Current partner codePEPTIDESDE
NCT07697144·Not applicable·OBSERVATIONAL

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

Status

Not yet recruiting

Phase

Not applicable

Enrollment

200

Locations

8

Results

Not posted

Publications

0

Study summary

What the protocol is testing.

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.

Full 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.

Interventions

Treatment arms and agents.

No intervention details reported.

Timeline

From registration to results.

  1. First posted

    Jul 13, 2026

  2. Study start

    Aug 1, 2026

  3. Primary completion

    Sep 1, 2029

  4. Study completion

    Sep 1, 2029

  5. Results posted

    Not reported

  6. Registry updated

    Jul 13, 2026

Outcomes

What the study measures.

Primary outcomes

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

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).

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.

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).

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).

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).

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.

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.

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)

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.

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.

Eligibility

Who can take part.

Minimum age
18 Years
Maximum age
Not reported
Sex
ALL
Healthy volunteers
No

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 locations

8 registered sites.

France. Showing up to 24 locations stored in the fast local snapshot.

CHU d'Angers

Angers, France

CH de Dieppe

Dieppe, France

Hôpital Bicêtre

Le Kremlin-Bicêtre, France

GHE, Hôpital Louis Pradel, HCL

Lyon, France

GHS - Hôpital Lyon Sud, HCL

Lyon, France

Hôpital Nord, AP-HM

Marseille, France

CHU Rennes - Site Pontchaillou

Rennes, France

Hôpital Hautepierre, Hôpitaux Universitaires de Strasbourg

Strasbourg, France

Publications

Results and literature.

No PMID-linked publications were present in this registry snapshot.

Primary links

Continue at the source.

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More studies on Vasopressin.

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