title: Association of Early Hemodynamic Profile and the Development of Systolic Dysfunction Following Traumatic Brain Injury.
abstract: BACKGROUND
  While 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.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  Thirty-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.
  
  
  CONCLUSIONS
  Patients 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.
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, BB-1469, Seattle, WA, 98195, USA. vkrish@u.washington.edu.|Department of Epidemiology, University of Washington, Seattle, WA, USA. vkrish@u.washington.edu.|Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA. vkrish@u.washington.edu.
authors.forename: Vijay
authors.identifier: http://orcid.org/0000-0003-4153-2348
authors.initials: V
authors.lastname: Krishnamoorthy
authors.affiliation: Department of Epidemiology, University of Washington, Seattle, WA, USA.|Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Ali
authors.initials: A
authors.lastname: Rowhani-Rahbar
authors.affiliation: Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Nophanan
authors.initials: N
authors.lastname: Chaikittisilpa
authors.affiliation: Division of Cardiology, Department of Medicine, University of Washington, Seattle, WA, USA.|Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Edward F
authors.initials: EF
authors.lastname: Gibbons
authors.affiliation: Department of Epidemiology, University of Washington, Seattle, WA, USA.|Department of Pediatrics, University of Washington, Seattle, WA, USA.|Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Frederick P
authors.initials: FP
authors.lastname: Rivara
authors.affiliation: Department of Neurosurgery, University of Washington, Seattle, WA, USA.|Department of Biostatistics, University of Washington, Seattle, WA, USA.|Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Nancy R
authors.initials: NR
authors.lastname: Temkin
authors.affiliation: Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Alex
authors.initials: A
authors.lastname: Quistberg
authors.affiliation: Department of Anesthesiology and Pain Medicine, University of Washington, 1959 NE Pacific Street, BB-1469, Seattle, WA, 98195, USA.|Harborview Injury Prevention and Research Center, University of Washington, Seattle, WA, USA.
authors.forename: Monica S
authors.initials: MS
authors.lastname: Vavilala
mesh_terms: D000328:Adult; D062186:Arterial Pressure / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D000070642:Brain Injuries, Traumatic / Q000150:complications*; D004452:Echocardiography; D005260:Female; D006339:Heart Rate / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology; D006801:Humans; D007022:Hypotension / Q000209:etiology*; D008297:Male; D008875:Middle Aged; D018487:Ventricular Dysfunction, Left / Q000209:etiology*; D055815:Young Adult
keywords: Echocardiography; Hemodynamics; Stress cardiomyopathy; Trauma; Traumatic brain injury