Evidence map›Paper›PMID 35046124›Full record

Observational studyOpen heart2022

Characteristics of circulatory failure after out-of-hospital cardiac arrest: a prospective cohort study.

Halvor Langeland, Daniel Bergum, Magnus Løberg, Knut Bjørnstad, Thomas R Skaug, Trond Nordseth, Pål Klepstad, Nils Kristian Skjærvold

Registry-linked trialOpen access · goldAbstract readObservational Study
In one paragraph

Observational study in Open heart, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02648061 (Transitions Between Clinical Circulatory States After Out-of-hospital Cardiac Arrest), which is not on this map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
3.3field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT02648061 completednot on this map

Transitions Between Clinical Circulatory States After Out-of-hospital Cardiac Arrest

TypeobservationalSponsorNorwegian University of Science and TechnologyRan2016 to 2017Enrolled50ConditionsOut-of-Hospital Cardiac Arrest
3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 14 citations in OpenAlex.

  1. Trial
  2. CytoSorbBiomedicines · 2026
    Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Halvor LangelandDepartment of Anesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway halvor.langeland@ntnu.no.ORCID 0000-0001-8155-1514
Daniel BergumDepartment of Anesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway.
Magnus LøbergClinical Effectiveness Research Group, University of Oslo, Oslo, Norway.
Knut BjørnstadDepartment of Cardiology, St. Olav's University Hospital, Trondheim, Norway.
Thomas R SkaugDepartment of Cardiology, St. Olav's University Hospital, Trondheim, Norway.
Trond NordsethDepartment of Anesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway.
Pål KlepstadDepartment of Anesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway.
Nils Kristian SkjærvoldDepartment of Anesthesiology and Intensive Care Medicine, St. Olav's University Hospital, Trondheim, Norway.ORCID 0000-0002-0085-7042
Norwegian University of Science and Technology · NOSt Olav's University Hospital · NOOslo University Hospital · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCirculatory 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.

methodsWe 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.

resultsCPO, 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.

conclusionThe 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 registrationNCT02648061.

Indexed as

AgedComaFemaleFollow-Up StudiesHumansMaleMicrocirculationNorepinephrineOut-of-Hospital Cardiac ArrestProspective StudiesVasoconstrictor AgentsVasodilationNorepinephrineVasoconstrictor Agentsbiomarkersepidemiologyheart arrestheart failure

Identifiers

PMID35046124
PMCPMC8772457
OpenAlexW4205883861

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.