Cardiac syncope can be divided into two basic pathophysiologic categories: dysrhythmias and structural cardiopulmonary lesions. In both settings, the heart is unable to provide adequate cardiac output to maintain cerebral perfusion.
Although both brady- and tachydysrythmias may lead to transient cerebral hypoperfusion, there is no absolute high or low heart rate that will produce syncope. Symptoms depend on both the autonomic nervous system's ability to compensate for a decrease in cardiac output and the degree of cerebrovascular atherosclerotic disease. A variety of dysrythmias may lead to syncope (Tab.!e..46z1). A bradydysrhythmia is more likely to be an incidental finding on EKG rather than the actual cause of syncope.6 Dysrhythmias are most likely to occur in the setting of ischemic heart disease but also may occur in other disease processes, such as in prolonged QT syndrome (torsades de pointes) and Lyme disease (heart blocks). Syncope from dysrhythmias is typically sudden, with prodromal symptoms lasting less than 3 s. Many patients report lack of any warning or premonition when questioned.
A wide variety of structural cardiopulmonary lesions may lead to an obstruction to flow and syncope. Syncope due to underlying structural cardiopulmonary disease often occurs in the setting of physical exertion but also may be seen in response to an acute vasodilation from medication or a hot environment. The resultant decrease in systemic vascular resistance is normally compensated by an increase in cardiac output to maintain arterial perfusion. In the presence of obstruction to flow, the upper limit of cardiac output is relatively fixed, limiting the compensation for decreased systemic vascular resistance and leading to a decrease in arterial perfusion and possible syncope. Aortic stenosis, a disease primarily of the elderly, is the most common structural cardiac abnormality causing syncope. In aortic stenosis there may be an additional component of abnormal reflex response, with increased ventricular pressures leading to inappropriate vasodilatation. Hypertrophic cardiomyopathy also leads to outflow obstruction and high ventricular pressures. It is characterized by asymmetric left ventricular hypertrophy and occurs most commonly in the young, although this entity is frequently present in persons over the age of 60. Pulmonary outflow obstruction may also lead to syncope. Up to 13 percent of patients diagnosed with pulmonary embolism have an initial syncopal episode that is likely secondary to the acute obstruction to flow by a large embolus.7
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