The Impact of Propofol and Ketamine on Cardiovascular Collapse During Induction for Intubation

September 16, 2025 updated by: Kocaeli City Hospital

The Impact of Propofol and Ketamine on Cardiovascular Collapse During Induction for Endotracheal Intubation in Critically Ill Patients: A Prospective Observational Study

This prospective observational study evaluates the impact of propofol and ketamine on the risk of cardiovascular collapse during induction for endotracheal intubation in critically ill patients. Induction agents play a crucial role in managing hemodynamic stability, particularly in this vulnerable population. Propofol, known for its vasodilatory and myocardial depressant effects, has been associated with significant hypotension during induction. Conversely, ketamine, with its sympathomimetic properties, is often considered a safer alternative for hemodynamic stability.

In addition to comparing the incidence of cardiovascular collapse-defined as severe hypotension or cardiac arrest-this study examines the relationship between these induction agents and shock indices, including systolic shock index, diastolic shock index, age-adjusted shock index, and modified shock index. These parameters will provide a more detailed understanding of the hemodynamic effects of each agent and their clinical implications. The findings aim to guide induction agent selection to optimize outcomes in critically ill patients.

Study Overview

Study Type

Observational

Enrollment (Estimated)

128

Contacts and Locations

This section provides the contact details for those conducting the study, and information on where this study is being conducted.

Study Contact

Study Locations

    • Kocaeli
      • Köseköy, Kocaeli, Turkey (Türkiye), 41060
        • Recruiting
        • Kocaeli City Hospital
        • Contact:
          • +90 262 225 27 00 3853 Kocaeli City Hospital
          • Phone Number: +90-262-225-27-00
          • Email: omeremgin@yahoo.com

Participation Criteria

Researchers look for people who fit a certain description, called eligibility criteria. Some examples of these criteria are a person's general health condition or prior treatments.

Eligibility Criteria

Ages Eligible for Study

  • Adult
  • Older Adult

Accepts Healthy Volunteers

No

Sampling Method

Non-Probability Sample

Study Population

Patients admitted to the intensive care unit (ICU) who undergo endotracheal intubation during their ICU stay will be included.

Description

Inclusion Criteria:

  • Patients aged over 18 years
  • Patients admitted to the intensive care unit (ICU) who undergo endotracheal intubation during their ICU stay will be included.

Exclusion Criteria:

  • Patients who did not provide consent to participate in the study
  • Patients intubated due to cardiac arrest
  • Patients intubated outside the intensive care unit

Study Plan

This section provides details of the study plan, including how the study is designed and what the study is measuring.

How is the study designed?

Design Details

Cohorts and Interventions

Group / Cohort
Intervention / Treatment
Cardiovascular collapse

"- At least one documented episode of SpO₂ < 80%, ensuring accuracy of measurement.

  • At least one episode of systolic arterial blood pressure (SAB) < 65 mmHg.
  • SAB < 90 mmHg sustained for a duration of 30 minutes.
  • Initiation of norepinephrine therapy.
  • Escalation of pre-existing norepinephrine infusion dose.
  • Administration of >15 mL/kg crystalloid fluids to achieve SAB > 90 mmHg.
  • Occurrence of cardiac arrest." The occurrence of any of the above-mentioned events within the first 30 minutes following the initiation of the intervention will be considered as cardiovascular collapse.

The hemodynamic effects of propofol and ketamine are well-documented in the general patient population, yet the incidence and characteristics of cardiovascular collapse induced by these agents in critically ill patients remain underexplored. Cardiovascular collapse, a severe and potentially life-threatening event, may arise due to the unique physiological stressors present in the critical care setting, including pre-existing hemodynamic instability, comorbidities, and the administration of high-risk pharmacological agents. Despite the theoretical understanding of these drugs' pharmacodynamics, there is limited evidence assessing their differential impact on cardiovascular function in this vulnerable population.

This study aims to contribute novel insights to the literature by exploring the association between these widely used sedative-hypnotic agents and the development of cardiovascular collapse. While propofol is known for its potent vasodilatory and myocardial depressive effects,

The hemodynamic effects of propofol and ketamine are well-documented in the general patient population, yet the incidence and characteristics of cardiovascular collapse induced by these agents in critically ill patients remain underexplored. Cardiovascular collapse, a severe and potentially life-threatening event, may arise due to the unique physiological stressors present in the critical care setting, including pre-existing hemodynamic instability, comorbidities, and the administration of high-risk pharmacological agents. Despite the theoretical understanding of these drugs' pharmacodynamics, there is limited evidence assessing their differential impact on cardiovascular function in this vulnerable population.

This study aims to contribute novel insights to the literature by exploring the association between these widely used sedative-hypnotic agents and the development of cardiovascular collapse. While propofol is known for its potent vasodilatory and myocardial depressive effects,

No Cardiovascular collapse

The hemodynamic effects of propofol and ketamine are well-documented in the general patient population, yet the incidence and characteristics of cardiovascular collapse induced by these agents in critically ill patients remain underexplored. Cardiovascular collapse, a severe and potentially life-threatening event, may arise due to the unique physiological stressors present in the critical care setting, including pre-existing hemodynamic instability, comorbidities, and the administration of high-risk pharmacological agents. Despite the theoretical understanding of these drugs' pharmacodynamics, there is limited evidence assessing their differential impact on cardiovascular function in this vulnerable population.

This study aims to contribute novel insights to the literature by exploring the association between these widely used sedative-hypnotic agents and the development of cardiovascular collapse. While propofol is known for its potent vasodilatory and myocardial depressive effects,

The hemodynamic effects of propofol and ketamine are well-documented in the general patient population, yet the incidence and characteristics of cardiovascular collapse induced by these agents in critically ill patients remain underexplored. Cardiovascular collapse, a severe and potentially life-threatening event, may arise due to the unique physiological stressors present in the critical care setting, including pre-existing hemodynamic instability, comorbidities, and the administration of high-risk pharmacological agents. Despite the theoretical understanding of these drugs' pharmacodynamics, there is limited evidence assessing their differential impact on cardiovascular function in this vulnerable population.

This study aims to contribute novel insights to the literature by exploring the association between these widely used sedative-hypnotic agents and the development of cardiovascular collapse. While propofol is known for its potent vasodilatory and myocardial depressive effects,

What is the study measuring?

Primary Outcome Measures

Outcome Measure
Measure Description
Time Frame
cardiovascular collapse
Time Frame: The occurrence of any of the above-mentioned events within the first 30 minutes following the initiation of the intervention will be considered as cardiovascular collapse.
  • At least one documented episode of SpO₂ < 80%, ensuring accuracy of measurement.
  • At least one episode of systolic arterial blood pressure (SAB) < 65 mmHg.
  • SAB < 90 mmHg sustained for a duration of 30 minutes.
  • Initiation of norepinephrine therapy.
  • Escalation of pre-existing norepinephrine infusion dose.
  • Administration of >15 mL/kg crystalloid fluids to achieve SAB > 90 mmHg.
  • Occurrence of cardiac arrest.
The occurrence of any of the above-mentioned events within the first 30 minutes following the initiation of the intervention will be considered as cardiovascular collapse.

Collaborators and Investigators

This is where you will find people and organizations involved with this study.

Study record dates

These dates track the progress of study record and summary results submissions to ClinicalTrials.gov. Study records and reported results are reviewed by the National Library of Medicine (NLM) to make sure they meet specific quality control standards before being posted on the public website.

Study Major Dates

Study Start (Actual)

July 15, 2024

Primary Completion (Estimated)

November 1, 2025

Study Completion (Estimated)

November 1, 2025

Study Registration Dates

First Submitted

December 5, 2024

First Submitted That Met QC Criteria

December 25, 2024

First Posted (Actual)

December 27, 2024

Study Record Updates

Last Update Posted (Actual)

September 22, 2025

Last Update Submitted That Met QC Criteria

September 16, 2025

Last Verified

September 1, 2025

More Information

Terms related to this study

Plan for Individual participant data (IPD)

Plan to Share Individual Participant Data (IPD)?

NO

IPD Plan Description

We regret to inform that the data from this study will not be shared due to constraints related to authorization and time limitations. However, those interested may contact the study's corresponding author to request access to the data.

Drug and device information, study documents

Studies a U.S. FDA-regulated drug product

No

Studies a U.S. FDA-regulated device product

No

product manufactured in and exported from the U.S.

No

This information was retrieved directly from the website clinicaltrials.gov without any changes. If you have any requests to change, remove or update your study details, please contact register@clinicaltrials.gov. As soon as a change is implemented on clinicaltrials.gov, this will be updated automatically on our website as well.

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