You Can't Stop The Beat

Hey there and welcome back to Pulse Check. This is Episode 4 on A Rhythmia's. This is my longest episode and the final episode of my BPD Cardiology series. Thank you so much for joining me for the ride. This episode's got your AF, your SVTs, your VT, your anti-othermics and your pacemakers. If you listen to this all in one sitting, you will fry your brain. Please take your time and savor it like a fine coffee from Zuki. My shout. Please enjoy. Let's talk about A Rhythmia's, starting with atrial fibrillation. Don't let anyone tell you that AF is easy, it is highly nuanced. We'll start with anti-coagulation. We refer to the Chad's Var score now. The ESC 2024 guidelines have moved away from Chad's Vask and now it's just Chad's Var removing the sex category. A Chad's Var of one or more merits long term anti-coagulation. One exception is trigger-injuiced AF, which is transient AF caused by a clearly reversible trigger such as sepsis or surgery. In these cases, the ESC 2024 AF guidelines provide a class to be recommendation to consider anti-coagulation, particularly if the Chad's Var is higher. I'm more inclined to anti-coagulate these patients long term if their Chad's Var is high, i.e. four or greater, or if they have severe left atrial enlargement, which suggests a high likelihood that they'll go into AF again in the future. On the flip side, I'm less likely to anti-coagulate these patients long term if they have a higher bleeding risk or if they're very elderly and frail. The other exception is device detected AF, which I'll talk about shortly. If you're going to cardiopvert a patient with AF, you want to avoid doing this if the patient has intra-cardiac thrombus, which is often hiding in the left atrial appendage. It's safe to cardiopvert patients with AF if they meet one of the following three criteria. One, it's been less than 48 hours of clear symptom onset, which is usually palpitations. Two, after three weeks of uninterrupted therapeutic anti-coagulation, and three, the patient has had a toe to exclude intra-cardiac thrombus. Patients receiving cardioversion in ED often fall into one of the first two scenarios. The most common reason we do inpatient toe DCR is in those patients with AF, or more commonly atrial flutter, where we can't get the rate under control with medications. So it's unsafe to send the patient home on rate control meds with the plan for outpatient DCR. So we do a toe DCR as an inpatient and get them back into sinus. You must be anti-coagulated for at least one month post cardioversion, even if the chadsvar is zero. The ACC guidelines do advise that if AF duration was less than 24 hours and your chadsvar is zero, you don't need that one month anti-coagulation. The reason we anti-coagulate for one month after cardioversion is that for some period of time after a version from AF to sinus, the atria are stunned and at high risk of forming clot. The mechanism of reversion is also irrelevant, whether that be DC cardioversion or chemical cardioversion with say oral flickernide. This is debatable, but even with self-reversion, many would anti-coagulate for a month due to that atrial stunning. We generally use a pixaban as our anti-coagulant over river-oxaban. A pixaban has a lower risk of major bleeding and both a pixaban and a river-oxaban actually have 12 hour half-lives. So the BD dosing of a pixaban better reflects this 12 hour half-life compared to river-oxabines daily dosing which does not. In the past people used aspirin instead of an anti-coagulant, but we don't do that at all anymore. The Avarose study published 2011 in Nedgym, randomized 5,000 patients with atrial fibrillation deemed unsuitable for warfront to a pixaban versus aspirin. The trial had to be stopped early because a pixaban was clearly better at stroke prevention and all caused mortality, but also there was no statistical difference in major bleeding between the two groups, 1.4% in the pixaban group and 1.2% in the aspirin group. So don't be scared to put your AF patients on a pixaban because aspirin isn't any safer. Also, if your patient with a label of a schemic heart disease or prior stent is on aspirin and they have a new indication for dolec, whether that be AF or a DVT or PE, you don't need both the dolec and the aspirin. The aspirin can usually be changed to a dolec, so long as they haven't had an infarct in the past 12 months or a stent in the past six months as a general rule. What about anti-coagulation in device detected AF? The major studies that provided data on stroke risk in AF based on Chad's VASC score, now Chad's VAR, included patients diagnosed with AF in the 90s and 2000s. Back when AF, bi and large, was only diagnosed when you captured it on a 12 lead ECG. These days, we captured transient AF on telemetry, smartwatches, loop recorders, heart bugs, pacemakers and ICDs, i.e. device detected AF. The standard annual stroke risk for these patients is much lower than their corresponding Chad's VAR number, so the question is when do we anti-coagulate these patients? There have been two recent large-scale RCTs on device detected AF. There's NOAA, which was published 2023 in NIDGEM, looking at Edoxaban versus placebo, in 2500 patients with device detected AF, which was termed "atrial high rate episodes" in the paper, and there's Artisia, which was published 2024 in NIDGEM, looking at a pixel band versus placebo, in 4000 patients with device detected AF. Patients had a median Chad's VASC score of four in both studies. If you look at a meta-analysis of the two, anti-coagulation reduced the risk of stroke with a relative risk of 0.85 and 95% confidence interval 0.73 to 0.99, so just meeting significance, but increased the risk of major bleeding with relative risk 1.62 and 95% confidence interval 1.05 to 2.50. There was no significant difference in all-cause mortality, so the guidelines are yet to provide a clear stance on anti-coagulation in the device detected AF cohort. My general approach is to anti-coagulate device detected AF in the following four scenarios. Symptomatic AF, long duration AF, more than 24 hours, history of prior stroke or TIA, or higher Chad's VASC greater than 4. As I've said, a pixel band is the most commonly prescribed DOAC, but if another clinician has started riveroxabine or debigatrian, I wouldn't make any changes. There are three main indications where we still use warfarin. The first is mechanical valve. The second is rheumatic mitral stenosis in the presence of either AF, prior embellic event, or intracuriac thrombus. Rheumatic MS of its own accord doesn't require anti-coagulation, but patients with severe rheumatic MS very often have AF, and these are the patients where we often find giant left atria on echo. The third is left ventricular thrombus. Warfarin is the gold standard for ALV thrombus, but recent studies have suggested that DOAC might be non-inferior to warfarin. The guidelines are yet to provide a firm stance on this, but if there are any concerns for not adherence with warfarin or with iron R-checks, DOAC is probably a reasonable alternative. We treat ALV thrombus with three months of anti-coagulation, six months if there's ALV dysfunction, with a repeat echo at the end of treatment to see if ALV thrombus has resolved. Left atrial appendage closure has been advertised as an alternative to anti-coagulation in AF patients with higher bleeding risk, but this is controversial. Curgical left atrial appendage occlusion has better evidence, which can be performed with an atroclip or another ligation method. This is routinely performed in patients with AF on anti-coagulation undergoing cardiac surgery for some other reason. The last three trial showed that surgical left atrial appendage occlusion reduced stroke risk by a third and only took six minutes on average. In contrast, percutaneous left atrial appendage occlusion, which is the watchman device, has not clearly been demonstrated to be a safe alternative to standard anti-coagulation. The closure AF trial, which is yet to be published, randomized 912 patients with AF and higher risk of stroke and bleeding, to watchmans versus standard of care, and the study failed to meet non-inferiority for the watchmans. Watchman's patients typically need to be on single agent anti-platelet, usually aspirin, because it's bioprostatic tissue. And as I explained earlier, aspirin and epixabane have similar bleeding risk anyway. So it's a bit of a tricky one, but that's enough about anti-coagulation. Let's move on to rhythm versus rate control. Patients with atrial fibrillation are classified as having one of the three P's. That's paroxysmal AF, which is intermittent AF, persistent AF, which is sustained AF for more than seven days, and permanent AF, which is simply sustained AF with a decision not to pursue a rhythm control strategy. Rhythm control should be your default approach to managing AF these days. Let me tell you about two major RCTs that tell the tale of rate versus rhythm control in AF. The first is a firm published in 2002, which randomized 4,000 patients with AF and mean age 70 to rate versus rhythm control with follow up 3.5 years. A firm showed no difference in all cause mortality between the rate and rhythm control groups. The conclusion was that rhythm control offered no survival advantage and some physicians to this day will still quote the affirmed trial in justifying their decision for rate control. The second study is the East AFNet 4 study published in 2020, which randomised 2,700 patients with AF diagnosed within the past 12 months, mean age 70 as well, to rate versus rhythm control with follow up of 5 years. East AFNet showed reduced cardiovascular death in the rhythm control group which met statistical significance. This provided significant assurance in pursuing a rhythm control strategy in these patients with AF detected early within the past 12 months. The other reasons we prefer a rhythm control approach is firstly to reduce symptom burden and hence improve quality of life and secondly to reduce the risk that RV failure occurs due to being left in AF for decades wherein the patients develop progressive RA dilation, causing dilation of the tracuspid anulus, progressively more severe TR, RV dilation and finally RV failure. So how do we enact a rhythm control strategy? If a patient is in atrial fibrillation, we arrange a DCR to get them back into sinus. Most commonly that involves anticoagulating them for at least three weeks, controlling their rate with an agent like Metoprolol during this period until they're therapeutically anticoagulated and bringing them back for an elective DCR. Remember you shouldn't start a rhythm control agent such as Flickonide, Sotolol or Amioderoin before they've been therapeutically anticoagulated. Once they've hit that three week mark of anticoagulation, which is probably while they're still on the DCR weight list, you can safely switch them across to a rhythm control agent. Rhythm control drugs are less effective at cardioverting patients rather they are more effective at maintaining sinus rhythm and keeping patients out of AF. If a patient is now on a rhythm control agent when they turn up for their DCR, most of the time they're still being in AF and when we shock them back into sinus, they have a greater likelihood of maintaining sinus compared to if you were to shock them while they were still on the rate control agent like Metoprolol. The success rate for DCR in persistent AF is very high, it's around 95%. With success rate being lower, the more dilated the atria are and the longer the patient has been in AF. DCR involves sedating the patient, usually with propyl, and then delivering up to three synchronised shocks. You press sync for the atrial tachyrothmias, like AF and Flutter, so that the machine times the shock so that it isn't delivered on top of a T-wave, which could cause R on T phenomenon and VT. You don't need to press sync in VT or VF. Guidelines vary significantly, but my general approach is that in AF, I would give around 200 joules for the first shock, 250 joules for the second, and if no luck, then I'll give them one final hit with 360 joules, timed for end exploration, while someone is providing external manual compression using some non-conducting object to push down onto the anterior D-fib pad. I usually put my pads into a posterior, but you can put them on anthera lateral. If a patient is very thin, I might start with 150 joules. Atrial Flutter on the other hand is much more responsive to DCR, so I would often start with 100 or 150 joules for these patients, though I've seen success with just 50 joules as well. Sometimes, if a patient has an ICD in SITU, we can use the ICD to deliver the shock at about 40 joules. Though this will deplete some of the battery, so you can just use the pads to shock and preserve the ICD battery life. Now that our patient is in sinus rhythm, we want to use a rhythm control agent to maintain sinus rhythm. There are three options for AF rhythm control in Australia. So to lol, Flaconide and Abioterone. So to lol is a Class III anti-arhythmic. It blocks potassium channels and has a weak, non-selective beta blocking effect. Its contraindications can be remembered with the rule of 40s, EGFR Less than 40, LV ejection fraction less than 40, and a QTC of more than around 440 to 460 milliseconds. So to lol prolongs the QTC, and in some people it can cause the QTC to blow out more than others, so you need to repeat an ECG one week after starting SOTOL, or after increasing the dose to ensure that the QTC hasn't prolonged to greater than 500 milliseconds. SOTOL is taken twice daily on an empty stomach, usually starting at 40mgbd up to a max dose of 160mgbd. We often quote 40mgbd as being subtherapeutic, and aim to get patients to 80mgbd to have a good effect. With that said, in elderly patients with low burden paroxysmal AF, it's not unreasonable to stay on 40mgbd and monitor. Flickonite is a Class I-C anti-arhythmic, which blocks sodium channels. Its contraindicated, Instructural or Aschemic Heart Disease, i.e. any scar in the heart. Scar is a fibre-bredic tissue in the heart that is picked up on cardiac MRI as late-gadolinium enhancement, and any infarcts or structural heart disease like hockum or dilated cardiomyopathy's can have scar. The cast trial published in 1991 on Class I-C agents like Flickonite for PVC suppression after myocardial infarction showed increased mortality and cardiac arrests in the Flickonite arm. So, we avoid Flickonite if patients have a history of myocardial infarction and if there's any structural heart disease. Flickonite should be co-administered with an AV nodal blocker when used in AF rhythm control to avoid atrial flutter with one-to-one conduction. How does this happen? Well, Flickonite slows atrial conduction and can convert disorganized AF into an organised atrial flutter. Normally, atrial flutter has an atrial rate of 300 beats per minute, and that's too fast for the AV node to conduct every beat due to its refractory period, which is why we often see 2-to-1 atrial flutter with a rate of 150 beats per minute. When you take Flickonite, you slow the atrial conduction, and if the patient goes into flutter, given that Flickonite doesn't affect the AV node, the atrial flutter rate could be 200-250 beats per minute instead of 300, and the AV node could conduct all 200-250 beats one-to-one through to the ventricles, essentially leading to ventricular fibrillation. So, we always call it Minister Flickonite with an AV nodal blocker, like Metoprolol, Attanol, Diltisem, or DeJoxon, when using it for AF rhythm control. So-to-Lol and Flickonite are both reasonable first-line anti-orethmic drugs for AF. I personally use more So-to-Lol, given its one tablet for the patient, compared to Flickonite, which also requires the AV nodal blocker, but if the patient is intolerant to one for whatever reason, I'd switch them over to the other. The third anti-orethmic is Amioderoan, which is only used if the other two are contraindicated. Amioderoan is predominantly a class 3 anti-orethmic, but has multi-channel effects, including sodium channel blocking, beta blocking, and calcium channel blocking. It also has side effects that you can remember with the Nomonic Ich, interstitial lung disease, requiring yearly chest X-rays, thyroid, both hyper and hypothyroidism, requiring 6-monthly TSH, corneal and cutaneous micro-deposits, so they should have a baseline corneal eye exam, and be aware to use sunscreen due to photosensitivity, and hepatitis, requiring 6-monthly LFTs. Amioderoan is the most effective of the three anti-orethmics at maintaining sinus rhythm. The most common reason we use Amioderoan in AF rhythm control is AF in the setting of heart failure. AF can be the cause of Heffreff, i.e. tacky cardia mediated cardiomyopathy, where AF sustained at a high rate, generally greater than 110, for several weeks, causes a global non-eschemic cardiomyopathy. Heffreff, from some other etiology, can also cause AF, because the atria tend to dilate in Heffreff due to increased left and right atrial pressure when the ventricles are stuffed. In Heffreff, the LV ejection fraction is less than 40%, so you can't use so-to-loll, and there is structural heart disease, so you can't use flickernight. It's extra important to strive for rhythm control in these patients, so we typically put them on Amioderoan, in addition to the four pillars of heart failure therapy, and arrange an outpatient DCR to get them back into sinus. Amioderoan has a half-life of 58 days, and requires loading. The loading regime requires 6-10 grams, which can be achieved by using either 200 milligram TDS for a week, and then BD for a week, or you can use 400 milligram TDS for 5 days, and then BD for 5 days. For an elderly patient in outpatient clinic, 200 milligram BD for 2 weeks would be reasonable. Then you commence a maintenance dose of 100-400 mg once daily. For AF, we usually use 100-200 milligram daily, the lowest effective dose, and for VT suppression, you might use either 200 or 400 milligram daily. The bioavailability of oral Amioderoan is around 100%. Some people get confused about IV Amioderoan, thinking that the standard IV regime of 300 milligram over 1-2 hours, followed by 900 milligram over 24 hours, is a loading regime. This is incorrect. It's simply 1.2 grams over 24 hours, which is equivalent to 400 milligram oral TDS over 24 hours. You still need the full oral loading regime when you switch them from IV to oral, just subtract one day's worth. The reason we use IV Amioderoan is because of its faster onset of action in patients with VT or borderline unstable AF. Remember that if AF is truly hemodynamically unstable, regardless of anti-coagulation status, they score a shock. However, in my experience, the most common reason why a patient in a fast AF is hemodynamically unstable is because either they're septic or they're dry. So make sure you give them antibiotics and push fluids before you sedate them with profile or medicine. to facilitate a shock. AF-Fablation is the other approach from rhythm control. AF most commonly derives from the tissue in the left atrium, just beyond the four pulmonary veins. Pulmonary vein isolation is the standard AF-Fablation approach, whereby the tissue around the four pulmonary veins is ablated, thus preventing any AF signals from propagating through to the rest of the atria. Access is via the right femoral vein, and toe guidance is used to puncture through the intatural system to get the ablation catheter from right atrium to left atrium. We used to do mostly radiofrequency ablation or RFA, which is a thermal technique, but we're gradually shifting to using Pulse field ablation or PFA, which is a non-thermal technique, it's quicker, and it virtually eliminates the risk of thermal complications, like the dreaded atria esophageal fistula or pulmonary vein stenosis. There are two class-one indications for AF-Fablation. The first is optimized HF-F with an LV ejection fraction of 35% or less, where the patient has paroxysmal or persistent AF. This was based on the Castle AF study published in 2018. The second is symptomatic AF that has failed first line anti-orethmic therapy. Access to AF-Fablation in the public system is the main barrier to more widespread use in Australia. In the private system, it's not a problem, because if you've got private health insurance with cardiac cover, and you've seen an electrophysiologist who does ablations, you can get one done very quickly. In the public system, however, weight lists can be one year and beyond, depending on the hospital network. I'd be remiss if I didn't tell you about the lifestyle factors for AF prevention, which are arguably more important than ablation or anti-orethmics. There are three big lifestyle factors that affect both your risk of AF and your chance of maintaining sinus rhythm for those with an AF-rhythm control strategy. These are weight, alcohol excess, and sleep apnea. To round off AF, let's talk about rate control. A rate control strategy is reserved for permanent AF, which is typically if the patient is elderly and asymptomatic. There are four main rate control agents, metoprolol, diltizem, dejoxen, and amyodorin. Metoprolol is the first line for most people, with diltizem being a common alternative in patients with side effects from metoprolol, like exercise intolerance. Metoprolol has twice daily dosing and is metabolised by the liver. In contrast to a tenelol, which has the advantage of being once daily dosing, but is renaly excreted, so we often avoid it in the oldies and those with renal impairment. Diltizem can be given either as the twice daily immediate release, or the once daily slow release formulation. Dejoxen is generally given in addition to another agent when it's used long term, rather than just as monotherapy. For example, AF with rate above target, despite the highest tolerated dose of metoprolol. In hospital, we commonly prescribe dejoxen for elderly patients with fast AF and decoupensated heart failure, i.e. fluid overload, to control the heart rate while the patient is being diaries to uvelemia, before switching them across to another agent like metoprolol. Dejoxen loading is 1 milligram if the eG of R is greater than 60, and 500 microg if less than 60. For 1 milligram loading, you can give 500 microg stat, and then 250 microg 6 hourly for two doses, before putting them on a maintenance daily dose of 62.5 to 125 microg daily. For 500 microg loading, give 250 microg stat, and then 125 microg 6 hourly for two doses, and then 62.5 microg daily. You don't need to routinely check serum dejoxen levels, especially if you're only using it for a short period of time. You might check dejoxen levels if you plan to use it long term, and the patient has either renal impairment, or they're on a drug that inhibits p-glycoprotein, such as amoeodirone, verapermil, fluoxetine, chlorothromycin, or ketoconazole, which can increase your dejoxen levels. If you do check serum dejoxen levels, it should be checked around 6 hours post-dose, and aim less than 1 nanogram per mil, though except to less than 2 nanogram per mil. The toxic levels to consider digibind for are greater than 10 nanogram per mil after acute overdose, or greater than 6 nanogram per mil for chronic toxicity. Though the most important trigger to give digibind should be life-threatening brady arrhythmias, like complete heart block, in a patient on dejoxen. Sometimes we encounter this in dejoxen patients who present with severe AKI, because dejoxen is renaly excreted. Regardless of the rate control agent, you titrate the dose to achieve your target heart rate. The Race 2 trial, published in 2010, showed that a lenient, resting heart rate target of less than 110 was non-inferior to a strict heart rate target of less than 80. Personally, I target a resting heart rate less than 100, and I check that the heart rate doesn't blow out too much when the patient exerts themselves, either with inpatient telemetry or with an outpatient halter. Because if the patient spends a lot of a day on their feet with a heart rate greater than 100, that's not very good heart rate control, and I would increase the rate control agent further. As I said before, metoprolol is the most commonly used rate control agent. Moving on to a true flutter. Flutter is a macro-reentrant taekycardia. Typical atrial flutter involves the K-VIRT-HUSBIT-ETHMIS, or CTI, in the right atrium. The electrical current travels in an anti-clockwise direction in 90% of cases, producing inverted flutter waves in leads to 3 and AVF, referred to as the SOAR-tooth pattern. Whilst 10% of the time it travels clockwise, with positive flutter waves inferiorly, you can also get a typical flutter, where the circuit appears elsewhere. For example, if you have an ASD patch, you can get a circuit where current travels around the patch. The best place to look for P-waves on an ECG is in V1, which is the closest lead to the right atrium. Sometimes you can see what appear as flutter waves in V1, but the rhythm is clearly irregular, and there are no other features of flutter, like a SOAR-tooth pattern. This is because AF can appear more organized in V1, where the AF waves form their own little circuit in the right atrial appendage. We sometimes call this "CORSE AF" or "flubber", but it's really just AF and is treated as AF. The management of atrial flutter is essentially the same as AF, with some nuances. Atrial flutter is more resistant to rate control, particularly in the young patient. Often we get younger patients in their 40s or 50s, with 2-to-1 atrial flutter, despite high doses of antirithmics, like amiodarone plus metoprolol 100mgb, plus dejoxin 250mg. These are the patients that require inpatient to DCR. Atrial flutter also has higher rates of success with ablation, and typically this takes the form of CTI ablation, or KV-tricuspid-ethamus ablation, where you're a part of that CTI circuit in the right atrium, theoretically curing the atrial flutter. Moving on to superventricular tecicardia. There are 3 main types of SVT, and we regard AF and flutter as being separate entities, despite technically being tecicardias that arise from above the ventricles. These are AV nodal reentrant tecicardia, AVN-RT, atrial ventricular reentrant tecicardia, AVRT, and ectopic atrial tecicardia, or ATAC. AVN-RT can occur in people that have what's called dual AV nodal physiology. About 10 to 35% of people have two pathways in their AV node for electrical current to conduct through, a slow pathway, and a fast pathway. Most people have just one pathway, and so aren't going to ever get AVN-RT. But some people have two pathways. In these people, normally, when sinus node fires, electrical conduction will reach the AV node, it will start to travel down both pathways, i.e. both the fast pathway and the slow pathway. But the fast pathway will be much quicker, and when it reaches the end of the fast pathway, current will diverge with some traveling down the his bundle to other ventricles, and some current will circle around and travel back up the slow pathway. When this retrograde current strikes, the forward current wave in the slow pathway, they cancel each other out, and it's a non-issue, and the heart goes on beating as normal. However, if you were to have an atrial ectopic beat, at just the right moment where the fast pathway is in a refractory period, then this atrial ectopic current can travel down the slow pathway, and then back up the fast pathway. Then it will depolarise the atrial retrograde, travel back down the slow pathway, and repeat itself in a circuit. This is AVN-RT. Which is the most common cause of SVT. AVRT occurs in patients who have an accessory pathway. An accessory pathway can be present at any point along the AV groove, either the left side or the right side. Patients with an accessory pathway have wolf pockets and white, and AVRT is one manifestation of WPW, the other manifestation being pre-excited AF. In patients with an accessory pathway, with a normal sinus beat, the electrical impulse hits the accessory pathway in the AV node at roughly the same time, travels down the accessory pathway quicker than the AV node, starts to depolarise the ventricles. But then the AVN-RT wave takes over, as the current takes the faster highway down the his and left and right bundle branches. The end result is an ECG showing pre-excitation, i.e. delta wave, with a shortened PR interval less than 120 milliseconds, followed by a normalish looking QRS pattern. A left-sided accessory pathway will have a delta wave visible across V1 to 6, including V1 to V2, whilst a right-sided pathway will not be visible in V1 to 2, but is more visible in V3 to 6. AVRT in patients with an accessory pathway, just like with AVN-RT in patients with dual AV node or physiology, is initiated with a well-timed or rather ill-timed ectopic beat. There are two directions that it can travel. In orthodromic AVRT, an atrial ectopic beat conducts down the AV node, reaches the ventricles and travels retrograde up the accessory pathway to get to the atria, then travels back down the AV node. This produces a narrow complex takicardia. In anti-dromic AVRT, usually it's a ventricular ectopic beat that travels in the opposite direction, up the AV node, and back down the accessory pathway, producing a wide complex takicardia because the ventricles are depolarised by the accessory pathway without travelling down the faster AV node, his bundle, bundle branch highway. Ectopic atrial takicardia or ATAC is an ectopic focus in the atria firing rapidly to produce a takicardia. The p-wave morphology will be different from sinus takicardia. You can also have multifocal atrial takicardia or MAT. When you have three different p-wave morphologies on the one ECG, if the rate is greater than 100, it's MAT, while if the rate is less than 100, it's termed "wondering atrial pacemaker" or "wap". Based on an ECG alone, it can be difficult to distinguish which type of SVT the patient has. An EP study can be performed to make the diagnosis. An EP study is performed by an electrophysiologist and involves putting catheters in the heart by the femoral vein, trying to reproduce the SVT, and doing a sequence of very smart techniques to prove that it's one type of SVT and not one of the other ones, before performing the ablation by ablating the slow pathway in AVNRT, the accessory pathway in WPW/AVRT, or the ectopic atrial focus in ATAC. Let's talk about management. When a patient is an SVT, first start with a modified valve-salver maneuver. This involves the patient blowing into a 10-mil syringe to push the plunger forward for about 15 seconds, then lying flat with their legs lifted to about 45 degrees. If this fails, and it usually fails, you give a denocene. A denocene is a pure AV nodal blocker, which has quick onset and offset, and is given as a bolus. You start at 6 milligrams, if that fails, give 12 milligrams, and if that fails, give 18 milligrams. Be sure to warn the patient about a brief feeling of just discomfort, shortness of breath, and a sense of impending doom. It's very important to have the patient on telemetry when giving the adenosine, and reviewing the telemetry if it fails. A denocene is effective for AVRT and AVNRT, where the AV node is involved in the circuit, so blocking the AV node will break the circuit. It's not effective in atrial flutter or ATAC, where you'll see P-Waves marching through during the period of acistually, so if you see this, don't give any more adenosine because it won't work. If a denocene fails and it isn't ATAC or a flutter, you can try giving IV metoprolol in a 5-milligram aliquots every 5 minutes up to a total of 15 milligrams. If that fails, try sedation and DCR, and if that fails, admit them and pop them on an amoeuot or an infusion, and they should come back into sinus eventually. There is one scenario where you shouldn't give adenosine, and that's pre-excited AF. This is AF in a patient with wolf Parkinson-white, which looks irregular and bizarre in morphology, with some impulses conducted via the AV node, and some conducted through the accessory pathway, leading to a mixture of narrow and wide Q-A-S complexes. If you give these patients a pure AV nodal blocker, such as adenosine or metoprolol, then all the impulses will be directed through the accessory pathway, which can lead to VF. For pre-excited AF, the best acute treatment is DCR. Let's talk about SVT prevention. There are several options that all depend on symptom burden. In low symptom burden, let's say SVT once per year, you could do a pill in the pocket method, where if the patient fears themselves going to SVT, they take metoprolol 50 or 100 milligrams, which may or may not be followed by flecanide at 100 milligrams or so. If the SVT persists, then they come into hospital for adenosine. If symptom burden is more frequent, let's say every month, or every week, they should have daily metoprolol and or flecanide. At this point, patients will often prefer to be weight-listed for an SVT ablation. WPWSVT profile axis is a bit different. In WPWSVT, which has the accessory pathway, you risk both SVT in the form of AVRT, as well as pre-excited AF, if they were to develop AF. Hence, you want to avoid using a pure AV nodal blocker, like metoprolol for SVT profile axis, which would work quite well at preventing AVRT, but if they happened to develop pre-excited AF while on it, they could develop VF with all the impulses shunted down the accessory pathway. So, we use anti-rhythmics that slow atrial conduction, without being pure AV nodal blockers. The three main options are flecanide, so-to-lol and amyoderoan. Flecanide monotherapy is most commonly used, because class-1c agents like flecanide directly prolong the refractory period and slow conduction through the accessory pathway. A symptomatic WPWSVT aka WPWSVT, which is an incidentally found delta wave on ECG, doesn't require SVT profile axis. Symptomatic WPWSVT aka WPWS syndrome, where the patient has advanced of helpetations, as a class-1 recommendation for EP study and ablation of the accessory pathway. Hence, flecanide is typically only used while the patient is on the weight list for their ablation, then it can be stopped. Moving on to ventricular tecarchia VT. Wide complex tecarchia is either VT or SVT with aberrant conduction, which includes AF or atrial flutter with aberrant conduction. Aburant conduction means either an accessory pathway or a left or right bundle branch block, which could be a preexisting bundle branch block or a functional bundle branch block triggered because the rate is so fast. It's often challenging to distinguish between VT and SVT with aberrant conduction. The Brigada criteria is the most well-known criteria for distinguishing between the two. If you have any of the following four features, it's VT. You can remember these features with the Nomonic Cram, C-R-A-M-C, for concordant monophase Q-R-S in all pre-cordial leads. I.E. the Q-R-S is positive throughout V1-6, or negative throughout V1-6. R stands for onset of R to an ADR of S greater than 100 milliseconds in any pre-cordial lead. The reason for this is because in SVT you would expect a shorter onset of R to an ADR of S because the conduction is traveling straight down the his and bundle branches, so the start of the Q-R-S complex should be very short, whereas VT has slower conduction through ventricular myocardium. A is for AV dissociation, where you can see regular P-waves, completely dissociated from the Q-R-S complexes, and M stands for Q-R-S morphology inconsistent with bundle branch block. For example, a Q-S pattern in V45. Some other things that might make you think about VT is if you see capture beats, which is where you get a sinus beat occurring amongst VT beats. This implies that a sinus beat has actually managed to travel through the AV node and conduct to the ventricles. A fusion beat is a hybrid ventricular sinus beat, also suggestive of VT. A positive Q-R-S complex in AVR also suggests VT, but not always. Be on the lookout for an irregularly irregular wide complex tagic area, which suggests AF with aberrant conduction. And pre-excited AF is that irregularly irregular rhythm, with a mix of both wide and narrow complexes. Moving on to anti-o rhythmics, there are four different anti-o rhythmic drug classes. You can remember the mechanisms with the mnemonic sum block potassium channels, i.e. SBPC. Class 1 is sodium channel blockers, class 2 is beta blockers, class 3 is potassium channel blockers, and class 4 is calcium channel blockers. For the subsets of class 1, remember double quarter pander, tomato lettuce mayo, fries please. Best audio self a few burgers for study purposes to help you remember. Class 1C is dysopyramide, guinardine and procanamide, double quarter pander, class 1B is token-eyed, light-acane, and mixillotine, lettuce tomato mayo, and class 1C is flecanide and pro-papherone, fries please. Let's go through these one by one. Dysopyramide we used to use in symptomatic hockum hypertrophic obstructive cardiomyopathy, as the second line agent after beta blocker or vericamil. Now it's rarely used in favor of jumping straight to mavercampton. Quinardine has a few uses, it has a special mechanism of blocking the transient outward potassium current or IKTO. We use it for VTVF suppression in Brigada syndrome, and for short coupled idiopathic VF, which is where you get PVCs that are really close to the T-wave, which can lead to R on T phenomenon. Procanamide and light-acane, aka lignane, we use a second line agents in refractory VT after IV amoeoderoine. Token-eyed and pro-papherone we don't have in Australia, and lastly, mixillotine we use as a second line oral agent for VT suppression after oral amoeoderoine, but GI and neurological side effects can be an issue. Now let's talk about the three channel lobathees. Brigada syndrome, longcutie syndrome, and cataclylominergic polymorphic ventricular tachycardia or CPVT. Brigada syndrome is a sodium channelopathy due to SCN 5A loss of function mutation or to a lesser extent, Cachna1c mutation, CACNA1c. You might remember the Brigada patterns on ECG, types 1, 2 and 3. Type 1 looks like an RSR pattern with a coved ST elevation and T-wave inversion in V1-3. The diagnostic criteria of Brigada syndrome has two requirements. First, you need to have a Type 1 pattern, either spontaneous or induced. Spontaneous means a Type 1 pattern present on resting ECG or a Brigada ECG, which is where you put V1 and V2 leads up one into coastal space, which can make the Type 1 pattern look more pronounced. Induced is a Type 1 pattern that manifests after giving a Class 1 sodium channel blocking agent, like Agmaline, a Class 1A agent, or Flaconide, a Class 1c agent. Even if you have a Type 2 or 3 Brigada pattern, if you can't induce a Type 1 pattern, they don't have Brigada syndrome. The second requirement is that the patient meets some clinical criterion. For example, they've had cardiac syncopy, VT or VF. They have a first degree relative with Brigada Syndrome or they have an SCN 5A mutation on genetic testing. For patients with Brigada Syndrome, if they have cardiac syncopy or a deemed high risk of sudden cardiac death, they score a pacemaker. We often use Quinnadeen on top of that for VT-Prophilexus. They need to avoid sodium channel blocking agents like tricyclic antidepressants and flakonide. A full list of drugs to avoid can be found on the BrigadaDrucks.com website. They also need to avoid fevers and hypothermia which can induce the type 1 pattern and increase the risk of VT. So if they develop fever, they should promptly and regularly take paracetamol. They obviously should also avoid cocaine. The next channel up at the is LongQT Syndrome. There is more than a dozen different types of LongQT Syndrome and lots of different genes involved. The first three are probably the most common. LongQT Syndrome type 1 is triggered by exercise and swimming and is a KCNQ1 loss of function mutation. LongQT Syndrome type 2 is triggered by auditory stimuli like alarm clocks and also the postpartum period and is a KCNQ2 loss of function mutation. And LongQT Syndrome type 3 is triggered by sleep and is an SCN5A gain of function mutation. Recall that Brigada Syndrome is an SCN5A loss of function mutation whilst LongQT Syndrome type 3 is an SCN5A gain of function mutation. LongQT Syndrome patients are at increased risk of polymorphic VT. We implant an ICD if they're deemed high risk for VT such as if they have syncopy while on beta blockade or if their QTC is greater than 550 milliseconds. We also use a non-selective beta blocker like natalol or proprenolol for VT prophylaxis. The third channel up at the is catechlaminurgic polymorphic ventricular tagicardia. CPVT is a ryanidine receptor mutation, RYR2, leading to diastolic calcium leak and these patients get exercise induced by directional VT. These patients score an ICD if they have cardiac syncopy or a high risk for sudden cardiac death. We use natalol or proprenol for VT prophylaxis. We then add a flecanide if they have recurrent symptoms, VT or induced VT on an exercise stress test. I mentioned bi-directional VT which is unique to CPVT. VT is generally monomorphic or polymorphic aka torsards. If you see monomorphic VT, think scar such as from previously infected myocardium. When you see polymorphic VT, think of the four main causes. First is ischemia. Second is QT prologation. Third is severe bradycardia, often with pauses, for example, complete heart block is at risk of developing polymorphic VT and fourth is an underlying channelopathy. Patients with polymorphic VT should first be shocked out of it, then give an IV mag sulfate and correct the underlying cause. The reason we give magnesium first before potassium is because magnesium rapidly stabilizes the cardiac membrane. If someone is in conscious VT, they should have 300 milligrams of IV amiodroin, which can be delivered rapidly over five minutes. If that fails, you can try IV lidocaine, 100 milligrams stat, followed by 50 milligrams, Q5 medently, up to a maximum dose of 3 milligrams per kilogram. If that fails, or they become unstable or unconscious at any time, they need a DCR, with sedation if they're conscious. Once they're out of VT, the focus should be treating the underlying cause of VT. If there's nothing reversible and they have a structurally abnormal heart, they generally score an ICD. These patients are often loaded with amiodroin, plus some toprolol XL for VT peripheral axis. Let's talk about syncopy. Cardiac syncopy is classically no warning syncopy, i.e. sudden loss of consciousness with no preceding presyncopy and with prompt return to normal consciousness. If they're at rest, such as lying, sitting, or driving, that makes us even more suspicious. History is really important. If someone says they got up from bed at night and as they were walking back from the bathroom, they blacked out, that makes us think about some orthostatic cause, like orthostatic hypertension or vaservagal syncopy. You can think of cardiac syncopy as being either a structural problem, like Hocke or Mosovir AS, or an electrical problem, like complete heart block or VTVF. Then there's orthostatic blood pressure intolerance, which is a family of conditions that include pots, vaservagal syncopy, and orthostatic or postural hypertension. These patients generally have presyncopal symptoms, like lightheadedness, dizziness, and visual changes, triggered by posture change, leading into loss of consciousness and followed by a gradual return to normal consciousness over a few minutes. There's significant overlapping symptoms between the three entities of all the static blood pressure intolerance, and whilst the treatment is similar, there are some subtle differences that make nailing the diagnosis helpful to your patient. A tilt table test is the gold standard for diagnosis. The access can be limited and weightless are often long. The way we do tilt table testing at my institution is by two phases. The passive phase is a 10 minute head-up tilt, at 70 degrees, with blood pressure and heart rate measured each minute. Patients usually tolerate this phase reasonably well. The provocation phase is a repeat phase one, with ISO Prennelan running. The alternative we use is 800 microg sublingual GTN for elderly patients. If patients have syncopy, we stop the test and assess the hemodynamics to make a diagnosis. Postural orthostatic tachycardia syndrome, or pots, is defined by a 30-bit per minute heart rate rise during passive tilt. Clinically, this also requires at least six months of postural symptoms. A vasovagal response is a fall in heart rate by 20 beats per minute, plus a fall in blood pressure of 20 mmHG. Postural heart retention is a gradual fall in systolic blood pressure by 20 mmHG. The other thing you'll sometimes hear is the subsets of vasovagal syncopy, aka neurocharyogenicsycopy, aka reflex syncopy. These subsets are charyoinhibitory, which is a heart rate drop, with or without a systolic, with sustained blood pressure, vasodopressa, which is blood pressure drop with sustained heart rate, and mix, which is a drop in both heart rate and blood pressure. Patients with pots are often very relieved to receive a diagnosis. There may be a number of reasons for that which I won't go into. Certainly, those patients crippled by months of severe postural symptoms feel a massive sense of validation when you tell them that they have pots. The classic demographic is the young adult female in their late teens to early 20s. Patients with pots will often grow out of their pots, whether that be because of maturation of the autonomic nervous system, I'm not sure, but it becomes less common to diagnose pots in patients in their mid-30s onwards. So the goal is to manage their symptoms until that time. We give the same advice to all patients with orthostatic blood pressure intolerance, which is to drink three liters of fluid per day, plus add salt generously to foods, where waist-tire compression stockings, we show them the physical counter-pressure maneuvers to use during a pro-dome, which includes sitting down, marching their legs, and clenching their hands to generate some venous return, and we advise progressive exercise training to build up some muscle tone. Yoga and Pilates are good options, and you'll find all sorts of physios and facilities that specialise in dysordinomia, which is essentially another synonym for orthostatic blood pressure intolerance. Also, make sure your pots patient is eating enough, because eating disorders can manifest as pots, but not all pots is due to eating disorder. Pharmacotherapy is more nuanced and tailored. In pots with high symptom burden, a vabridine, or a beta blocker like Prefrontalol, are first line options if the blood pressure is robust. If blood pressure is a bit on the lower side, like systolic in the 80s or 90s, fledric autosone is a better option. If you still have refractory symptoms, despite these, you can think about adding mitodren, or even pirido stigma, but mitodren is expensive, and piridose digmin has side effects. For recurrent vasovagal syncope, your best options are fledric autosone, mitodren, SSRIs, or in refractory, kadu inhibitory cases with acestory greater than 3 seconds demonstrated on tilt table testing, pacing. If your patient has recurrent unexplained syncope, think about a loop recorder, which is a small device placed in the chest wall under local anaesthetic. The battery life is about 5 years, after which time we can remove it, but if it's not bothering the patient, sometimes we just leave it in. While a loop recorder is in, we do 6 monthly checks to check for conduction disease, or VT, and if the patient has any syncope during this period, the device can be checked sooner. If you find evidence of conduction disease, like transit complete heart block, that patient scores a pacemaker. Regarding out of hospital cardiac arrests, whether they be VT, VF or PEA arrest, routine immediate angiography is not recommended unless they have ST elevation on the post-rosque ECG. This is based on the results of the co-act study published in 2019, which showed no difference in outcomes when you compare immediate angiography versus waiting until the patient shows favorable neurological recovery before doing the angiography. Let's talk about ICDs, implantable cardiac vertebrae ledders. The purpose of an ICD is to reduce the risk of sudden cardiac death. There are primary prevention and secondary prevention ICDs. The indications for primary prevention ICDs are firstly, a Schema Cardiomypti, with an LV ejection fraction of 35% or less, despite guideline directed medical therapy, i.e. the four pillars, at 40 days post MI, if they are not re-vascularized, or 90 days if they are re-vascularized. They should also be NYHR class 2-3. If they are NYHR class 1, we use EF 30% as the cutoff. Non-eschemic Cardiomypti is more of a gray zone. The Danish trial randomized non-eschemic Cardiomypti patients with EF 35% or less, despite optimized GDMT and NYHR 2+ symptoms to ICD versus NO ICD. The 10-year follow-up results were published in 2022, which showed mortality benefit in those aged less than 70, but no mortality benefit in those aged more than 70. The other indications for primary prevention ICDs are high risk groups with inherited Cardiomypti and channel opities like Brigada, Longcuti syndrome, CPVT, ARVC, which is a Rhythmitronic right ventricular Cardiomypti and high risk Hocomemore. patients. In young patients, for example, those age less than 40, we often perform a subcutaneous ICD rather than a standard transvenous ICD. The battery life of both an ICD and a pacemaker is about 10 years. In a young patient, if you do transvenous systems for decades, you increase the risk of vascular complications and trachuspid regurgitation compared to a subcutaneous device. A secondary prevention ICD is indicated if a patient has sudden cardiac arrest or sustained if VT or VF with a structural abnormal heart, with the cause not being readily reversible. For example, a VT arrest due to a blocked LED, treated with an LED stint, doesn't need an ICD. However, if that same patient comes back five years later with a VT arrest and the LED is open, the VT was probably due to LED territory scar, and that patient merits a secondary prevention ICD. Sustained VT is VT that lasts for 30 seconds or more, as opposed to non-sustained VT, which is anywhere between 4 beats to 30 seconds. A single beat is a PVC, 2 beats is a ventricular couplet, 3 beats is a triplet, and 4 beats or more we call VT, which can be non-sustained if less than 30 seconds, or sustained if more than 30 seconds. Let's round all of this off with a big discussion on pacemakers. Feel free to pause and take a breather if you're still hanging in there well done. There are four main indications for a pacemaker. The first is symptomatic sinus node dysfunction. SND, previously called 6-cynacinthrome, is characterized by any combination of a sinus rate less than 50, sinus pauses of 3 seconds or more, and coronatropic incompetence, i.e. failure to adequately increment the heart rate with exertion. Symptomatic sinus node dysfunction, symptomatic meaning precyncope, syncopy, or poor exercise tolerance, merits a pacemaker. A symptomatic sinus node dysfunction does not merit a pacemaker, regardless of how long the pauses are. If the pauses are long enough, that patient will have symptoms. The second indication is high grade AV block, i.e. MOBITS 2 or complete heart block. On that note, a triphysicular block is the combination of a right bundle branch block, left anterior or posterior vesicular block, and a first degree AV block, i.e. PR interval greater than 200 milliseconds. Left anterior vesicular block is unexplained left axis deviation on ECG, and left posterior vesicular block is unexplained right axis deviation. I say unexplained, because left axis deviation can be caused by LVH and inferior myocardial infarction, whilst right axis deviation can be caused by RVH and lateral MI, among other causes. An asymptomatic triphysicular block doesn't need pacing and can be monitored, whilst symptomatic triphysicular block, i.e. a history of syncopy or precyncope, merits pacing, because that suggests that the patient has had transient complete heart block and will probably develop it again in the future. Also on that note, ventricular standstill is a subset of complete heart block, where in ECG or telemetry you have a period of time with p-waves, but no ventricular activity, until you get either a junction or a ventricular escape beat. Ventricular standstill merits a pacemaker. The third indication for pacemaker is slow AF. This is AF with a very slow rate, saying the 30s or 40s, with symptoms, while on no rate lowering medications. This is essentially AF with high grade AV block, because the AF rate stays the same, it's just that less beats are getting through to the ventricles. If on telemetry or halter you see slow AF with junctional or ventricular escape beats, which appear as regular beats with a different morphology to the standard irregular AF beats, that patient scores a pacemaker. The other AF related indication for pacing is tacky Brady syndrome. Tacky Brady is where you've got sinus node dysfunction, meaning a very slow sinus rate at baseline, alongside paroxysmal AF. In these patients you can't use any rate or rhythm control agents, because this will lower the baseline sinus rate to dangerously low levels, so you need a pacemaker. It also doesn't necessarily need to be sinus node dysfunction with AF. It could be sinus node dysfunction with paroxysmal flutter or SVT as well. The fourth indication for pacemaker is cardiac recent colonization therapy or CRT. This is the bi ventricular pacemaker or ICD, indicated in optimized half-ref with an ejection fraction of 35% or less, a wide left bundle, 150 milliseconds or more, MIHA class 2, 3 or ambulatory class 4 symptoms, and sinus rhythm or very well-rate controlled AF. There are other indications for pacing beyond these four main indications, but these are less common. These include carotid sinus hypersensitivity with a systole of more than three seconds on carotid massage, as well as recurrent bays of agol syncopy with a systole for more than three seconds on tilt table testing. Now let me tell you about pacemaker settings. The pacemaker or ICD mode is designated by a four-letter code, the most common being VVIR and DDDR. An ICD is simply a pacemaker that has the capacity to defibrillate, with a defibrill coil present on the RV lead. In other words, an ICD has all of the functions of a pacemaker plus a defibrill function. When we place a pacemaker or ICD, these days we either do a dual chamber RA and RV device or a single chamber RV device. CRT also has an LV lead, which sits in a cardiac vein accessed via the coronary sinus in the radiotrium. A single chamber RV pacemaker is generally only performed if the patient has permanent AF, so would never use an RA lead, or if they're very elderly and the proceduralist wants to minimize procedure time and risk. Otherwise, it's a dual chamber RA and RV pacemaker. Coming back to the four-letter code, the first letter is what is being paced, which is either AF, atria, V for ventricle, or D for duel, which is both. The second letter is what is being sensed, also AF, V or D. The third letter is what happens when something is sensed, which can be T for trigger, IF for inhibit, or D, meaning capacity for either. The last letter is rate response, meaning whether the pacemaker can be programmed to increase its pacing rate when the patient exerts themselves, and most pacemakers are programmed with the rate response turned on. Some people do get uncomfortable symptoms when it's turned on, in which case we can turn it off. VVIR is the most common setting in a single chamber RV pacemaker. It paces the ventricle, which is the first letter. It senses the ventricle, second letter. If it senses ventricular activity, it inhibits pacing, that's the third letter, and has rate response on. VVIR. This creates a pacing system that encourages intrinsic activity of the heart, with the pacemaker only there to act as a backup if it doesn't detect any intrinsic activity for a period of time. Often we'll set the lower limit for the pacemaker, aka the backup rate, at about 50 or 60 beats per minute. DDDR is the most common setting in a dual chamber, RA RV pacemaker. It paces both atrium and ventricle, that's the first letter, D. It senses both atrium and ventricle, that second letter, D, and has capacity to trigger or inhibit either chamber, depending on what it senses, third letter, D. For example, if it senses the atrium firing, but nothing getting through to the ventricle, then it'll just paste the ventricle. If it senses nothing coming from the atrium, but the AV node and ventricle are working just fine, then it'll paste just the atrium. With a standard pacemaker or ICD, we adjust the settings to maximise the heart's own intrinsic activity and minimise the work of the pacemaker. This reduces the risk of RV dysfunction and pacing induced cardiomyopathy, as well as the risk of pacemaker syndrome, which tends to occur in single chamber RV devices. When the pacemaker fires at the same time as the atrium contracts, meaning the atrium can't eject blood through the cresped valve because it's closed, which impairs forward flow of blood and causes symptoms. In contrast, a CRT device aims to maximise pacing, ideally greater than 92%, so that a greater proportion of time is spent with synchronous RV and LV contractions. We commonly get calls from ED or other teams with concerns that the pacemaker isn't pacing properly. 99% of the time, the pacemaker is working properly, it's just naturally inhibiting itself when the heart is beating at a sufficient rate and kicking in only when it needs to. A special mode is called CLS or closed loop stimulation, which is unique to biotronic devices, though Medtronic have a similar setting called RDR or rate drop response. Both of these settings are used in patients with recurrent vasovagal syncopy. CLS senses RV impedance and when that drops, indicating a vasovagal event is about to occur, the pacemaker fires rapidly at about 120 beats per minute for about a minute, and this can abort a vasovagal syncopy. Rate drop response, sensors the rate and when that drops, indicating the start of a vasovagal, it delivers rapid pacing. Patients with complete heart block sometimes need temporary transvenous pacing. Most patients with complete heart block can be monitored on the ward, resting in their bed, until they get their pacemaker on the next available pacing list. Sometimes they need isoprenaline, which increases the junctional rate. We start an isoprenaline fusion at a rate of somewhere between 2 and 10 microgh per minute, if the heart rate is less than 30 as a general rule, or if the heart rate is less than 35, with some feature of cardiogenic shock, such as rising lactate, creatinine or LFTs, reduced GCS, or cold peripheries. Patients with a very wide pulse pressure, say blood pressure of 200 over 50, are at high risk of developing some feature of shock and should be monitored closely, because the wide pulse pressure is a compensatory response to try to maximise tissue perfusion. It's really important to avoid lowering the systolic blood pressure with GTN or M lot of pain, otherwise the patient will go into shock. Patients with hemodynamic instability, ventricular stance still, or ventricular arrhythmias, whilst on Isoprenaline, merit temporary transvenous pacemakers. This takes about 10 minutes in the cath lab and involves advancing the temp wire up through the femoral vein, into the RV and suturing it in place. We put the settings as VVI and then select the rate and the output, the output measured in milliamps. We usually set the rate somewhere between 60 and 80 beats per minute. We usually start with the output at about 10 milliamps and then work our way down to try to find the threshold, which is the lowest current setting before we get loss of capture, i.e. pacing spikes without a QRS complex. The threshold is usually around 1 or 2 milliamps. Then we set the current at least 2 times that number. When a temporary pacing wire is in, you can stop the Isoprenaline and change it over to a permanent pacemaker on the next pacing list. Finally, let me tell you about magnets. If you put a magnet on a pacemaker, it will inhibit sensing. It switches the mode to either DOO for dual chamber devices or VOO for a single chamber device. This is called asynchronous pacing. It doesn't sense, it just paces at what's called the magnet rate, which is usually around 80 beats per minute, the differs for different pacemaker models. If you put a magnet on an ICD, it will inhibit shocks, but it does not alter the pacing function. In other words, the pacemaker component of the ICD will function as normal. It will sense and it will pace, but it won't shock. The distinction is important for how you manage devices periodically, because diothermic can cause electromagnetic interference or EMI with devices. If the surgery is below the umbilicus, regardless of whether it's a pacemaker or an ICD, you don't need to do anything. No magnet, no reprogramming required. This is because the diothermic will be far enough away that EMI shouldn't affect the device. If surgery is above the umbilicus, if it's a pacemaker, you should place a magnet. If it's an ICD and the patient is not pacing dependent, you can use a magnet. This is because even if EMI disrupts the sensing of the ICD, it shouldn't be an issue because the patient's conduction disease isn't so advanced that it is dependent on the pacing function of the ICD. However, if the patient has an ICD and is pacing dependent, the ICD needs reprogramming. A magnet probably isn't safe. This is easily performed by pacing tech who can reprogram it to asynchronous pacing before the surgery and then change it back to the normal settings post-op. A magnet is easier because as soon as you remove it, the device automatically returns to its pre-magnet settings. What do you do if someone is dying and they've got a device in? If it's a pacemaker, you don't need to do anything. Just leave it alone. It doesn't need a magnet. If the patient is dying for whatever reason, whether that be sepsis, respiratory failure, whatever, the pacemaker won't prolong life. It'll just keep pacing even after the patient dies and it will continue to pace in the grave until the battery dies. If it's an ICD, you should place a magnet until a tech can come and switch it off in hours. This will inhibit unwanted shocks that can occur when the patient develops ventricular arrhythmias, which can occur as part of the dying process. A pacemaker or ICD only needs to be removed after death if the patient is going to be cremated, otherwise it will explode. And that's it for my Cardiology BPD mini-series. You've all been a great audience. I've loved the feedback. I hope you enjoyed the journey. Good luck with your exams and I'll see you around.