Pathophysiology of Reflex Syncope: A Review

Wayne O. Adkisson MD; David G. Benditt MD

Disclosures

J Cardiovasc Electrophysiol. 2017;28(9):1088-1097. 

In This Article

Specific Pathophysiologic Features of Reflex Syncope

As previously noted, reflex syncope includes: VVS, carotid hypersensitivity syncope, as well as several, so-called, "situational" syncope syndromes (Table 1). The efferent limb of the reflex is somewhat better understood than the afferent limb(s) or the central cerebral interconnections. Also, while the afferent limb may differ among the various forms of reflex syncope, the efferent limb is seemingly relatively similar.[9] For these reasons, we will begin by briefly reviewing the efferent pathways.

Efferent Pathways

As noted above, syncope, except in rare circumstances such as hypoxia, results from transient failure of CBF to meet the metabolic needs of the brain and nearby structures. This occurs when MAP falls below that required even in the presence of healthy CA to ensure adequate CBF (Figure 2).

MAP depends on the relation of CO to systemic resistance. CO (Figure 1) may fall as a result of a fall in stroke volume (SV) (decrease contractility and/or preload) or a fall in the heart rate (HR), or both. However, even if CO remains unchanged, a sudden drop in systemic vascular resistance (SVR) can also result in a collapse of MAP (Figure 1).

As alluded to earlier, a fall of MAP is an essential feature in all forms of syncope. If the primary cause is arterial or venous dilation (thereby tending to trap blood in the lower extremities and/or splanchnic beds) with little or no bradycardia, the syncope is deemed as "vasodepressor." Thus, the term "vasodepressor" implies an in-depth knowledge of the syncope mechanism and should not be used as a synonym for reflex syncope or a descriptor of VVS unless that additional insight into the mechanism of syncope is known.

In the majority of cases, reflex syncope is accompanied by a marked or relative decrease in heart rate. When the heart rate slows dramatically, the faint may be referred to as "cardioinhibitory." However, even in the setting of cardioinhibition, most reflex fainters also exhibit vasodepressor physiology. Consequently, such faints are most often of "mixed" origin (i.e., vasodepressor and cardioinhibitory). Only if a vasodepressor element is not evident should the term "cardioinhibitory" reflex faint be used.

Cardioinhibition results from increased vagal input to the sinus node (Figure 1) and/or atrioventricular node (AV) node. In syncope resulting from either mixed or cardioinhibitory pathophysiology, asystole may develop and continue for many seconds. Even if vascular tone remains intact, asystole results in a sudden and dramatic fall in MAP. BP may decline by roughly half within a few seconds, especially in the upright victim.[10] After 10–15 seconds of asystole, circulation comes to a standstill with a uniform static BP of 10–20 mmHg.[11] Even if vascular tone is preserved, such a marked fall in MAP will result in syncope. Less dramatic heart rate slowing may also result in a sufficient decline in MAP for syncope to ensue. The failure of the heart rate to increase as would normally occur in the face of a fall in MAP also reflects a degree of cardioinhibition.

Unlike cardioinhibition, which results from an increase in vagal stimulation of the sinus node or AV node or both, vasodepression results from a decrease in sympathetically mediated arteriolar and/or venous vasoconstriction (Figure 1). The resulting decline in SVR, even if CO is maintained, leads to a fall in MAP. In fact, even in the absence of cardioinhibition, CO often falls as well. A fall in CO results because the decrease in vasoconstriction is not confined to the arterial bed. Veno-constriction is also affected. The resulting increase in venous capacitance leads to a fall in venous return to the heart, and hence a fall in SV. Since CO is the product of SV and HR, even if HR is maintained a fall in SV will result in a fall in CO. Recent work suggests that the primary cause of hypotension in reflex syncope is not, in fact, a fall in SVR, but rather a fall in CO due to a reduction in SV resulting from an increase in venous capacitance.[12] Further, it follows that maneuvers that diminish venous congestion in the large muscle groups of the legs (e.g., counter-pressure muscle straining) or the abdomen (e.g., abdominal binders) may help prevent hypotension and syncope.

The highly variable nature of the cardioinhibitory feature of reflex syncope led to the belief that TLOC was primarily a vasodepressor, and in particular a diminution of SVR event. However, recent investigations suggest that this view is too simplistic. Verheyden and colleagues[13] demonstrated that SVR was maintained, or fell only slightly, and only shortly before syncope occurred. Whereas, a marked fall in CO was observed in the period leading up to the event. Similar investigations suggest that although a loss of sympathetically mediated vasoconstriction does occur, it only occurs during or just before syncope, and that a decline in CO is the primary factor in the fall in MAP.[14]

It appears that reflex syncope can be terminated in a variety of ways. A common feature is the restoration of central volume. Clinically, this occurs when TLOC leads to the loss of postural tone and the patient falls down. The horizontal (gravity neutralizing) position and various physical counter-maneuvers (e.g., lower body muscle tensing and leg crossing) alluded to earlier[15] achieve the same effect, namely, enhancing venous return. Presumably, the increase in venous return leads to interruption of the afferent pathways that triggered the reflex in the first place.

Afferent Pathways

The afferent pathways triggering the various forms of reflex syncope are less well understood. While space does not permit comprehensive review of the various proposed mechanisms, we will touch upon the leading theories in our discussion of the specific syndromes below.

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