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May 20, 2026American Journal of Respiratory and Critical Care Medicine0 citations

D104-04 Misinterpreted Tachypnea Due to Auto-Triggering From Cardiogenic Oscillation During Veno-Venous Extracorporeal Membrane Oxygenation Under Deep Sedation

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LJL Cheng JungLKL -T KengHLH Lin

Key Points

  • This research investigates the phenomenon of auto-triggering due to cardiogenic oscillation in VV-ECMO patients receiving sedation.
  • Patient diagnosed with respiratory failure initiated on VV-ECMO under sedation with fentanyl and midazolam.
  • Ventilator settings adjusted from flow-triggered to pressure-triggered to address the persistent tachypnea.
  • Assessment of cardiogenic oscillations was performed using flow-time and pressure-time curves.
  • Auto-triggering due to cardiogenic oscillation was identified, with an RR of 30 breaths/min on the ventilator observed.
  • Adjusting the ventilator settings successfully resolved auto-triggering, leading to improved patient-ventilator synchrony.
  • Recognition of auto-triggering can help prevent excessive sedation and reduce risks like pulmonary injury.

Abstract

Abstract Introduction Sedation is routinely administered to veno-venous extracorporeal membrane oxygenation (VV-ECMO) patients. However, auto-triggering caused by cardiogenic oscillation (CO) is not easily recognized in clinical practice. This phenomenon could lead medical staff to mistakenly interpret the patient as experiencing severe dyspnea or insufficient sedation. Case Presentation A 57-year-old male with a medical history of chronic obstructive pulmonary disease, hyperlipidemia, non-obstructive coronary artery disease, and congestive heart failure presented with intermittent dyspnea and developed respiratory failure requiring intubation. After prone positioning, he had persistent poor oxygenation, so VV-ECMO was initiated. Continuous sedation with Fentanyl, Midazolam, and Cisatracurium was administered. However, persistent tachypnea was observed, with a respiratory rate (RR) of 30 breaths/min on the ventilator. The ventilator mode was flow-triggered pressure control-assist control with an inspiratory pressure of 12 cmH2O, a positive end-expiratory pressure (PEEP) of 10 cmH2O, a fraction of inspired oxygen of 40%, an RR of 12 breaths/min, and a flow-trigger sensitivity of 2 L/min. Scaling up the flow-time and pressure-time curves revealed CO that led to auto-triggering (Fig.1). To resolve this phenomenon, the patient’s ventilator was adjusted from a flow trigger to a pressure trigger with a gradual titration to an adequate trigger level, which successfully resolved the auto-triggering. Discussion CO generated by the heartbeat transmitted to the lungs is mainly related to the transmission of pulmonary pulsatility. Patient-ventilator asynchrony can be associated with a longer duration of mechanical ventilation and an extended ICU stay. Patients with auto-triggering tend to have physiological characteristics, including larger cardiogenic oscillations, higher cardiac output, elevated ventricular filling pressures, and an enlarged heart size. Early recognition of these features in sedated patients and adjustments to ventilator settings or sedation doses can help improve patient-ventilator synchrony. A past study showed that for every 1 cmH2O increase in cardiogenic oscillation, the ventilator's flow trigger needs to be raised by approximately +2.5 L/min to prevent auto-triggering. Accurate identification of auto-triggering can prevent patients from receiving excessive sedatives, avoid hyperventilation, and reduce the risk of additional pulmonary injury, preventing secondary barotrauma and atelectrauma. This abstract is funded by: None

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Cite This Study

Jung et al. (2026) studied this question.

synapsesocial.com/papers/6a0d4f62f03e14405aa9ab99https://doi.org/10.1093/ajrccm/aamag162.4757
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