A dead stop: Vasovagal mediated asystole

LEARNING OBJECTIVE #1: Recognize that vasovagal syncope is a diagnosis primarily based on a thorough history LEARNING OBJECTIVE #2: Recognize vasovagal syncope can cause profound vasodiliatory and cardioinihibitory responses including complete sinus arrest. CASE: A 58-year-old female with medical history of prior syncope and breast carcinoma now in remission presented for elective breast reconstruction surgery. Post-operative day #2 she was working with physical therapy and developed extreme shoulder and chest wall pain at surgical site followed by nausea, lightheadedness and diaphoresis. Continuous telemetry monitoring during the event showed sinus rhythm transition to junctional bradycardia followed by 20.7 s of asystole associated with loss of consciousness. After regaining consciousness she complained of fatigue and malaise with gradual recovery over several minutes. Cardiac evaluation with ECG, TTE and LHC 2 months prior were all normal. Past workup for prior episodes of syncope included multiple ambulatory ECG monitors without evidence of causative arrhythmia. The patient noted symptoms of lightheadedness, nausea, diaphoresis occurring every few months, all associated with moments of severe emotional distress or pain. Occasionally, if severe, they will progress to transient loss of consciousness. She has always been able to feel the event coming on, lies down and never been injured due to these episodes. She had no personal or family history of heart disease and no family history of sudden death. DISCUSSION: Syncope is the transient loss of consciousness and remains a common diagnosis, with over 20 % of cases considered to be vasovagally mediated. A thorough history will elicit a diagnosis in nearly 50 % of syncope events. In the setting of an appropriate history and negative cardiac workup, a diagnosis of neurally-mediated vasovagal syncope was made. Vasovagal syncope occurs classically in setting of orthostatic or emotional stress resulting in inappropriate autonomic reflexes causing either a significant cardioinhibitory, vasodilatory process, or both. The cardioinhibitory response can result in sinus slowing or arrest, AV delay or block, or both. In our case the patient had a long asystolic pause due to sinus slowing/arrest and transient atrioventricular block, likely from extrinsic autonomic changes rather than intrinsic conduction disease. It is important to include all forms of syncope in the differential diagnosis. Forms of neurally mediated syncope include vasovagal, situational, carotid sinus hypersensitivity and postexertional, which account for up to two-thirds of etiologies behind syncope. These are largely considered benign. Orthostatic hypotension account for approximately 10 % of cases. Cardiogenic syncope accounts for an additional 10-20% of cases and occurs in the setting of structural heart disease, cardiomyopathy, outlet obstruction, and arrhythmias. Cardiogenic syncope is unlikely in the setting of a normal ECG and a structurally normal heart on echocardiography, as abnormal findings on ECG are seen in up to 90 % of patients with cardiac syncope. Other important etiologies include medication effect, seizure, hypovolemia, hemorrhage, hypoglycemia, aortic dissection, pulmonary embolism, cardiac tamponade and psychogenic. Vasovagal syncope has not been associated with an increase risk of cardiovascular morbidity or mortality. Conservative management principles revolve around physical maneuvers to help increase peripheral vascular resistance and venous return including lying supine with legs raised above the heart, leg-crossing and arm gripping with muscle tension, or squatting. Remaining well hydrated for volume expansion or increasing dietary salt as tolerated is recommended. Thigh-high compression stockings can also be used. There has been no clear evidence in favor of pharmacologic therapies. While once thought to be theoretically beneficial, beta-blockers have fallen out of favor and are no longer recommended. Fludrocortisone, a mineralocorticoid to promote volume expansion, and midodrine, a vasoconstrictor, are the most commonly prescribed but have not shown consistent evidence of benefit. Other agents have been proposed but have indeterminate evidence to support their use. In our case, the prologed cessation of electrical cardiac activity was of concern. Cardiac pacing can correct the cardioinhibitory process but does not correct the vasodilatory process, leaving many patients prone to recurrent events despite an invasive procedure. A 2009 meta-anaylsis on pacemaker implantation in vasovagal syncope showed no overall benefit but did suggest an “expectation effect” on patients after pacing. A more recent trial of pacing in neurally mediated syncope and asystolic pauses showed a borderline statistically significant reduction in syncope recurrence at two years. Options were presented to our patient who elected against further testing or permanent pacemaker implantation. She had an otherwise uncomplicated hospital course without further arrhythmias or syncopal events.