---start---- anesth 3.30.98 klein when should an arrhythmia be treated? did everyone read those chapters from that textbook? people are saying yes...er...uh...okaaaayyyyy. we stopped last time when she was trying to explain when you would want to treat an arrhythmia and when you wouldn't. she is referencing dr. Knight's handout which talks about old theories, and she says he believes in letting some stable arrhythmias go without treatment. but he's talking about animals that come in healthy and happen to have arrythmias that are stable and not putting the animal at risk of sudden death. she's talking today about arrhythmias that occur suddenly during anesthesia as a result of concurrent disease, injury, electrolyte abnormalities, blood loss, chest injury, drug use, etc. so the same arrhythmia that dr. knight wouldn't treat in the office might need to be treated if it occured suddenly during anesthesia. some criteria: is it getting worse? affecting cardiac output? affecting coronary perfusion? if yes, treat. slide: premature atrial complexes in this EKG from horse. there are normal PQRST complexes. there are some double peaked P waves. but there is no real difference b/w the complexes of the normal beats or the premature beats. there is little effect on hemodynamics. the baseline variation is an artifact of respiration. the lungs fill, change the configuration of the chest, so baseline moves around, because electrode position changes a little. a more rapid, prolonged atrial tachycardia then returning to sinus rhythm. HR is about 100 (5*20) during the run of tachycardia. probably wouldn't treat this either. other examples of atrial arrhythmias. here we see normal complex followed by atrial premature beat, then that pattern continues. sometimes we see one regular beat plus one premature beat, sometimes two regular beats then one premature beat, or one regular and then two premature beat. atrial bigeminy, trigeminy. might not notice it in a small animal. if these occur, look for a reason, but do not worry too much about it. check if animal is alkalotic, hypoxemic, but it's hemodynamically insignificant since cycle lengths are pretty normal, filling and conduction seem to be normal, so you don't have to worry that much. you don't have to think too hard to assume that this one is bad. she says if you look closely, you might see an R wave now and then. it's very rapid, over 200 bpm. it's hard to say if it is atrial or ventricular tachycardia, b/c it is so rapid that the P and T waves would merge. it could be very rapid sinus tachycardia. not all complexes look alike, so there may be probems with conduction or ectopic foci firing at random times. there may be relative conduction blocks. rates this fast in a horse (that isn't racing - racehorse could have 200 bpm ok) (this horse was dying of blood loss during anesthesia) indicates sudden iatrogenic administration of catecholamine, or sudden drop in BP reducing coronary perfusion, you would have to treat immediately. equine base-apex ekg. normal beat - double peaked P, R, S, T, then another P - but then, there is an abnormally early Q wave - an early firing. there could be some effect on stroke valume - palpate a pressure to see if it is strong enough. or look at pressure wave if you have the right machine hooked up. then, there is a pause before the next beat. if you see one of these early beats now and then you do not have to treat it. another equine EKG - this horse had a run of ventricular ectopic beats - paroxysmal ventricular tachycardia. no P waves, sometimes buried within QRS complex. hemodynamic consequnce - at least there is no atrial component of the stroke volume, and possibly, there is an affect on ventricular ability to pump due to abnormal conduction. duration of QRS is normal. probably, for an anesthetized animal, there is little hemodynamic consequence to this type of v-tach. you can feel pulses and look at pressure waves if you are concerned. when you see abnormal things on a rhythm strip, and you aren't sure if they are real or artifacts, look for T waves. if there is a ventricular depolarization, there must be repolarization. artifacts do not have to repolarize. if there is no T wave, it's possible that there was isoelectric repolarization within the lead you are using, so you would switch leads and see if you saw a t wave on another lead. ventricular ectopic activity that is not acceptable: this horse has a couple of what could be normal PQRST, and it also has bunches of wide QRST complexes. the upper strip shows a rate approaching 300 which would probably not be causing normal cardiac output. heart is going too fast, probably hypoxic due to rapid rate of firing and falling BP. this is approaching ventricular fibrillation. T wave changes - in advanced cardiac life support classes they teach that people who have MIs are often diagnosed when unipolar chest leads are used and you look for a t wave inversion, associated with ischemia. the lead closest to the area of damage will show T wave inversion. in our domestic animals esp under anesthesia - first of all, MI very unlikely. myocardial ischemia usually not focal, usually due to global myocardial hypoxia, or regional, but not a discrete area associated with specific arteries. so don't worry too much about T wave inversion. can occur in awake horses due to changes in sympathetic tone - if you scare a horse, his T waves may invert. this happens during anesthesia and isn't really that important. another sign of myocardial hypoxia is an ST segment shift. again, in the human, the direction and lead configuration is really well worked out for certain focal areas of myocarial ischemia. in animals, usually global hypoxia is causing this. ST segment depression is hard to understand when a global situation is causing it - the damaged cells have membrane potentials which aren't maintained b/c their ion pumps are malfunctioning - so instead of staying at -90 it starts rising toward threshold =- it's less polarized than normal. so current could flow from damaged area to normal area. this is happening during diastole - a P wave comes and atria depolarize, rest of heart depolarizes, and then there is 0 or sl positive potential across the membrane. now there is no current flowing from damaged area to normal area - so that is the normal baseline. the part that looks like the baseline is really elevated due to abnormal current flow. now, some areas of the heart are very subject to problems from inadequate perfusion due to low diastolic pressure. so they call this ST segment shift, but it is really a baseline shift. don't have to remember all that, just try to understand where it is coming from. so this can be evidence of something bad. here there appears to be normal conduction through ventricles. not sure what other circumstances can cause this in animals. in humans, esp young parturient women with spinal or high epidural anesth - when you give an epidural, you give a dose and get a level of block somewhere in midthorax. some women who had epidurals that went high ended up having ST segment shifts. but these were healthy women having babies, and why would they be having MIs? so they thought maybe it is sympathetic block. dog studies seem to back this up. it might be true. the problem is, we don't know why it would create this or what the significance is. but you might see it in an animal with a high epidural. if you see it you should worry that something is wrong, and should check BP and ensure that heart is getting perfused adequately. ventricular ectopic foci - look at how early they occur. sick goat came in with almost no palpable pulse and nearly inaudible heart. there is a wide, long, T wave. he had many episodes of ventricular ectopic foci occuring - and one of them then degenerated into ventricular fibrillation. early PVC - "R on T" - may be dangerous. now, many people walk around with PVCs and no problems, but it CAN be a problem especially if there are other things going on which might increase susceptibility to fibrillation. very early pvcs suddenly occuring during anesthesia should be treated. markedly slow conduction through ventricles, bizarre conduction patterns - here we see an asiatic lion EKG during a root canal. we see what might be a ventricular escape rhythm with sinus arrest due to high vagal tone due to stimulation of trigeminal nerve.there are no P waves anywhere. we have seen this occur in three big cats so far. if this is vagal phenomenon, it may or may not respond to atropine. if it doesn't, you may want to use a sympathomimetic. you would also want to feel pulses to see if output was high enough - if there is no pulse, do CPR. if you need to treat a rhythm disturbance - look for an underlying cause. check rates of fluid administration. remember diastolic pressure is important for coronary perfusion. so increase fluid rate to keep up BP, tilt head down - may improve venous return from hind quarters. change body position as needed. decrease depth of anesthesia if hypotensive, perhaps treat hypotension with inotropic or vasopressic drugs. some arrhythmias are exacerbated by respiratory acidosis or alkalosis so changing ventilatory pattern may help. increased oxygen concentration may help turning off nitrous oxide may help - nitrous causes some arrhythmias increasing depth of anesthesia will help if problem is due to surgical stimulation and you are really really brave, if arrhythmia is due to vagal or sympathetic reflex from light anesthesia during surgical stimulation... if you think the arrhythmia is due to surgical stimulation, stop stimulating it, and give local anesthetics, if you are afraid to increase depth of anesthesia. you might want to change the anesthetic being used also carotid sinus pressure - may slow some supraventricular tachyarrhythmias by eliciting a vagal reflex treat electrolyte or acid base disturbances drugs: mechnisms are complicated and confusing. don't remember them. but know what you treat slow rhythms with, what you treat fast rhythms with, and whether they are likely to work on atrial or ventricular arrhytmias for bradycardias: atropine - anticholinergic drugs like atropine or glycopyrrolate are used for rhythms induced by vagal reflex. sometimes they don't work dobutamine - sympathomimetic dopamine - sympathomimetic isoproterenol - pure beta agonist sympathomimetic for rapid rhythms: quinidine or procainamide for supraventricular rhythms (or ventricular but not first choice for that) - quinidine more negative inotropic effect, but will work for arrhythmias refractory to lidocaine. procainamide also causes decreased contractility. lidocaine for ventricular tachyarrhythmias - rapid onset, little inotropic effect, short duration, can be infused. shortens refractory period for arrhythmias due to excess catecholamines (pheochromocytoma, hyperthyroid) beta blockers - propranolol, esmolol. also used for ventricular arrhythmias of unknown origin that don't respond to lidocaine. some neg inotropic effect. bretylol - markedly prolongs refractory period - used to tx ventricular arrhythmias that are extremely refractory, nonresponsive to tx. can convert ventricular fibrillation to normal rhythm. sometimes. maybe. worth a try anyway. exam would never ask for doses of these drugs, but you should look at an EKG and have ability to choose a drug. do not say "use lidocaine" for a flatline EKG, and do not say "use atropine" for a horse with a rate of 300. other drugs: verapamil - Ca++ channel blocker to slow ventricular response during a-fib or tx atrial arrhythmia edrophonium - cholinesterase inhibitor - creates a large quantity of ACH that persists at NMJ - like giving ACH - used to break atrial tachyarrhythmias. digoxin - used to slow ventricular response rate during a-fib, causes AV block phenylephrine and methoxamine, by suddenly raising BP via vasoconstriction, cause vagal response that might break an AV junctional tachycardia potassium induced arrhythmias: calcium - to tx hypocalcemia glucose and insulin - move potassium into cells from ECF to temporarily rapidly lower extracellular potassium bicarb - also used to tx high serum potassium - because it pulls H+ out of cells and pushes K+ in potassium - used to tx hypokalemia-induced arrhythmias or acute digitalis toxicity (in humans, not anymore, b/c they give digitalis antibodies) monitoring leads used for different species - different patterns of depolarization in dog vs horse heart were discussed earlier slide: drawing of a rat in dorsal recumbency black dot on right shoulder and left knee white dot on left shoulder dog, cat, small mammals - major wave of depolarization goes cranial to caudal and right to left. think about how heart sits in chest - it goes dorsal to ventral, base to apex. lead II - measures potential change b/w right arm electrode and left leg electrode. right arm - left leg. you want to get a system which produces a positive P wave, and a consistent QRS, so that we can quickly and consistently evaluate sudden, acute changes in the EKG. so by convention, we put the negative electrode on the right arm. you hook up the wires and dial lead II and you measure the changes in potential. during depolarization, this wave moves toward the back - you see it as a tall positive deflection - the R wave - the first positive wave. the Q wave is the negative wave preceding the R wave. the S wave occurs after that. the horse is different as are other large mammals although we aren't sure about whales - there is an extensive purkinje system. the heart is huge. you need all the muscle to depolarize simultaneously. so when god made big hearts, she made big purkinje systems. the rapidly conducting fibers go way in there and major depolarization occurs all at once, and looks like nothing, b/c ther eis no directional component. there is a tiny R wave,it's mostly electrically silent. but there is a large part of depolarization going from apex to base, to get the last part of myocardium - this goes ventral to dorsal, and a bit caudal to cranial. so to see that, put the right arm lead on the right side of the neck,a dn the left arm lead behind left elbow. look at lead one. you see a big negative S wave. there is no Q wave. it's just RS. but you still call it QRS. ---end----