Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5189_Библиотеки_им_академика_М_И_Перельмана.pdf
14 Atrial Size andFunction
191
between intracardiac and intrapulmonary
shunt. With a PFO during the agitated saline
contrast study, there is an early appearance of
the bubbles from right to left within three to
four cardiac cycles. This can be provoked by
physiological maneuvers like Valsalva or
cough, which causes a transient increase in
the right atrial pressures. In the case of intrapulmonary shunt, there is a late appearance of
the bubble on the left heart with bubble study,
usually after ve to seven cardiac cycles and
there is no change with the maneuvers mentioned above [24].
References
1. Ho SY, Cabrera JA, Sanchez-Quintana D.Left atrial
anatomy revisited. Circ Arrhythm Electrophysiol.
2012;5(1):220–8. https://doi.org/10.1161/
CIRCEP.111.962720.
2. Lang RM, Badano LP, Mor-Avi V, Alalo J,
Armstrong A, Ernande L, Flachskampf FA, Foster E,
Goldstein SA, Kuznetsova T, Lancellotti P, Muraru
D, Picard MH, Rietzschel ER, Rudski L, Spencer
KT, Tsang W, Voigt JU. Recommendations for cardiac chamber quantication by echocardiography
in adults: an update from the American Society of
Echocardiography and the European Association of
Cardiovascular Imaging. J Am Soc Echocardiogr.
2015;28(1):1–39.e14. https://doi.org/10.1016/j.
echo.2014.10.003.
3. Mitchell C, Rahko PS, Blauwet LA, etal. Guidelines
for performing a comprehensive transthoracic echocardiographic examination in adults: recommendations from the American Society of Echocardiography.
J Am Soc Echocardiogr. 2019;32(1):1–64. https://doi.
org/10.1016/j.echo.2018.06.004.
4. Hoit BD, Litwin SE. The new normal: how should
we assess cardiac chamber sizes and proportionality across the full spectrum of body sizes with varying degrees of adiposity? J Am Soc Echocardiogr.
2021;35(2):151–3. https://doi.org/10.1016/j.
echo.2021.11.013.
5. Olsen FJ, Møgelvang R, Modin D, Schnohr P, Jensen
GB, Biering-Sørensen T. Association between isometric and allometric height-indexed left atrial
size and atrial brillation. J Am Soc Echocardiogr.
2022;35(2):141–50.e4. https://doi.org/10.1016/j.
echo.2021.10.010.
6. Hoit BD.Left atrial size and function: role in prognosis. J Am Coll Cardiol. 2014;63(6):493–505. https://
doi.org/10.1016/j.jacc.2013.10.055.
7. Mor-Avi V, Yodwut C, Jenkins C, etal. Real-time 3D
echocardiographic quantication of left atrial volume:
multicenter study for validation with CMR. JACC
Cardiovasc Imaging. 2012;5(8):769–77. https://doi.
org/10.1016/j.jcmg.2012.05.011.
8. Shin SH, Claggett B, Inciardi RM, etal. Prognostic
value of minimal left atrial volume in heart failure
with preserved ejection fraction. J Am Heart Assoc.
2021;10(15):e019545. https://doi.org/10.1161/
JAHA.120.019545.
9. Appleton CP, Galloway JM, Gonzalez MS, Gaballa
M, Basnight MA. Estimation of left ventricular lling pressures using two-dimensional and
Doppler echocardiography in adult patients with
cardiac disease. Additional value of analyzing
left atrial size, left atrial ejection fraction and the
difference in duration of pulmonary venous and
mitral ow velocity at atrial contraction. J Am
Coll Cardiol. 1993;22(7):1972–82. https://doi.
org/10.1016/0735- 1097(93)90787- 2.
10. Haji K, Huynh Q, Be KK, Wright L, Marwick
TH. Interobserver agreement of left atrial strain
assessment by two-dimensional speckle echocardiography. J Am Soc Echocardiogr. 2022;35(2):228–9.
https://doi.org/10.1016/j.echo.2021.10.008.
11. Mochizuki A, Yuda S, Fujito T, etal. Left atrial strain
assessed by three-dimensional speckle-tracking echocardiography predicts atrial brillation recurrence
after catheter ablation in patients with paroxysmal
atrial brillation. J Echocardiogr. 2017;15(2):79–87.
https://doi.org/10.1007/s12574- 017- 0329- 5.
12. Singh A, Carvalho Singulane C, Miyoshi T, et al.
Normal values of left atrial size and function and the
impact of age: results of the world Alliance societies
of echocardiography study. J Am Soc Echocardiogr.
2022;35(2):154–164.e3. https://doi.org/10.1016/j.
echo.2021.08.008.
13. Tsang TS, Abhayaratna WP, Barnes ME, Miyasaka Y,
Gersh BJ, Bailey KR, Cha SS, Seward JB.Prediction
of cardiovascular outcomes with left atrial size: is volume superior to area or diameter? J Am Coll Cardiol.
2006;47(5):1018–23. https://doi.org/10.1016/j.
jacc.2005.08.077.
14. Moller JE, Hillis GS, Oh JK, Seward JB, Reeder
GS, Wright RS, Park SW, Bailey KR, Pellikka
PA. Left atrial volume: a powerful predictor of survival after acute myocardial infarction. Circulation.
2003;107(17):2207–12. https://doi.org/10.1161/01.
CIR.0000066318.21784.43.
15. Beinart R, Boyko V, Schwammenthal E, Kuperstein
R, Sagie A, Hod H, Matetzky S, Behar S, Eldar M,
Feinberg MS. Long-term prognostic signicance
of left atrial volume in acute myocardial infarction.
J Am Coll Cardiol. 2004;44(2):327–34. https://doi.
org/10.1016/j.jacc.2004.03.062.
16. Tsang TS, Barnes ME, Gersh BJ, Bailey KR, Seward
JB.Left atrial volume as a morphophysiologic expression of left ventricular diastolic dysfunction and relation to cardiovascular risk burden. Am J Cardiol.
2002;90(12):1284–9. https://doi.org/10.1016/
s0002- 9149(02)02864- 3.
192
T. Ahmed et al.
17. Morris DA, Takeuchi M, Krisper M, Köhncke C,
Bekfani T, Carstensen T, Hassfeld S, Dorenkamp
M, Otani K, Takigiku K, Izumi C, Yuda S, Sakata K,
Ohte N, Tanabe K, Osmanoglou E, Kühnle Y, Düngen
HD, Nakatani S, Otsuji Y, Haverkamp W, Boldt
LH.Normal values and clinical relevance of left atrial
myocardial function analysed by speckle-tracking
echocardiography: multicentre study. Eur Heart J
Cardiovasc Imaging. 2015;16(4):364–72. https://doi.
org/10.1093/ehjci/jeu219.
18. Kurt M, Wang J, Torre-Amione G, Nagueh SF.Left
atrial function in diastolic heart failure. Circ
Cardiovasc Imaging. 2009;2(1):10–5. https://doi.
org/10.1161/CIRCIMAGING.108.813071.
19. Yoon YE, Oh IY, Kim SA, Park KH, Kim SH, Park
JH, Kim JE, Lee SP, Kim HK, Kim YJ, Sohn DW,
Cho GY.Echocardiographic predictors of progression
to persistent or permanent atrial brillation in patients
with paroxysmal atrial brillation (E6P study). J Am
Soc Echocardiogr. 2015;28(6):709–17. https://doi.
org/10.1016/j.echo.2015.01.017.
20. Obokata M, Negishi K, Kurosawa K, Tateno R, Tange
S, Arai M, Amano M, Kurabayashi M. Left atrial
strain provides incremental value for embolism risk
stratication over CHA
-VASc score and indi-
2DS2s
cates prognostic impact in patients with atrial brillation. J Am Soc Echocardiogr. 2014;27(7):709–716.e4.
https://doi.org/10.1016/j.echo.2014.03.010.
21. Di Salvo G, Caso P, Lo Piccolo R, Fusco A, Martiniello
AR, Russo MG, D’Onofrio A, Severino S, Calabro P,
Pacileo G, Mininni N, Calabro R.Atrial myocardial
deformation properties predict maintenance of sinus
rhythm after external cardioversion of recent-onset
lone atrial brillation: a color Doppler myocardial
imaging and transthoracic and transesophageal echocardiographic study. Circulation. 2005;112:387–95.
22. Motoki H, Dahiya A, Bhargava M, Wazni OM, Saliba
WI, Marwick TH, Klein AL.Assessment of left atrial
mechanics in patients with atrial brillation: comparison between two-dimensional speckle-based strain
and velocity vector imaging. J Am Soc Echocardiogr.
2012;25(4):428–35. https://doi.org/10.1016/j.
echo.2011.12.020.
23. Yang H, Marwick TH, Fukuda N, Oe H, Saito M,
Thomas JD, Negishi K. Improvement in strain
concordance between two major vendors after
the strain standardization initiative. J Am Soc
Echocardiogr. 2015;28(6):642–8.e7. https://doi.
org/10.1016/j.echo.2014.12.009.
24. Goerlich E, Minhas A, Gilotra N, Barth AS, Mukherjee
M, Parziale A, Wu KC, Hays AG.Left atrial function
in patients with coronavirus disease 2019 and its association with incident atrial brillation/utter. J Am
Soc Echocardiogr. 2021;34(10):1106–9. https://doi.
org/10.1016/j.echo.2021.05.015.
25. Gudmundsson GS, Smull DL, Pisani BA, Bane CD,
Mendez JC, Mullen GM, Jacobs WR. Increase in
atrial size in long-term survivors of heart transplant.
J Am Soc Echocardiogr. 2003;16(10):1043–8. https://
doi.org/10.1016/S0894- 7317(03)00591- 1.
26. Silvestry FE, Cohen MS, Armsby LB, et al.
Guidelines for the echocardiographic assessment of
atrial septal defect and patent foramen ovale: from the
American Society of Echocardiography and Society
for Cardiac Angiography and Interventions. J Am
Soc Echocardiogr. 2015;28(8):910–58. https://doi.
org/10.1016/j.echo.2015.05.015.
27. Hanley PC, Tajik AJ, Hynes JK, etal. Diagnosis
and classification of atrial septal aneurysm
by two- dimensional echocardiography: report
of 80 consecutive cases. J Am Coll Cardiol.
1985;6(6):1370–82. https://doi.org/10.1016/
s0735- 1097(85)80228- x.
28. Attaran RR, Ata I, Kudithipudi V, Foster L, Sorrell
VL. Protocol for optimal detection and exclusion
of a patent foramen Ovale using transthoracic echocardiography with agitated saline microbubbles.
Echocardiography. 2006;23:616–22. https://doi.
org/10.1111/j.1540- 8175.2006.00272.x.
29. Rudski LG, Lai WW, Alalo J, et al. Guidelines
for the echocardiographic assessment of the right
heart in adults: a report from the American Society
of Echocardiography endorsed by the European
Association of Echocardiography, a registered
branch of the European Society of Cardiology, and
the Canadian Society of Echocardiography. J Am
Soc Echocardiogr. 2010;23(7):685–788. https://doi.
org/10.1016/j.echo.2010.05.010.
30. Alboliras ET, Edwards WD, Driscoll DJ, Seward
JB. Cor triatriatum Dexter: two-dimensional
echocardiographic diagnosis. J Am Coll Cardiol.
1987;9(2):334–7. https://doi.org/10.1016/
s0735- 1097(87)80385- 6.
31. Peters PJ, Reinhardt S. The echocardiographic
evaluation of intracardiac masses: a review. J Am
Soc Echocardiogr. 2006;19(2):230–40. https://doi.
org/10.1016/j.echo.2005.10.015.
32. Nagueh SF, Kopelen HA, Zoghbi WA. Relation of
mean right atrial pressure to echocardiographic and
Doppler parameters of right atrial and right ventricular function. Circulation. 1996;93(6):1160–9. https://
doi.org/10.1161/01.cir.93.6.1160.
Left Ventricular Diastolic Function
RyotaSato andSiddharthDugar
15
Learning Objectives
1. Understand the physiology of diastole, including the four phases of diastole (isovolumic
relaxation, early diastolic lling, diastasis,
and late diastolic lling) and its mechanisms.
2. Understand how to measure parameters used
to dene and grade left ventricular diastolic
function (E/e′, e′, tricuspid regurgitation jet
peak velocity, and left atrial volume index).
3. Understand the caveats on the denition of
diastolic dysfunction in critically ill patients.
Introduction
Cardiac function critically depends on diastole to
provide an adequate left ventricular (LV) lling
for maintenance of cardiac output and tissue perfusion. Over the last decade, it has become appar-
Supplementary Information The online version contains supplementary material available at https://doi.
org/10.1007/978- 3- 031- 80038- 2_15.
ent that LV diastolic dysfunction, independent of
LV systolic dysfunction, is a signicant contributor to morbidity, prolonged hospital stay, and
even mortality in critically ill patients [1–5]. The
denition of diastolic dysfunction and the echocardiographic parameters utilized for its characterization continue to evolve. The current method
of uncovering and grading diastolic dysfunction
in critically ill patients is derived from the denition used in the general population. Few have
questioned if the denition needs to be modied
and simplied to t the pathophysiology of critical illness where impaired relaxation may be
acute/subacute with constantly changing loading
conditions from uids, inotropic agents, and
mechanical ventilation [6–8]. In this chapter, we
detail our current understanding of the pathophysiology of diastolic dysfunction during critical illness, elucidate parameters used to dene
and grade left ventricular diastolic function, and
caveats to their application in critically ill
patients.
R. Sato
The Queen’s Medical Center, Honolulu, HI, USA
John A.Burns School of Medicine, University of
Hawai’i Manoa, Honolulu, HI, USA
S. Dugar (*)
Department of Critical Care, Cleveland Clinic Lerner
College of Medicine, Respiratory Institute,
Cleveland Clinic, Cleveland, OH, USA
e-mail: dugars@ccf.org
© The Author(s), under exclusive license to Springer Nature Switzerland AG 2025
M. J. Lanspa, A. T. Levinson (eds.), Echocardiography and Ultrasonography in the ICU,
Respiratory Medicine, https://doi.org/10.1007/978-3-031-80038-2_15
Diastole
Diastole is the cardiac cycle interval between the
aortic valve (AV) closure and mitral valve (MV)
closure. Diastole constitutes the phase of transporting blood from one chamber (the left atrium
[LA]) to another chamber (the left ventricle
[LV]). This ow of blood is determined by the
193
194
R. Sato and S. Dugar
pressure gradient between these two chambers,
which in turn are determined by the characteristics of those chambers. At the end of systole, LV
bers start actively relaxing, reducing the LV
pressure, and increasing the LA-LV pressure gradient, which allows the opening of the MV.During
diastole, the LV, LA, and pulmonary venous system act as a single chamber allowing the blood in
the pulmonary capillary bed to ow into LA and
nally to LV.The diastole is partitioned into four
phases: (1) Isovolumic relaxation, (2) Early diastolic lling, (3) Diastasis, and (4) Late diastolic
lling. On visual assessment, the myocardium
functions as a muscle-powered oscillator, seamlessly transitioning through these phases without
discrete transition points. However, these four
phases are essential for understanding the diastole as a hemodynamic parameter (Fig.15.1).
Isovolumic Relaxation
Isovolumic relaxation occurs between the AV closure and MV opening. During this phase, the LV
initiates relaxation to its resting unstressed length
against closed MV and AV. The effect of this
relaxation of the cardiac muscle bers is a sudden
drop in LV pressure. The rate of pressure decrease
during the isovolumetric relaxation period directly
reects on the velocity of cardiac muscle relaxation and LV compliance. Once the LV pressure
drops below the LA pressure, MV opens allowing
initiation of the early diastolic lling [9].
Early Diastolic Filling
An early diastolic lling is characterized by the
rapid lling of blood to the LV from LA without a
signicant increase in LV pressure. The relaxation
of LV, which begins during isovolumic relaxation,
continues in the initial phase of early diastolic lling generating the early diastolic LA-LV pressure
gradient. This pressure gradient draws in the
blood from LA to LV.The velocity of this blood
ow is a measure of the rate of LV relaxation and,
hence, compliance. Mitral inow velocity (the
ow velocity between LA and LV) during early
diastolic lling measured using echocardiography
is called a peak E wave velocity.
Diastasis
Diastasis is the stable phase, where the ventricular lling slows down due to the equalization of
pressures between the LA and LV.During diastasis, the normal LV is composed of entirely relaxed
Fig. 15.1 Phases of
diastole. Wiggers
diagram of intra-cardiac
pressures during the
cardiac cycle showing
simultaneous pressure
tracings of the left
ventricle, left atrium,
and the aorta. Ao aorta,
AVc aortic valve closure,
AVo aortic valve closure,
IVCT isovolumic
contraction time, IVRT
isovolumic relaxation
time, LA left atrium, LV
left ventricle
15 Left Ventricular Diastolic Function
195
cardiomyocytes. The duration of diastasis
depends on heart rate; longer at slow heart rates
and shorter to completely absent at higher heart
rates. The blood ow from LA to LV in diastasis
may occur in a highly compliant LV, or if LA
pressure is markedly elevated. However, in most
normal individuals, minimal lling occurs in
diastasis.
Late Diastolic Filling
The late diastolic lling is produced by atrial
contraction, as LA pressure rises again from
atrial contraction and exceeds LV pressure. Atrial
contraction near the end of diastole contributes
20–30% to the total LV lling volume. Under
normal conditions, the LV diastolic pressure
increases by less than 5 mmHg. LV lling can
usually be accomplished by very low lling pressures in the LA and pulmonary veins, preserving
a low pulmonary capillary pressure (<12mmHg)
and a high degree of lung distensibility. Mitral
inow velocity during these phases measured
using echocardiography is called a peak “A
wave” velocity.
As noted, the normal diastolic function comprises LV with vigorous relaxation to pull blood
from LA during early diastolic lling and high
compliance, to minimize increase in the LV
pressure with the ow of blood from LA.The
loss of normal LV diastolic relaxation and compliance from structural and functional causes
impairs LV pressure decline and lling necessitating a rise in LA and pulmonary venous
pressures to maintain perfusion. This translates
to an increase in pulmonary capillary pressure,
an increase in lung water, and heart failure
symptoms.
Unfortunately, there exists no single parameter that can encompass the pathophysiological
markers of LV diastolic dysfunction namely, LV
relaxation, LV and LA compliance, and lling
pressure. Therefore, the assessment of diastolic
function requires a comprehensive approach
using a combination of several different echocardiographic parameters to assess these abnormalities (Table15.1) [10].
196
leaet tip.
imperative
• Measured in A4C
• Place the pulse wave Doppler at the mitral
• Measure peak E velocity and A velocity
• Optimization of the gain and lter setting is
• Cannot measure it accurately in the setting of
R. Sato and S. Dugar
atrial brillation due to beat-to-beat variation
• Deceleration time of E wave
Normal
E wave velocity<50cm/s
E/A>0.8
Mitral inow velocity pattern
Table 15.1 Parameters for the assessment of diastolic function
15 Left Ventricular Diastolic Function
197
(continued)
septal or lateral mitral annulus
• Measured in A4C
• Place the tissue Doppler imaging (TDI) on the
• Measure peak septal and lateral e′ tissue
Normal
Septal e′≥7
Lateral e′≥10
Average E/e′<10
Therefore, it represents systole (s′)
velocities
• Positive wave is the motion toward the probe.
• On the other hand, the subsequent negative
Abnormal
Septal e′<7
Lateral e′<10
Average E/e′≥10
wave represents LV relaxation during early
diastolic relaxation (e′)
both lateral and septal annulus and averaged
• Ideally the measurements should be taken from
(Average E/e′≥14=grade
3)
Mitral annular motion velocity
198
respectively
accurate measurements
end-systolic phase
• The measurements should be done in the
• Endocardium needs to be visualized for
• The Simpson method: LA needs to be traced in
the back wall of LA=L
apical four-chamber and two-chamber
• The area-length method:
The diameter from the mitral annular plane to
LA areas in A4C and A2C=A1 and A2,
LAV=0.85×A1×A2/L
• LAVI=LAV/BSA
R. Sato and S. Dugar
LAVI:
Normal: 16–34
Mildly abnormal: 35–41
Moderately abnormal:
42–48
Severely abnormal: > 48
Left atrial volume index
Table 15.1 (continued)
15 Left Ventricular Diastolic Function
199
(continued)
wave (D), and atrial contraction wave (Ar)
• Measured in A4C
• PV ow consists of systolic wave (S), diastolic
• Place the pulse wave Doppler on the PV
• During systole, LA cavity is expanded and the
Normal
S wave > D wave
Diastolic dysfunction
D wave > S wave
blood ows into LA from PV (toward the
probe). So, the S wave is a positive wave
into LA from PV (toward the probe). So, D
• During diastole, LV relaxes and the blood ows
wave is positive
PV.So, Ar is negative wave.
• Ar represents the regurgitation from LA to
Pulmonary venous ow
200
can be underestimated if doppler not properly
aligned to the blow ow
• Measured from RV inow, PSAX, A4C views
• Measures the RV-RA gradient
• Utilized to measure SPAP
• Highest value is considered as the measurement
R. Sato and S. Dugar
Normal
(continued)
≤2.8m/s
Abnormal
>2.8m/s
TR velocity
RV inow CW TR jet measurement
Table 15.1
PSAX CW TR jet measurement
Apical four-chamber CW TR jet measurement
A4C apical four-chamber view, RV right ventricle, TDI tissue Doppler imaging, PLAX parasternal long axis, PSAX parasternal short axis, LA left atrium, BSA body surface area,
LV left ventricle, PV pulmonary vein, TR tricuspid regurgitation, SPAP systolic pulmonary arterial pressure