Clinical trial NCT06936839: Optimal ECMO Flow in the Critical Phase of Cardiogenic Shock to Optimize Peripheral Organ Perfusion and Myocardial Stress
Official title: Optimal ECMO Flow in the Critical Phase of Cardiogenic Shock to Optimize Peripheral Organ Perfusion and Myocardial Stress
Study type: OBSERVATIONAL
Overall status: NOT_YET_RECRUITING
Conditions: Cardiogenic Shock
Keywords: ECMO
optimal flow
cardiogenic shock
echocardiography
organ perfusion
myocardial recovery
human
adult
left ventricular overload
Lead sponsor: University Hospital, Montpellier
Sponsor class: OTHER
First posted: 2025-04-20
Enrollment: 55
Sex: ALL
Minimum age (years): 18
Standard ages: ADULT
OLDER_ADULT
Accepts healthy volunteers: no
Observational model: COHORT
Time perspective: PROSPECTIVE
Sampling method: NON_PROBABILITY_SAMPLE
Study population: Adult patients with cardiogenic shock treated with VA ECMO for less than 48 hours without any of the exclusion criteria.

Brief summary: 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).


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

Primary outcomes:
measure: optimal flow
timeFrame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).
Secondary outcomes:
measure: optimal flow according to echocardiography
timeFrame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).
measure: optimal flow according to the patient's native cardiac output
timeFrame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).
measure: optimal flow in subgroup 1 (low pulse pressure)
timeFrame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).
measure: optimal flow in subgroup 2 (normal pulse pressure)
timeFrame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).
measure: Correlation between flow and other perfusion indicators
timeFrame: Day 1 (ECMO initiation), Day 2 (24 hours after ECMO initiation), and Day 3 (48 hours after ECMO initiation).
Other outcomes:
Locations:
city: Montpellier
country: France
facility: Montpellier University Hospital
state: Occitanie
Study officials:
affiliation: Montpellier University Hospital
name: Aurore Ughetto, MD
role: PRINCIPAL_INVESTIGATOR
References:
citation: 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.
citation: 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.
citation: 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.
citation: 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.
citation: 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.
citation: 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.
citation: 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.
citation: 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.
citation: Bakker J, Vincent JL, Gris P, Leon M, Coffernils M, Kahn RJ. Veno-arterial carbon dioxide gradient in human septic shock. Chest. 1992 Feb;101(2):509-15. doi: 10.1378/chest.101.2.509.
citation: Mecher CE, Rackow EC, Astiz ME, Weil MH. Venous hypercarbia associated with severe sepsis and systemic hypoperfusion. Crit Care Med. 1990 Jun;18(6):585-9. doi: 10.1097/00003246-199006000-00001.
citation: Groeneveld AB. Interpreting the venous-arterial PCO2 difference. Crit Care Med. 1998 Jun;26(6):979-80. doi: 10.1097/00003246-199806000-00002. No abstract available.
citation: Faden H. Prophylactic antibiotics in pediatrics cardiovascular surgery: current practices. Ann Thorac Surg. 1981 Mar;31(3):211-3. doi: 10.1016/s0003-4975(10)60928-9.
citation: Moller JE, Sionis A, Aissaoui N, Ariza A, Belohlavek J, De Backer D, Farber G, Gollmann-Tepekoylu C, Mebazaa A, Price S, Swol J, Thiele H, Hassager C. Step by step daily management of short-term mechanical circulatory support for cardiogenic shock in adults in the intensive cardiac care unit: a clinical consensus statement of the Association for Acute CardioVascular Care of the European Society of Cardiology SC, the European Society of Intensive Care Medicine, the European branch of the Extracorporeal Life Support Organization, and the European Association for Cardio-Thoracic Surgery. Eur Heart J Acute Cardiovasc Care. 2023 Jul 7;12(7):475-485. doi: 10.1093/ehjacc/zuad064.
citation: Chiolero RL, Revelly JP, Leverve X, Gersbach P, Cayeux MC, Berger MM, Tappy L. Effects of cardiogenic shock on lactate and glucose metabolism after heart surgery. Crit Care Med. 2000 Dec;28(12):3784-91. doi: 10.1097/00003246-200012000-00002.
citation: Khosravani H, Shahpori R, Stelfox HT, Kirkpatrick AW, Laupland KB. Occurrence and adverse effect on outcome of hyperlactatemia in the critically ill. Crit Care. 2009;13(3):R90. doi: 10.1186/cc7918. Epub 2009 Jun 12.
citation: Valenza F, Aletti G, Fossali T, Chevallard G, Sacconi F, Irace M, Gattinoni L. Lactate as a marker of energy failure in critically ill patients: hypothesis. Crit Care. 2005;9(6):588-93. doi: 10.1186/cc3818. Epub 2005 Sep 28.
citation: Laine GA, Hu BY, Wang S, Thomas Solis R, Reul GJ Jr. Isolated high lactate or low central venous oxygen saturation after cardiac surgery and association with outcome. J Cardiothorac Vasc Anesth. 2013 Dec;27(6):1271-6. doi: 10.1053/j.jvca.2013.02.031. Epub 2013 Sep 5.
citation: Abrams D, Combes A, Brodie D. What's new in extracorporeal membrane oxygenation for cardiac failure and cardiac arrest in adults? Intensive Care Med. 2014 Apr;40(4):609-12. doi: 10.1007/s00134-014-3212-0. Epub 2014 Jan 29. No abstract available.