Download successful rescue of sustained ventricular tachycardia/ventricular

Extracorporeal Membrane Oxygenation for Ventricular Tachyarrhythmia
CASE REPORTS
SUCCESSFUL RESCUE OF SUSTAINED VENTRICULAR
TACHYCARDIA/VENTRICULAR FIBRILLATION AFTER
CORONARY ARTERY BYPASS GRAFTING BY
EXTRACORPOREAL MEMBRANE OXYGENATION
Robert J. Chen, Wen-Je Ko, and Fang-Yue Lin
Abstract: Extracorporeal membrane oxygenation (ECMO) can be set up quickly at
the bedside and provides reliable temporary mechanical circulatory support for
severe heart failure. We report the case of a 56-year-old female with circulatory
collapse due to sustained ventricular tachycardia and ventricular fibrillation (VT/
Vf) after coronary artery bypass grafting (CABG) who was successfully resuscitated
using ECMO. The sustained VT/Vf might have been secondary to myocardial
stunning, ischemia, infarction, or reperfusion. There were 40 cardioversions within
the first 5 postoperative days. The patient improved after 8 days of ECMO in addition
to use of an intraaortic balloon pump and administration of inotropic agents for
profound heart failure. Left ventricular ejection fraction improved from 28%
preoperatively to 54.5% on the 20th postoperative day. Cardiogenic shock due to
sustained VT/Vf after CABG may be an indication for ECMO support. Immediate
establishment of circulatory support using ECMO provides valuable time for spontaneous and interventional correction of reversible causes of sustained VT/Vf.
Simple ventricular arrhythmias are not uncommon
after coronary artery bypass grafting (CABG) and may
not considerably affect the patient’s prognosis [1].
However, sustained ventricular tachycardia and ventricular fibrillation (VT/Vf), defined as those lasting
more than 30 seconds, are among the most dreadful
events after CABG [1, 2], and carry an in-hospital
mortality rate of around 25 to 44% [1, 3]. In post-CABG
patients, the estimated incidence of new-onset sustained VT/Vf is around 0.41 to 3.1% [1, 2]. Associated
factors include myocardial ischemia, post-infarction
scarring, and profound heart failure [1–4].
Extracorporeal membrane oxygenation (ECMO)
should be considered in patients with drug-resistant
sustained VT/Vf [5]. For reversible heart failure, ECMO
is the mechanical circulatory support of choice after
(J Formos Med Assoc
2002;101:283–6)
Key words:
extracorporeal membrane
oxygenation
coronary artery bypass grafting
ventricular tachycardia
ventricular fibrillation
intraaortic balloon pumping (IABP) [6]. ECMO might
save more than half of patients with cardiogenic shock
after coronary artery surgery, allowing them to survive
to the point of hospital discharge [7, 8].
Rescue of sustained VT/Vf using ECMO or a
ventricular assist device (VAD) has been reported
before [5, 9, 10]. These cases included post-CABG
adults [5, 10] and non-CABG children [9]. The
duration of ECMO support ranged from 6 hours to 3
days [5, 10]. Survival after recurrent, sustained, and
refractory VT/Vf after a relatively long duration of
ECMO support is unusual. We report the case of an
adult patient who was successfully rescued using ECMO
support for 8 days. She had 40 cardioversions for
recurrent sustained VT/Vf within the first 5 days after
CABG.
Department of Surgery, National Taiwan University Hospital, Taipei.
Received: 2 July 2001.
Revised: 8 August 2001.
Accepted: 5 February 2002.
Reprint requests and correspondence to: Dr. Wen-Je Ko, Department of Surgery, National Taiwan University Hospital, 7
Chung-Shan South Road, Taipei, Taiwan.
J Formos Med Assoc 2002 • Vol 101 • No 4
283
R.J. Chen, W.J. Ko, and F.Y. Lin
Case Report
A 56-year-old woman was sent to the emergency room due to
worsening chest pain and dyspnea for 6 months. She had
undergone percutaneous transluminal coronary angioplasty
(PTCA) of the left anterior descending artery (LAD) and right
coronary artery (RCA) at another medical center 2 months
previously.
Physical examination showed regular heartbeat, fine lung
crackles, and mild leg edema. Laboratory data were unremarkable except for hyperglycemia (283 mg/dL). Electrocardiogram (ECG) showed sinus rhythm, Q waves at inferior limb
leads, ST elevation at anterior precordial leads, a corrected
QT interval of 370 ms, and a QRS duration of 80 ms. Coronary
angiography found 95% stenoses over the proximal LAD, left
circumflex artery, and RCA. Echocardiography showed a left
ventricular ejection fraction (LVEF) of 28%, global hypokinesia,
a left ventricular (LV) end-diastolic dimension of 53 mm, and
no significant valvular dysfunction. In the cardiac surgery
ward, she received infusion of nitroglycerin but no
catecholamine.
She underwent elective CABG under cardiopulmonary
bypass. The left internal mammary artery was grafted to the
obtuse marginal artery. Two greater saphenous veins were
grafted to the LAD and the RCA. However, immediately after
decannulation, a sustained attack of VT/Vf developed
unexpectedly. Intravenous lidocaine (1 mg/kg) and magnesium sulfate (64 mEq) failed to reverse the arrhythmias. Ten
cardioversions were given to restore the sinus rhythm. Profound cardiogenic shock followed. Amiodarone (6 mg/kg
–1
–1
loading), dopamine (13.25 µg⋅kg ⋅min ), epinephrine
–1
–1
(0.085 µg⋅kg ⋅min ), norepinephrine (0.26 µg⋅kg–1⋅min–1),
milrinone (25 µg/kg loading), and emergency IABP all failed
to control the cardiogenic shock. Veno-arterial ECMO was
then urgently set up via the right femoral route. ECMO rapidly
stabilized the circulation. In the intensive care unit,
the patient’s hemodynamic status under ECMO was maintained by the infusion of amiodarone (12 µg⋅kg –1⋅min –1),
milrinone (0.5 µg⋅kg –1 ⋅min –1), norepinephrine (0.052
–1
–1
–1
–1
µg⋅kg ⋅min ), nitroglycerine (3.4 µg⋅kg ⋅min ), and dopam–1
–1
ine (6.6 µg⋅kg ⋅min ). Within the first 4 hours postoperatively
after ECMO, sustained VT/Vf relapsed and she received eight
cardioversions. During this time, electrolytes and hemoglobin were intensively monitored and interventions were given
to maintain them within normal ranges. During the fifth
postoperative hour, emergency surgery was performed to
control bleeding. A 2-mm tear in the middle portion of the
greater saphenous vein grafted to the RCA was found and
repaired. Lidocaine infusion was started (50 mg loading, then
2 mg/min) but there were still four more attacks of sustained
VT/Vf that required cardioversions.
Two additional cardioversions for VT/Vf were required on
postoperative day 1 (POD1) and one on POD2. There was no
sustained VT/Vf on POD3. On POD4, discontinuation of
lidocaine infusion was attempted, but a further sustained VT/
Vf attack required 15 cardioversions, so lidocaine infusion
was resumed. Later on that day, ECMO flow declined and
marked hemoglobinuria was also noted. Plasma leakage and
284
thrombi were found inside the ECMO oxygenator. ECMO
support had to be continued because of the low LVEF (30%)
and the high risk of sustained VT/Vf. We replaced the oxygenator immediately with a flow interruption of less than 30
seconds. The ECMO flow resumed and became stable, with
no more hemoglobinuria.
On POD5, further surgery for cardiac tamponade was
performed. Pericardial hematoma was evacuated and meticulous hemostasis was done at the aorta and the split
sternum. On inspection, all coronary grafts were patent and
there was a myocardial infarct of 2 cm in diameter over the
territory of the distal diagonal artery (LAD branch). Electrolytes and hemoglobin were kept within normal limits. Over
the next 3 days, there were no more sustained VT/Vf attacks.
The patient was weaned from ECMO on POD8. Her hemodynamics remained stable under support with IABP and infu–1
–1
sions of dopamine (3.3 µg⋅kg ⋅min ), lidocaine (3 mg/min),
–1
–1
and nitroglycerin (1.7 µg⋅kg ⋅min ).
The patient was weaned from IABP on POD12, but
–1
–1
pharmacologic support with dopamine (3.3 µg⋅kg ⋅min ),
–1
–1
nitroglycerin (2 µg⋅kg ⋅min ), and lidocaine (1.6 mg/min)
was maintained. These medications were all tapered off on
POD26. She was weaned from mechanical ventilation and
transferred to the cardiac surgery ward on POD30. She
recovered and was discharged 3 months later after a rehabilitation program. During outpatient follow-up over 15 months,
she had New York Heart Association function class I, with no
more chest pain, and was free from the need for antiarrhythmia drugs. Her LVEF remained around 55%. Echomeasured LVEF was 28% preoperatively, 28.9% on POD1,
33.6% on POD5, 48.6% on POD6, and 54.5% on POD20.
The patient received 40 cardioversions for sustained VT/
Vf during the first 5 days postoperatively. Her pre- and
postoperative ECGs were similar except for anterior ST elevation that disappeared on POD12. There were two clusters of
sustained VT/Vfs (Figure). The first occurred within the first
few postoperative hours, and the second was on POD4. Peak
concentration of myocardial-bound creatine kinase (CK-MB;
1,309 U/L) followed the first cluster (Figure).
Discussion
Sustained VT/Vf after coronary artery surgery may be
treated using electric cardioversion [3, 11], anti-arrhythmic drugs [3, 11], elimination of etiologies [3,
11], electrophysiologic study (EPS)-guided antiarrhythmic (AA) therapy [3], or implantable cardioverterdefibrillators (ICD) [3, 11]. The use of a VAD [10] and
ECMO [5, 9] to stabilize the hemodynamics may be
required. ECMO is usually used for temporary cardiogenic shock such as myocardial stunning and favorable
results have been shown in post-CABG patients [7–9].
In this case of unanticipated sustained VT/Vf, the
major reason for choosing ECMO was its easy set-up at
the bedside during an emergency [8]. ECMO stabilizes
the hemodynamics to allow the search for difficult
J Formos Med Assoc 2002 • Vol 101 • No 4
Extracorporeal Membrane Oxygenation for Ventricular Tachyarrhythmia
25
1,400
1,309 ◆
22
VT/Vf (/d)
◆
20
1,200
CK-MB (U/L)
15
15
800
678 ◆
516
10
600
CK/MB (U/L)
VT/Vf (/d)
1,000
Figure. Myocardial-bound
creatine kinase (CK-MB)
concentration and ventricular tachycardia/ventricular
fibrillation (VT/Vf) frequency in the postoperative
period. ECMO = extracorporeal membrane oxygenation.
400
5
◆
284
2
92
0
◆
194
201
◆
◆
189
156
44
1
10
◆
◆
*OR
*0
*1
*2
200
◆
*3
*4
*5
*6
*7
Postop day (*ECMO use)
etiologies under emergency conditions and also provides a safe bridge to another treatment modality such
as EPS-guided AA therapy, VAD, ICD, or heart transplantation [5, 8]. Under ECMO-stabilized
hemodynamics, we had time to investigate the etiology
of sustained VT/Vf that might have included
perioperative myocardial ischemia, focal infarction
scarring, reperfusion effect, and hemodynamic instability [1–4].
The first cluster of VT/Vf attacks could be explained as the effects of ischemia, infarction, and
reperfusion. Post-CABG VT/Vf might be a sign of
myocardial ischemia [2, 3]. Cardiac tamponade and
graft defects might cause and aggravate myocardial
ischemia. The focal infarct at the diagonal artery could
serve as a fixed anatomic substrate for arrhythmogenesis
[3]. Patients with new-onset sustained VT are more
likely to have prior myocardial infarction [1, 3]. When
infarction is extensive, sustained VT/Vf might result
from electrical instability secondary to LV remodeling
or aneurysm formation [12]. However, when the infarct is focal, as in this case, ventricular arrhythmia
develops via reperfusion [1, 3, 4]. Steinberg et al found
that reperfusion was crucial in the pathogenesis of newonset sustained VT in a prospective study that enrolled
382 patients [1]. They also found that the risk of
sustained VT increased significantly when an infarct
zone was revascularized, and that when an infarct was
not reperfused, VT was very unlikely to develop during
the in-hospital period [1]. Reperfusion by CABG might
restore electrical function in the hibernating myocarJ Formos Med Assoc 2002 • Vol 101 • No 4
*8
9
29
17
◆
◆
10
11
16
◆
0
12
dium around an infarct and, thus, create reentrant
circuits for the genesis of VT [1, 4].
The second cluster on POD4 in this patient might
have resulted from LV dysfunction or premature withdrawal of lidocaine. Preoperative low LVEF and hemodynamic instability (the need for IABP) are associated
with the development of sustained VT/Vf after CABG
[2]. This patient needed IABP for low LVEF. LV dysfunction led to coronary hypoperfusion and then aggravated the myocardial ischemia. Ischemia-associated
ventricular arrhythmia may have caused LV dysfunction again and, thus, created a vicious cycle. Lidocaine
re-infusion and ECMO replacement broke this vicious
cycle and the cluster of VT/Vf attacks was diminished.
The peak CK-MB concentration (1,309 U/l) on
POD2 could be explained by the repeated electric
cardioversions [13]. This high CK-MB concentration
did not necessarily indicate extensive myocardial
infarction. The infarct, which was visualized during the
repeated surgery, was focal with a diameter of 2 cm.
The reversible nature of the heart failure also suggested an absence of extensive post-infarction scarring.
The baseline ECG Q-waves might imply that the infarct
existed before the CABG. The repaired graft defect was
in the territory of the RCA that had little anatomical
relationship with the infarct at the diagonal artery
(LAD branch). The focal infarct probably contributed
to generate sustained VT/Vf [1–3].
ECMO played a pivotal role in the treatment of this
patient with sustained VT/Vf after CABG. Lidocaine
and amiodarone, as the standard treatment for post-
285
R.J. Chen, W.J. Ko, and F.Y. Lin
CABG VT/Vf [3, 11], did not produce an immediate
response, so we decided to set up ECMO promptly at
bedside for cardiac rescue. Under ECMO support and
with removal of pro-arrhythmic factors, lidocaine and
amiodarone successfully suppressed sustained VT/Vf
in this case. If they had not suppressed the arrhythmia,
procainamide could have been added next [11].
This patient developed unanticipated sustained
VT/Vf attacks during the post-cardiopulmonary bypass
period. After repeated defibrillation, high doses of
inotropic agents and IABP failed to restore hemodynamics.
ECMO was needed for emergency cardiac support. The
LVEF improved and VT/Vf became less frequent under
ECMO support. The ECMO fulfilled its role as a transient
support and was weaned off on POD8.
In conclusion, this patient had profound heart
failure due to sustained VT/Vf. The possible etiologies
included myocardial stunning, ischemia, infarction,
and reperfusion. To stabilize the hemodynamics, ECMO
was chosen for its simplicity and rapidity of set-up. It
bridged this patient successfully to recovery.
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