Tachycardia: Difference between revisions
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=====Pathophysiology:===== | =====Pathophysiology:===== | ||
The pathophysiology of AF is complex and incompletely understood.<cite>24</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>25</cite> This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (i.e. the autonomic nerve system).<cite>26</cite> These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change and move through the atria. The ability of the atria to sustain AF is dependable on atrial structural changes (fibrosis/inflammation). AF induces electromechanical changes in the atrium. These changes make it easier for AF to perpetuate; AF begets AF.<cite>27</cite> Due to the fast and rapid activation of the atria, there is no functional mechanical activity left. This results in the most feared complication of AF, namely forming of blood clots (with for instance stroke as a result). During atrial standstill the atria does not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.<cite>28</cite> The strokes resulting from AF are often more severe than other causes of stroke. Another complication of AF is a tachycardiomyopathy. Due to the constant chaotic activity in the atria, the AV-node can conduct these signals at high rate. The result is an irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>29</cite> | The pathophysiology of AF is complex and incompletely understood.<cite>24</cite> In most patients the trigger of AF results from extra beats in from the pulmonary veins.<cite>25</cite> This is due to myocardial sleeves growing into the pulmonary veins, which are triggered to fire extra beats due a variety of modulators (i.e. the autonomic nerve system).<cite>26</cite> These triggers can trigger the atria into forming multiple self-perpetuating re-entry circuits. These multiple wavelets, are self-perpetuating circuits than constantly change and move through the atria. The ability of the atria to sustain AF is dependable on atrial structural changes (fibrosis/inflammation). AF induces electromechanical changes in the atrium. These changes make it easier for AF to perpetuate; AF begets AF.<cite>27</cite> Due to the fast and rapid activation of the atria, there is no functional mechanical activity left. This results in the most feared complication of AF, namely forming of blood clots (with for instance stroke as a result). During atrial standstill the atria does not effectively pump blood to the ventricle, and blood can coagulate the left atrium or left atrial appendage.<cite>28</cite> The strokes resulting from AF are often more severe than other causes of stroke. Another complication of AF is a tachycardiomyopathy. Due to the constant chaotic activity in the atria, the AV-node can conduct these signals at high rate. The result is an irregular fast ventricular activation. These fast activation of the ventricle can lead to a (reversible) dilated cardiomyopathy.<cite>29</cite> | ||
{| class="wikitable" border="0" cellpadding="0" cellspacing="0" width="600px" | |||
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|colspan="2" bgcolor="#cfefcf"|'''Classification of Atrial Fibrillation (AF) related symptoms based on the European Heart Rhythm Association (EHRA) score are: <cite>EHRA</cite>''' | |||
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!EHRA I | |||
|No symptoms | |||
|- | |||
!EHRA II | |||
|Mild symptoms; normal daily activity not affected | |||
|- | |||
!EHRA III | |||
|Severe symptoms; normal daily activity affected | |||
|- | |||
!EHRA IV | |||
|Disabling symptom; normal daily activity discontinued | |||
|} | |||
=====Clinical diagnosis:===== | =====Clinical diagnosis:===== | ||
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=====Pathophysiology:===== | =====Pathophysiology:===== | ||
AVNRT is a regular arrhythmia relying on the dual AV-physiology for its maintenance. The AV-node usually has two pathways in these patients; a fast pathway with fast conduction times and a slow pathway, which conducts slowly. The fast pathway has a longer refractory period than the slow pathway. Due to these characteristics re-entry formation is possible. Normally the impulse from the atria is conducted through the fast pathway to the ventricle. The impulse also travels through the slow pathway, but reaches tissue still in the refractory period at the end of the AV-node (as the fast pathway has already conducted the impulse and activated this part of the AV-node). When an extra premature atrial contraction occurs it encounters a refractory fast-pathway (which has a longer refractory period). It enters the slow pathway and when it reaches the end of this pathway it can conduct to the (now restored) end of the AV-node to the ventricles | AVNRT is a regular arrhythmia relying on the dual AV-physiology for its maintenance. The AV-node usually has two pathways in these patients; a fast pathway with fast conduction times and a slow pathway, which conducts slowly. The fast pathway has a longer refractory period than the slow pathway. Due to these characteristics re-entry formation is possible. Normally the impulse from the atria is conducted through the fast pathway to the ventricle. The impulse also travels through the slow pathway, but reaches tissue still in the refractory period at the end of the AV-node (as the fast pathway has already conducted the impulse and activated this part of the AV-node). When an extra premature atrial contraction occurs it encounters a refractory fast-pathway (which has a longer refractory period). It enters the slow pathway and when it reaches the end of this pathway it can conduct to the (now restored) end of the AV-node to the ventricles | ||