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.

Identifying patients with epilepsy at high risk of cardiac death: signs, risk factors and initial management of high risk of cardiac death

“…With further BP decline, subjects have difficulty concentrating and become unaware of their surroundings. A brief period of staring and an inability to act may occur prior to complete syncope [22]. Eventually, when BP reaches the critical closing pressure, patients will fall and lose consciousness.…”

Predicting Vasovagal Responses: A Model-Based and Machine Learning Approach

“…Consistent with this, there is also an immediate loss of the baroreflex-generated Muscle Sympathetic Nerve Activity (MSNA) at the onset of syncope ( 40 – 42 ). The pathophysiological mechanism and significance of the baroreflex disengagement in producing bradycardia and hypotension have been conjectured to be the basis for VVS ( 3 , 4 ), but no specific mechanism has been identified that could produce these changes. As such, despite being relatively common ( 1 , 12 , 43 ), the origin and neural basis of VVR s, which are related to VVS are not known ( 2 , 36 , 38 ) and there are no physical signs of neurogenically mediated VVR .…”

“…A neurogenically induced vasodilation and corresponding inappropriate bradycardia can lead to hypotension and transient loss of body tone and consciousness, that is, fainting. This condition has been termed neurogenic or vasovagal syncope ( VVS ) ( 1 – 4 ). Many nerves connect to the heart and blood vessels, which help control the beat frequency of the heart and the dilation and contraction of the blood vessels that control blood pressure ( BP ).…”

“…This maneuver usually brings on the symptoms of fainting and returning subjects to a reclining position makes them go away. Treatment of recurrent VVS using implanted pacemakers or beta blockers is often ineffective ( 6 – 10 ), because the underlying changes in the cardiovascular system that lead to the syncope are still incompletely understood ( 11 , 12 ), although there has been an acknowledgment that the relative timing of BP and HR plays an important role in VVS generation ( 3 , 4 ). The role of the vestibular system in generating the timing has only recently been explored and has suggested ways of habituating VVS as a treatment option ( 13 ).…”

Cardiovascular fingolimod effects on rapid baroreceptor unloading are counterbalanced by baroreflex resetting

“…Since cardiovascular autonomic function is frequently compromised in patients suffering from multiple sclerosis (MS) [10,15,18,23,31], immune-modulating therapies with effects on cardiovascular function might aggravate autonomic dysregulation in MS patients [10]. Particularly orthostatic intolerance and syncope [10] might be triggered by vagomimetic fingolimod effects since reflex syncope typically results from cardiovagal activation and sympathetic withdrawal [39]. As central autonomic modulation and baroreflex function may be compromised in MS patients [10,18,40], vagomimetic fingolimod effects might further alter centrally mediated or baroreflex dependent cardioinhibitory responses and thus increase the risk of syncope in MS patients.…”