CASE REPORT |
https://doi.org/10.5005/jp-journals-11006-0059 |
A Rare Case Report: VA ECMO Support for Cardiogenic Shock Caused by Arrhythmia-induced Cardiomyopathy
1-6Department of ICU, Mediclinic Parkview Hospital, Dubai, United Arab Emirates
Corresponding Author: Sanjay K Nihalani, Department of ICU, Mediclinic Parkview Hospital, Dubai, United Arab Emirates, Phone: +971502834510, e-mail: sanjaynihalani76@gmail.com
Received on: 24 December 2022; Accepted on: 27 May 2023; Published on: 23 June 2023
ABSTRACT
Herein we report a rare case of venoarterial extracorporeal membrane oxygenation (VA ECMO) support in a patient with arrhythmia-induced cardiomyopathy and cardiogenic shock. The patient had a lactate of more than 20 at the time of initiation of ECMO. Arrhythmia-induced cardiomyopathy is a potentially reversible state in which atrial or ventricular tachycardia/arrhythmias results in a decrease in left ventricular (LV) function, causing systolic heart failure and in rare cases, cardiogenic shock.1 VA ECMO is now increasingly used for various forms of cardiogenic shock, including the above condition that is unresponsive to conventional therapy.
This is a case report of middle age man who presented with atrial fibrillation (AF) and rate related cardiomyopathy resulting in severe cardiogenic shock. He failed to respond to conventional management, including rate control medications, inotropic, and vasopressor agents. He had a cardiac arrest and was revived postcardiopulmonary resuscitation. Only with the early initiation of VA ECMO could the stabilization of hemodynamics be maintained. Further, ECMO support gave us the time for the reversible cardiomyopathy to resolve, and the patient survived who otherwise may not have in view of poor ejection fraction (EF) of 10%.
How to cite this article: Nihalani SK, Singhal AB, Capatos G, et al. A Rare Case Report: VA ECMO Support for Cardiogenic Shock Caused by Arrhythmia-induced Cardiomyopathy. Indian J Crit Care Case Rep 2023;2(3):82-84.
Source of support: Nil
Conflict of interest: None
Patient consent statement: The author(s) have obtained written informed consent from the patient for publication of the case report details and related images.
Keywords: Atrial fibrillation, Cardiomyopathy, Extracorporeal membrane oxygenation.
CASE DESCRIPTION
A 51-year-old male with no known comorbidities presented with a 3-week history of chest pain, shortness of breath. There was no fever or signs of upper respiratory tract infection. His past medical history included palpitations of longstanding duration for which he had not sought medical attention. Upon initial assessment, he was found to be tachycardic in atrial fibrillation (AF) up to a rate of 160/minute, hypotensive (80/40 mm Hg), and tachypnea (35 breaths/minute), and a lactate of 2.4 in arterial blood gas (ABG) with a pH of 7.47.
He was given adequate fluids and 150 mg of amiodarone following which his AF reverted to sinus rhythm and a transient improvement in blood pressure (BP) (110/65). Following admission to ICU, the patient developed signs of shock with hypotension, tachypnea, and evidence of systemic hypoperfusion with increasing lactate (9.2) and a metabolic acidosis for which he was started on norepinephrine and dobutamine infusion.
A bedside echocardiography performed showed global hypokinesia with ejection fraction (EF) of 10–15%, no regional wall motion abnormalities, left ventricular (LV) hypertrophy, and severe mitral regurgitation. At this point, he required significant support for hemodynamic stability, and the need for mechanical support in the form of extracorporeal membrane oxygenation (ECMO) was considered (Fig. 1).
Fig. 1: Echo view on day 1 showing global hypokinesia
Clinically the patient continued to deteriorate with hypotension and systemic hypo perfusion despite significant doses of noradrenaline and dobutamine. The patient was intubated in view of worsening clinical status following which the patient developed pulseless electrical activity followed by asystole. Cardiopulmonary resuscitation was initiated promptly as per ACLS protocol, and return of spontaneous circulation (ROSC) was achieved after 20 minutes. Post-ROSC BP was maintained on high doses of adrenaline, norepinephrine, dobutamine, and ventilatory support continued.
Post-return of spontaneous circulation (ROSC), he was moving spontaneously; pupils remained bilaterally equal and reactive. Patient was kept sedated.
As he remained unstable requiring high doses of inotropes, with a lactate of 21, venoarterial ECMO (VA ECMO) was initiated. A drainage cannula (23 Fr) in the right internal jugular vein and a return cannula (19 Fr) in the right femoral artery were inserted with an 8 Fr reperfusion cannula. Initial ECMO settings were flow—2 L/minute, revolutions per minute 2500, with which we were able to achieve a SvO2 > 75. An immediate improvement was seen clinically with stable BP and lactate levels decreasing satisfactorily, and was able to wean off adrenaline and decrease norepinephrine infusion (Table 1).
| ABG | pH | PCO2 | PO2 | HCO3 | Lactate |
|---|---|---|---|---|---|
| Before ECMO initiation | 7.25 | 19.8 | 273 | 12.5 | 21 |
| After ECMO 12 hours | 7.54 | 32.9 | 96.7 | 30 | 3.7 |
The patient required renal replacement therapy for 3 days and multiple cardioversions for refractory AF in addition to amiodarone infusion. On day 4, the patient was extubated and put on a high flow nasal cannula. He was started on levosimendan infusion as his EF remained low, and by day 5, his EF had increased to 30%, which allowed us to successfully decannulate on day 6 after a successful trial off from ECMO.
Patient was then shifted out of ICU to the ward on day 11 and was later discharged home on day 18 on carvedilol, amiodarone, and apixaban with no neurological deficit (Fig. 2).
Figs 2A and B: (A) Worsening of chest X-ray (CXR) day 2; (B) CXR before discharge of patient
DISCUSSION
This is the first reported case of VA ECMO support for Arrhythmia-induced cardiomyopathy in UAE. In the present case report, we treated a 51-year-old man suffering from cardiomyopathy due to rate related AF with EF of 10%, successfully with VA ECMO support. Arrhythmia induced cardiomyopathy (AIC) is a state in which atrial or ventricular tachyarrhythmias decrease the LV function, resulting to systolic heart failure (HF).1 The main aspect of this state is partial or complete reversibility once arrhythmia is controlled.
On review of the literature, we found that AF with uncontrolled ventricular rate can cause a decrease in LV function, heart failure, or ischemia of the heart (when primary computer-aided design is present).2,3 AF is the most common cause of AIC in adults.
The relation between arrhythmia and cardiomyopathy can be hard to determine because an arrhythmia could be present for years before it is recognized and before cardiomyopathy results. The presentation can be delayed only after obvious systolic HF occurs. AF is associated with palpitations (acute onset) or fatigue (chronic). Our patient had complained of chest discomfort and shortness of breath for 3 weeks which had increased over the past 3 days. These symptoms are explained by cardiomyopathy and heart failure due to rate related AF.
We further excluded the possibility of acute myocarditis as one of the differential diagnosis. There was no elevation in myocardial enzyme levels, and the patient did not have any precedent upper respiratory infection. His viral screen for myocarditis was negative. Therefore, acute myocarditis was unlikely.
Three attempts of restoring sinus rhythm with direct current cardioversion as an inpatient —all were successful, but the patient did not remain in sinus rhythm. Echocardiogram before discharge showed EF ~45% in sinus rhythm and ~40% when in atrial fibrillation. He was discharged on amiodarone, carvedilol for rate control, and apixaban for anticoagulation. The patient was seen 3 months after the admission with a normal EF in sinus rhythm and subsequently had an ablation procedure for AF a year later.
In a new retrospective study by Hékimian et al., it was found that between 2004 and 2018, 35 patients had received VA ECMO for severe, nonischemic cardiogenic shock and new onset supraventricular arrhythmia (77% AF). In 21 patients (60% of patients), cardiogenic shock was the initial disease presentation. In 12 of the 35 patients, amiodarone and/or electric cardioversion successfully decreased arrhythmia, increased LVEF, and allowed to wean off VA ECMO.4
As mentioned, the patient required dialysis due to acute kidney injury, and an ultrasound of his kidneys performed was normal. His creatinine returned to normal over the next few weeks.5
Extracorporeal cardiopulmonary resuscitation (ECPR) refers to VA ECMO during cardiac arrest, including ECMO and cardiopulmonary bypass. The use of ECPR may give physicians time to treat reversible primary causes of cardiac arrest (e.g., acute coronary syndrome, pulmonary embolism, refractory VF, cardiac injury, myocarditis, cardiomyopathy, congestive heart failure, drug toxicity, etc.) or may act as a bridging device for LV assist device insertion or heart transplantation. American Heart Association 2015 recommendation—in settings where it can be rapidly done, ECPR may be advised for select cardiac arrest patients for whom the suspected cause of the cardiac arrest is likely reversible during a limited time of mechanical cardiorespiratory assistance (Class IIb, level of evidence C-limited data).4 VA ECMO can also be used postcardiac arrest to treat postcardiac arrest syndrome which is a result of total body ischemia and reperfusion injury.
CONCLUSION
In our case, we treated our patient with AF rate related cardiogenic shock with VA ECMO support. ECMO support was used as a destination therapy in this case but may act as a bridge to a more permanent mechanical circulatory device or transplant in other cases. Cardiogenic shock as a result of the cardiomyopathy caused by arrhythmia recovered fully, which may not have been possible without the bridging afforded by ECMO. The patient was seen 3 months after the admission with a normal EF in sinus rhythm. VA ECMO in postcardiac arrest syndrome may also be lifesaving, as seen in this case.
ORCID
Sanjay K Nihalani https://orcid.org/0000-0003-0732-2064
Apoorva B Singhal https://orcid.org/0000-0001-8132-3415
Gerasmos Capatos https://orcid.org/0000-0003-4527-3179
Kalpana Krishnareddy https://orcid.org/0000-0003-2445-2629
Seemin Shiraz https://orcid.org/0000-0002-0994-2550
Anil Agarwal https://orcid.org/0000-0002-3696-1861
REFERENCES
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2. Maisel WH, Stevenson LW. Atrial fibrillation in heart failure: epidemiology, pathophysiology, and rationale for therapy. Am J Cardiol 2003;91(6A):2D–8D. DOI: 10.1016/s0002-9149(02)03373-8
3. Papadakis M. Atrial fibrillation. current medical diagnosis and treatment. 2018; 57th ed., pp. 394–395. Mc Graw Hill education, New York.
4. Hékimian G, Paulo N, Waintraub X, et al. Arrhythmia-induced cardiomyopathy: a potentially reversible cause of refractory cardiogenic shock requiring venoarterial extracorporeal membrane oxygenation. Heart Rhythm 2021;18(7):1106–1112. DOI: 10.1016/j.hrthm.2021.03.014
5. Link MS, Berkow LC, Kudenchuk PJ, et al. Part 7: adult advanced cardiovascular life support: 2015 American Heart Association Guidelines update for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation 2015;132(18 Suppl 2):S444–S464. DOI: 10.1161/CIR.0000000000000261
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