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Post exercise vasovagal syncope: Difference between revisions
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{{case_present| | {{case_present| | ||
A 28 years old male fire fighter with an excellent general condition lost transiently consciousness after termination of a routine check-up exercise test | A 28 years old male fire fighter with an excellent general condition lost transiently consciousness after termination of a routine check-up exercise test <cite>Krediet</cite> | ||
. The episode occurred, while he was sitting motionless on the bicycle ergometer after the test, and his skin fold thickness was being measured. The patient was declared unfit for his job. The patient was referred to our syncope unit for further analysis of the episode. | |||
The exercise test was repeated using continuous non-invasive blood pressure monitoring. The figure shows the original continuous blood pressure and instantaneous heart rate tracing. | The exercise test was repeated using continuous non-invasive blood pressure monitoring. The figure shows the original continuous blood pressure and instantaneous heart rate tracing. | ||
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== Editor's Comments == | == Editor's Comments == | ||
The majority of cases of syncope occurring after exercise fall into two related categories: 1) an exaggerated form of the normal post-exercise hypotension response, and 2) neurally mediated syncope (i.e., vasovagal reactions). It is probable that the former triggers the latter. | The majority of cases of syncope occurring after exercise fall into two related categories: 1) an exaggerated form of the normal post-exercise hypotension response, and 2) neurally mediated syncope (i.e., vasovagal reactions). It is probable that the former triggers the latter. <cite>Krediet</cite> | ||
=== Post-exercise hypotension === | === Post-exercise hypotension === | ||
During post-exercise hypotension, the mechanisms that regulate arterial pressure drive a modest but sustained reduction in arterial pressure. The cause of PEH is two-fold, involving both neural and local vascular mechanisms | During post-exercise hypotension, the mechanisms that regulate arterial pressure drive a modest but sustained reduction in arterial pressure. The cause of PEH is two-fold, involving both neural and local vascular mechanisms <cite>Kenney</cite> | ||
<cite>Halliwill</cite>. In comparison to rest, PEH is characterized by a persistent drop in systemic vascular resistance that is not completely offset by increases in cardiac output <cite>Kenney</cite><cite>Halliwill</cite>. The vasodilatation that underlies PEH is not restricted to the sites of active skeletal muscles, but involves inactive regions as well. The associated rise in arterial blood inflow through the vasodilated regions contributes to an increase in venous pooling of blood. | |||
During exercise, rhythmically contracting skeletal muscles in the lower part of the body reduce the degree of venous pooling by squeezing veins, in effect, pumping blood back to the heart. This phenomenon is known as the ‘muscle pump’. This “pump” is absent during passive recovery from exercise. The increase in venous pooling, in conjunction with the loss of plasma volume associated with exercise, leads to a reduction in central venous pressure (~ 2 mmHg supine) and cardiac filling | During exercise, rhythmically contracting skeletal muscles in the lower part of the body reduce the degree of venous pooling by squeezing veins, in effect, pumping blood back to the heart. This phenomenon is known as the ‘muscle pump’. This “pump” is absent during passive recovery from exercise. The increase in venous pooling, in conjunction with the loss of plasma volume associated with exercise, leads to a reduction in central venous pressure (~ 2 mmHg supine) and cardiac filling <cite>Halliwill</cite><cite>Halliwill2</cite>. Despite this fall in cardiac preload, stroke volume is maintained due to the reduction in cardiac after-load and a probable increase in cardiac contractility <cite>Kenney</cite><cite>Halliwill2</cite>. The net result of these influences on the blood vessels and heart is that cardiac output is elevated (heart rate is higher with unchanged stroke volume). Thus PEH is due to a persistent drop in systemic vascular resistance that is not completely offset by increases in cardiac output. | ||
The main point is that PEH is common after moderate-intensity dynamic exercise. In general, this is a benign process and in the majority of individuals PEH is insufficient to cause syncopal symptoms. | The main point is that PEH is common after moderate-intensity dynamic exercise. In general, this is a benign process and in the majority of individuals PEH is insufficient to cause syncopal symptoms. | ||