Evidence map›Paper›PMID 28000133›Full record

ArticleNeurocritical care2017

Association of Early Hemodynamic Profile and the Development of Systolic Dysfunction Following Traumatic Brain Injury.

Vijay Krishnamoorthy, Ali Rowhani-Rahbar, Nophanan Chaikittisilpa, Edward F Gibbons, Frederick P Rivara, Nancy R Temkin, Alex Quistberg, Monica S Vavilala

Abstract read
In one paragraph

Article in Neurocritical care, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
4.7field-weighted citation impact, top 5% 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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
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  4. Eight rules for the haemodynamic management of traumatic brain-injured patients.European journal of anaesthesiology and intensive care · 2023
    Article
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  10. Observational
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  15. Article
  16. The authors reply.Critical care medicine · 2017
    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 1 institution in 1 country.

Vijay KrishnamoorthyDepartment of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, BB-1469, Seattle, WA, 98195, USA. vkrish@u.washington.edu.ORCID http://orcid.org/0000-0003-4153-2348
Ali Rowhani-RahbarDepartment of Epidemiology, University of Washington, Seattle, WA, USA.
Nophanan ChaikittisilpaHarborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
Edward F GibbonsDivision of Cardiology, Department of Medicine, University of Washington, Seattle, WA, USA.
Frederick P RivaraDepartment of Epidemiology, University of Washington, Seattle, WA, USA.
Nancy R TemkinDepartment of Neurosurgery, University of Washington, Seattle, WA, USA.
Alex QuistbergHarborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
Monica S VavilalaDepartment of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, BB-1469, Seattle, WA, 98195, USA.
University of Washington · US

Funding

Anesthesiology & Perioperative Medicine Training GrantT32GM086270 · NIGMS · UNIVERSITY OF WASHINGTON · PI Tonya M Palermo · 2009 to 2026
$4.3M
NIGMS NIH HHS T32 GM086270NINDS NIH HHS L30 NS084420
6 · The paper itself

Abstract

backgroundWhile systolic dysfunction has been observed following traumatic brain injury (TBI), the relationship between early hemodynamics and the development of systolic dysfunction has not been investigated. Our study aimed to determine the early hemodynamic profile that is associated with the development of systolic dysfunction after TBI.

methodsWe conducted a prospective cohort study among patients under 65 years old without cardiac comorbidities who sustained moderate-severe TBI. Transthoracic echocardiography was performed within the first day after TBI to assess for systolic dysfunction. Hourly systolic blood pressure (SBP), mean arterial pressure (MAP), heart rate, and confounding clinical variables (sedatives, fluid balance, vasopressors, and osmotherapy) were collected during the first 24 h following admission. Multivariable linear mixed models assessed the early hemodynamic profile in patients who developed systolic dysfunction, compared to patients who did not develop systolic dysfunction.

resultsThirty-two patients were included, and 7 (22 %) developed systolic dysfunction after TBI. Patients who developed systolic dysfunction experienced early elevation of SBP, MAP, and heart rate, compared to patients who did not develop systolic dysfunction (p < 0.01 for all comparisons). Patients who developed systolic dysfunction experienced a greater rate of decrease in SBP [-10.2 mmHg (95 % CI -16.1, -4.2)] and MAP [-9.1 mmHg (95 % CI -13.9, -4.3)] over the first day of hospitalization, compared to patients who did not develop systolic dysfunction (p < 0.01 for both comparisons). All sensitivity analyses revealed no substantial changes from the primary model.

conclusionsPatients who develop systolic dysfunction following TBI have a distinctive hemodynamic profile, with early hypertension and tachycardia, followed by a decrease in blood pressure over the first day after TBI. This profile suggests an early maladaptive catecholamine-excess state as a potential underlying mechanism of TBI-induced systolic dysfunction.

Indexed as

AdultArterial PressureBlood PressureBrain Injuries, TraumaticEchocardiographyFemaleHeart RateHemodynamicsHumansHypotensionMaleMiddle AgedVentricular Dysfunction, LeftYoung AdultEchocardiographyHemodynamicsStress cardiomyopathyTraumaTraumatic brain injury

Identifiers

PMID28000133
PMCPMC5444944
OpenAlexW2561098984

What OpenQuestion holds

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Registered trials

None linked

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.