The interaction between the heart and the brain has been well established. A tragic example is the frequently seen symptomatic bradycardia following cervical spinal cord injury (CSCI). We present a case report and review of the limited literature on this subject.
A 45-year-old male without significant past medical history was admitted to the University of Missouri hospital after falling from a height of 35–40 feet. There was no history of any prodromal symptoms prior to the fall. The patient subsequently lost consciousness and was brought to the hospital. Magnetic resonance imaging (MRI) of the cervical spine revealed a C5–6 dislocation.
Despite an urgent discectomy and anterior cervical arthrodesis, he developed partial quadriplegia. He subsequently developed respiratory failure requiring mechanical ventilation. On hospital day seven, his heart rate decreased to 30 beats per minute (bpm) and his blood pressure (BP) to 90/60mmHg without any symptoms. This episode resolved spontaneously after one minute. Telemetry revealed sinus bradycardia, followed by sinus arrest, a ventricular escape rhythm, and, subsequently, restoration to normal sinus rhythm.
On hospital day 10, he developed asystole lasting 20 seconds with loss of consciousness. This episode resolved spontaneously with restoration of sinus bradycardia at 50–55bpm. Due to severe hemodynamic collapse caused by this event, a transvenous pacemaker was placed. The patient required continuous ventricular pacing at a rate of 60bpm for the next four days, after which his intrinsic rate increased to 60–70bpm without further episodes of asystole. He did not require any more pacing support over the next three days and on hospital day 17 the pacemaker was discontinued.
The patient did well from a cardiac standpoint at follow-up four weeks after the injury, with no further documented episodes of bradyarrythmias, syncope, or pre-syncope.
There are an estimated 10,000–12,000 spinal cord injuries every year in the US. A quarter of a million Americans are currently living with spinal cord injuries. Cervical spine injuries constitute nearly half of all these injuries. Fifty-five percent of spinal cord injury victims are between 16 and 30 years of age.1 Most of these patients have a prolonged rehabilitation course. Cardiovascular complications are a leading cause of death in patients with CSCI.2,3
Neural pathways play an important role in the dynamics of cardiovascular physiology. The heart receives both sympathetic and parasympathetic innervation. The parasympathetic fibers travel from the pre-ganglionic neurons in the medulla (nucleus ambiguus and dorsal motor nucleus of the vagus) with the vagus nerve to supply the heart. The sympathetic fibers travel from neurons in the intermediolateral columns of the spinal cord at the T1–T4 levels and synapse in the (stellate) cervical ganglia, and from here the post-ganglionic sympathetic neurons reach the heart.
Parasympathetic neurons have an inhibitory effect on heart rate and the conduction, excitability, and contractility of myocardial cells, while the sympathetic stimulation has the opposite effect.
Sinoatrial and atrioventricular nodes and the atrioventricular conduction system have abundant parasympathetic innervation. The arteries and veins of the systemic circulation are innervated primarily by the sympathetic system. In normal circumstances there is parasympathetic predominance in the heart physiology. The autonomic nervous system receives its sensory input from the baroreceptors located in the major vessels, and this forms part of the arterial baroreflex feedback mechanism, which ultimately regulates the heart rate and blood pressure.4,5
Severe bradycardia and hypotension as a complication of acute CSCI are common as a result of post-injury imbalance in the autonomic nervous system caused by dissociation of spinal cardiac and vasomotor sympathetic fibers, while the parasympathetic fibers that travel with vagus nerve remain intact.
There is experimental evidence suggesting two mechanisms by which these patients may develop bradycardias. One mechanism is that of autonomic imbalance with predominance of the parasympathetic nervous system due to anatomic sympathetic denervation. A second mechanism that may have relevant long-term manifestations is autonomic dysreflexia, which causes sympathetic surges. This manifests with sudden rise in BP, which may cause activation of the baroreflex pathway resulting in vagal stimulation and resultant bradycardia.2 The role of the vagal-mediated pathway in experimental animal models is evidenced by termination of bradyarrythmias with vagotomy.6
Bradycardia has been reported in almost all cases of CSCI, with asystole in 15% of these patients. The time of onset is variable, but the incidence is highest in the first two to four weeks following CSCI and may decrease subsequently as the spinal shock and edema resolve.7 The incidence and hemodynamic impact may be directly related to the severity of the injury. Billelo et al. report no significant difference in the frequency of neurogenic shock (bradycardia with hypotension) in patients with a high CSCI (C1–C5) compared with low CSCI (C6–C7), but the former had a significantly greater requirement for cardiovascular interventions, including pacemakers, regardless of age or concomitant injuries.8
There are a number of inciting events that may precipitate bradyarrythmias, e.g. rolling in bed or any movement, endotracheal intubation, endotracheal suctioning, and hypoxia. All may lead to vagal nerve stimulation resulting in unopposed parasympathetic surge.7,9 However, the event may not be related to any precipitating cause, as occurred with our patient.
All patients with spinal cord injury regardless of the level and severity should be closely monitored. Treatment modalities include atropine, epinephrine, aminophylline, and pacemaker insertion.10 The criteria for pacemaker use in this population are not well defined. Permanent pacemaker placement should be strongly considered in patients with refractory or recurrent bradyarrhythmias, those with high or complete CSCI, or those requiring long-term mechanical ventilation.11,12
In the case we describe, the patient had bradycardia leading to hemodynamic collapse, thus requiring brief temporary transvenous pacing. Patients who continue to have bradyarrythmias more than two weeks after the initial injury should be considered for permanent pacemaker implantation.11
There are a few case reports reporting the occurrence of bradycardia/asystole and related deaths months after the initial injury.11,13 The choice of pacing mode for treatment of bradycardia and asystole would be determined by the underlying cardiac rhythm. If patients were in sinus rhythm, a DDD(R) pacing system would be indicated; if in atrial fibrillation, a VVI(R) mode would be used. If a DDD(R) were used, a feature unique to some models (rate drop response intervention; used primarily for patients with vasovagal syncope) could be considered.
A device that combines an internal cardiac defibrillator (ICD) may be used if there is additional indication from unexplained sudden death or poor left ventricular function (typically left ventricular ejection fraction <35%) suggesting a substrate for ventricular arrhythmias.14
The aforementioned treatment options are based on anecdotal reports and small retrospective analyses. Currently, there are no evidence-based guidelines regarding permanent pacemaker implantation in patients similar to ours who do not have further bradycardiac episodes, at least for the time period for which he was under observation in the hospital. The decision about permanent pacemaker implantation in this situation has to be tailored on a case-by-case basis.