Treating Incessant Tachyarrhythmia-Induced Cardiogenic Shock With Emergent Atrioventricular Node Ablation

Abstract

Background

Tachycardia-induced cardiogenic shock (TICS) is a life-threatening condition requiring prompt intervention.

Case Summary

An elderly patient with chronic atrial fibrillation and multiple comorbidities developed refractory cardiogenic shock secondary to rapid ventricular rate. Initial management with antiarrhythmics, electrical cardioversion, and vasopressors failed to restore hemodynamic stability. Emergent atrioventricular node ablation (AVNA) with temporary biventricular pacemaker implantation was performed, resulting in immediate heart rate control and subsequent hemodynamic stabilization and heart failure recovery.

Discussion

This case highlights a rare mechanism of cardiogenic shock predominantly driven by diastolic dysfunction secondary to rapid atrial fibrillation. It also demonstrates the potential of emergent AVNA to serve as a life-saving strategy in critically ill patients with refractory TICS.

Take-Home Message

Emergent AVNA can be a life-saving intervention for critically ill patients experiencing refractory TICS.

Graphical Abstract

History of Presentation

A 73-year-old man presented with shortness of breath, lethargy, and altered mental status. On arrival, he was found to be in atrial fibrillation with rapid ventricular response. Vital signs included pulse 130 beats/min, blood pressure 80/48 mm Hg, respiratory rate 26 breaths/min, oxygen saturation 84% on room air, lactic acid 2.4 mmol/L, and maximum temperature 100.8 °F. Complete blood count and renal function tests were unremarkable. Chest radiographs were concerning for pneumonia.

Take-Home Message

• •Emergent AVNA can be a life-saving intervention for critically ill patients experiencing refractory TICS.

Past Medical History

The patient had a past medical history of chronic atrial fibrillation (anticoagulated on apixaban), chronic heart failure with preserved ejection fraction, liver cirrhosis, primary hypertension, and hyperlipidemia.

Differential Diagnosis

Given preliminary laboratory and diagnostic findings, unstable atrial fibrillation with rapid ventricular response secondary to underlying sepsis was the primary concern. Pulmonary embolism, alcohol withdrawal, decompensated cirrhosis, and antihypertensive overdosing were considered in the differential diagnosis; however, these were ruled out on further history taking and physical examination.

Management

The patient was given boluses of intravenous amiodarone, metoprolol tartrate, normal saline, and broad-spectrum antibiotics. Owing to progressive hemodynamic instability and worsening ventricular rate, a decision was made to perform emergent cardioversion, but despite multiple attempts, his tachyarrhythmias persisted. He was transferred to the intensive care unit where norepinephrine was initiated, and he was ultimately sedated and intubated for airway protection and to inhibit autonomic propagation of arrhythmia. Transthoracic echocardiography revealed no major valvular or wall motion abnormalities. However, severe diastolic dysfunction was noted along with a dilated left atrium measuring 4.9 cm in diameter (left atrial volume index of 46 mL/m²). On day 3, the patient was receiving high doses of norepinephrine, epinephrine, and vasopressin, and his heart rate continued to climb as inotropes were uptitrated, resulting in a malignant cycle. Bedside transesophageal echocardiography was performed, which did not reveal any regional wall motion abnormalities or structural abnormalities (Video 1). However, it was clear that owing to severity of the tachycardia, diastolic filling times were inadequate, thus hindering end-organ perfusion.

Attempts to replace epinephrine with α-agonists such as phenylephrine were unsuccessful and resulted in worsening hemodynamic decline. Swan-Ganz catheterization revealed cardiac index of 1.7, pulmonary artery pressures of 45 mm Hg (systolic) and 23 mm Hg (diastolic), and pulmonary capillary wedge pressure of 25 mm Hg, with systemic vascular resistance of 1,190 dyn/s/cm⁻⁵. The patient’s clinical decline continued with worsening lactic acidosis and mixed septic and cardiogenic shock on multiple pressors, intubation/sedation, and continuous renal replacement therapy with refractory atrial fibrillation with rapid ventricular rates as high as 174 beats/min (Figure 1A). Electrophysiology services were promptly consulted, and a shared decision was made at bedside to proceed with a temporary biventricular pacemaker (Figures 1B and 2A) and emergent atrioventricular node ablation (AVNA) for immediate rate control in hopes of stabilizing this unstable patient with mixed shock.

Figure 1.

Electrocardiograms Pre- and Post-Emergent AV Node Ablation

Electrocardiogram revealing supraventricular tachycardia at a rate of 156 beats per minute (A) followed by successful rate control with biventricular pacing and emergent AV node ablation (B).

Figure 2.

Procedural Fluoroscopy

Fluoroscopy demonstrating temporary lead placement (A) prior to final positioning of permanent pacemaker pulse generator at time of discharge (B).

The pacemaker was programmed to VVIR. Using EnSite X EP System (Abbott Cardiovascular), the patient underwent successful three-dimensional mapping followed by radiofrequency ablation of the atrioventricular node. During the procedure, the patient experienced 2 episodes of ventricular tachycardia, both of which were promptly terminated with external cardioversion. In subsequent days his cardiac function and hemodynamics improved, his lactic acidosis resolved, and he was weaned off all vasopressors (Table 1). Repeat transthoracic echocardiography revealed normal ejection fraction with no regional wall motion abnormalities or valvopathies. He was provided with supportive care and underwent device exchange to a permanent pacemaker immediately before discharge (Figure 2B).

Table 1.

Hemodynamics Before and After Emergent Biventricular Pacemaker Implantation and AVNA (Day 3)

	Day 1	Day 2	Day 3a	Day 4	Day 5
CI, L/min/m2	—	2.2	1.7	3.8	3.2
CO, L/min	—	5.6	3.2	5.2	4.7
CVP, mm Hg	—	15-18	9-17	13-17	9-12
EF, %	40-45	—	25-29	—	55-60
HR, beats/min	114-130	127-144	156-187	90	90
Lactic acid, mmol/L	2.4	5.2	6.8	2.2	1.2
PA saturation, %	—	56	52	70	—
PAP, mm Hg	—	40/25	45/23	42/23	35/18
PCWP, mm Hg	—	19	25	23	17
SVR, dyn/s/cm−5	—	742	1,190	982	955
Vasopressors	—	Norepinephrine	Epinephrine Norepinephrine Vasopressin	Norepinephrine Vasopressin	—

AVNA = atrioventricular node ablation; CI = cardiac index; CO = cardiac output; CVP = central venous pressure; EF = ejection fraction; HR = heart rate; PA = pulmonary artery; PAP = pulmonary artery pressure; PCWP = pulmonary capillary wedge pressure; SVR = systemic vascular resistance.

^aDay of AVNA.

Outcome and Follow-Up

The patient was discharged home in stable medical condition. He is now 9 months status post pacemaker placement and has done very well thus far with no cardiopulmonary or neurologic limitations to date.

Discussion

Tachycardia-induced cardiogenic shock (TICS) is a condition characterized by heart failure with end-organ hypoperfusion due to a persistent rapid heart rate. The most common causative tachyarrhythmias are supraventricular such as atrial fibrillation, atrial flutter, and atrial tachycardia.¹ Health care providers continually endeavor to recognize and address the underlying reversible factors contributing to cardiogenic shock. However, the clinical reality is that precisely identifying the specific etiology can prove challenging, particularly in underserved or smaller institutions and in time-sensitive situations where timely action is necessary. Although the recognition of shock may occur rapidly, determining the root cause frequently requires a more prolonged and comprehensive evaluation, often spanning hours or even days. In these life-threatening scenarios, clinicians may be compelled to pursue definitive, though potentially aggressive, interventions. Notably, the existing literature lacks robust data on the efficacy of the pace-and-ablate strategy for managing hemodynamically unstable patients.²

The literature contains limited reports highlighting the life-saving potential of emergent AVNA in patients with refractory supraventricular tachyarrhythmia–induced cardiogenic shock.^3,4 Treatment for this condition typically involves a stepwise approach, starting with pharmacologic suppression of the ventricular rate using antiarrhythmic drugs or atrioventricular node–blocking agents, followed by rhythm control and electrical cardioversion. Ultimately, AVNA with pacemaker implantation may be necessary as a last resort. In our patient, the chronic nature of the atrial fibrillation likely contributed to the persistent failure of pharmacologic and electrical interventions to restore normal sinus rhythm. Furthermore, as the patient's vasopressor requirements increased, the worsening tachyarrhythmia exacerbated the shock state. Therefore, we determined that permanent AVNA was the most appropriate step to achieve rate control for this critically ill patient.

A factor that also complicated our work-up and assessments was the patient's history of hepatic cirrhosis. This comorbidity frequently contributes to vasodilatory or distributive shock by reducing systemic vascular resistance, a factor that should be considered when interpreting the hemodynamic profile for these patients, potentially leading to a compensatory mechanism of increased cardiac output via an elevated heart rate. This phenomenon is well established and multifactorial, involving increased splanchnic and peripheral blood flow, a hyperdynamic circulatory state, and augmented production of vasodilatory mediators.⁵ Consequently, in cirrhotic patients with cardiogenic shock, systemic vascular resistance may paradoxically be within normal ranges. Clinicians should therefore integrate systemic vascular resistance values within the broader clinical context and other indices of tissue perfusion.

In cases of TICS, the use of mechanical circulatory support to provide additional hemodynamic assistance can be a tempting option.⁴ However, several things need to be considered—the first is that in the setting of mixed shock, it is challenging to fully ascertain the extent of pump failure. It is well established that faster heart rates can lead to lower ejection fractions. Second, the use of mechanical circulatory support would have delayed care in a patient who urgently needed definitive rate control. It was crucial to identify the primary driver of the progressive hemodynamic decline for our patient to simply be the lack of adequate diastolic filling time. Despite this, an Impella CP (Abiomed) was initially considered for left ventricular support. Nevertheless, we ultimately decided to first address what we believed was the main underlying cause based on the hemodynamic findings. Finally, it is important to emphasize that in the absence of mechanical circulatory support, pulmonary vein isolation is not a feasible option in unstable patients in need of definitive and timely intervention, especially patients with chronic or permanent atrial fibrillation.

Conclusions

Larger-scale studies on various preventive and resuscitative strategies are ongoing and necessary to help clinicians better understand the efficacy, feasibility, and realistic expectations in managing patients with TICS.

Funding Support and Author Disclosures

This research was supported (in whole or in part) by HCA Healthcare and/or an HCA Healthcare affiliated entity. The views expressed in this publication represent those of the authors and do not necessarily represent the official views of HCA Healthcare or any of its affiliated entities. The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Appendix

Video 1

Severely Impaired Diastolic Function on Transesophageal Echocardiography