Effect of Adding Vasopressin on Cardiac Output, Blood Pressure, Diuresis, and Tissue Perfusion Indices in Patients With Septic Shock
For patients and families
In plain language
An automatic summary of structured registry data. It is an orientation aid, not a substitute for the official protocol or a physician assessment.
- What is being studied
- This is an observational study: the protocol does not assign a study treatment.
- Who it may be relevant to
- Registry conditions: Septic Shock and Use of Vasopressin. Basic parameters: from 18 years · All.
- What needs checking
- Age, condition and sex are only basic indicators. Prior treatment, laboratory values and other mandatory requirements appear in the eligibility criteria below.
- Where it takes place
- France
- Next step
- Save the trial, show it to the treating physician, and confirm current recruitment with the study center. Costs, documents and travel →
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Overview
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.
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.
Primary outcome measures
- 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 [Time frame: T0 = inclusion. T20 = 20 minutes after the introduction of the vasopressin]
Secondary outcome measures (10)
- To describe the evolution of cardiac index between inclusion (T0), T1h, T3h, and T24h after vasopressin initiation [Time frame: 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 [Time frame: 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. [Time frame: 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 [Time frame: 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. [Time frame: 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 [Time frame: 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 [Time frame: 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 [Time frame: 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 [Time frame: 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. [Time frame: 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]
Eligibility criteria
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.
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 · 8 centers
- CHU d'Angers — Angers
- CH de Dieppe — Dieppe
- Hôpital Bicêtre — Le Kremlin-Bicêtre
- GHE, Hôpital Louis Pradel, HCL — Lyon
- GHS - Hôpital Lyon Sud, HCL — Lyon
- Hôpital Nord, AP-HM — Marseille
- CHU Rennes - Site Pontchaillou — Rennes
- Hôpital Hautepierre, Hôpitaux Universitaires de Strasbourg — Strasbourg
Identifiers
NCT: NCT07697144 · APHP260204 · 2026-A00568-43