Timing of Circulatory and Neurological Events in Syncope

Abstract

Syncope usually lasts less than a minute, in which short time arterial blood pressure temporarily falls enough to decrease brain perfusion so much that loss of consciousness ensues. Blood pressure decreases quickest when the heart suddenly stops pumping, which happens in arrhythmia and in severe cardioinhibitory reflex syncope. Loss of consciousness starts about 8 s after the last heart beat and circulatory standstill occurs after 10-15 s. A much slower blood pressure decrease can occur in syncope due to orthostatic hypotension Standing blood pressure can then stabilize at low values often causing more subtle signs (i.e., inability to act) but often not low enough to cause loss of consciousness. Cerebral autoregulation attempts to keep cerebral blood flow constant when blood pressure decreases. In reflex syncope both the quick blood pressure decrease and its low absolute value mean that cerebral autoregulation cannot prevent syncope. It has more protective value in orthostatic hypotension. Neurological signs are related to the severity and timing of cerebral hypoperfusion. Several unanswered pathophysiological questions with possible clinical implications are identified.

Keywords: pathophysiology; syncope; tilt table test; transient loss of consciousness; vasovagal syncope.

Figure 1

Factors affecting cerebral blood flow. Blood will only flow through the brain if two criteria are met: there must be a pressure difference between the arteries and veins supplying the brain, and the vessels in between must be open. The latter depends on a summation of forces opening and closing the vessels. The main opening force is the pressure in the lumen of the vessel. The two closing forces are intracranial pressure and vessel wall tension.

Figure 2

Signs in tilt-induced VVS. Each bar represents the mean value and the 95% confidence intervals for a range of signs, determined by analysis of video-EEG records of 69 cases of tilt-induced VVS [These data conform to Table 2 in Van Dijk et al. (3)].

Figure 3

Explanation of signs in syncope and sudden cardiac death. In syncope cerebral perfusion (bold line) temporarily decreases below the normal level (A). Clinical signs depend on the severity of cerebral hypoperfusion. Dysfunction becomes apparent in two ways: normal function can be decreased or completely lost, and new actions may appear, caused by neuronal disinhibition. With mild hypoperfusion this occurs for the cortex, while the basal ganglia and brainstem still function normally: state (B) appears at the beginning and end of syncope. With more severe hypoperfusion all cortical function is lost, and new signs concern a decrease of function and disinhibition of the brainstem (C). If recovery takes too long, there will be cerebral damage such as the postanoxic coma; if there is no circulatory recovery at all, the result is sudden cardiac death (D).

Figure 4

Signs in slow and quick cerebral hypoperfusion. In cOH, BP decreases after standing up to a varying degree and with varying speed in different people (A). The general tendency is for BP to decrease quickly at first and slower later. Whether symptoms and signs appear depend on whether a symptom threshold of cerebral perfusion is crossed. One result of this is that BP may stabilize at a level too high for syncope to occur, yet too low for patients to act volitionally, causing an “inability to act” (B). In VVS, BP decreases slowly at first, but accelerates thereafter. This means that the critical level at which symptoms such as the inability to act occur, is crossed very quickly that this phase is usually not noted (C).