Discussion-
Spinal cord injury particularly above T6 vertebra level cause disruption of sympathetic system and unopposed vagal stimulation which can lead to several effects on CV system. Major effects are persistent bradycardia, neurogenic shock, rarely asystole. Some patients develop atrial fibrillation and flutter. Patients with partial spinal cord disruption may sometimes develop autonomic dysreflexia which is characterised by sudden increase in blood pressure in response to triggering events (2). Most common dysrhythmia in acute cervical cord injury is persistent sinus bradycardia which peaks at day 4 and generally resolves at 4 to 6 weeks. Rarely patients develop severe bradycardia and cardiac arrest. Ventricular tachycardia has not been described in spinal cord injury patient in literature but may develop if patient has certain risk factor like previous cardiac disease or if patient develops stress induced cardiomyopathy or electrolyte imbalance or on multiple QT prolonging drugs. Our patient had no history of any significant illness, structurally normal heart during event and on discharge, and was not on any QT prolonging drugs.
Polymorphic ventricular tachycardia is uncommon and can occur in setting of normal or increased QT interval (3). Polymorphic VT in setting of normal QT interval occurs in acute myocardial ischemia, brugada syndrome, catecholaminergic PVT and electrolyte imbalance, digitalis toxicity and hypertrophic cardiomyopathy (4). Polymorphic VT in setting of increased QT interval is a special category called Torsades de pointes and has acquired or congenital causes. This distinction is important because treatment options for both categories are different. Polymorphic VT with normal QT interval can be treated with lidocaine or amiodarone whereas amiodarone is contraindicated in second category. Intravenous magnesium sulfate, isoprenaline infusion and rapid pacing at rate of 100 to 120 with temporary pacemaker to decrease QT interval are treatment options in torsades.
Bunten D C et al have shown that Heart rate variability (HRV) is altered in cervical spinal cord trauma patients and may have prognostic significance (5). Further Hillebrand Stefanie et al have shown than loss of HRV is associated with increased risk of cardiovascular events in population with no cardiovascular disease (6). So autonomic imbalance along with loss of heart rate variability may be triggering factors in initiation of polymorphic VT in our patient.