Septic Shock and Use of VasopressinVASO-PHENONCT07697144
Effect of Adding Vasopressin on Cardiac Output, Blood Pressure, Diuresis, and Tissue Perfusion Indices in Patients With Septic Shock
An observational study of Septic Shock and Use of Vasopressin, run by Assistance Publique - Hôpitaux de Paris at 8 sites in France.
Trial summary
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. Read more about this study
- Who is it for?
- Ages 18 years and older
- Conditions the study is for
- Septic Shock and Use of Vasopressin
- How many people
- 200 participants
- Where
- 8 sitesFrance
- Study dates
- 1 Aug 2026to 1 Sep 2029
- Phase
- Observational
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 years and older
- All sexes
- No healthy volunteers
- Adult, Older adult
Study population: Adult patients hospitalized in the intensive care unit for septic shock and with use of vasopressin
Who may be able to join
- 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.
Who cannot join
- Patient already receiving vasopressin;
- Pregnancy;
- Patient under legal protection;
- Patient unwilling to participate in the study.
Trial locations and contacts
8 sites in 1 country. Contact the study team or a site near you to ask about taking part.
Nicolas FAGE, MD PhD contact
8 sites in 1 country
France8 sites
CHU d'Angers
Angers
Pierre ASFAR, PiAsfar@chu-angers.fr
CH de Dieppe
Dieppe
Marion BEUZELIN, MBeuzelin@ch-dieppe.fr
Hôpital Bicêtre
Le Kremlin-Bicêtre
Xavier MONNET, xavier.monnet@aphp.fr
GHE, Hôpital Louis Pradel, HCL
Lyon
Matthias JACQUET-LAGREZE, matthias.jacquet-lagreze@chu-lyon.fr
GHS - Hôpital Lyon Sud, HCL
Lyon
Jean-Luc FELLAHI, jean-luc.fellahi@chu-lyon.fr
Hôpital Nord, AP-HM
Marseille
Marc LEONE, Marc.LEONE@ap-hm.fr
CHU Rennes - Site Pontchaillou
Rennes
Mathieu LESOUHAITIER, Mathieu.LESOUHAITIER@chu-rennes.fr
Hôpital Hautepierre, Hôpitaux Universitaires de Strasbourg
Strasbourg
Julien DEMISELLE DEMISELLE, julien.demiselle@chru-strasbourg.fr
About this study
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.
Read the 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.
- Conditions
- Septic Shock and Use of Vasopressin
- Keywords
- Septic shock, Vasopressin, Cardiac output, Hemodynamic
- Medical subject headings
- Shock, Septic, Diabetes Insipidus
What is being measured
The primary outcome is the main question the study is designed to answer.
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).
Measured: T0 = inclusion. T20 = 20 minutes after the introduction of the vasopressin
Secondary outcomes (10)
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).
Measured: 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.
Measured: 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).
Measured: 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).
Measured: 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).
Measured: 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.
Measured: 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.
Measured: 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)
Measured: 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.
Measured: 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.
Measured: 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
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted13 Jul 2026
- Study start1 Aug 2026 (estimated)
- Primary completion1 Sep 2029 (estimated)
- Study completion1 Sep 2029 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Septic Shock and Use of VasopressinStudies of the same condition, open and under way.
- More trials run by Assistance Publique - Hôpitaux de ParisThe sponsor's other registered studies.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Observational
- Observational model
- Cohort
- Time perspective
- Prospective
- Enrolment
- 200 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Assistance Publique - Hôpitaux de Paris
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT07697144
- Sponsor's protocol ID
- APHP260204
- Other IDs
- 2026-A00568-43
- Acronym
- VASO-PHENO
- Status last verified
- Jun 2026
- First submitted
- 22 Jun 2026
- Last updated
- 13 Jul 2026
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
Study at a glance
From the registry record, last updated by the sponsor on 13 Jul 2026. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Effect of Adding Vasopressin on Cardiac Output, Blood Pressure, Diuresis, and Tissue Perfusion Indices in Patients With Septic Shock
- ClinicalTrials.gov ID
- NCT07697144
- Acronym / sponsor ID
- VASO-PHENO / APHP260204
- Conditions
- Septic Shock and Use of Vasopressin
- Keywords
- Septic shock, Vasopressin, Cardiac output, Hemodynamic
- Study type
- Observational
- Recruitment status
- Not yet recruiting
- Enrolment
- 200 participants (estimated)
- Lead sponsor
- Assistance Publique - Hôpitaux de ParisUniversity, hospital or other
- Study start
- 1 Aug 2026 (estimated)
- Primary completion
- 1 Sep 2029 (estimated)
- Study completion
- 1 Sep 2029 (estimated)
- First posted
- 13 Jul 2026 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
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.
Study design
- Observational model
- Cohort
- Time perspective
- Prospective
Who may qualify
- Ages
- 18 years and older
- Sex
- All
- Healthy volunteers
- Not accepted
- Age groups
- Adult, Older adult
- Study population
- Adult patients hospitalized in the intensive care unit for septic shock and with use of vasopressin
Key inclusion criteria (5 listed)
- 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.
Key exclusion criteria (4 listed)
- Patient already receiving vasopressin;
- Pregnancy;
- Patient under legal protection;
- Patient unwilling to participate in the study.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Primary outcome
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
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).
10 secondary outcomes
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
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 13 Jul 2026.
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
Nicolas FAGE, MD PhD contact
8 sites in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
An observational study of Septic Shock and Use of Vasopressin, run by Assistance Publique - Hôpitaux de Paris at 8 sites in France.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 5 inclusion and 4 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: opening soon, as of the sponsor's last update on 13 Jul 2026. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 8 sites in France. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Xavier MONNET, MD PhD (+33(0)145213539, xavier.monnet@aphp.fr), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
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). It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 13 Jul 2026.