A 27-year-old woman comes to the emergency department after losing consciousness for 2 minutes while standing in line at a supermarket. She recalls nausea and a feeling of warmth spreading over her body immediately before she passed out. Her friend, a nurse who was with her during the episode, noted a weak pulse of 40/min. The patient was not confused after the episode and has never experienced a similar event. She takes sertraline for generalized anxiety disorder, and the dosage was recently increased. She does not use tobacco, alcohol, or illicit drugs. The patient's father had a heart attack at age 50, and her sister has a seizure disorder. Vital signs are within normal limits. ECG shows normal sinus rhythm with no other abnormalities. Which of the following most likely contributed to this episode?
Clues to etiology of syncope | ||
Reflex | Vasovagal |
|
Situational |
| |
Carotid |
| |
Orthostatic | Medications |
|
Hypovolemia |
| |
Autonomic |
| |
Cardiac | LV outflow |
|
Ventricular |
| |
Conduction |
| |
*Sick sinus syndrome or advanced atrioventricular block. DM = diabetes mellitus; HD = heart disease; LV = left ventricular. | ||
This patient experienced a syncopal event with a trigger (eg, prolonged standing), a prodrome (eg, nausea, feeling of warmth), and a rapid recovery (eg, within 1-2 min). This clinical presentation is suggestive of vasovagal syncope, a type of reflex syncope. Other common triggers include pain, anxiety, and strong emotion. When vasovagal syncope is repeatedly triggered by a certain activity (eg, coughing, micturition), it is referred to as situational syncope.
The pathophysiology of reflex syncope is not completely understood. The initial signal is likely triggered in the cerebral cortex or within various baroreceptors or mechanoreceptors (eg, cardiopulmonary, genitourinary) and then sent via afferent neuronal pathways to the brainstem. On receipt in the brainstem's cardioregulatory center, some combination of the following efferent responses occurs:
Cardioinhibitory response: Increased parasympathetic stimulation to the sinoatrial and atrioventricular (AV) nodes slows heart rate. In addition, decreased sympathetic output to the myocardium decreases myocardial contractility.
Vasodepressor response: Decreased sympathetic output to vascular smooth muscle causes vasodilation of venous capacitance veins (ie, decreased cardiac preload) and systemic arterioles (ie, decreased perfusion pressure).
The result of these responses is a brief but profound decrease in cardiac output with hypotension and markedly decreased cerebral perfusion; when this decrease overcomes the limits of cerebral autoregulation, syncope occurs. Vasovagal syncope is generally benign and usually has an excellent prognosis.
(Choice A) Increased, rather than decreased, baroreceptor activity in the carotid sinuses (ie, carotid hypersensitivity) is a potential cause of reflex syncope. However, this typically occurs due to direct pressure on the carotid sinus (eg, neck extension, shaving) and usually affects older patients.
(Choice C) Intrinsic disease of the sinoatrial node (ie, sick sinus syndrome) can cause bradycardia and syncope. However, affected patients are typically older with comorbid conditions and often have transient symptoms of fatigue, light-headedness, palpitations, and dyspnea. ECG abnormalities (eg, sinus pauses) are often present.
(Choices D and E) A number of medications can cause orthostatic syncope by impairing vascular tone or AV node conduction to disrupt the normal baroreceptor response; however, selective serotonin reuptake inhibitors (eg, sertraline) do not significantly affect the AV node or vascular tone.
Educational objective:
Vasovagal syncope, a type of reflex syncope, typically involves a trigger (eg, emotional stress, prolonged standing), a prodrome (eg, nausea, warmth), and a rapid recovery (eg, within 1-2 min). It results from a transient, autonomic nervous system–mediated cardioinhibitory and vasodepressor response.