---start---- anesth 4/2/98 klein cardiac rhythm disturbances regarding tuesday's exams - will have to ID some arrhythmias on EKG. on the final, since Dr. Soma lives in a "different space", there will be more questions on this material for the final. the arrhythmias will be on this exam, though. on the final, will be more problem solving stuff. not essay, but multiple short answer or multiple guess. will have to count rate, say what rhythm is. there is a review session tuesday am, and she'll be here for that too. today we'll see some normal EKGs from various spp, some artifacts, some slow rhythms,some fast rhythms,and how to tell them apart. 1. horse EKG - double P wave. could be zebra or rhino, but is horse. base-apex lead. double P wave, tiny R, big S, big positive T. equine base apex lead usually see double P, tiny or medium R, then big S, then T that is positive or negative, or biphasic. when heart speeds up, we usually do not see the double P wave - conduction speeds up across atria so it isn't bifid like this. 2. dog, lead II ekg - normal - P, QRS, negative T - normal. when animal changes position, moving legs apart, there is a bigger Q wave, and some other differences. the point is, make sure to check the EKG in the same position each time so you don't see spurious "changes". 3. ostrich lead III - long axis lead placement involving L wing and L leg instead of R wing and L leg. P wave is biphasic (not sure how common that is in birds). then, big S wave, then positive T wave. normal for birds. HR about 100. smaller birds have similar EKG but much much faster up to 500-600. Lead I has biphasic P, big R, neg T 4. remember - baseline variation can occur due to respiration 5. k9 lead II: extreme baseline variation - mimics much more abnormal rhythm. but this is really same as 4 but due to panting. dog was panting, resisting ventilator. this is artifact. 6. feline lead II - wave forms that look really abnormal are present. looks like v-fib. but, animals do not go into v-fib and then have normal complexes in a regular pattern. this must be artifact. this cat was awake. it was purring. there were normal complexes but regular intervals of squiggles from purring. 7. horse - 2nd degree AV block with dropped beats. a couple of P waves lack QRS complexes. otherwise normal. also, PR interval gets gradually longer and then there is complete block. this is type I/wenkebach 2nd degree AV block. common in resting, young athletic horses with high vagal tone. they have big hearts, very efficient, don't need to pump all the time. also seen after alpha2 agonists are given IV. xylazine and detomidine are alpha2 agonists and they cause a sudden increase in BP, a vagal reflex, and a vagal bradycardia with AV block. this occurs 1-2min post drug admin. HR can go to 11 or 12, and this is normal response to the drug. not so normal to see this resting block in older or unfit horse. still get response to drug in those horses, though. also in horse anesthetized with volatile inhalants, this is unusual, suggests conduction problem. if in horse with higher HR, older, or metabolic dz - think abnormal. during the pause when there is no QRS, you hear the 4th heart sound. 8. dog - pauses b/w some beats, but not all the same length. no P waves in the pauses. this is not AV block. this is sinus arrhythmia. characterized by variable periods of normal complexes with the rate changing - here it is ocming in pairs, but usually it speeds up, slows down, associated with respiration. speeds up as it inhales, slows as it exhales. common in resting, fit dog, large breeds. vagal tone in dog, man causes sinus arrhythmia, in horse causes AV block. 9. AV block in dog - two normal cycles, then a whole bunch of P waves at regular intervals w/o QRS. this is a period of third degree AV block. for 4.5 seconds, no ventricular depolarization - coronary perfusion and cerebral perfusion would be poor. this was a dog given an opiate for induction and no anticholinergic prior to that, and had AV block that needed to be treated. tx with atropine rather than glycopyrrolate b/c it works faster but some would argue that. ben asks: what is the official distinction b/w second and third degree av block? 3rd degree is when there is never conduction; 2nd degree is when there is sometimes conduction. maybe 9 is "advanced 2nd degree block"? depends how long you look at it. really, just know if it needs to be treated, know the consequences of the rhythm. this one needs to be treated, whatever you call it. 10. another vagal phenomenon in horse. pauses b/w QRS, with no P waves in them. this looks like respiratory sinus arrhythmia sseen in dog. what it really is is, and we don't see it that well here, but we see that the cycle lengths that are normal are all the same - and then there are pauses of 2x normal cycle length. this is a recurrent pattern, independent of respiration. pauses always multiples of normal cycle length. this is a sinus block.- SA block. you dx by measuring pause of length. assume sinus node is firing,but there is sinoatrial exit block. unusual in horse. inconsequential if rare, if happening a lot might treat 11. P wave not followed by QRS - AV block 12. horse under anesthesia, being overdosed unbeknownst to anesthetist. had very little change in normal clinical parameters like eye reflex, position, muscle tone (hard to asses), so student was worried about having it wake up and then suddenly, there was a long period of no heartbeat. could be SA block or arrest. you can't tell. you can't stop and get calipers and measure it. assume arrest. long period of arrest - 11 seconds with no contraaction. why didn't this animal have any ventricular ectopic activity in that interval? the inhalants depress automaticity all over the heart. they can see this in vitro by blowing halothane over cells. so, you have to turn off the gas, flush with O2 right away, might give some atropine, do CPR - this is a dead horse while heart isn't breathing. atropine didn't work -this wasn't vagally induced. they gave ephedrine or epinephrine, not sure. ephedrine takes longer to work but CPR might work in a pony ok, so maybe they used it - anyway, he recovered and EKG looked ok afterwards. 13. artifact - out of phase - k9 lead II- looks like multiple upside down P waves - but if you look at them, there are normal complexes occuring in the background. some variation in QRS amplitude. this is a change occuring with respiration. QRS complexes get smaller on inspiration. but superimposed on this rhythm are a number of squared off blips. electrical interference. most common type is 60 cycle interference from poorly grounded equipment, poor contacts, etc. this isn't that but it is some kind of interference. 14. bird - short eared owl - lead II. tiny bird - HR 300 bpm. normal,funky looking EKG - beats every 0.2 sec. looks like an ST segment deviation - not sure about significance of that. look for reasons for myocardial hypoxia if you see this; might be normal in small degrees. 15. horse. 2nd degree AV block - every other beat. horse under anesthesia. this is concerning. problem - ventricles have a lot longer time to fill during skipped beat - when HR slow, bigger stroke volume, when muscle is stretched more it contracts w/more vigor, but not during anesthesia with volatile gases. so rates that are tolerated in awake animals are not tolerated during anesthesia. fluid loading doesn't work to increase BP in anesthetized animals getting volatile anesthetics b/c heart doesn't pump harder. this HR of 20 isn't good during anesthesia b/c CO is depressed. might treat this. 16. 3rd degree AV block. extreme vagal rxn to administration of vasopressor in horse. rolled on back for surgery (cryptorchid neuter), BP dropped very low after a while, horse was very peripherally dilated, and was given a vasopressor, methoxymine, to get mean BP up. his BP went from 58 to 63, still inadequate, and he got AV block immediately. since it's vagal, you would think heart would start again on its own as vagal tone went away, but under anesthesia you have to tx. so they gave an anticholinergic which didn't work, then ephedrine or epinephrine worked and heart started pumping again. CPR is nearly impossible in a dorsally recumbent horse with abdomen open. actually, it is impossible. this horse did conduct a few beats, enough to get drug through. internal cardiac massage isn't done in the horse. horse chests are very intolerant of invasion under less than perfectly aseptic conditions. dogs can be resuscitated by cutting hairy chest wall and doing bare handed cardiac massage without getting infected. horses can't. anyway, should have infused the vasopressor instead of giving bolus to avoid this problem in this horse. 17. k9 lead II - no P waves at first. then, some P waves show up and QRS is a little smaller. and hey, wait a second, there are some others, buried in the QRS complexes. there is sinus activity and conduction to atria, and sometimes there is conduction to ventricles. the normal PQRST is a captured beat. the others are ventricular or AV junctional in origin, and those P waves in there aren't working b/c ventricles are refractory. this is isorhythmic AV dissociation (atrioventricular dissociation). the hemodynamic consequence? well, ventricles are only filling passively - is that ok? depends on the patient. how would you treat this? if you want AV conductance to occur - well, you have to suppress the ventricular or AV junctional focus that is firing more quickly than the sinus node. you can either slow the ectopic focus or speed up the sinus node. if worried about CO, speed up the sinus node. here, the sinus rhythm is slow anyway, so speeding it up is a good idea. this dog was given atropine and reverted to normal sinus rhythm with a rate of 94. to slow ventricular focus, you might give lidocaine. for supraventricular focus, might use quinidine, which also improves AV conduction. also - if your HR is slow due to vagal stimulation and you stop the vagal stimulation to speed up SA node, would that also speed up ectopic focus? not really - less vagal influence on ventricular foci. "captured beat" means that the P wave was conducted to ventricles - it "captured" the ventricles. wouldn't use bretyllium for this - that is a scary drug. 18. equine AV dissociation - P waves occur at weird intervals. now and then a normal complex follows it. most of the beats are ventricular origin and look weird. isorhythmic AV dissociation again. fast rhythms: consider the criteria for identifying these and look at the ones in the handout. 19. baseline variation due to respiration; horse ekg. normal bifid P wave, decreasing P-P interval occurs, P wave changes shape, so consider the P wave is coming from ectopic focus. it's early and abnormal. it's premature atrial complex. 3 or more in a row is paroxysmal atrial tachycardia. why isn't this just an increase in sinus rate and then a decrease? it's a different shape - indicates different focus. also, real distinction b/w sinus and atrial tachycardia is that when sinus rate increases - normally - due to exercise, or whatever - it's a slow increase, and slow decrease. but with paroxysmal atrial tachycardia, it gets suddenly fast, then suddenly reverts. nothing gradual about it. this is a key factor. this rate of 90 in an anesthetized horse is probably not worrisome. QRS look normal, BP probably going up a bit during tachycardia...might not treat this. not very rapid. ventricles still pumping ok. 20. dog with different rhythm. paper speed 50 mm/sec. there are a lot of P waves at regular intervals, about every big box, so atrial rate is about 600/min. very rapid rate. the QRS look wide but that's due to paper speed. variable conduction. the ventricular complexes probably are coming from previous P wave. this is atrial flutter. sometimes the ventricular response is regular and sometimes it isn't. here, ventricular rate is about 150. if palpating pulse, you might not know this rhythm was present. how do you know these aren't ventricular ectopic beats? a ventricular rate of 150 is possible with ventricular ectopic activity, but commonly with a-fib or a-flutter there is some AV conduction, just not every impulse is conducted. tripp wants to know how you know the P waves aren't artifacts. artifacts do not look like p waves, usually. also, then, there would be zero p waves, weird artifacts, and a ventricular rate of 150 - unlikely. also - if you can identify P waves, it isn't fibrillation. the ventricular response depends on enough AV conduction to get signal through - so resposne might be regular, or might not - now, you do not want ventricles to contract 600 times/min. with a-fib, there is always variable penetrance of signal,b/c with a-fib, a variable amount of atrial tissue is firing, and that affects which impulses get through. with atrial flutter, there is a regular pattern. 21. atrial premature complexes of little significance. coming in group sof two or three - bigeminy or trigeminy. bigeminy - abnormal complex follows normal one in a fixed coupling. you see the P wave coming early, closer to the previous T wave. the P wave is a different shape from the other one. it is always coupled at the same interval to the normal one, suggesting a circuit of reentry or something, some conduction block somewhere triggering this abnormal impulse. trigeminal - two normal then abnormal, or one normal and two abnormals. 22. tachycardia in dog on isoflurane- can't really tell b/w rapid sinus rhythm of 300 or atrial tachycardia. 23. a-fib - compare with a-flutter. there are no obvious p waves. there is an Fwave pattern - amplitudes are irregular, it's chaotic jiggling, not regular P waves. could be motion artifact, but the ventricular rhythm is also irregular. it's an irregular irregular rhythm - no fixed irregularity. cycle lengths vary widely. no P waves precede the QRS. but the QRS do look normal. these complexes are the result of conduction through AV node occuring at irregular intervals. no ventricular escape beats seen. not sure why. one explanation may be that they are constantly suppressed by being driven from the atria. after atria stop driving them,may take a long time before they depolarize back to threshold. animals with complete AV block will collapse before an escape rhythm occurs - or, some animals will have escape rhythms. ask a cardiologist about it. you can pace hearts rapidly, stop pacing, and have long periods before SA node will kick in again. 24. horse - P waves not followed by QRST. then, we see something weird. theres a normal PQRST,then a P, then nothing, then a weird thing. the thing looks like ventricular ectopic beat, but has no T wave. look at pressure wave and see if it generates a pulse- didn't - was an artifact. a ventricular ectopic focus must have a T wave. 25. VPC situated b/w two normally spaced complexes. unusual. 26. another example of ventricular ectopic activity - in a dog. normal complexes occur, then every once in a while there is an ectopic one. could be abnormal conduction through ventricles. could be abnormal focus firing now and then. 27. dog w/ventricular bigeminy - normal PQRST followed each time by high amplitude negative deflecting complex with T wave - ventricular bigeminy common after barbiturate induction. this is a reentrant rhythm due to a unidirectional conduction block -impulse wanders around ventricles, finds a nonrefractory area and triggers depolarization. probably no hemodynamic consequence if these are generating pulses. if they weren't generating pulses, might want to treat. 28. ventricular unifocal tachycardia in horse. paroxysmal. about 60 bpm. BP normal. don't have to treat. look for cause for enhanced ectopic activity - hypoventilation, hypoxemia. 29. bird - halothane anesth- P, R, S, T seen. also a bunch of other ventricular complexes are seen, some with higher amplitude, some positive, some biphasic - suggests ectopic foci and fusion complexes or a third focus. this is multifocal ventricular tachycardia suggesting significant irritability in the heart. probably halothane induced catecholamine induced arrhythmia - treat with lidocaine. or switch to isoflurane. 30. two examples of ugly rhythms. one case of v-tach in a horse - rate is about 150. also a period of v-flutter with fused QRST - meaning depolarization and repolarization are happening coincidentally in different araes. could easily become fibrillation. tx lidocaine or if refractory try quinidine. lidocaine less negative inotropic effect. 31. slow ventricular rhythm with ominous features. T wave very long. so repolarization takes a long time, allowing areas of heart to be out of sync, allowing, allowing abnormal rhythms to occur. this animal was dying of blood loss. heart is hypoxic. prolonged repolarization phase, then slowed ventricular conduction, ineffective pumping. 32. similar EKG in lion being anesthetized - unknown etiology - tx with epinephrine, sinus rhythm restored. so if a sudden onset of this occurs, do something to increase rate of impulse formation and improve conduction through heart. anticholinergic won't help = need sympathomimetic or catecholamine. ---break---- soma GA and resp function dr klide will have bulk of exam - classically he uses multiple choice questions. soma will give an essay question. 30 points. one hour. handout - exam questions of anesthesia cases - look at them starting in about a week. something like this will be on the final. respiratory function- effects of anesthesia on ventilation, perfusion, abnormalities, changes in compliance and resistance, changes in resp rate, and how you control ventilation under anesthesia. for first few minutes, go back and review basic stuff like inspired concnetration of O2. room air - 21% O2 under anesth - give 50 - 100% O2 usually you give only O2 plus anesthetic agent. so under anesth, O2 tensions, partial pressure of O2 you anticipate in alveoli that you consider normal, is not referenced to 21% O2. it's referenced to the concentration you are inhaling. so you ask a question - you say, look at the blood gas, and the partial pressure of O2 is 100, is that normal? yes on 20% O2, but not on 100% O2. it's still adequate, but isn't normal, indicates a problem. there is a big gradient b/w what is being delivered, and what is in the aterial blood. probably that is reversed when animal wakes up. when animal is waking up and has an O2 tension of 60 on 100% O2, where do you go from there? no wiggle room. you are in a deteriorating situation. but if O2 tension is 60 on room air, you can add 50% more O2 and increase O2 tension. this is why we need to know normal concentrations/O2 tension in alveoli and arteries. fractional concetration of inspired O2 20% - that means the %FIO2 fractional inspired O2 concentration - that's room air. if FIO2 is 100%, you're on 100% O2. how do you convert the FIO2 to PO2? use atmospheric pressure times the fractional concentration, minus water vapor. you have to take out water. so if 1 atmosphere is 760 mmHg why are you subtracting water vapor pressure? because you are inhaling water. at 37 C the PH20 is 47 mmHg. so take 760 - 47 and you get 713. multiply that times fractional concentration to get the partial pressure. if body temp is 38, water vapor is higher. maybe 49. not a huge difference. start out with one partial pressure, and in the lung you end up with lower concentration b/c it's diluted with water vapor. same thing with PCO2 in alveoli. about 40 mmHg is normal in alveoli and in arteries - this is about 5%. you're exhaling about 5% CO2, and about 79% N2 on room air. under anesth, exhale about 5% CO2, very very minimal N2 (assuming high enough flow initially to replace the N2 with O2 and anesthetic vapor - if you close your system down before denitrogenating animal, you might have lower FIO2 than anticipated. you can't induce and close down to closed circuit immediately.) time to denitrogenate depends on flow rate, metabolic rate, size of animal. ---end----