Skip to main content
OpenTrials
Not Yet Recruiting

NCT Number: NCT07697144

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

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.

Not Yet Recruiting

Trial opening soon.

Get Notified

Key information

Conditions

Septic Shock and Use of Vasopressin Diabetes Insipidus Endocrine System Diseases Female Urogenital Diseases Female Urogenital Diseases and Pregnancy Complications Infections Inflammation Kidney Diseases Male Urogenital Diseases Pathologic Processes Pathological Conditions, Signs and Symptoms Pituitary Diseases Sepsis Shock Shock, Septic Systemic Inflammatory Response Syndrome Urogenital Diseases Urologic Diseases

Age range

18 year and older

Sex eligibility

All sexes

Study type

Observational

Primary location

CHU d'Angers, Angers, France

Loading trial locations.

About this study

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.

Who can participate

Healthy volunteers accepted: No

Only the study team can determine whether someone qualifies for participation.

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.

Treatment and study plan

Primary outcomes

  1. 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).

Secondary outcomes

  1. 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

    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).

  2. 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

    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.

  3. 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

    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).

  4. 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

    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).

  5. 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

    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).

  6. 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)

    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.

  7. 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

    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.

  8. 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

    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)

  9. 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

    Arterial lactate will be assessed by a arterial blood gaz sample, if available at this different time point.

  10. 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

    Cardiac output will be assessed with PICCO2 device or pulmonary artery catheterization. Left ventricular ejection fraction will be asssessed before adminstration of the vasopressin.

Study contacts

Contact information is provided by the study sponsor or research team.

Nicolas FAGE, MD PhD

CONTACT

[email protected]

Xavier MONNET, MD PhD

CONTACT

[email protected]

+33(0)145213539

Sponsors and collaborators

Lead sponsor

Assistance Publique - Hôpitaux de Paris

Other

Registry information

Acronym: VASO-PHENO

Important dates

Study start
2026
Primary completion
2029
Study completion
2029
First posted
Jul 13, 2026
Registry last updated
Jul 13, 2026

OpenTrials presents study information sourced from ClinicalTrials.gov. The official registry record should be consulted for the latest information.

View the official ClinicalTrials.gov record (opens in a new tab)

This listing is for discovery and informational purposes only. It is not medical advice, does not guarantee that a study is recruiting, and does not determine eligibility. Contact the study team and a qualified healthcare professional when considering participation.

Related clinical trials

Published trials that share one or more normalized conditions with this study.