Professional Documents
Culture Documents
DISCUSSION
This patient underwent the Mustard procedure for correction of d-transposition of the great arteries, which
directs systemic venous blood through the left atrium,
left ventricle, and into the PA and directs pulmonary
venous blood through the right atrium, the morphologic
RV and into the aorta (Fig. 1B). Over time, the Mustard
procedure can lead to dysfunction of the morphologic
RV because it lacks sufficient contractile reserve and
atrioventricular valve function to generate systemic pressures long-term.
For many individuals with either congenital or acquired
forms of heart disease that result in decreased cardiac
function, cardiac transplantation is the final treatment
option for those who cannot recover with other therapies.1
RV failure continues to have significant morbidity for
patients undergoing cardiac transplantation, especially
those with high pulmonary vascular resistance preoperatively.2 RV failure after transplantation has been caused by
preexisting pulmonary hypertension, poor RV myocardial
protection, air embolism, or rare anatomic/anastomotic
complications. Such causes of postoperative RV dysfunction secondary to outflow tract obstruction have been
reported after anastomotic stricture after lung transplantation and kinking of the PA after heart transplantation.3,4 Pretransplant heart catheterization on our patient
demonstrated PA pressures of 40/25 mm Hg (mean 35
mm Hg) and pulmonary vascular resistance of 2.56
Woods units, which was appropriate to attempt cardiac
transplantation.
Postoperative treatment with a VAD has been used after
heart transplantation and for individuals with heart failure
after acute myocardial infarction.5 VAD therapy allows
recovery of ventricular function over time and eventual
removal of the device, as it occurred in this patient.
Examination after the RVAD was paused demonstrated
improved RV function and normal tricuspid annulus plane
systolic excursion before RVAD extraction on posttransplant day 27.
Regarding the intraoperative findings, a normal diameter of the PA at the level of the stricture is 1.5 to 2.1 cm and
normal flow through the PA and pulmonic valve should be
100 cm/second.6,7 Because the diameter of stricture on 2D
imaging was 1.14 cm, it was a smaller than expected
diameter for the PA. A focused evaluation using 2D echo in
2 orthogonal planes, midesophageal ascending aorta shortaxis view and midesophageal ascending aorta long-axis
view, was important for confirmation that a stenotic area
was present and not artifact. Manipulation of the TEE
probe depth in these 2 views allowed visualization of the
PA in long-axis and short-axis, respectively, though visualization of the PA with these views is not always available.
The use of CFD to demonstrate flow acceleration at the
www.anesthesia-analgesia.org
257
ECHO ROUNDS
r2 area
0.572 1.02 cm2
A diameter of 1.14 cm gives a CSA of 1.02 cm2. Interrogation of stenotic lesions can use the PISA radius (r), the
aliasing velocity (Valias), the maximum velocity across
the region (Vmax) and the interface angle () to solve the
estimated orifice area:
2r2 Valias
Vmax
180
21.39 cm 2 50 cm/s
343 cm/s
113
180
1.11 cm2
The estimated area using both the CSA and PISA calculations supports the presence of the anastomotic stricture
seen on 2D imaging. Given a normal PA diameter of 2 cm,
CSA would be 3.14 cm2. A CSA of 1.0 to 1.1 cm2 would be
a moderate to severe stenosis.
Without identification of this anastomotic stricture it is
possible the patient would not have recovered appropriate
RV function to allow RVAD removal. PA anastomosis
visualization was not reported during transplantation with
area
258
www.anesthesia-analgesia.org
www.anesthesia-analgesia.org
259
ECHO ROUNDS
Right ventricular (RV) dysfunction after heart transplantation may result from pulmonary hypertension, inadequate
myocardial preservation, coronary air embolism, or anastomotic complications. Anastomotic complications include
kinking, torsion, or protruding suture lines. In cases of severe posttransplantation RV dysfunction, support with an RV
assist device may be necessary.
Multiple transesophageal echocardiography (TEE) views and imaging modalities should be routinely used to examine the RV
after heart transplantation. A qualitative assessment of RV size and systolic function may be obtained using the
midesophageal 4-chamber, RV inflow-outflow, and transgastric views. Color flow Doppler can be used to detect tricuspid
regurgitation (TR) and flow acceleration due to stenosis at the pulmonary artery (PA) anastomosis while continuous wave
Doppler (CWD) allows measurement of the TR velocity and pressure gradient across the PA anastomosis.
In this case, narrowing of the PA anastomosis was identified by 2-dimensional imaging and confirmed by color flow
acceleration; abnormally high flow velocities in the PA were noted during CWD examination. Later, off-line calculations
of the effective PA anastomotic area using the proximal isovelocity surface area (PISA) method correlated well with the
anastomotic area calculated using the measured diameter of the stricture. Revision of the PA anastomosis facilitated
recovery of RV function.
Although rare, anatomic irregularities of anastomoses after heart transplantation may contribute to cardiac dysfunction. A
comprehensive posttransplant TEE examination should include 2-dimensional and color Doppler imaging of anastomotic
areas along with spectral Doppler interrogation when needed.
260
www.anesthesia-analgesia.org