Download Relationship Between Tricuspid Annular Excursion and Velocity in

Relationship Between Tricuspid Annular Excursion and Velocity
in Cardiac Surgical Patients
Raymond Hu, MBBS, FANZCA, C. David Mazer, MD, FRCPC, and Claude Tousignant, MD, FRCPC
Objectives: The primary objective of this study was to
establish the relationship among tricuspid annular velocity
(S’), tricuspid annular plane systolic excursion (TAPSE), and
stroke volume (SV) in a cardiac surgical population with and
without right ventricular (RV) dysfunction. The secondary
objective was to assess the effect of ephedrine on these
relationships in a population without RV dysfunction.
Design: Prospective, nonrandomized, unblinded study.
Setting: Single tertiary-level, university-affiliated hospital.
Participants: Twenty-seven patients undergoing elective
coronary artery bypass grafting with no evidence of RV
dysfunction (Group 1). Sixteen ventilated postcardiac surgical patients with suspected RV dysfunction (Group 2).
Interventions: Ten mg of intravenous ephedrine to Group
1 only.
Measurements and Main Results: Using transthoracic
echocardiography, S’ and TAPSE were measured using color
tissue Doppler applied at the RV base in a 4-chamber view.
SV was calculated using thermodilution. Six patients in
Group 1 and 6 patients in Group 2 were excluded because
of poor imaging or ineligibility.
Modest correlation was found between TAPSE and SV in
Group 1 (R ¼ 0.50, p o 0.001). There was no correlation
between TAPSE and SV in Group 2. There was no correlation between S’ and SV in both groups.
In Group 1, the relationship between TAPSE and S’ was
curvilinear (R ¼ 0.74 pre-ephedrine, p o 0.001; R ¼ 0.64, p ¼
0.009 post-ephedrine). There was no relationship between
TAPSE and S’ in Group 2. Ephedrine increased S’ and TAPSE.
The TAPSE-S’ relationship was not significantly altered.
Conclusions: In the presence of RV dysfunction, TAPSE
did not correlate with cardiac output. In the absence of RV
dysfunction, the relationship between TAPSE and S’
described a curvilinear relationship.
& 2014 Elsevier Inc. All rights reserved.
K
The goal of this study was to assess the relationship among
TAPSE, S’, and SV using TTE and color-tissue Doppler
imaging in elective cardiac surgical patients under general
anesthesia before and after the administration of ephedrine, a
weak inotrope. This relationship also was examined in a
critically ill postoperative cardiac surgical population with
RV dysfunction and elevated pulmonary artery pressures
(PAP) who required inotropic support.
NOWLEDGE OF right ventricular (RV) function in the
perioperative setting may have important prognostic
implications, especially in the presence of left ventricular
(LV) dysfunction.1 Tricuspid annular plane systolic excursion
(TAPSE) has become a popular surrogate marker for global RV
systolic function because of its ease of application2 and good
correlation with RV stroke volume (SV) in cardiac patients
undergoing catheterization or surgery.3,4 It is measured using
an M-mode technique.
Tissue-Doppler imaging allows for enhanced measurements
of RV myocardial performance in addition to TAPSE.5 Peak
systolic velocity at the tricuspid annulus (S’) and isovolumic
acceleration (IVA) both provide further insight into RV
function. The correlation between S’ and RVFAC or SV has
been variable.6–9 S’ may be more sensitive to load and inotropic
state and relate more to rate of work as opposed to amount of
work.10,11 The comparison of S’ to RV geometric markers or
output variables, thus, may be misleading. In the RV, IVA
appears to be a more load-insensitive marker of RV function.10
Most studies have examined TAPSE, S’, and IVA using
transthoracic echocardiography (TTE) at the lateral wall of the
RV. Good tissue Doppler alignment using transesophageal
echocardiography (TEE) is only possible in the transgastric RV
inflow–outflow view.12 However, there is no correlation
between TAPSE and SV using this method.4 Using TTE, on
the other hand, Uhrheim et al found a good correlation between
TAPSE by color-tissue Doppler and SV.3 Furthermore, TAPSE
could track SV changes associated with epoprostenol infusions.3 TTE, thus, appears to be the preferred modality to
assess RV function by TAPSE, S’, and IVA.
Both TAPSE and S’ are influenced by loading conditions.5
Although knowledge of loading conditions remains important,
the combination of TAPSE and annular velocity (S’) may offer
simultaneous insights into RV work and rate of work. Additionally, their relationship in each patient may prove superior to
either one alone.
KEY WORDS: right ventricular function, color-tissue Doppler,
TAPSE, tricuspid annular velocity
METHODS
The study protocol was approved by the St. Michael’s Hospital
Research Ethics Board. There were 2 groups of patients. In Group 1,
eligible patients undergoing elective coronary artery bypass graft
surgery (CABG) were approached preoperatively, and a signed,
informed consent was obtained before conducting any study-related
procedures. Patients were excluded if they were not in sinus rhythm, if
the LVEF by preoperative echocardiography was less than 45%, and if
there was evidence of RV dysfunction or more than mild tricuspid
regurgitation (TR). Each patient had an ECG and invasive monitoring,
including indwelling radial arterial and pulmonary artery catheters (7.5French Paceport, Edwards Lifesciences, Irvine, CA) as part of clinical
routine. Approximately 15 minutes after the induction of anesthesia
(sufentanil, midazolam, and rocuronium), a TTE was performed with
the patient supine and tilted slightly to the left (GE Vivid 7 system,
Milwaukee, WI). Echocardiography measurements were made simultaneously with hemodynamic measurements before and after the administration of ephedrine, 10 mg IV. No inhalation agents were used during
the study period.
From the Department of Anaesthesia, St Michael’s Hospital,
University of Toronto, Toronto, Ontario, Canada.
Address reprint requests to Claude Tousignant, MD, Department of
Anaesthesia, St Michael’s Hospital, 30 Bond Street, Toronto, ON M5B
1W8, Canada. E-mail: [email protected]
© 2014 Elsevier Inc. All rights reserved.
1053-0770/2601-0001$36.00/0
http://dx.doi.org/10.1053/j.jvca.2013.10.005
Journal of Cardiothoracic and Vascular Anesthesia, Vol ], No ] (Month), 2014: pp ]]]–]]]
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HU, MAZER, AND TOUSIGNANT
Group 2 patients (with suspected RV dysfunction) were identified
by the attending physician in the intensive care unit. They were
included if the mPAP was above 25 mmHg and if they required
inotropic support. They were excluded if the TAPSE on initial TTE
examination was normal (41.6cm) or if there was more than mild TR.
Written informed consent for the study was obtained from the next of
kin. A TTE examination and hemodynamic measurements were
performed simultaneously.
The following peak hemodynamic measurements were recorded in
all groups: Heart rate (HR), mean arterial blood pressure (SBPm), and
mean pulmonary artery pressure (PAPm). Cardiac output (CO)
measurements were done using thermodilution and recorded as the
average of 3 consecutive measurements from 10 mL saline boluses at
room temperature. SV was calculated by dividing the CO by the HR
and expressed in mL.
Using a GE Vivid 7 system (GE, Milwaukee, WI) with a phased
array M4S or M3S TTE probe using harmonics, a 4-chamber view was
obtained in which the RV annular motion was aligned with the Doppler
plane. A color-tissue Doppler sector was applied to the RV annulus and
basal segment, ensuring that the annulus remained within the sector
throughout the cardiac cycle. The 2D sector was narrowed to optimize
the tissue Doppler frame rate (4200 fps). Five consecutive beats were
recorded digitally for offline analysis. Image acquisition was performed
simultaneously with hemodynamic measurements.
Using Quantitative Analysis software (GE, Milwaukee, WI) a 6 6
mm sample volume was applied to the color-tissue Doppler sector at
the basal segment of the RV as close to the annulus as possible. The
sample volume was placed such that the highest possible velocity was
ensured and that the sample volume remained within the myocardium
at the base. The peak systolic velocity at the tricuspid annulus (S’) and
the isovolumic acceleration (IVA) were recorded as previously
described.10,12 Tissue tracking then was used to measure displacement
(TAPSE). The average of 3 consecutive values was used.
The sample size was a convenience sample based on previous
studies. All values were expressed as mean ⫾ standard deviation
(SD). Changes in hemodynamic and echocardiographic parameters
were expressed as mean ⫾ 95% confidence interval (CI). A paired
Student’s t test was used to assess pre- and postephedrine values for
echocardiographic and hemodynamic variables. An unpaired t test
was used to assess between-group variables. A p value o0.05 was
considered significant. The relationship between TAPSE and SV
as well as S’ and SV was assessed using linear regression. The
relationship between TAPSE and annular velocity (S’) was examined
using second order polynomial regression, because it was clear from
examining the data that it would not fit a straight line. To examine the
changes as a result of the administration of ephedrine, the TAPSE-S’
relationship was log-transformed for TAPSE and linear regression
was performed.
RESULTS
Twenty-seven patients were recruited in Group 1 (CABG
patients), and 16 patients were recruited in Group 2 (critically
ill patients). Six patients were excluded in Group 1: 3 due to
poor images and 3 due to poor LV function (EFo 45%). Six
patients were excluded in Group 2 due to poor imaging. The
demographic characteristics for each group are presented in
Table 1.
Patients in Group 2 were receiving various combinations of
norepinephrine, vasopressin, dobutamine, and milrinone. There
was a significant difference in HR and PAPm between Group 2
and the pre-ephedrine values in Group 1 (Table 2). There was
no significant difference in SBPm and SV. The echocardiographic parameters TAPSE, IVA, and S’ were significantly
Table 1. Demographic Data
Group 1
Group 2
Characteristic
(CABG)
(n ¼ 21)
(Critically Ill)
(n ¼ 10)
Age (years)
Sex (M/F)
Height (cm)
Weight (kg)
64 ⫾ 9
20/1
173 ⫾ 8.4
89 ⫾ 22
67 ⫾ 12
5/5
166 ⫾ 13
78 ⫾ 20
NOTE. Values are expressed as means ⫾ SD.
Abbreviations: CABG, coronary artery bypass graft surgery; F,
female; M, male.
lower in Group 2 compared with Group 1 pre-ephedrine values
(Table 3).
A modest correlation between TAPSE and SV was seen in
Group 1 when all data were combined (R ¼ 0.50, p o 0.001)
(Fig 1A). There was no correlation between TAPSE and SV in
Group 2 (R ¼ 0.30, p ¼ 0.39) (Fig 1A).
There was no significant relationship between S’ and SV
in Group 1 (R ¼ 0.28, p ¼ 0.08) or in Group 2 (R ¼ 0.16,
p ¼ 0.66).
Ephedrine administration resulted in significant increases in
all hemodynamic variables (Table 2). There were significant
increases in S’ and TAPSE as a result of ephedrine administration (Table 3, Fig 1B). However, ephedrine did not result
in any appreciable rise in IVA; the 95% CI was larger than the
mean IVA change (Table 3).
The relationship between TAPSE and S’ for Group 1
described a curvilinear relationship, in which TAPSE increased
along with S’ to a point at which no further appreciable
increase in TAPSE was observed despite further increases in S’
(Fig 2). Using second order polynomial regression, a good
correlation was found in Group1, pre-ephedrine (R ¼ 0.74,
p o 0.001), and Group1, postephedrine (R ¼ 0.64, p ¼ 0.009)
(Fig 2). In Group 2, increases in S’ were not statistically significantly associated with any appreciable increase in TAPSE
(Fig 2).
The postephedrine TAPSE versus S’ relationship curve
appeared shifted up when compared with the pre-ephedrine
curve (Fig 2). Using linear regression of a log transformation of
TAPSE vs S’, a good correlation was found in both the preand postephedrine groups (R ¼ 0.68, p o 0.001 and R ¼ 0.55,
p ¼ 0.01, respectively). There was, however, significant
Table 2. Hemodynamic Changes in Group 1 and Group 2
Group 1
Pre-ephedrine Postephedrine Change (⫾95% CI)
HR (bpm)
SBPm (mmHg)
PAPm (mmHg)
SV (mL)
58 ⫾ 9
78 ⫾ 13
20 ⫾ 6
75 ⫾ 18
64 ⫾ 11*
95 ⫾ 14*
23 ⫾ 5*
85 ⫾ 21*
6⫾3
17 ⫾ 5
4⫾2
10 ⫾ 5
Group 2
82 ⫾ 16†
75 ⫾ 14
35 ⫾ 4†
72 ⫾ 27
NOTE. Values are expressed as means ⫾ SD. The changes in Group
1 are expressed as mean ⫾ 95%CI.
Abbreviations: CI, confidence interval; HR, heart rate; bpm, beats
per minute; PAPm, mean pulmonary artery pressure; SBPm, mean
arterial blood pressure; SV, stroke volume.
*Denotes p o 0.001 compared with pre-ephedrine values.
†Denotes p o 0.001 compared with Group 1 pre-ephedrine values.
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TRICUSPID ANNULAR EXCURSION AND VELOCITY
Table 3. Tissue Doppler Parameters for Group 1 and Group 2
Group 1
Pre-ephedrine Post-ephedrine Change (⫾95% CI)
IVA (m/sec2) 2.18 ⫾ 0.80 2.45 ⫾ 0.97
S’ (cm/sec) 9.59 ⫾ 2.3 11.15 ⫾ 2.3*
TAPSE (mm)
19.18
22.32*
0.27 ⫾ 0.38
1.55 ⫾ 0.71
3.14 ⫾ 1.2
Group 2
0.95 ⫾ 0.47†
5.00 ⫾ 1.42†
6.68 ⫾ 1.43†
NOTE. Values are expressed as mean ⫾ SD. The changes in Group
1 are expressed as mean ⫾ 95% confidence interval.
Abbreviations: CI, confidence interval; IVA, isovolumic acceleration;
S’, peak systolic velocity at the tricuspid annulus; TAPSE, tricuspid
annular plane systolic excursion.
*Denotes p o 0.001 compared with pre-ephedrine values.
†Denotes p o 0.001 compared with Group 1 pre-ephedrine values.
overlap of the 95% CI for both regression curves. Furthermore,
the y intercepts (at S’ ¼ 0 cm/sec) were not significantly
different between the pre- (1.04 mm, 95% CI [0.89, 1.19]) and
postephedrine (1.18 mm, 95% CI [1.03, 1.33]) values.
DISCUSSION
A reduced TAPSE has been associated with poor RV
function and has been shown to predict depressed SV and
Fig 1. (A) Relationship between TAPSE and SV using linear
regression for Group 1 (open circles, solid line, R ¼ 0.50, p o 0.001)
and Group 2 (open triangles and dashed line, R ¼ 0.30, p ¼ 0.39). (B)
Relationship between S’ and SV using linear regression for Group 1
(open circles, solid line, R ¼ 0.28, p ¼ 0.08) and Group 2 (open
triangles and dashed line, R ¼ 0.16, p ¼ 0.66).
Fig 2. Relationship between TAPSE and S’ and corresponding
second order polynomial regressions for Group 1 pre-ephedrine
(empty circles, dotted line, R ¼ 0.74, p o 0.001); Group 1 postephedrine (dark circles, solid line, R ¼ 0.64, p ¼ 0.009); and Group 2
(empty triangles, dashed line, R ¼ 0.74, p ¼ 0.06).
RVFAC;2,3,7,13–16 values less than 16 mm are considered
abnormal.17 Normal values for S’ depend on the methodology.
Using spectral pulsed-wave tissue Doppler, values less than
10 cm/sec are considered abnormal.18 Using color-tissue
Doppler imaging, the reported normal values range from
8.3 ⫾ 2.1 cm/sec to 10.0 ⫾ 2.0 cm/sec.6,19–21 A depressed S’
has been shown to reveal RV dysfunction in a range of
situations,22,23 similar to the differences seen between these 2
groups. Normal values for IVA using TTE in an anesthetized
cardiac surgical population have been reported as 1.81 ⫾ 0.83
m/sec2.19
The present study of elective cardiac surgical patients
confirmed a modest correlation that has been found previously
between TAPSE and SV.3 Similar to other studies, no
significant relationship between S’ and SV was found.7,12
TAPSE may be more robust, because it correlates with
geometric changes in RV size or length associated with the
volume of blood that is moved during systole. On the other
hand, the lack of a relationship between TAPSE and SV in the
critically ill population shows that when TAPSE is indicative of
depressed RV function, it does not necessarily mean depressed
output performance. Other conformational changes may be
responsible for the ejection volume. In an animal study, Leather
et al found that RV longitudinal function correlated best with
RV preload-recruitable stroke work.24 However, numerous
studies suggested that in the abnormal RV (eg, congenital
heart disease), longitudinal function may not fully represent
global function; circumferential fibers and transverse motion
appear to become more important.13,25,26
The RV may be divided into 3 components: Inlet (sinus),
apical trabecular, and outlet.27 The RV muscle fibers are
predominantly longitudinal; however, circumferential fibers
are found in the subepicardial layers.27 TAPSE is representative
of the sum of the longitudinal function of the lateral wall that
includes the inlet and apex. The function of the RV has been
compared with that of a bellows, and the short-axis motion of
the mid-RV wall likely contributes a significant portion of
ejected RV volume.25 This may represent the function of the
outlet, because it has been found to contribute up to 20% of the
ejected volume.28 Septal and LV systolic function also are
4
HU, MAZER, AND TOUSIGNANT
important contributors to RV function.29-31 The investigation of
all these components (including tissue Doppler-derived values)
should be undertaken in a complete assessment of RV function,
especially in patients with abnormal function or loading
conditions.
In a cardiac surgical population with normal RV function, the
relationship between TAPSE and annular velocity (S’) describes
a concurrent rise in both values until a point is reached beyond
which only minimal increases in TAPSE are observed. At this
point, only efficiencies in annular velocity (S’) are observed.
This curve may provide useful information on the relationship
between surrogates for work (TAPSE) and rate of work (S’) and,
by extension, power.10,11 Some patients may show a depressed
TAPSE in response to abnormal loading conditions and disease.
An associated depressed rate of annular descent (S’) may reflect
inadequate inotropic compensation in addition to a move away
from optimal loading conditions.11 Knowing how this conceptual “work-rate” relationship changes and defining maximum
values may be helpful in assessing the status of the RV and
predicting how it will cope with further stress.
In the critically ill patients, TAPSE and S’ were reduced
significantly, and there was no relationship between TAPSE and
S’ (Fig 2). Patients with a depressed and fixed TAPSE due to
various constraints, such as pulmonary hypertension or systolic
dysfunction, may achieve efficiencies only through increases in
rate of excursion (Fig 2). This may occur as a result of increased
inotropic stimulation.10 In the Group 2 population, the use of
inotropic drugs did not restore either the TAPSE or the S’
velocity to normal values. This suggested both significant constraints and significantly depressed systolic function.
Induction of anesthesia frequently results in a decrease in
sympathetic tone. In addition, the frequent use of β-blockers in
cardiac patients results in a slower heart rate and a depressed
inotropic state. These factors may contribute to an apparent
depression of RV function when examined under echocardiography. Ephedrine, a weak inotrope, may help determine
whether the depressed RV under anesthesia is recruitable or
depressed. The authors previously have found that measurements of TAPSE using M mode and Speckle tracking with TEE
could not reliably reflect changes following ephedrine administration.4 This is contrary to what was found in the present
study at the lateral wall using TTE. Using color-tissue Doppler,
Curren et al found that RV basal S’ increased significantly from
8.3 ⫾ 2.1 cm/sec to 12.7 ⫾ 2.5 cm/sec after exercise.6 Using
ephedrine, significant increases in S’ as well as TAPSE were
found in the CABG group (Table 3). However, ephedrine did
not influence significantly the TAPSE-S’ relationship (Fig 2). A
clinically significant rise in PAPm was not observed (Table 2).
However, interventions that would influence significantly the
PAPm could certainly affect this relationship.
The IVA has been described as a load-independent measure
of contractility.11 In an animal study using color-tissue
Doppler, dobutamine 10 μg/kg/min, raised the IVA from
3.0 ⫾ 1.4 m/sec2 to 4.7 ⫾ 1.5 m/sec2.11 In the present study,
the administration of ephedrine did not result in any significant
increase in IVA (Table 3). It is possible that ephedrine was not
potent enough to effect a significant change in IVA. Alternatively, the variability in the measurement of IVA was due to
measurement difficulties, a large interpatient variability or
simply large beat-to-beat variability.18 The IVA was significantly lower in Group 2 compared with the pre-ephedrine
patients in Group 1. This difference likely represented a
significant reduction in RV inotropic state in this critically ill
patient group despite the intravenous inotropic support.
There were several limitations in this study. The number of
patients was small. Larger numbers may have resulted in a
significant difference between the pre- and postephedrine data.
Furthermore, ephedrine may not have had sufficient inotropic
potency to elicit the response necessary to assess the echo
changes in RV function. The effects of general anesthesia and
cardiac medications also may have influenced the RV response.
Modification of volume status was not undertaken; describing
the TASPE-S’ relationship after volume modification would
have been a useful adjunct to this study.
CONCLUSIONS
This study supported the utility of color-tissue Dopplerderived TAPSE, S’, and IVA to distinguish between a cardiac
surgical population with good RV function and one with
significantly depressed RV requiring inotropic support. However, in patients with depressed RV function, TAPSE is not
related closely to global RV cardiac output. Additional parameters of RV function should be investigated under these circumstances. The relationship between TAPSE and S’ describes a
curvilinear relationship, which may offer insight into baseline
RV function and response to stimulation. This particular
relationship is lost in patients with significant RV dysfunction.
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