Hemodynamic Assessment in Cardiogenic Shock Regarding the Etiology

The classic physiopathology of cardiogenic shock is explained by a systolic ventricular failure, responsible for a decrease in cardiac output associated with high systemic vascular resistances (SVR). This theory is currently challenged in light of the data collected in the SHOCK study, which assessed outcome of early revascularization versus initial medical stabilization, in cardiogenic shock following myocardial infarction.13 A sub-study highlighted depressed SVR in the population with ischemic cardiogenic shock, related to a systemic inflammatory response syndrome.14 Furthermore, mean FEVG was 30% in the SHOCK trial,13 with a similar distribution with post myocardial infarction heart failure patients without signs of shock.15-19 Thus, alteration of myocardial contractility can be only moderate in cardiogenic shock and isn't the only cause responsible for the hemodynamic instability.20 Recent studies suggest the important roles of the peripheral vascular system and neurohormonal system in the genesis and prolongation of cardiogenic shock.12 Vasodilation caused by nitrous oxide synthase activation27 explains the absence of compensating vasoconstriction observed during the SHOCK trial13, and leads to decreased systemic and coronary perfusion, thus increasing myocardial ischemia and initial ventricular dysfunction. 28,29 Cotter et al. conducted an interesting study of hemodynamic evaluation of various cardiac conditions where they observed a significant variability in the peripheral vascular status, with systemic vascular resistances collapsed in certain patients (similar to those observed in septic shock) and rather close to normal or very high resistances in other patients.21 However these data were obtained from a selected group of patients without differentiating the etiology of cardiogenic shock. Finally, the majority of available studies were limited to cardiogenic shock whose etiology was myocardial infarction.

Therapeutic management of cardiogenic shock is based in first intention on an inotropic support by Dobutamine.11,23 However, better outcomes on contractility and microcirculatory state have been observed with the use of a vasopressor support by Norepinephrine, suggesting the importance of SVR decreasing in genesis of cardiogenic shock.14,24 Recent reviews showed very few data on inotropic treatment and association with vasopressor support,22 hence the low level of recommendations in current guidelines.11,23

So far it is crucial to accurately characterize hemodynamic status and in particular the systemic vascular resistance for patients with cardiogenic shock. Important variabilities in hemodynamic profiles observed in Cooter's trial could explain the difficulty in defining an optimal therapeutic strategy.

the investigators hypothesize that the hemodynamic profile, particularly SVR, of patients with cardiogenic shock is different depending on their etiology. Ischemic cardiogenic shock should be characterized by lower SVR, in relation to a major role of systemic inflammatory response syndrome. On the contrary, non-ischemic cardiogenic shock could be associated with normal or elevated SVR, and thus could explain the variability in distribution of SVR.

Study Overview

• Status: Unknown
• Conditions: Cardiogenic Shock
• Intervention / Treatment: Other: Cardiac Volume Monitoring VolumeView; Device: echocardiography

• Study Type: Observational
• Enrollment (Anticipated): 64

Contacts and Locations

Study Locations

• France
  • Marseille, France
    • Recruiting
    • Assisatnce Publique Hopitaux de Marseille
    • Contact: JEAN-OLIVIER ARNAUD; Email: drci@ap-hm.fr
    • Principal Investigator: LAURENT BONELLO

Participation Criteria

Eligibility Criteria

• Ages Eligible for Study: 18 years and older (Adult, Older Adult)
• Accepts Healthy Volunteers: No
• Genders Eligible for Study: All

• Sampling Method: Non-Probability Sample

Study Population

patients with cardiogenic shock.

Description

Inclusion Criteria:

• Persistent hypotension (systolic blood pressure <90 mmHg for at least 30 minutes or need for vasopressor support)
• Signs of visceral hypoperfusion (confusion, marbling, oliguria, hyperlactataemia), 11
• Lower heart rate (<1.8 L / min / m2) Adap Suitable or high filling pressures12

Exclusion Criteria:

• Pregnant or nursing women
• Major under guardianship
• Person staying in a health or social facility
• Non-beneficiaries of a social security scheme
• Persons deprived of liberty
• No one is able to give consent.

Study Plan

How is the study designed?

Number of groups / cohorts

4

Cohorts and Interventions

Group / Cohort	Intervention / Treatment
cardiogenic shock without SCA	Other: Cardiac Volume Monitoring VolumeView; hemodynamic measure; Device: echocardiography; hemodynamic measure
cardiogenic shock with SCA	Other: Cardiac Volume Monitoring VolumeView; hemodynamic measure; Device: echocardiography; hemodynamic measure
SCA,	Device: echocardiography; hemodynamic measure
acute left heart failure with severe alteration of LVEF	Device: echocardiography; hemodynamic measure

What is the study measuring?

Primary Outcome Measures

Outcome Measure	Time Frame
Monitoring by transpulmonary thermodilution (VolumeView	2 days

Collaborators and Investigators

• Sponsor: Assistance Publique Hopitaux De Marseille

Study record dates

Study Major Dates

• Study Start (Actual): September 6, 2017
• Primary Completion (Anticipated): September 1, 2018
• Study Completion (Anticipated): March 1, 2019

Study Registration Dates

• First Submitted: September 13, 2017
• First Submitted That Met QC Criteria: September 13, 2017
• First Posted (Actual): September 15, 2017

Study Record Updates

• Last Update Posted (Actual): April 11, 2018
• Last Update Submitted That Met QC Criteria: April 10, 2018
• Last Verified: April 1, 2018

More Information

Terms related to this study

• Additional Relevant MeSH Terms: Ischemia; Pathologic Processes; Necrosis; Myocardial Ischemia; Heart Diseases; Cardiovascular Diseases; Vascular Diseases; Myocardial Infarction; Infarction; Shock; Shock, Cardiogenic
• Other Study ID Numbers: 2017-15; 2017-A00563-50 (Other Identifier: n°IDRCB)

Drug and device information, study documents

• Studies a U.S. FDA-regulated drug product: No
• Studies a U.S. FDA-regulated device product: No