Optimal ECMO Flow in the Critical Phase of Cardiogenic Shock to Optimize Peripheral Organ Perfusion and Myocardial Stress

Overview

Veno-arterial ECMO (VA ECMO) is considered the ultimate lifesaving technique in refractory cardiogenic shock (CS). However, VA ECMO is associated with potentially serious adverse effects and complications. Many authors have demonstrated that VA ECMO increases left ventricular (LV) afterload, leading to increased LV stress, left ventricular end-diastolic pressure (LVEDP), and left atrial pressure (LAP). This pressure increase frequently results in pulmonary oedema and higher myocardial oxygen consumption. These complications are critical to patient survival and myocardial recovery and can lead to prolonged hospital stays and increased healthcare costs. In the absence of clinical studies and strong recommendations, the optimized management of VA ECMO in clinical practice involves finding an ECMO flow that balances adequate organ perfusion with preserved ventricular ejection, while minimizing LV stress. Since the optimal flow changes with myocardial recovery, ramp tests are regularly performed to adjust ECMO flow. To date, the optimized management of VA ECMO has been guided empirically. The aim of this study is to describe the consequences of variations in VA ECMO flow during the critical phase of cardiogenic shock on peripheral organ perfusion and LV stress. By analyzing the relationships between VA ECMO flow rate, peripheral perfusion, and myocardial stress, investigators aim to optimize flow settings-particularly by minimizing the potential complications of VA ECMO. During the daily ramp tests, investigators plan to collect hemodynamic data (cardiac output, SvO₂, pulse pressure, EtCO₂, vasopressor and inotrope dosing), echocardiographic measurements, and organ perfusion indicators (NIRSS, CO₂ gap, respiratory quotient, lactate levels). Data will be collected on Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).

Interventions

• Other Obversation
  Observing the optimal flow rate to reduce left ventricular stress and enhance peripheral organ perfusion during ramp tests (conducted at QECMO levels of 100%, 75%, 50%, and 25%, provided that SVO₂ remains \>55% and NIRS rSO₂ remains \>50%)

Primary outcome measures

• optimal flow [Time frame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).]

Secondary outcome measures (5)

• optimal flow according to echocardiography [Time frame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).]
• optimal flow according to the patient's native cardiac output [Time frame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).]
• optimal flow in subgroup 1 (low pulse pressure) [Time frame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).]
• optimal flow in subgroup 2 (normal pulse pressure) [Time frame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).]
• Correlation between flow and other perfusion indicators [Time frame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).]

Eligibility criteria

Inclusion criteria

• cardiogenic shock
• treated with VA ECMO for less than 48hours

Exclusion criteria

• ECMO initiated for refractory cardiac arrest
• Cardiac arres prior to the cardiogenic shock with Low-Flow > 30 min
• Noradrenaline dose > 1μg/kg/min, vasopressin dose > 2IU/h, dobutamine dose > 15μg/kg/min, adrenaline dose > 1μg/kg/min, or unstabilized vasopressors or inotropes
• Post-cardiotomy cardiogenic shock
• Septic shock
• Left ventricular unloading by Impella (CP/5) or atrioseptostomy
• Atrial septal defect
• Ventricular septal defect
• Pregnant or breast-feeding women
• Patients protected by law (under guardianship or curatorship),
• Patient participating in another research study with an exclusion period still in progress
• Opposition to participation after having been informed
• Patient not affiliated to any health care system
• Patient unable to express non-opposition without available trusted person

Criteria are shown verbatim from the registry (in English). Final eligibility is always assessed by the study center.

Healthy volunteers: No

Study design

Observational model

Cohort

Study locations

France · 1 center

• Montpellier University Hospital — Montpellier

Publications

• Ostadal P, Mlcek M, Kruger A, Hala P, Lacko S, Mates M, Vondrakova D, Svoboda T, Hrachovina M, Janotka M, Psotova H, Strunina S, Kittnar O, Neuzil P. Increasing venoarterial extracorporeal membrane oxygenation flow negatively affects left ventricular performance in a porcine model of cardiogenic shock. J Transl Med. 2015 Aug 15;13:266. doi: 10.1186/s12967-015-0634-6. PMID 26275717
• Burkhoff D, Sayer G, Doshi D, Uriel N. Hemodynamics of Mechanical Circulatory Support. J Am Coll Cardiol. 2015 Dec 15;66(23):2663-2674. doi: 10.1016/j.jacc.2015.10.017. PMID 26670067
• Fuhrman BP, Hernan LJ, Rotta AT, Heard CM, Rosenkranz ER. Pathophysiology of cardiac extracorporeal membrane oxygenation. Artif Organs. 1999 Nov;23(11):966-9. doi: 10.1046/j.1525-1594.1999.06484.x. PMID 10564298
• Burkhoff D, Sagawa K. Ventricular efficiency predicted by an analytical model. Am J Physiol. 1986 Jun;250(6 Pt 2):R1021-7. doi: 10.1152/ajpregu.1986.250.6.R1021. PMID 3717375
• Mallat J, Pepy F, Lemyze M, Gasan G, Vangrunderbeeck N, Tronchon L, Vallet B, Thevenin D. Central venous-to-arterial carbon dioxide partial pressure difference in early resuscitation from septic shock: a prospective observational study. Eur J Anaesthesiol. 2014 Jul;31(7):371-80. doi: 10.1097/EJA.0000000000000064. PMID 24625464
• Mesquida J, Saludes P, Gruartmoner G, Espinal C, Torrents E, Baigorri F, Artigas A. Central venous-to-arterial carbon dioxide difference combined with arterial-to-venous oxygen content difference is associated with lactate evolution in the hemodynamic resuscitation process in early septic shock. Crit Care. 2015 Mar 28;19(1):126. doi: 10.1186/s13054-015-0858-0. PMID 25888382
• Routsi C, Vincent JL, Bakker J, De Backer D, Lejeune P, d'Hollander A, Le Clerc JL, Kahn RJ. Relation between oxygen consumption and oxygen delivery in patients after cardiac surgery. Anesth Analg. 1993 Dec;77(6):1104-10. doi: 10.1213/00000539-199312000-00004. PMID 8250298
• Vallet B, Teboul JL, Cain S, Curtis S. Venoarterial CO(2) difference during regional ischemic or hypoxic hypoxia. J Appl Physiol (1985). 2000 Oct;89(4):1317-21. doi: 10.1152/jappl.2000.89.4.1317. PMID 11007564

Identifiers

NCT: NCT06936839 · RECHMPL24_0215

Primary sources (government registries)

• ClinicalTrials.gov (US NIH)

View this study on ClinicalTrials.gov ↗