Tachycardia and Arrhythmias

Intro SVT and tacky arrhythmias. Just a quick reminder that every podcast episode is mapped to a written article on anaesthesia.com where you can find more self-assessment questions, resources and references. Let's start with those take home messages #1 shock needs a shock. Two, be very cautious with your sedation. And three, don't get sucked into ownership of the cardiovascular management ABC. In our line of work, we usually see a tachycardia in the context of an emergency during an operation or whether another medical professional has asked us to come and help out. So we'll start with the resuscitation approach for a patient where the only thing you know is help. They've got a really fast heart rate. I'm going to be completely honest here, My approach to a weird heart rhythm looks a bit like this. Give oxygen if they need it, check the blood pressure and wheel out the D fib. If it's crashing, give some fluid. Assuming there's no heart failure, check a blood gas and replace whatever's low and give some empirical magnesium. Very rarely has this not worked, so we're sticking to it. But for the exam, you need to be able to explain your actions. Hence we've got this podcast and a post on anesthesia.com. The algorithm Start as you always do, ABC and fix as you go. If the heart rate is fast because of anaphylaxis, life threatening asthma or attention pneumothorax, Hopefully this will become apparent before you start reaching for adenosine or syringes to blow in. We've got the Resource Council's algorithm on anaesthesia.com for you to have a look at now. You might get asked, please can you come and sedate this patient? SVT and Tachyarrhythmias This is a classic call, often from CCU or resus patients in SVT or other tachyarrhythmia. They're signs of shock or ischemia and they need electrical medicine. It's much nicer to undergo DC cardioversion with some sort of sedation on board, but this is possibly the hardest sedation to get right. Sedating a patient with life threatening cardiovascular compromise that already has an arrhythmia is real tiger country, so you need your wits about you. If you feel like you're giving a ridiculously small dose of midazolam, ketamine, or propofol, then you're doing it right. These patients need very little indeed. Remember they're not having a joint manipulated or anything in size. They just need to not be fully aware. The most important thing is that they don't really remember their millisecond jolt of chest lightning. Try naughty .5 milligrams midazolam. Often this is more than enough. Make sure you have all your airway kit ready and be ready to manage as AVF arrest. Cardioversion is synchronized to the QRS complexes, while Defibrillation just blasts the myocardium whenever the button is pressed. Managing a stable tachycardia. Managing a stable tachycardia We tend to do less of this as anaesthetist, largely because by definition there generally isn't any requirement for ABC sport. Now this might crop up as an intraoperative scenario with a tachycardia in an anaesthetized patient. Again, we've got the Resource Council's guidelines on anaesthesia.com. Now is the QRS narrow, IE less than nought .12 seconds or broad? If you've got a narrow QRS then you ask yourself is it regular or irregular? Regular. You try some vagal manoeuvres and then if that's ineffective you'd give your adenosine and irregular, then you're probably looking at AF and things like rate control is important, so things like beta blockers. You'd also want to consider anticoagulation if the duration's been longer than 48 hours. If you've got a broad QRS, then you ask yourself again, is this irregular or regular? Irregular broad QRS can include things like AF with a bundle branch block or polymorphic Vt, for example Torsard's DuPont or Dupois. If you're looking at a regular broad complex QRS, then you're considering Vt. So let's try some vagal manoeuvres. I've seen ice work, but it usually doesn't. I've seen blowing into a syringe work, but it usually doesn't. Adenosine rarely fails if the problem is a legitimate AV node issue. If you're using adenosine, be ready to use a laryngoscope and a defibrillator, and if that doesn't work, by this point you're either not involved as an anaesthetist or you're being called to come to date a patient for a DC cardioversion, as we've just described. Again, easy on the sleepy meds, please. So what exactly is SVT? This is any fast heart rhythm that is dependent on nodal tissue to keep it going. So things like AF and multifocal atrial tachycardia aren't technically SVT as the AV node isn't the causative issue. So we've sort of mentioned some others, but let's talk about other atrial tachyarrhythmias, the regulars sinus tachycardia. Other Atrial Tachyarrhythmias This is a normal autonomic response to some sort of stressor on the cardiovascular system. It's fixed by fixing the cause. So things like hypovolemia, sepsis, pain, anxiety, the usuals. Then we've got atrial flutter. This is pathological. It's a narrow, complex organized rhythm, usually from a re entrance circuit around the tricuspid valve. The Atria depolarize at around 300 beats per minute. You can see variable AV node conduction, usually around 2 to one, and this gives a heart rate of around 150 beats per minute. It's often quite hard to spot because of the speed and overlap between T&P waves. The conduction ratio can also change between 2:00 to 1, three to one, etcetera, making it look irregular. Then we've got our AV re entrant tachycardia. Now this has an accessory pathway that's congenitally abnormal. It bypasses the AV node and can conduct forwards or backwards just for fun. There are three types of AVRT. Orthodromic, which is a regular narrow complex tachycardia anterograde via the AV node and back up the accessory pathway. Antidromic, which is a regular broad complex tachycardia anterograde via the accessory pathway and back up the AV node and AF with rapid anterograde conduction via the accessory pathway. We're going to be talking about Wolf, Parkinson White in a minute. AV nodal re entrant tachycardia. Now there's no accessory pathway. The re entrant circuit is via the posterior and anterior pathways to the AV node, where one is conducting significantly faster than the other. An atriolectropic starts during the refractory period of the fast pathway. This then tracks down the slower pathway, then back up the fast pathway once it's ready to go again. And as a result the P wave is buried in the QRS complex. Usually this is seen in young adults. That rarely causes major hemodynamic compromise unless there's another cardiac vadnais somewhere underneath. So Wolf, Parkinson, White. It's a very particular type of AVRT and it can be orthodromic or antidromic. There has to be pre excitation on the ECG as well as them having symptomatic tachyarrhythmias. Aberrant conduction between Atria and ventricles via bundle of Kent. Now the major ECG changes are that you see short PR and this is because the accessory node bypasses the AV node. You've got broad QR s s with delta waves due to fusion of early depolarization down the accessory pathway and late depolarization through the AV node. And the reason why Wolf Parkinson White is so dangerous is because the patient loses the natural rate limiter of the AV node. The accessory pathway can conduct ridiculously rapidly to the ventricles, so if the Atria go too fast, the ventricles will do the same and you end up in VF. You don't want to give these patients verapamil focal atrial tachycardia. Next. This is a regular atrial tachycardia and it starts somewhere in the Atria but not in the SA node. The P waves just look slightly different and it's usually quicker onset than sinus tachycardia. So we've covered the regulars. Now let's look at the irregulars and let's start with the good old one, atrial fibrillation. Irregular Atrioventricular Fibrillation Now this is where you get multiple little electrical triggers throughout the Atria. You get irregular conduction to the ventricles, no P waves. You get an irregular RR interval and narrow complexes. Assuming that there's no bundle branch block as well, then we've got multifocal atrial tachycardia or MAT. Now usually this is only in really really unwell elderly patients, and it's sometimes seen in theophylline toxicity. Usually it does progress to AF and it's characterized by irregular atrial impulses with at least three different looking P ways. This is usually best managed by treating the cause rather than the arrhythmia itself. Now the clue is to look at the P waves. You can't see them and they're irregular. AFI can't see them, but they're regular and really fast. Then triadenosine. The P waves are all weird. You're looking at mat sawtooth P waves at 250 to 300 beats per minute flutter, normal P waves, AVRT or AVNRT, weird P waves with long PR fat and definitely no P waves and regular. Then you're looking at junctional tachycardia. Now let's talk about adenosine. Adenosine First of all, we don't advise telling the patient they're about to feel an impending sense of doom. Tell them they're going to feel strange, like they're skipping a beat for a few seconds. Adenosine induces a hopefully transient AV. No block for a few seconds. Adenosine hits the A1 receptor, it inhibits adenyl cyclase, and it reduces CAMP. It allows potassium out of the cell and therefore hyperpolarizes the cell. It needs to be injected through a large proximal cannula and flushed very quickly as it gets metabolized rapidly in the blood. The contraindications for adenosine would be things like a known accessory pathway. So in Wolfe, Parkinson, White as this can induce AFVT or VF if you've got asthma or severe COPD because it can induce bronchospasm. If you've got a broad complex tachycardia or you've got sick sinus syndrome, a few other drugs to know. So by this point you're usually involving some sort of cardiological person, but you need to be able to list the second and third line options of SVT and these would be verapamil, beta blockers, flecainide and procainamide. Perioperative AF. Perioperative AF Some patients either have AF anyway and just flick in and out of it throughout their perioperative stay and others develop new AF for the first time. Follow the algorithm and focus on treating the underlying trigger. Rate Control is the priority as this increases duration of diastole and therefore oxygen delivery to the myocardium. ESMALL is fast acting and easy to titrate but is a negative inotrope. Amiodarone is always there just waiting for you, and if a patient is on a beta blocker, verapamil, or diltiazam, then generally speaking these should be continued perioperatively. Remember to consider the thromboembolic risk of postoperative AF, which needs a Chad's 2 score and a decision regarding anticoagulation. So let's ask ourselves, what if the tachyrhythmia is broad? It's safer to treat a broad complex tachycardia as Vt and be wrong than it is to treat as SVT with bundle branch block and be wrong. As always, we hope you found that useful. There are some useful tweets, resources, and further reading on anesthesia.com. Thanks for listening and we'll see you next time. Take care.