OBJECTIVE: Neurogenic shock considered a distributive type of shock secondary to loss of sympathetic outflow to the peripheral vasculature. In this study, we examine the hemodynamic profiles of a series of trauma patients with a diagnosis of neurogenic shock. METHODS: Hemodynamic data were collected on a series of trauma patients determined to have spinal cord injuries with neurogenic shock. A well-established integrated computer model of human physiology was used to analyze and categorize the hemodynamic profiles from a system analysis perspective. A differentiation between these categories was presented as the percent of total patients. RESULTS: Of the 9 patients with traumatic neurogenic shock, the etiology of shock was decrease in peripheral vascular resistance (PVR) in 3 (33%; 95% confidence interval, 12%-65%), loss of vascular capacitance in 2 (22%; 6%-55%) and mixed peripheral resistance and capacitance responsible in 3 (33%; 12%-65%), and purely cardiac in 1 (11%; 3%-48%). The markers of sympathetic outflow had no correlation to any of the elements in the patients' hemodynamic profiles. CONCLUSIONS: Results from this study suggest that hypotension of neurogenic shock can have multiple mechanistic etiologies and represents a spectrum of hemodynamic profiles. This understanding is important for the treatment decisions in managing these patients.
OBJECTIVE:Neurogenic shock considered a distributive type of shock secondary to loss of sympathetic outflow to the peripheral vasculature. In this study, we examine the hemodynamic profiles of a series of traumapatients with a diagnosis of neurogenic shock. METHODS: Hemodynamic data were collected on a series of traumapatients determined to have spinal cord injuries with neurogenic shock. A well-established integrated computer model of human physiology was used to analyze and categorize the hemodynamic profiles from a system analysis perspective. A differentiation between these categories was presented as the percent of total patients. RESULTS: Of the 9 patients with traumatic neurogenic shock, the etiology of shock was decrease in peripheral vascular resistance (PVR) in 3 (33%; 95% confidence interval, 12%-65%), loss of vascular capacitance in 2 (22%; 6%-55%) and mixed peripheral resistance and capacitance responsible in 3 (33%; 12%-65%), and purely cardiac in 1 (11%; 3%-48%). The markers of sympathetic outflow had no correlation to any of the elements in the patients' hemodynamic profiles. CONCLUSIONS: Results from this study suggest that hypotension of neurogenic shock can have multiple mechanistic etiologies and represents a spectrum of hemodynamic profiles. This understanding is important for the treatment decisions in managing these patients.
Authors: Richard L Summers; James M Harrison; James R Thompson; John Porter; Thomas G Coleman Journal: Acad Emerg Med Date: 2011-09-26 Impact factor: 3.451
Authors: Richard L Summers; William C Shoemaker; W Franklin Peacock; Douglas S Ander; Thomas G Coleman Journal: Acad Emerg Med Date: 2003-06 Impact factor: 3.451
Authors: Constantin Popa; Florian Popa; Valentin Titus Grigorean; Gelu Onose; Aurelia Mihaela Sandu; Mihai Popescu; Gheorghe Burnei; Victor Strambu; Crina Sinescu Journal: J Med Life Date: 2010 Jul-Sep
Authors: Valentin Titus Grigorean; Aurelia Mihaela Sandu; Mihai Popescu; Mihai Aurelian Iacobini; Rares Stoian; Catalin Neascu; Victor Strambu; Florian Popa Journal: J Med Life Date: 2009 Apr-Jun
Authors: Thomas Standl; Thorsten Annecke; Ingolf Cascorbi; Axel R Heller; Anton Sabashnikov; Wolfram Teske Journal: Dtsch Arztebl Int Date: 2018-11-09 Impact factor: 5.594