterload reducing the LV lling at
normal LA pressure and hence, reducing stroke
volume. In the early phase of diastolic
dysfunction, LA contraction increases to surpass
this reduction of stroke volume. With the progression of diastolic dysfunction, this compensatory mechanism fails to maintain cardiac output.
LA remodeling ensues with chamber dilation to
increase LA lling pressure to overcome the
increased afterload. Therefore, left atrial volume
(LAV) has been known to be associated with
both the severity and chronicity of diastolic dysfunction, as well as increased risks of death, cardiovascular events, and stroke [11, 12]. LAV can
be measured with the Simpson method or the
Area- length method in the end-systolic phase. In
the Simpson method, LA needs to be traced in
apical 4 and 2 chambers. In the Area- length
method, the diameter from the mitral annular
plane to the back wall of LA (L) and LA areas in
apical 4 and 2 chambers (A1 and A2, respectively) are used to calculate LAV with the following formula: LAV=0.85×A1×A2÷L. The
echocardiographic planes should be adjusted to
ensure that the maximal area of the left atrium is
captured without foreshortening. LAVI, the
value of LA volume divided by body surface
area, is recommended as a parameter to determine the presence of diastolic dysfunction. If
LAVI is >34mL/m
2
, it is considered moderately
dilated LA.
Tricuspid Regurgitation (TR) Jet Peak Velocity
The measurement of TR jet velocity can provide
an estimate of pulmonary systolic arterial pressure (PASP) when combined with right atrial
pressure, which can be measured by a central
venous catheter or estimated by the inferior vena
cava measurement. An elevated PSAP can support the presence of chronic elevated LA pressure
from impaired LV relaxation and decreased LV
compliance. Therefore, the presence of TR can
204
R. Sato and S. Dugar
reect the presence of diastolic dysfunction. TR
jet velocity can be measured at RV inow view,
parasternal short-axis view at aortic valve level,
or apical four-chamber view with continuous
wave Doppler. The color ow Doppler can be
used to guide the placement of continuous wave
Doppler. The highest recorded velocity from all
acquired views is usually reported. In case of a
weak TR jet signal, agitated saline can be used to
improve the delineation of the TR jet [13]. There
is also a study describing that the mixture of 10%
blood-10% air-80% saline further improves the
delineation of TR [14]. TR jet velocity of
>2.8m/s is considered abnormal and associated
with elevated right-sided pressures.
Pulmonary Vein Flow
The increase in LA pressure due to impaired LV
relaxation and elevated LV lling pressure in
diastolic dysfunction impedes the ow from the
pulmonary venous system into LA.Hence, the
pulmonary venous ow waveform pattern has
been used to facilitate the diagnosis of diastolic
dysfunction. Pulmonary vein (PV) ow consists
of systolic wave (S), diastolic wave (D), and
atrial contraction wave (Ar). It can be measured
with PW Doppler at the pulmonary vein in the
apical four-chamber view. Since this is typically
measured in the apical four-chamber view in
TTE, PVS and PVD reect the blood ow coming into LA from PV during systole and diastole
respectively, while PVAr reects the regurgitant
blood from LA to PV during atrial contraction.
The PVS wave is determined by LA relaxation
and compliance, while the PVD wave is determined by LV relaxation and compliance, hence,
PVD follows a similar pattern to the E wave. In
other words, in normal cardiac function, the pulmonary venous ow to LA is predominantly
systolic with peak pulmonary vein systolic ow
velocity/with peak pulmonary vein diastolic
ow velocity (S/D) ratio>1. With diastolic dysfunction with impaired LV relaxation and elevated LA lling pressure, the ow from the
pulmonary vein to LA predominately occurs in
diastole. An S/D ratio< 1 in the presence of
impaired LV relaxation is highly suggestive of
elevated LAP.
Diastolic Dysfunction Denition
Over Years
ASE Recommendation 2009
ASE guidelines 2009 dened the presence of diastolic dysfunction based on mitral annulus e′ and
LAVI [15]. The severity was graded based on
E/A, DT, and E/e′. In this guideline, diastolic
dysfunction is diagnosed if
1. Septal e′<8cm/s
2. Lateral e′<10cm/s
3. LAVI≥34mL/m
2
The severity of diastolic dysfunction is graded as.
Parameter Grade 1 Grade 2 Grade 3
E/A ratio <0.8 0.8–1.5
DT (ms) >200 160–200 <160
Average E/e′
PVAr-A <30
Valsalva ΔE/A
≤8
<0.5
9–12
≥30 ≥30
≥0.5 ≥0.5
≥2
≥13
ASE Recommendation 2016
ASE guidelines 2016 dened the presence of diastolic dysfunction based using E/e′, e′, TR jet
velocity, and LAVI [10]. The severity was graded
based on E/A.
In this guideline, diastolic dysfunction is diagnosed if more than 50% of the following criteria
are positive.
1. Septal e′<7cm/s
2. Lateral e′<10cm/s
3. LAVI≥34mL/m
with addition of
4. TR velocity>2.8m/s.
E/A ≤0.8 and E≤ 50 cm/s are considered
Grade 1. If E/A≤0.8 and E> 50cm/s or E/A
0.8–2.0, then, there are three criteria to be evalu-
2
15 Left Ventricular Diastolic Function
205
ated. If more than two of the following three criteria are positive, then, it is considered Grade 2
(1, Average E/e′>14; 2, TR velocity>2.8m/s; 3,
LAVI >34 mL/m2). If only 1 or 0 out of these
three criteria is positive, it is considered Grade 1.
If E/A≥2.0, then this is considered Grade 3.
Comparison ofASE 2009 and2016
In 2016, the diastolic dysfunction was simplied
by minimizing the parameters required to grade
the severity of diastolic dysfunction. Sanchis
et al. evaluated LV diastolic function initially
based on ASE 2009 guidelines followed by ASE
2016 guidelines. ASE 2016 guidelines were able
to classify patients more accurately according to
brain natriuretic peptide levels, the diagnosis of
heart failure, and cardiovascular outcomes. In
this study, most patients diagnosed with grade 1
diastolic dysfunction based on ASE 2009 guidelines were reclassied as normal diastolic function based on ASE 2016 guidelines [16]. Other
studies also reported that the prevalence of diastolic function signicantly decreased when
using ASE 2016 guidelines as opposed to ASE
2009 guidelines [17, 18]. These ndings support
that ASE 2016 guidelines seem to be able to diagnose only the advanced cases in the general
population.
On the other hand, Clancy etal. reported that
the prevalence of diastolic dysfunction was signicantly higher when using ASE 2016 compared to ASE 2009in patients with severe sepsis
and septic shock [19]. Similarly, Lanspa etal.
reported that ASE 2016 guidelines categorized
more sepsis and septic shock patients to have diastolic dysfunction than ASE 2009 guidelines [7].
In critically ill patients, DT and LAVI appear to
be less relevant given that these parameters represent chronic changes rather than acute changes.
This might explain the reason why the diagnostic
characteristics of ASE 2009 and 2016 guidelines
differ between relatively stable patients and critically ill patients. While ASE 2016 guidelines’
grading system predicted elevated LVEDP and a
poor prognosis more accurately than that of ASE
2009 in stable cardiac patients [20], it is still
unclear whether the grading of diastolic dysfunction correlates with the prognosis in the critically
ill population [5, 7].
Caveats ontheUse ofASE
Recommendations intheICU
Caveats on the use of ASE recommendations in
the ICU also need to be mentioned. ASE 2016
recommends using E/e′, e′, LAVI, and TR jet
velocity. Among these parameters, LAVI and
TR jet velocity may be less reliable in the critical care setting. For instance, LA dilatation is
likely to reect chronically elevated LA pressure. The acute nature of impaired LV relaxation during critical illness may not result in
LA dilation. In addition, LA volume is affected
by loading conditions, which can change rapidly in the critical care setting. TR jet sometimes could be difcult to assess accurately in
the critical care setting due to suboptimal positioning, positive pressure ventilation, etc.
Furthermore, peak TR jet velocity can occur or
alter acutely by positive pressure ventilation,
positive end-expiratory pressure, and uid
loading limiting its utility as a surrogate of
chronically elevated left-sided lling pressure
[21]. While E/e′ is also affected by several conditions, E/e′ may suffer less than other parameters from the confounding inuence enhancing
its utility in the assessment of elevated lling
pressure along with the use of e′ as parameters
of LV relaxation [22].
Conditions That Require Caution
intheAssessment ofDiastolic
Dysfunction
1. Arrhythmias such as atrial brillation will
result in loss of atrial kick and absence of A
wave velocity. In addition, the RR interval
may vary affecting the accurate assessment of
Mitral inow velocity pattern and LV relaxation limiting the utility of these parameters in
the assessment of diastolic dysfunction
(Fig.15.3).
2. Valvular pathologies such as mitral stenosis
and regurgitation affect mitral inow velocity
due to increased volume or pressure from valvular disease instead of LV and LA relaxation
206
Fig. 15.3 Diastolic
function assessment in
presence of arrhythmia
Fig. 15.4 Diastolic
function assessment in
presence of mitral valve
pathology
R. Sato and S. Dugar
properties. Therefore, if patients have any of
these, mitral inow velocity may not be reective of the LA-LV pressure gradient and hence
cannot be used to assess diastolic function.
These pathologies may also result in dilation
of the left atrium limiting the utility of LA
dilation as criteria for diastolic dysfunction
(Fig.15.4).
3. Hypertrophic cardiomyopathy, severely
reduced LV systolic function, and regional wall
motion abnormality may regionally affect
mitral annular motion velocity limiting the utility of these parameters as surrogates of global
LV relaxation. Therefore, in such patients,
comprehensive assessments including other
parameters are required to assess the presence
and severity of diastolic dysfunction.
4. Mitral or Aortic valve repair or replacement
and mitral annulus calcication may also
impair mitral annular motion and invalidate the
15 Left Ventricular Diastolic Function
Fig. 15.5 Diastolic function assessment in presence of tachycardia
207
mitral inow measurements. Therefore, in such
patients, comprehensive assessments including
other parameters are required to assess the
presence and severity of diastolic dysfunction.
5. Age: Aging is associated with increased LV
stiffness and slowing of myocardial relaxation
resulting in a decrease in E/A ratio and e′ values and resembling diastolic dysfunction.
Hence age-appropriate normative values
should be utilized for the detection and grading of diastolic dysfunction.
6. Pericardial effusion/Constrictive pericarditis:
Due to external restriction of LV relaxation,
the lling pressure will be elevated despite
normal myocardial tissue relaxation and
compliance.
7. Tachycardia: Tachycardia may lead to the
fusion of the E and A waves, resulting in an
inaccurate assessment of peak E and A wave
velocities (Fig.15.5).
8. Acute cor pulmonale: The paradoxical septal
motion from interventricular dependence will
impair LV relaxation assessment, especially
septal e′ velocity measurement.
Diastolic Function intheICU
The prevalence of LV diastolic dysfunction is
reported between 40.4% and 84%. Therefore, it
is important for critical care practitioners to know
the clinical situations where diastolic dysfunction
could play a role in critically ill patients. These
situations include estimation of lling pressure to
facilitate uid management, acute respiratory
distress syndrome (ARDS), sepsis, and liberation
from mechanical ventilation.
Estimation ofPulmonary Artery
Occlusion Pressure
E/e′ has been evaluated as a surrogate to noninvasively estimate PAOP, especially in heart failure populations. Although transesophageal
echocardiogram (TEE) appears to have a better
predictive value of PAOP than transthoracic
echocardiogram (TTE) [23, 24], the access to
TEE in the general/medical ICU may be limited.
While several estimation formulas are known
[e.g., Nagueh formula: PAOP=1.24 (E/e′)+1.9]
[25], these formulas have not been validated in
the ICU population. In mechanically ventilated
critically ill patients, Doppler TTE indices were
highly specic but not sensitive to estimate
PAOP [26]. In this study, lateral E/e′ >15 was
predictive of PAOP ≥18mmHg with a sensitivity of 25% and specicity of 95%, whereas lateral E/e′<7 was predictive of PAOP <18mmHg
with a sensitivity of 32% and specicity of 81%.
A more recent study suggested that simple
Doppler measurements such as lateral e′ or E/A
ratio provide a similar level of diagnostic per-
208
R. Sato and S. Dugar
formance of PAOP compared to the denition of
diastolic function by the guidelines [27].
Diastolic Function andARDS
There is no direct evidence showing the relationship between diastolic dysfunction and the
prognosis of ARDS. On the other hand, in
patients with ARDS, high PAOP and BNP are
known to be associated with higher mortality
[28–30]. In the FACTT trial, conservative uid
management improved lung function and shortened the duration of mechanical ventilation and
ICU stay in patients with acute lung injury [31].
Given this evidence, it may be important to use
E/e′ to guide the loading condition and diuretic
therapy.
Diastolic Function andSepsis
Diastolic dysfunction is commonly seen in septic
patients and a meta-analysis reported that 48% of
septic patients had diastolic dysfunction diagnosed by TDI. Diastolic dysfunction was also
associated with higher mortality [3, 32] while
systolic dysfunction is less common and deemed
not to be associated with higher mortality in septic patients [33]. Especially a meta-analysis
emphasizes the close correlation between lateral
e′<10cm/s and E/e′>14 with increased mortality. Given that e′ is partially inuenced by volume loading, these values may suggest volume
overload, which is known to be associated with
higher mortality [34].
in patients who failed to wean compared with
those who succeeded [36, 37]. Moschietto etal.
reported that patients who succeeded in the
weaning maintained the same E/e′ level with
SBT while the patients who failed to wean had
the elevation of E/e′, suggestive of an increase in
left ventricular lling pressures [38]. Therefore,
knowing diastolic dysfunction before SBT may
be helpful in identifying high-risk patients for
cardiogenic weaning failure.
Summary Points
• Diastole consists of four phases (isovolumic
relaxation, early diastolic lling, diastasis,
and late diastolic lling).
• The current American Society of
Echocardiography guidelines dene the presence of diastolic dysfunction based using E/e′.
e′, tricuspid regurgitation (TR) jet velocity,
and left atrial volume index (LAVI). Then, the
severity is graded based on E/A.
• It may not be possible to reliably assess diastolic function in some situations. These situations include tachycardia, arrhythmia such as
atrial brillation, and valvular diseases, especially mitral valve pathology. In addition, it is
also important to note that aging, hypertrophic
cardiomyopathy, pericardial effusion, and
acute cor pulmonale will affect the measurements of diastolic function.
• Diastolic dysfunction is known to be associated with unfavorable outcomes in critically
ill patients such as ARDS or sepsis.
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weaning-induced PAOP elevation [35]. Similarly,
several studies showed that higher E/e′ was seen
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