 Hello and welcome to Physiology Open. In this video, we will see how various types of tachyarhythmias may be treated. First, let us recall a bit about anti-arhythmic drugs. Well, there are four classes of anti-arhythmic drugs. Class 1 drugs block sodium channels. Class 2 are beta blockers. Class 3 are potassium channel blockers and class 4 drugs are calcium channel blockers. Also, class 1 drugs further have three subclasses. Class 1A drugs block sodium channels in open state. Class 1B drugs block sodium channels in inactivated state. Since sodium channels inactivate on depolarization, the most important effect of these drugs occurs on already depolarized tissue as seen in Estemia. Class 1C drugs block sodium channels in open state and also prolong the recovery time of the channels. Now, here is a diagram showing action potential of contractile cells that is atrium ventricles as well as pacemaker cells, which includes an SA node, AV node, bundle of his. There are some significant differences between these action potentials. Phase 0 of action potential of pacemaker cells is caused by entry of calcium due to opening of calcium channels. While phase 0 of contractile cells is caused by entry of sodium due to opening of sodium channels. Phase 4 of action potential of pacemaker cells slowly drips towards threshold without any external stimulus and its slope may be increased by sympathetic activity and decreased by parasympathetic activity. Thus, increasing or decreasing the number of impulses generated respectively. In contrast, you see phase 4 of contractile cell action potential it is constant. Phase 3, that is phase of repolarization occurs due to exit of potassium in both contractile as well as pacemaker cells. Okay, now let's come to strategies for treating tachyarythmias. Fundamentally, in any tachyarythmia, what is important clinically is increased ventricular rate. If ventricular rate is too much, cardiac output will decrease tremendously because filling of the ventricles will be affected. Now for treating, we should know whether this increased ventricular rate is due to problems in ventricle itself or due to problems above the ventricle, which may be at level of SA node, atria or AV node. So based on their origin, they are known as either ventricular arrhythmias or supraventricular arrhythmias, that is due to origin above the ventricles. To take one example of supraventricular arrhythmias, increased number of impulses generated in atria will be conducted ultimately to ventricles causing increased ventricular rate and thus affecting the cardiac output. So treatment strategy will differ depending on the cause of increased ventricular rate. First, some fundamentals on treatment strategy. See, any interference if you have to do for atria or ventricular cells, you have to use class 1 drugs or class 3 drugs. Class 1 drugs that is sodium channel blockers will affect the phase 0 because it is occurring due to entry of sodium ions and class 3 drugs that is potassium channels blockers will affect phase 3. That is slow it down because it is occurring due to exit of potassium through potassium channels. In arrhythmias which occur due to pacemakers that is SA node or involved AV node, in that case it is class 2 drugs that is beta blockers that are used. They basically act on phase 4 and decrease its slope. Or class 4 drugs that is potassium channel blockers are used which act on phase 0. So basically these two classes of drugs are used for supraventricular arrhythmias that are caused in SA node or involved AV node. Now let's discuss individual arrhythmias. First we will see supraventricular causes of tachyarrhythmias. In case of supraventricular arrhythmias cause can be at the level of SA node, or atria or AV node pathway. At the level of SA node first cause of tachyarrhythmias is inappropriate tachycardia. It occurs due to increased number of impulses generated by SA node at rest or out of proportion to the intensity of exertion. So as we have seen earlier for treating SA node arrhythmias we may use either class 2 drugs that is beta blockers which will act here and decrease its slope. Or class 4 drugs that is potassium channel blockers which will act here in phase 0. Ultimately they will decrease the number of impulses that are being generated. Now second cause is atrial. It may be either atrial flutter or fibrillation. Atrial flutter or fibrillation occur due to some ectopic focus in atria that generates an impulse and this impulse finds reentry path in atria itself. So it keeps on moving in circle causing tachyarrhythmias. Now some of these impulses reach to ventricles thus increasing the ventricular rate also. In atrial flutter atrial rate is 240 to 300 beats per minute and ventricular rate may be about 150 beats per minute. While in atrial fibrillation ventricular rate may be as high as 200 beats per minute. So what should you do to treat this arrhythmias? Fundamentally you need to decrease the number of impulses being conducted to ventricle. So you need to act on AV node which has action potential of pacemaker cells. So again the drugs in class 2 that is beta blockers and class 4 that is calcium channel blockers like parappermill and diltiasm may be used. So basically the arrhythmias is not terminated. The number of impulses generated will be more only but they won't be conducted to ventricles thus preventing the deterioration of function of heart despite continued increase generation of impulses. Second thing if ventricular rate cannot be controlled or the patient experiences symptoms like palpitation despite the control of the ventricular rate or the patient is hemodynamically unstable we need to revert back to sinus rhythm that is terminate the arrhythmias. So if it is an emergency condition when the patient is hemodynamically unstable we need to use electrical cardioversion to bring back the rate to sinus rhythm quickly. In case if it is not an emergency but the patient is experiencing the symptoms or in case the condition is recurrent then after reverting to original rhythm we should use drugs to maintain sinus rhythm. For both these cases we need drugs which act on contractile cells action potential. So either class 1c drugs that is propophenone or class 3 drugs that is dophitalite may be used. Now remember that for prolonged treatment for recurrent atrial fibrillation or frutter another class 3 drug that is amiodarone is used because it has a long duration of action and has very low pro arrhythmic potential. Most of the anti arrhythmic drugs are useful for one type of arrhythmias but predisposed to other types of arrhythmias. Amiodarone on the other hand has very low pro arrhythmic potential and is preferred for chronic therapy. However it may lead to some other side effects on chronic therapy and need to be monitored for that. Also ablation of the focus with radio frequency waves may be done. Third cause of supraventricular arrhythmias is reentry arrhythmias. It may be either avianodal reentry arrhythmia or itchuventricular reentry arrhythmias. In avianodal reentry both past and slow pathways are present in the conducting pathways involving avi node. So again we need to use drugs which act on pacemaker action potential. In case of reentry keeping the cells refractory for longer time terminates the arrhythmias. Initially vagal manoeuvres are recommended which decrease the resting membrane potential. Another very useful drug may be used that is adenosine. Adenosine hyperpolarizes the tissue making them less excitable and it acts for very very short duration. So it is used for acute therapy to terminate the reentry. Because of it so fast and very very short duration of action it is also known as chemical defibrillator. Then class 2 and class 4 drugs may also be used because avianod is involved. For atrioventricular reentry where there is an accessory pathway between the atria and the ventricles we need to act on ventricular cells and keep them refractory for longer time or make them less excitable. This is done by using potassium channel blockers that is class 3 drugs which will prevent the cells from getting repolarized and class 1 drugs which will increase the threshold. Again vagal manoeuvres and adenosine will hyperpolarize the tissue and may be used for termination of atrioventricular reentry arrhythmias just like avianodal reentry. In fact vagal manoeuvres and adenosine are the first choice treatment for terminating these reentry arrhythmias. Now let's come to ventricular arrhythmias. By this time you might have understood that for ventricular arrhythmias we need to use class 1 drugs or class 3 drugs because these drugs act on contact cells action potential. For ventricular tachycardia if the person is hemodynamically unstable we need to urgently use electrical cardioversion to revert him back to sinus rhythm. If ventricular tachycardia is rising in an ischemic tissue we can use class 1B drugs especially Lidocale which is given by intravenous root. We have discussed earlier that class 1B drugs are used mainly for arrhythmias arising in ischemic tissue. In case of recurrent ventricular tachycardia we need to resort to long term treatment. Again for long term we have to use class 3 drugs especially amyadarol. For ventricular fibrillation which is caused by reentry for hemodynamically unstable cases again we need to use electrical cardioversion to revert them to sinus rhythm. In case of recurrent ventricular fibrillation we need to implant a cardiac defibrillator i.e. ICD in patients heart which senses the origin of ear and delivers shocks to restore normal sinus rhythm. If the patient is not an ideal candidate for ICD we may use class 3 drug amyadarol to increase the refractory period and make the cells unresponsive so that reentry is not possible. So these were the approach for the treatment of various types of tachyarrhythmias. Hopefully you have seen the video on mechanism of generation of arrhythmias if not you can check out this playlist which also talks about the classes of antiarrhythmic drugs. Okay, thanks for watching the video. If you liked it don't forget to subscribe to the channel Physiology Open. Thank you.