Related Experiment Video
Updated: Oct 6, 2025
Technical Refinement of a Bilateral Renal Ischemia-Reperfusion Mouse Model for Acute Kidney Injury Research
Published on: November 3, 2023
Characteristics of circulatory failure after out-of-hospital cardiac arrest: a prospective cohort study
Halvor Langeland1,2, Daniel Bergum3, Magnus Løberg4,5
1Department of Anesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway halvor.langeland@ntnu.no.
Insights
Circulatory failure after cardiac arrest is primarily due to heart dysfunction, not inflammation. Heart failure biomarkers, not inflammatory ones, predicted the need for longer circulatory support in patients.
Area of Science:
- Cardiology
- Critical Care Medicine
- Hemodynamics
Background:
- Post-cardiac arrest syndrome (PCAS) involves circulatory failure, potentially from myocardial depression and vasodilation.
- The roles of myocardial dysfunction and systemic inflammation in PCAS circulatory failure remain unclear.
- Detailed macrocirculatory and microcirculatory assessments are needed for PCAS patients.
Purpose of the Study:
- To investigate the macrocirculatory and microcirculatory failure in postcardiac arrest syndrome.
- To differentiate the contributions of myocardial dysfunction and systemic inflammation to circulatory failure in PCAS.
- To identify predictors of circulatory support duration in PCAS patients.
Main Methods:
- Invasive monitoring of circulatory variables in 42 comatose OHCA patients from admission to day 5.
- Measurement of cardiac power output (CPO), stroke work (SW), aortic elastance, microcirculatory metabolism, and biomarkers.
- Survival analysis and Cox regression to assess time to norepinephrine discontinuation and fluid balance, stratified by biomarkers.
Main Results:
- Cardiac power output, stroke work, and oxygen delivery increased within 48 hours.
- Macrocirculatory homeostasis was gradually restored, with decreasing norepinephrine need.
- Higher pro-brain natriuretic peptide levels predicted longer norepinephrine use; inflammatory markers did not.
- Microcirculatory distress markers normalized within 24 hours.
Conclusions:
- Circulatory failure in PCAS is initially characterized by reduced cardiac function but resolves within 48 hours.
- Biomarkers of acute heart failure, not inflammation, predicted the duration of circulatory support.
- Findings suggest early, resolving cardiac dysfunction rather than late vasodilation is key in PCAS circulatory failure.
Background:
Circulatory failure after out-of-hospital cardiac arrest (OHCA) as part of the postcardiac arrest syndrome (PCAS) is believed to be caused by an initial myocardial depression that later subsides into a superimposed vasodilatation. However, the relative contribution of myocardial dysfunction and systemic inflammation has not been established. Our objective was to describe the macrocirculatory and microcirculatory failure in PCAS in more detail.
Methods:
We included 42 comatose patients after OHCA where circulatory variables were invasively monitored from admission until day 5. We measured the development in cardiac power output (CPO), stroke work (SW), aortic elastance, microcirculatory metabolism, inflammatory and cardiac biomarkers and need for vasoactive medications. We used survival analysis and Cox regression to assess time to norepinephrine discontinuation and negative fluid balance, stratified by inflammatory and cardiac biomarkers.
Results:
CPO, SW and oxygen delivery increased during the first 48 hours. Although the estimated afterload fell, the blood pressure was kept above 65 mmHg with a diminishing need for norepinephrine, indicating a gradually re-established macrocirculatory homoeostasis. Time to norepinephrine discontinuation was longer for patients with higher pro-brain natriuretic peptide concentration (HR 0.45, 95% CI 0.21 to 0.96), while inflammatory biomarkers and other cardiac biomarkers did not predict the duration of vasoactive pressure support. Markers of microcirculatory distress, such as lactate and venous-to-arterial carbon dioxide difference, were normalised within 24 hours.
Conclusion:
The circulatory failure was initially characterised by reduced CPO and SW, however, microcirculatory and macrocirculatory homoeostasis was restored within 48 hours. We found that biomarkers indicating acute heart failure, and not inflammation, predicted longer circulatory support with norepinephrine. Taken together, this indicates an early and resolving, rather than a late and emerging vasodilatation.
Trial Registration:
NCT02648061.
Related Concept Videos
01:27Heart Failure I: Introduction
01:17Pathophysiology of Heart Failure
01:21Cardiopulmonary Resuscitation I: Adult
01:20Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...
01:30Coronary Artery Disease III: Clinical Manifestations
01:30Cardiomyopathy II: Dilated Cardiomyopathy