Effect of Adding Vasopressin on Cardiac Output, Blood Pressure, Diuresis, and Tissue Perfusion Indices in Patients With Septic Shock (VASO-PHENO)

In patients with septic shock, vasopressin is increasingly used in combination with norepinephrine, but its timing of initiation remains heterogeneous and its clinical hemodynamic effects are still insufficiently characterized. Available data suggest variable responses, which may depend on the hemodynamic phenotype at the time of treatment initiation. In particular, the effects of vasopressin may differ according to the presence of preload dependency, baseline cardiac output, impaired systolic function, or baseline diastolic arterial pressure, reflecting the degree of vasoplegia. In this context, the VASO-PHENO study aims to provide a detailed and dynamic description of the early hemodynamic and clinical effects of vasopressin initiation in septic shock.

To date, no clinical study has systematically and dynamically evaluated the effects of vasopressin on central and peripheral hemodynamic parameters according to the hemodynamic profile at the time of its initiation. Describing these effects appears essential to better understand the variability in clinical responses and to contribute to a more rational and personalized approach to vasopressor escalation in septic shock.

Study Overview

• Status: Not yet recruiting
• Conditions: Septic Shock and Use of Vasopressin

Detailed Description

In patients with septic shock, hemodynamic profiles are highly heterogeneous. From a pathophysiological perspective, three main hemodynamic phenotypic components may contribute to the septic shock state:

• preload dependency;
• impaired myocardial function, leading to a cardiac output that is inadequate to meet oxygen demand;
• vasoplegia.

In some of these contexts, the introduction of vasopressin, as a pure vasoconstrictor, may be inappropriate or even harmful, by impairing cardiac output or exposing the patient to excessive vasoconstriction and a subsequent risk of ischemia.

Thus:

• In the presence of impaired myocardial function, defined by reduced cardiac output and/or impaired left ventricular ejection fraction, vasopressin initiation may lead to a decrease in cardiac output;
• In the presence of vasoplegia, the effects of vasopressin on mean arterial pressure and microcirculatory indices, such as capillary refill time, mottling, and urine output, may vary according to the severity of the initial vasoplegia, notably reflected by diastolic arterial pressure;
• In the presence of persistent preload dependency, the initiation of a pure vasoconstrictor may either increase cardiac output by increasing venous return, or worsen microcirculatory alterations by enhancing vasoconstriction in a context of hypovolemia.

To date, no study has precisely described the effects of vasopressin on macrocirculatory hemodynamic parameters, including arterial pressure, cardiac output, and central venous pressure, and on routinely assessable microcirculatory parameters, including capillary refill time, mottling, and urine output, according to the different hemodynamic phenotypic components present at the time of vasopressin initiation.

Describing the evolution of these parameters appears essential to better understand the variability in clinical responses and associated outcomes. Such an approach could help identify at-risk profiles and provide objective elements to support a more rational and personalized escalation of vasopressor therapy in septic shock.

• Study Type: Observational
• Enrollment (Estimated): 200

Contacts and Locations

• Study Contact: Name: Xavier MONNET, MD PhD; Phone Number: +33(0)145213539; Email: xavier.monnet@aphp.fr
• Study Contact Backup: Name: Nicolas FAGE, MD PhD; Email: fage.nicolas@gmail.com

Study Locations

• France
  • Angers, France
    • CHU d'Angers
    • Contact: Pierre ASFAR; Email: PiAsfar@chu-angers.fr
  • Dieppe, France
    • CH de Dieppe
    • Contact: Marion BEUZELIN; Email: MBeuzelin@ch-dieppe.fr
  • Le Kremlin-Bicêtre, France
    • Hôpital Bicêtre
    • Contact: Xavier MONNET; Email: xavier.monnet@aphp.fr
  • Lyon, France
    • GHE, Hôpital Louis Pradel, HCL
    • Contact: Matthias JACQUET-LAGREZE; Email: matthias.jacquet-lagreze@chu-lyon.fr
  • Lyon, France
    • GHS - Hôpital Lyon Sud, HCL
    • Contact: Jean-Luc FELLAHI; Email: jean-luc.fellahi@chu-lyon.fr
  • Marseille, France
    • Hôpital Nord, AP-HM
    • Contact: Marc LEONE; Email: Marc.LEONE@ap-hm.fr
  • Rennes, France
    • CHU Rennes - Site Pontchaillou
    • Contact: Mathieu LESOUHAITIER; Email: Mathieu.LESOUHAITIER@chu-rennes.fr
  • Strasbourg, France
    • Hôpital Hautepierre, Hôpitaux Universitaires de Strasbourg
    • Contact: Julien DEMISELLE DEMISELLE; Email: julien.demiselle@chru-strasbourg.fr

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: Adult; Older Adult
• Accepts Healthy Volunteers: No

• Sampling Method: Non-Probability Sample

Study Population

Adult patients hospitalized in the intensive care unit for septic shock and with use of vasopressin

Description

Inclusion Criteria:

• Age ≥ 18 years;
• Hospitalized in an intensive care unit;
• Presenting with septic shock according to Sepsis-3 criteria;
• For whom the treating clinician wishes to initiate vasopressin as second-line therapy as part of routine care;
• Undergoing hemodynamic monitoring with a PiCCO2 device (Pulsion Medical Systems, Getinge, Feldkirchen, Germany) or pulmonary artery catheterization as part of routine care.

Exclusion Criteria:

• Patient already receiving vasopressin;
• Pregnancy;
• Patient under legal protection;
• Patient unwilling to participate in the study.

Study Plan

How is the study designed?

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Measure Description	Time Frame
To describe and compare the evolution of cardiac index between inclusion and 20 minutes after vasopressin initiation in patients with septic shock, according to hemodynamic profiles identified a posteriori from variables collected at the time of vasopre	Hemodynamic profiles will not be defined a priori. They will be identified a posteriori using a supervised clustering analysis based on variables measured at inclusion and selected for their pathophysiological relevance: presence of preload dependency at the time of vasopressin initiation (yes/no);; cardiac index at inclusion;; diastolic arterial pressure at inclusion;; left ventricular ejection fraction (LVEF).	T0 = inclusion. T20 = 20 minutes after the introduction of the vasopressin

Secondary Outcome Measures

Outcome Measure	Measure Description	Time Frame
To describe the evolution of cardiac index between inclusion (T0), T1h, T3h, and T24h after vasopressin initiation	Secondary objectives will be analyzed in the overall population and, for descriptive purposes, according to the hemodynamic profiles identified by clustering analysis and according to age at inclusion. Hemodynamic profiles will not be defined a priori. They will be identified a posteriori using a supervised clustering analysis based on variables measured at inclusion and selected for their pathophysiological relevance: presence of preload dependency at the time of vasopressin initiation (yes/no);; cardiac index at inclusion;; diastolic arterial pressure at inclusion;; left ventricular ejection fraction (LVEF).	T0 = inclusion, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
Change in mean arterial pressure after vasopressin initiation	Mean arterial pressure will be measured at inclusion before vasopressin initiation and at predefined time points after vasopressin initiation. The evolution of mean arterial pressure will be described in the overall population.	T0 = inclusion, T20 = 20 minutes after the introduciton of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
In patients monitored with a Swan-Ganz® pulmonary artery catheter: to describe the evolution of pulmonary artery occlusion pressure between inclusion (T0), T20, T1h, T3h, and T24h after vasopressin initiation3.	PAPO will be assessed with a standard occlusion of the ballon in the pulmonary arteries with the use of the Swan Ganz. Secondary objectives will be analyzed in the overall population and, for descriptive purposes, according to the hemodynamic profiles identified by clustering analysis and according to age at inclusion. Hemodynamic profiles will not be defined a priori. They will be identified a posteriori using a supervised clustering analysis based on variables measured at inclusion and selected for their pathophysiological relevance: presence of preload dependency at the time of vasopressin initiation (yes/no);; cardiac index at inclusion;; diastolic arterial pressure at inclusion;; left ventricular ejection fraction (LVEF).	T0 = inclusion, T20 = 20 minutes after the introduciton of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
In patients monitored with a transpulmonary thermodilution device combined with pulse contour analysis (PiCCO®): to describe the evolution of indexed extravascular lung water between inclusion (T0), T20, T1h, T3h, and T24h after vasopressin initiation	The indexed extravascular lung water will be assessed with a standard thermodilution in patients with PICCO. Hemodynamic profiles will not be defined a priori. They will be identified a posteriori using a supervised clustering analysis based on variables measured at inclusion and selected for their pathophysiological relevance: presence of preload dependency at the time of vasopressin initiation (yes/no);; cardiac index at inclusion;; diastolic arterial pressure at inclusion;; left ventricular ejection fraction (LVEF).	T0 = inclusion, T20 = 20 minutes after the introduciton of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
To describe the evolution of mean arterial pressure between inclusion (T0), T20, T1h, T3h, and T24h after vasopressin initiation, according to diastolic arterial pressure at inclusion.	Secondary objectives will be analyzed in the overall population and, for descriptive purposes, according to the hemodynamic profiles identified by clustering analysis and according to age at inclusion. Hemodynamic profiles will not be defined a priori. They will be identified a posteriori using a supervised clustering analysis based on variables measured at inclusion and selected for their pathophysiological relevance: presence of preload dependency at the time of vasopressin initiation (yes/no);; cardiac index at inclusion;; diastolic arterial pressure at inclusion;; left ventricular ejection fraction (LVEF).	T0 = inclusion, T20 = 20 minutes after the introduciton of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
Change in urine output during the first 24 hours after vasopressin initiation	Urine output will be collected every 2 hours during the first 24 hours after vasopressin initiation. The evolution of urine output will be described in the overall population.	Urine output will be assessed every 2 hours from the introduction of vasopressine (T0) to 24 hours after the introduction of the vasopressine (T24)
Change in capillary refill time after vasopressin initiation	Capillary refill time will be assessed at baseline and at predefined time points after vasopressin initiation using a standardized method. The evolution of capillary refill time will be described in the overall population.	T0 = inclusion, T20 = 20 minutes after the introduciton of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
To describe the evolution of the mottling between the introduction of vasopressin (T0), T20, T1h, T3h, and T24h after vasopressin initiation, according to the evolution of the mean arterial pressure, diastolic arterial pressure, and of the cardiac output	Mottling will be assessed in a standardized way, by the mottling score. The mottling score describe the intensy of the mottling, from 0 (no mottling) to 5 (mottling up to the abdominal skin)	T0 = inclusion, T20 = 20 minutes after the introduciton of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
To describe the evolution of arterial lactate between the introduction of vasopressin (T0), T20, T1h, T3h and T24h after vasopressin initiation, according to the evolution of the mean arterial pressure, diastolic arterial pressure and cardiac output	Arterial lactate will be assessed by a arterial blood gaz sample, if available at this different time point.	T0 = inclusion, T20 = 20 minutes after the introduction of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin
To describe the evolution of the cardiac output between the introduction of vasopressin (T0), T20, T1H, T3h and T24h after vasopressin initiation, according to the initial left ventricular ejection fraction.	Cardiac output will be assessed with PICCO2 device or pulmonary artery catheterization. Left ventricular ejection fraction will be asssessed before adminstration of the vasopressin.	T0 = inclusion, T20 = 20 minutes after the introduction of the vasopressin, T1h = 1 hour after the introduction of the vasopressin, T3h = 3 hours after the introduction of the vasopressin. T24h = 24 hours after the introduction of the vasopressin

Collaborators and Investigators

• Sponsor: Assistance Publique - Hôpitaux de Paris

Study record dates

Study Major Dates

• Study Start (Estimated): August 1, 2026
• Primary Completion (Estimated): September 1, 2029
• Study Completion (Estimated): September 1, 2029

Study Registration Dates

• First Submitted: June 22, 2026
• First Submitted That Met QC Criteria: July 6, 2026
• First Posted (Actual): July 13, 2026

Study Record Updates

• Last Update Posted (Actual): July 13, 2026
• Last Update Submitted That Met QC Criteria: July 6, 2026
• Last Verified: June 1, 2026

More Information

Terms related to this study

• Keywords: Hemodynamic; Septic shock; Cardiac output; Vasopressin
• Additional Relevant MeSH Terms: Urogenital Diseases; Endocrine System Diseases; Pathologic Processes; Male Urogenital Diseases; Kidney Diseases; Urologic Diseases; Female Urogenital Diseases; Female Urogenital Diseases and Pregnancy Complications; Infections; Sepsis; Systemic Inflammatory Response Syndrome; Inflammation; Pituitary Diseases; Shock; Pathological Conditions, Signs and Symptoms; Shock, Septic; Diabetes Insipidus
• Other Study ID Numbers: APHP260204; 2026-A00568-43 (Other Identifier: IDRCB)

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No