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.