Heart-Brain Connection: Role of the Central Nervous System

Scenario: This electrocardiogram is from a 28-year-old woman who came to an emergency department with generalized edema and shortness of breath. She had been in a motor vehicle accident 8 years prior, leading to a traumatic brain injury (TBI) causing seizures and a spinal cord injury (SCI) with spastic quadriplegia. Current comorbidities included obesity (body mass index [calculated as weight in kilograms divided by height in meters squared], 38), diabetes, and non-ischemic myocardial injury. She was nonverbal and bedbound, and her parents made all of her medical decisions. She was often admitted to the hospital because of inappropriate thermoregulation, anasarca, bradycardia, and respiratory failure, all consequences of the TBI and SCI. On arrival, her blood pressure was 102/65 mm Hg, respiratory rate 18/min, oxygen saturation 93% on room air, and temperature 36.4 °C. Atropine and a dopamine infusion did not improve her heart rate, so she was transferred to a tertiary hospital for a cardiac workup and potential pacemaker placement.Sinus arrest with junctional escape rhythm. Repolarization abnormalities seen globally with ST-segment depression and T-wave inversions.When automaticity in the sinus node decreases or fails, other areas in the conduction system that have pacemaker cells spontaneously depolarize and become the predominant pacemaker. Pacemaker cells are mainly found in the sinus and atrioventricular nodes but can also be found in the bundle of His and Purkinje fibers. When pacemaker cells outside the sinus node depolarize and become the predominant pacemaker, they initiate escape rhythms. Escape rhythms are not considered arrhythmias but rather are protective and occur in an attempt to compensate for the decreased automaticity of the sinus node. Junctional escape rhythm originates from the atrioventricular node or His bundle and has an inherent rate of about 40 to 60 beats per minute. This rhythm typically has a narrow QRS complex, and the P wave may not be seen if it is buried within the QRS complex or may be visible slightly before the QRS complex (short PR interval) or after the QRS complex. In normal sinus rhythm, the P wave is upright in lead II, but in junctional escape rhythm, the P wave is inverted or absent owing to retrograde conduction, as in this case.Many things can cause a decrease in sinus node function leading to junctional escape rhythms. Common causes include hypokalemia, myocardial infarction, and medications such as β-adrenergic blockers, to name a few. Slow heart rates, including escape rhythms, are not uncommon in patients with SCI, as in this case. Depending on the location of the SCI, there can be a total loss of sympathetic innervation, which controls cardiovascular functions including cardiac contractility and heart rate. In this population, only parasympathetic supraspinal control of the heart can occur by way of the vagus nerve, leading to bradycardias and other cardiac rhythm abnormalities. This patient had a history of bradycardia due to her SCI, but its origin was unclear. The mother did note that her daughter's heart rate had decreased about 10 beats per minute on this occurrence and she thus felt it prudent to bring her to the hospital.This patient's chest radiograph showed a slightly enlarged heart and some pulmonary congestion. Her echocardiogram showed normal wall thickness and chamber size, but her wall motion could not be assessed, although it was described as "grossly normal." To prevent further slowing of the heart rate, phenytoin for seizures was changed to oxcarbazepine and baclofen for muscle spasms was withheld. She began treatment with furosemide once daily to decrease the fluid volume overload and a trial of theophylline twice daily to see if it would increase the heart rate. Although well-controlled studies using theophylline for bradycardias in SCI have not been done, several anecdotal cases have shown that treatment and close monitoring for toxic effects have allowed pacemaker implantations to be avoided in the acute phase of SCI. Pacemaker implantation is most often performed in the acute phase of SCI (within 6 weeks of injury) and rarely is done after several months. It was unclear if the junctional escape rhythm was caused by the patient's volume overload because her SCI does not allow compensatory sympathetic activity to increase her heart rate and contractility. After discussing the risks of pacemaker implantation and acknowledging the positive effects of the current treatment regimen with the parents, a conservative approach was agreed on. The risks of pacemaker implantation include thromboembolism and infection, which is one of the leading causes of death in SCI patients. She continued treatment with theophylline and furosemide and was discharged home the following day to be followed up in the clinic.