title: Cardiac dysfunctions following spinal cord injury.
abstract: The aim of this article is to analyze cardiac dysfunctions occurring after spinal cord injury (SCI). Cardiac dysfunctions are common complications following SCI. Cardiovascular disturbances are the leading causes of morbidity and mortality in both acute and chronic stages of SCI. We reviewed epidemiology of cardiac disturbances after SCI, and neuroanatomy and pathophysiology of autonomic nervous system, sympathetic and parasympathetic. SCI causes disruption of descendent pathways from central control centers to spinal sympathetic neurons, originating into intermediolateral nuclei of T1-L2 spinal cord segments. Loss of supraspinal control over sympathetic nervous system results in reduced overall sympathetic activity below the level of injury and unopposed parasympathetic outflow through intact vagal nerve. SCI associates significant cardiac dysfunction. Impairment of autonomic nervous control system, mostly in patients with cervical or high thoracic SCI, causes cardiac dysrrhythmias, especially bradycardia and, rarely, cardiac arrest, or tachyarrhytmias and hypotension. Specific complication dependent on the period of time after trauma like spinal shock and autonomic dysreflexia are also reviewed. Spinal shock occurs during the acute phase following SCI and is a transitory suspension of function and reflexes below the level of the injury. Neurogenic shock, part of spinal shock, consists of severe bradycardia and hypotension. Autonomic dysreflexia appears during the chronic phase, after spinal shock resolution, and it is a life-threatening syndrome of massive imbalanced reflex sympathetic discharge occurring in patients with SCI above the splanchnic sympathetic outflow (T5-T6). Besides all this, additional cardiac complications, such as cardiac deconditioning and coronary heart disease may also occur. Proper prophylaxis, including nonpharmacologic and pharmacological strategies and cardiac rehabilitation diminish occurrence of the cardiac dysfunction following SCI. Each type of cardiac disturbance requires specific treatment.
authors.affiliation: "Bagdasar-Arseni" Clinical Emergency Hospital, Department of General Surgery, Bucharest, Romania.
authors.forename: Valentin Titus
authors.initials: VT
authors.lastname: Grigorean
authors.forename: Aurelia Mihaela
authors.initials: AM
authors.lastname: Sandu
authors.forename: Mihai
authors.initials: M
authors.lastname: Popescu
authors.forename: Mihai Aurelian
authors.initials: MA
authors.lastname: Iacobini
authors.forename: Rares
authors.initials: R
authors.lastname: Stoian
authors.forename: Catalin
authors.initials: C
authors.lastname: Neascu
authors.forename: Victor
authors.initials: V
authors.lastname: Strambu
authors.forename: Florian
authors.initials: F
authors.lastname: Popa
mesh_terms: D001281:Atrial Fibrillation / Q000209:etiology / Q000503:physiopathology; D001282:Atrial Flutter / Q000209:etiology / Q000503:physiopathology; D001919:Bradycardia / Q000209:etiology / Q000503:physiopathology; D003327:Coronary Disease / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D006331:Heart Diseases / Q000453:epidemiology / Q000209:etiology*; D006801:Humans; D015994:Incidence; D009420:Nervous System / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000150:complications / Q000453:epidemiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology; D013610:Tachycardia / Q000209:etiology / Q000503:physiopathology; D020246:Venous Thrombosis / Q000209:etiology / Q000517:prevention & control