Vol No: 4 Issue No: 2 eISSN:
Dear Authors,
We invite you to watch this comprehensive video guide on the process of submitting your article online. This video will provide you with step-by-step instructions to ensure a smooth and successful submission.
Thank you for your attention and cooperation.
PVS Prakash* , Selvakumar R, Shahenshah, Sanjay OP, Varun Shetty, Julius Punnen, Devi Prasad Shetty
Narayana Institute of Cardiac Sciences, A unit of Narayana Health, Bangalore.
*Corresponding author:
Mr. PVS Prakash, HOD & Consultant Perfusionist Perfusion Department Narayana Health Bangalore. E-mail: prakash.p.v.s@narayanahealth.org
Received date: October 26, 2021; Accepted date: December 28, 2021; Published date: April 30, 2022
Abstract
Background: The inflammation or degeneration of the heart muscle myocarditis may be fatal. This disease often goes undetected. It may also disguise itself as ischemic, valvular, or hypertensive heart disease. Here we report eight cases of acute fulminant viral myocarditis suffering from low cardiac output, ARDS (Acute respiratory distress syndrome) formation and successfully treated with ECMO (Extra corporeal membrane oxygenation).
Methodology: All the cases were admitted in the emergency coronary care unit with severe respiratory distress, poor hemodynamics and ECHO examination revealed low Left ventricle Ejection Fraction (LVEF,15-20%). Veno - Arterial ECMO was initiated with femoro-femoral cannulation with distal limb perfusion. On ECMO support, the hemodynamics were stabilized with no inotropic support. The heart and lungs were given adequate rest time for recovery by maintaining total cardiac output on ECMO. The average ECMO support was 84.2 ± 4 hours. Maquet Quadrox PLS / Sorin Dideco ECMO oxygenators with rotaflow centrifugal pump were used. Delta pressure, pre-pump pressures were continuously monitored.
Results: Out of the eight cases put on VA ECMO for viral myocarditis, seven were successfully weaned off and were discharged (success rate of 87.5%). Soon after the initiation of ECMO, the arterial saturation reached the normal levels. The serum lactate levels which were high (>6 mmol/L) prior to initiation of ECMO remarkably came down to <2 mmol/L after 24 hours. Seven patients were weaned off and decannulated in the operating room. One patient required LV decompression by Balloon Atrial Septostomy in the Hybrid OR and was successfully weaned off after 48 hours. One patient succumbed due to continuous low cardiac output which was irreversible with full blown septicemia and was not responding to ECMO and medications.
Conclusion: Peripheral VA-ECMO support is very effective in optimizing myocardial recovery for the treatment of refractory acute fulminant viral myocarditis when maximal conventional supports are ineffective.
Keywords
Downloads
-
1FullTextPDF
Article
Introduction
Acute fulminant viral myocarditis is a condition that precipitates as heart failure preceded by symptoms of viral infection.1 The condition can be worse sometimes that it requires immediate mechanical circulatory support ECMO (Extra corporeal membrane oxygenation) due to the deprived left ventricle function. The inflammation or degeneration of the heart muscle in myocarditis may be fatal.2 This disease often goes undetected. It may also disguise itself as ischemic, valvular, or hypertensive heart disease. Inflammatory processes in the myocardium can directly lead to fluctuations in membrane potential that can trigger recurrent arrhythmias (complete heart block, ventricular tachycardia/ventricular fibrillation).3
ECMO is a lifesaving treatment for these types of acute emergencies and has yielded better results in the recent past. The high flow ECMO provides full heart lung support for conditions of low cardiac output and severe respiratory failure ensuring optimal oxygen delivery to all the vital organs. During the ECMO, mechanical ventilation and inotropic medications can be stopped or minimized so as to avoid further barotrauma and myocardial damage, and active treatment targeting the primary disease can be provided which is vital for heart and lung recuperation.4 VA ECMO is shown to be effective in treating refractory acute fulminant myocarditis.5 Timely initiation of VA ECMO is a novel option in treating acute viral myocarditis and we have an experience of eight cases.
Methods and Patients
Case details
From the period of April 2008, eight cases were admitted in the emergency coronary care unit with severe respiratory distress with poor hemodynamics (systolic blood pressure ≤ 90 mm of Hg)and ECHO examination revealed low LVEF (Left ventricle ejection fraction 15- 20%). Five males and three females aged 18 to 36 years (median age of 23 years) and weighing 49-85 kg (mean - 67.3 kg) were included. On examination, they had a varied heart rate in the range of 110-155 bpm.
Four patients had cool clammy skin with tachypnea. In addition, laboratory data also revealed increased levels of cardiac biomarkers (Creatine kinase MB > 37.0 U/L; Troponin-I > 15.0 ng/mL) and leukocytosis (WBC > 11000/mm3 ) with mild increase in C-reactive protein (CRP > 7.5 mg/L). All the patients were administered large doses of inotropic support drugs including adrenaline (0.2-1 µg/kg/min), and/or Dobutamine (10- 20 µg/kg/min) prior to ECMO initiation.
Treatment
Patients were electively ventilated and consent was taken for instituting peripheral VA ECMO. After systemic heparinization 2mg/kg, ECMO was established at a dose maintaining the activated clotting time (ACT) between 180 and 220 seconds. On ECMO support, the hemodynamics were stabilized with no inotropic support. The heart and lungs were given adequate rest time for recovery by maintaining total cardiac output on ECMO. The average ECMO support was 84.2 ± 4 hours. Maquet Quadrox PLS / Sorin Dideco ECMO oxygenators with rotaflow centrifugal pump were used. Peripheral cannulation was achieved with 24 Fr Bard with 8 mm hemashield or 20 Fr Edwards femoral arterial cannula with 10 Fr distal limb perfusion cannula for arterial cannulation. Venous access was established with 24 Fr long femoral venous cannula. The routine tests on a daily basis included echocardiography, chest radiography, blood gas analysis, blood coagulation parameters, liver function tests, serum lactate, fibrin degradation products, D-Dimers, renal function tests. Once the cardiac function improved, the ECMO flows were decreased proportionately over a period of time. Heparin flows were increased as the ECMO flows were brought down. After documenting recovered LVEF > 30% by echocardiography and when the Troponin biomarker started to descend, the decision to wean off ECMO was taken.
Results
The heart rate, blood pressure, clinical parameters and tissue oxygen saturation significantly improved after the ECMO. The average ECMO support was 84.2 ± 4 hours (48-138 hours). One patient had LA hypertension for which he had to undergo Balloon Atrial Septostomy (BAS). After the BAS procedure, his condition improved. Three patients required intra aortic balloon pump just before weaning off from ECMO. Out of the eight patients, seven patients were successfully weaned from ECMO and survived to hospital discharge, resulting in an 87.5% (7/8) survival rate. One patient succumbed due to continuous low cardiac output which was irreversible with full blown septicemia and was not responding to ECMO and medications. During the follow-up period, cardiac function was found within the normal range in six patients. One patient who underwent BAS had a mild LV dysfunction with LVEF=42%, with mild mitral regurgitation. After one year of follow-up, seven patients were found to be doing well clinically and resumed their respective professional careers. All of the survived seven patients demonstrated normal neuro cognitive behavior.
Discussion
ECMO offers a very good supportive therapy and a lifesaving option in the acute emergencies like fulminant viral myocarditis. Timely initiation of the ECMO provides sufficient rest for the heart and lungs to recuperate from the cardiogenic shock triggered by this acute viral myocarditis.6 Early initiation of VA-ECMO, LV Decompression promotes myocardial recovery and the ECMO flows/cardiac output should be targeted towards maintaining end organ perfusion which can be achieved with revolutions per minute (2500-3000) on the circuit in order to maximize perfusion. Endo myocardial biopsy is not routinely performed in patients because of the risks of the procedure in patients in critical condition.7 ECMO contributes for the early recovery of myocardium by reducing myocardial wall tension, increasing coronary perfusion pressure, and providing adequate systemic perfusion.8 During ECMO support, the dose of inotropes can be decreased to prevent overload on the myocardium in the acute stage.9 Recurrent arrhythmias are frequently seen in these conditions which are encountered with cardarone. Klein et al., found that inflammatory processes in the myocardium can directly lead to fluctuations in membrane potential.10 Ectopic pacemakers, late potentials, and re-entry as a result of in homogeneous stimulus conduction can develop because of fibrosis and scarring of myocardial tissue, secondary hypertrophy and atrophy of myocytes. Furthermore, left ventricular dysfunction may aggravate wall tension, increase myocardial oxygen consumption, and diminish coronary reserve, increasing the risk of arrhythmias.11 Recurrent arrhythmias are frequently seen in these conditions which are encountered with cardarone.12 ECMO reduces the incidence of recurrent arrhythmias in these conditions by preserving the myocardial reserve.
One patient was suffering from LA hypertension on the second day of ECMO for which he required Balloon Atrial Septostomy. His condition remarkably improved after the BAS and we could wean him off on the sixth day of ECMO. On his one year follow-up visit, he was found to have mild LV dysfunction with LVEF >42%, mild MR with no signs and symptoms of heart failure.
Proper ECMO monitoring and periodic assessment of these patients on ECMO has yielded positive results in this critical condition. The serum lactate levels which were high (>6 mmol/L) prior to initiation of ECMO remarkably came down to <2 mmol/L after 24 hours.
Conclusion
VA-ECMO support is very effective in optimizing myocardial recovery for the treatment of refractory acute fulminant viral myocarditis when maximal conventional supports are ineffective.
Conflicts of Interest
None of the authors have any conflict of Interests
Supporting File
References
1. Lieberman EB, Herskowitz A, Rose NR, Baughman KL. A clinicopathologic description of myocarditis. Clin Immunol Immunopathol 1993;68:191-6.
2. Wang Q, Pan W, Shen L, Wang X, Xu S, Chen R et al. Clinical features and prognosis in Chinese patients with acute fulminant myocarditis. Acta Cardiol 2012;67:571-6.
3. Ning B, Zhang C, Lin R, Tan L, Chen Z, Yu J et al. Local experience with extracorporeal membrane oxygenation in children with acute fulminant myocarditis. PLoS One 2013;8:e82258.
4. Teele SA, Allan CK, Laussen PC, Newburger JW, Gauvreau K, Thiagarajan RR. Management and outcomes in pediatric patients presenting with acute fulminant myocarditis. J Pediatr 2011;158:638-643.
5. Wu MY, Lin PJ, Tsai FC, Chu JJ, Chang YS, Haung YK et al. Postcardiotomy extracorporeal life support in adults: the optimal duration of bridging to recovery. ASAIO J 2009;55:608-13.
6. Chung JC, Tsai PR, Chou NK, Chi NH, Wang SS, Ko WJ. Extracorporeal membrane oxygenation bridge to adult heart transplantation. Clin Transplant 2010;24:375-80.
7. Conrad SA, Rycus PT, Dalton H. Extracorporeal life support registry report 2004. ASAIO J 2005;51:4- 10.
8. Fleming GM, Gurney JG, Donohue JE, Remenapp RT, Annich GM. Mechanical component failures in 28,171 neonatal and pediatric extracorporeal membrane oxygenation courses from 1987 to 2006. Pediatr Crit Care Med 2009;10:439-44.
9. Aoyama N, Imai H, Kurosawa T, Fukuda N, Moriguchi M, Nishinari M, et al. Therapeutic strategy using extracorporeal life support, including appropriate indication, management, limitation and timing of switch to ventricular assist device in patients with acute myocardial infarction. J Artif Organs. 2014;17:33–41.
10. R.M. Klein, E.G. Vester, M.U. Brehm, H. Dees, F. Picard, D. Niederacher, et al. Inflammation of the myocardium as an arrhythmia trigger.Z Kardiol, 89 (2000), 24-35
11. J.R. Sharma, S. Sathanandam, S.P. Rao, S. Acharya, V. Flood Ventricular tachycardia in acute fulminant myocarditis: medical management and follow-up. Pediatr Cardiol, 29 (2008), 416-419
12. E.M. Delmo Walter, V. Alexi-Meskishvili, M. Huebler, M. Redlin, W. Boettcher, Y. Weng, et al. Rescue extracorporeal membrane oxygenation in children with refractory cardiac arrest Interact Cardiovasc Thorac Surg, 12 (2011), 929-934