Related Experiment Video
Updated: Dec 3, 2025

Standardized Hemorrhagic Shock Induction Guided by Cerebral Oximetry and Extended Hemodynamic Monitoring in Pigs
Published on: May 21, 2019
Hemodynamic Profiles of Cardiogenic Shock Depending on Their Etiology
Mélanie Gaubert1, Marc Laine1, Noémie Resseguier2
1Cardiology Department, APHM, Mediterranean Association for Research and Studies in Cardiology (MARS Cardio), Centre for CardioVascular and Nutrition Research (C2VN), Aix-Marseille Univ, INSERM 1263, INRA 1260, Hopital Nord, 13015 Marseille, France.
Insights
Cardiogenic shock (CS) patients have different hemodynamic profiles based on the cause. Acute myocardial infarction CS shows lower systemic vascular resistance and higher cardiac index compared to acute decompensated chronic heart failure CS.
Area of Science:
- Cardiology
- Critical Care Medicine
- Hemodynamics
Background:
- Cardiogenic shock (CS) pathophysiology differs by etiology, influencing hemodynamic profiles (HP) and treatment strategies.
- Understanding these variations is crucial for optimizing patient management and therapeutic interventions.
Purpose of the Study:
- To compare the hemodynamic profiles of CS patients with acute myocardial infarction (AMI) versus acute decompensated chronic heart failure (ADCHF).
- To determine if distinct HP warrant tailored therapeutic approaches based on CS etiology.
Main Methods:
- Prospective inclusion of 28 CS patients with either AMI or ADCHF.
- Measurement of Systemic Vascular Resistance index (SVRi), Cardiac Index (CI), and Cardiac Power Index (CPI) via trans-thoracic Doppler echocardiography before inotropic or vasopressor administration.
Main Results:
- CS secondary to AMI exhibited significantly lower SVRi (2010 vs. 2622 dynes-s·cm-5·m-2, p=0.002) compared to ADCHF.
- A trend towards a higher CI was observed in AMI CS (2.13 vs. 1.78 L·min-1·m-2, p=0.067).
- Demographics and shock severity were comparable between the two groups.
Conclusions:
- Significant differences in hemodynamic profiles exist between CS caused by AMI and ADCHF.
- These distinct HP, particularly lower SVRi and higher CI in AMI CS, should inform patient selection for future clinical research and guide therapeutic strategies.
Abstract:
The pathophysiology of cardiogenic shock (CS) varies depending on its etiology, which may lead to different hemodynamic profiles (HP) and may help tailor therapy. We aimed to assess the HP of CS patients according to their etiologies of acute myocardial infarction (AMI) and acute decompensated chronic heart failure (ADCHF). We included patients admitted for CS secondary to ADCHF and AMI. HP were measured before the administration of any inotrope or vasopressor. Systemic Vascular Resistances index (SVRi), Cardiac Index (CI), and Cardiac Power Index (CPI) were measured by trans-thoracic Doppler echocardiography on admission. Among 37 CS patients, 28 had CS secondary to ADCHF or AMI and were prospectively included. The two groups were similar in terms of demographic data and shock severity criteria. AMI CS was associated with lower SVRi compared to CS related to ADCHF: 2010 (interquartile range (IQR): 1895-2277) vs. 2622 (2264-2993) dynes-s·cm-5·m-2 (p = 0.002). A trend toward a higher CI was observed: respectively 2.13 (1.88-2.18) vs. 1.78 (1.65-1.96) L·min-1·m-2 (p = 0.067) in AMICS compared to ADCHF. CS patients had different HP according to their etiologies. AMICS had lower SVR and tended to have a higher CI compared to ADHF CS. These differences should be taken into account for patient selection in future research.
Related Concept Videos
Blood Pressure Imbalances and Circulatory Shock
Blood Pressure: Hypertension and Hypotension
Normal blood pressure is 120/80 mm Hg. Elevated blood pressure is 120-129/under 80 mm Hg. Hypertension, warranting treatment at 130/80 mm Hg, is often asymptomatic and can lead to severe cardiovascular events, aneurysms, peripheral arterial disease, chronic renal disease, or cardiac...
Pathophysiology of Heart Failure
Heart Failure II: Pathophysiology
Pathophysiology of Cardiac Performance
Cardiopulmonary Resuscitation IV: Pharmacological Management
Cardiomyopathy III: Hypertrophic Cardiomyopathy

