I want to talk today about acute aab with hemodynamic instability I want to discuss how to actually manage those patients that we see every single day in the ICU practically in real life unlike the theory stated in the guidelines you will hear this in all guidelines hemodynamically unstable aib requires emergent electrical cardioversion this is one of the least helpful cliche that is carried in all of medicine and guidelines and textbook this situation is practically more complex than just cardioversion and is marred by three major practical problems and I will dissect those problems one acute electrical or DC card verion is problematic as it requires sedation unless the patient is in extremist and near car arrest sedation by itself aggravates hypotension worsens shock or converts a pre-shock into fullblown shock why because sedation has a vasodilatory effect and it has a camine blunting effect so sedation has risk in the process of coverting the patient you may aggravate his situation in addition one problem of acute electrical cardion is that when there is an active trigger of a f such as acute heart failure or acute sepsis aib will likely recur immediately or soon after cardioversion so saying that those patients need emergent electrical cardioversion May signify aggravating their situation temporarily and knowing how to deal with that and it may mean that well it may come right back after you shock him and we've seen this over and over it's a very common situation that immediate recurrence a second set of major problem with that statement here is what is unstable a and one is aib the culprit of the unstability unstable aib is defined usually as aib with hypotension with shock clinical shock with low perfusion or massive heart failure not just pulm edema hypoxemia it's massive heart failure with a mass pulmonary edema often requiring intubation and when do we attribute this hemodynamic compromise to aib aib with a rate of 110 120 is not by itself a cause of hemodynamic compromise aib consistently reduces KC output at all rates even when it's rate control and is an aggravating factor in all heart failure and in all hemodynamic situations but it's not the cause of a full-blown shock a with a rate over 150 bat per minute is often a major contributor to the shock and is considered for emerging cardioversion in systolic heart failure the cut off for a fib induced major hemodynamic compromise is likely 120 130 instead of 150 bats per minute and I will explain why also in order to attribute hemodynamic compromise to a fib a fib must be newly diagnosed or newly recurrent not a known permanent aib a patient with a known permanent aib who comes with shock don't attribute shock to aib he's been living in aib forever why is it causing all of a sudden shock now so it's not usually a known permanent aib I've seen that mistake as well many times so why does a fib cause hemodynamic compromise at a lower heart rate in heart failure in heart failure the heart rate that provides the highest cardiac output in the acutely ill is around hundreds to 100 teens for decompensated heart failure with reduced EF and likely 110s to 120s for heart failure with preserved EF and why is that we know there is a bodage phenomena in normal heart and in the failing heart whenever the heart rate increases the intrinsic contractility increases up to a certain point this is what we call the bow effect that certain point is lower in heart failure with UCF and is about hundreds to 100 teens as opposed to a much higher rate in normal individuals in heart failure with reduc CF the maximal KC output and the maximal contractility seems to be achieved with a heart rate around hundreds to 100 teens whether in sinus rhythm or in aib and this is based on three bodage Revisited trials Beyond this rate kak output often does not rise because of the loss of the Bish effect in the energy and metabolically depleted systolic heart failure hence contractility and car output decline at higher rates and those are the three bage Revisited trials this is the second one of them and this one showed that the peak contractility is at a heart rate of 103 plus or minus 22 and heart failure versus 120s 240s in matched older patients now in heart fail with preserv VF pacing data and a beta blocker withdrawal trial suggests that higher Bas on heart rate of 75 to 80 and probably a peak heart rate in the 120s improves quality of life and symptoms compared to basine heart rate of 60s cardiac output and likely contractility and relaxation lit tropy improve up to a heart rate of 11 to 120s in the stiff LV of heart failure with PVF we know that stiff restrictive LV of heartfare with PVF needs a higher heart rate to maintain car output but it's also likely that contractility and lusitropy improve up to a heart rate of 11s 120s based on multiple studies but especially that nice inv vitro study of the myocardial cells of Di stolic heart failure and based on that pacemaker trial So In Sum to attribute hemodynamic compromise to a fiate must be over 150 in the general patient and over 120 to 130 in systolic heart failure probably over 130 for heart failure with PVF now a third major caveat of saying that unstable aib needs urgent cersion is that there are two types of aib where hemodynamic compromise does not warrant emergent cardioversion for example aib with border line blood pressure of 90 to 100 without fullblown shock and without low perfusion State and the second situation is a fib with a full-blown shock from another cause for example a clear septic shock or massive bleed with hemorragic shock you may have a faib with a rate of 110 120 or even 15 50 but there is a clear cause and that aib needs to be rate controlled but it doesn't need to be cardioverted acutely it's not a major contributor to that shock rate control is enough in those cases and anyway acute cardion is plagued with the hazard of sedation and the high rate of immediate recurrence of a fib so we'll aggravate the patient hemodynamic status with cersion without benefit and with high immediate recurrence there are special rate control meds that need to Us in the setting with hemodynamic compromise and I will explain those so in light of the major Hazard and poor efficacy of electrical cardioversion and after carefully knowing when to attribute hemodynamic compromise to a fib how do we perform cardioversion in those patients when a fib needs to be cardioverted emergently consider pharmacological cardion and or the safest pharmacological rate control meds with the least hemodynamic effect instead of electrical cardio verion electrical cardio version remains appropriate as per guidelines particularly in the patient who's in extrem he who's in profound shock precc arrest who's already obtunded where you need little to no sedation but even in that patient where you do electrical cardioversion it's not going to be enough because there is there is a high rate of immediate recurrence so even in that patient where you do electrical cardioversion you do need to use pharmacological anti rithmic drugs to sustain the sinus rhythm and you need to know that there are five options for pharmacological cardioversion in those hemodynamically compromised patients number one amiodaron it has an immediate rate controlling effect but a slower and less effective cardioversion effect at around 8 to 12 hours with about 50% efficacy at 8 to 12 hours more effectively it sustains electrical cardioversion if it is eventually needed and usually we give the ballis 150 mgram over 20 minutes to avoid hypotension do not give it in a shorter time frame fast Ballers will cause hypotension and aggravate shock in this patient these are some ideas about amiodaron amiodaron has a rate controlling effect because it has a sympotic effect which is a downstream effect of the beta adrenic pathway not a direct beta blocker effect despite this sympatholytic effect amiodaron has little to no negative inotropic effect by itself and it has little risk of hypotension less than 10% therefore it is well tolerated in heart failure and in those borine hemodynamics or in shock the issue is with the IV formulation of amiodaron which is mixed with with excipients that have lipids in them and that have a pronounced vasodilatory effects and some negative inotropic effects which cause hypotension this is particularly the case when you quickly administer the IV bols of Amon and it's reduced when you slowly give that bolus over 20 to 30 minutes hypotension is neither seen with oral Amon and is not seen with another aquous IV formulation instead of lipid formulation now the second major option beside IV Amon is IV procainamide which is given as as an IV infusion over 30 minutes 15 mgram per kilogram it can be used even in heart failure and it has 50 to 60% cardioversion rate at 30 to 60 minutes it's faster than Amon this is based on raap 2 trial procainamide is not popular in the US it is quite popular in Canada and it is quite effective and regarding its safety and heart failure there is another trial that studied procainamide in VT versus amod it's called the proo trial and actually procainamide proved effective against VT in patients most of whom had structural heart disease and an EF that was 40 plus or minus 133% so most of them had low EF yet it was effective and safe it was actually safer than amiodaron less H potential and less Mar Eda in VT so by extrapolation I think ipride is still relatively safe in heart failure again not popular in the US and not a lot of expertise with it in the US the third option is IV ibutilide which is a ballus that may be repeated at 10 minutes efficacy is around 30% with the first bers and up to 50% when you give the second ballus 10 minutes later and it's a quickly effective at 10 to 30 minutes the main risk is tors point of 3 to 4% and this is higher in patient with severely reduced EF importantly magnesium 2 G IV immediately before ibutilide mitigate this risk of torside the fourth option is IV magnesium this is very important in all acute a whether with hemodynamic compromise or not it has been shown that IV magnesium improves a fibrate control to less than 100 bits per minute in over 50% of treated patients it also mitigates the risk of torside with ibutilide so magnesium not to cardiovert a but to slow it Di and rate control it which is very important in those hemodynamically compromised patients until they get cardioverted by those drugs or in case they fail to be cardioverted IV magnesium has been shown beneficial in this meta analysis and usually the dose is around 5 g 2 G over 50 minutes then 3 G over 3 hours and actually magnesium IV is given class 2A in the ACC guidelines for rate control of acute aib a lot of us don't do that but we need to use more magnesium in acute a not just with hemodynamic compromise but it only works as a junct to Other Drugs not Standalone magnesium therapy now the fifth option is a very interesting option called IV LOLOL which is an ultra short acting intravenous very selective beta one blocker this is very effective for rate control of unstable patients that prove difficult to cardiovert again until they get cardioverted by the drugs or in case we fail citing them at least we need to achieve good rate control and IV LOLOL achieves this acute rate control with little to no negative inotropic effect and little to no hypotensive effect even though it is a beta blocker and I will explain that in a little bit it's a very new beta blocker it just got approved by the FDA it's not yet widely available in the US so those are the five option for the hemodynamically unstable ifip that needs card verion three of those option actually achieve C verion the other two achieve rate control while awaiting cardu version now for a Feb associated with borderline blood pressure not shock or associated with non aib shock such as aib at a rate of 120 140 beats per minute with septic shock you need to rate control this a you don't need to car it but you need to rate control it with safe drugs and when we say rate control the target aib rate is usually less than bat per minute in the acutely as per ESC it's a little bit higher than the Target in chronic stable atrial fibrillation the same applies to decompensated heart failure you don't need to cardiovert a fib with a rate over 120 130 bits per minute in De compensated heart failure unless there is fullblown cogenic shock or massive pulmonary edema if you have decompensated heart failure with an aib rate over 120 13 bats per minute without cogenic shock all you need is rate control acutely then you cardiovert later once the patient has been diares and has been in a compensated stage a couple of days later this will make cersion more effective more sustained and less risky sedation will be less risky and you can perform te before cersion as well and here are the four options for rate control of aib with questionable hemodynamics or non aib shock so five option in the aib induced hemodynamic compromise and four option for rate control in questionable hemodynamics the first option is IV amiodaron which is usually the top agent everybody gets concerned about using IV Amon acutely for rate control because there is a concern that amiodaron has a theoretical rate R of acutely cardi overing aib indeed it's an anti rythmic drug with some efficacy in acute cardioversion so there is a concern in acutely carding aib that doesn't need to be acutely cardioverted in a patient who may have an atal appendic thrombus however here is the thing with amiodaron the short term less than 12 24 hours likelihood of cardioversion with amiodaron is only slightly higher than that of spontaneous cardion it's only 20 25% higher for example when you give Amon to those patient the chance of coversion at 8 to 12 hours is 50% at 24 hours it's 70 to 80% but the chance of spontaneous cersion is in the 50s per keep that in mind especially in those ill patient as you start to control their illness so true there is a risk of acute cardioversion with amiodaron but it's not much higher than theis risk of spontaneous cardioversion and it's a risk that one may need to take the same way you take a risk of acute cardioversion in a patient who is hemodynamically compromised and here is a data from a recent metaanalysis regarding acute cardioversion rate with various drugs IV or P Amon the cersion rate at 24 hours is 70 to 80% versus a 50% spontaneously procainamide is about 70% at 9 hours fide and propon have the highest cardion rate 80% at 2 to 5 hours the second option for rate control is IV dejin load usually 500 microgram first balls then 250 in 6 hours and often another 250 in another 6 hours the problem with dig is that it has a slow onset of one to 5 hours and it's not effective in high camine State critical illness shock state where again you have a high camine tone the third option is I explained IV magnesium the fourth option is IV LOLOL again you need to know that option not widely available in the US yet and I don't have experience with it but from what I read about it it's likely to be a miracle drug in those critically ill patients with aib why it's an ultra short acting super selective betan blocker with a half lifee of four minutes with limited negative inotrope and hypotensive effect it may be used in cases of instability or decompensated heart failure with lowf even lower than 30 40% per ESC it has limited impact on myocardial contractility or blood pressure and this is more information lend your all at a dose of 1 to 10 microgram per kilogram per minute you start the lower dose and you slowly up tight rated watching your hemodynamics the beta 1 to Beta 2 effect IS 250 to one so it's very very beta one selective and maybe that could explain why it has very limit to to no negative inotropic effect yet it has more pronounced negative chronotropic effect than other beta blockers so less to no negative anatropin unaffected so the camines whether intrinsic or administ catamin continue to act on the beta 2 and continue to provide contractility and inotropism Via beta 2 receptor multiple studies in septic shock patient and various ICU medical and surgical ICU patients have shown that LOLOL has rare to no hypotensive effect less than 5% hypotensive effect no reduction of car output and actually an increase in stroke volume it has been commonly used in some some of those studies in patient receiving beta Agonist or dobutamine at various doses the latter continue to provide the inotropic effect and the Vaso constrictive effect despite LOLOL so you can use LOLOL with camine or epinephrine dobutamine and these are some of the references for LOL now I will move on to discuss an overlapping topic which is acute symptomatic aab along with decompensated heart failure a heart rate of 100 to 110 beats per minute may be helpful including in the patient with a fibb as it increases carak output and LV emptying by increasing the number of cardiac cycles per minute cardiac contractility also increases up to a heart rate of 100s 100 teens based on the bodit effect and the bodit Revisited trials takic cardia over 120 beats per minute is counterproductive and reduces the contractility of the energy depleted cardium the kak output and the P2 consumption particularly in heart failure with reduced EF now Tak card over 120 to 130 beats per minute with severe hemodynamic compromised often needs acute cardioversion in systolic and probably indolic heart failure to improve LV energetics LV contractility and LV filling now those who read my book will know that that I say that when you have the compensated heart failure restoring the atal kick does not improve car output much and that's true look at this figure when you have compensated heart failure you have a small e filling in the As and big AWA filling from the atrial kick when you're in decompensated heart failure you have a big e-wave and a the atrial kick cannot push too much flow because of the high LV diastolic pressure so really those patient do not benefit a whole lot from the atrial kick but they do benefit some so when you're in a fib and you're in decompensated heart failure restoring sinus rhythm makes you go from this to that you're not improving LV filling much by restoring the atal kick however when you're in compensated heart failure here and you restore the atal kick you're improving cardiac output a lot you're improving LV feeling a lot you have a huge airwave and actually restoring sinus rhythm in compensated heart failure dramatically improves symptoms of the patient because of that atal kick and dramatically reduces the risk of decompensation and improves correct output and improves EF and improves mortality in those patient as has been shown in many trials that's why we like to cardiovert a fib in heart failure after we've diores them and put them in a compensated stage however those patients who are in Shock along with a rate over 120 to 130 may still derive some benefit from acute cardiov verion why one you do establish some atrial kick which provides some car out output which is vital in those patient with critically redu car output and second and more importantly we know that aside from the loss of atrial kick the irregular heart rate in atrial fibrillation by itself reduces car output by 16% for the same heart rate having irregular rate versus a regular rate reduces car output by 16% so cardioversion not just establishes a small atal kick but it regularizes the heart rate which improves the car output also it slows the heart rate down which again in those patients with systolic heart F and an impaired bodage phenomena that improves LV energetics and improves myocardial contractility so for all those reasons even though cardion is not as effective as in compensated heart failure it remains effective in the decompensated heart failure with shock for those three reasons I explained the small atal kick the regular heart rate and improving LV energetics and the balage effect at lower heart rate in a fib the irregular heart rate by itself further reduces car output by 16% aside from the loss of atrial filling in fact LV filling and stroke volume sharply and exponentially decrease with a short RR cycle which is not made up by the longer RR cycle the very short RR interval less than 500 millisecond reduces stroke volume more than the long RR interval makes up for it and this is an illustration this is a reg rate of 90 beats per minute this is an irregular rate of 90 beats per minute and this is another irregular rate the more irregular you are like here alternation between very short and very long RR the more you drop your car output because you dramatically drop your stroke volume with this and you don't make up for it with this much longer RR interval because you're only able to fill during a certain period of that long RR interval especially in a decompensated heart failure with a narrow e-wave so that's why kak output drops on average by 16% with an irregular heart rate and W pressure goes up by 20% based on several Landmark studies from the '90s and when you need urgent cardioversion in acute a with decompensated heart failure you have those same five options I discussed earlier amiodaron procainamide ibutilide magnesium and LOLOL LOLOL and magnesium mainly to rate control you safely while awaiting cardioversion keep in mind that procainamide and ibutilide have higher hazards in heart failure patients and you have those same four rate control options in acute decompensated heart failure with acute aab you have the IV Amon IV dein magnesium and LOLOL which will become very handy once available and for rate control when you have that heart rate of over 120 bits per minute without severe hemodynamic compromise you use rate control to achieve a heart rate less than 100 110 bats per minute and you have those same four options I discussed before I Amon IV dejin IV magnesium and IV LOLOL which will become very handy once widely available in the US the ESC and ACC guidelines allow in half failure with preser ef and even in heart failure with mid-range EF 41 to 50% allow the use of beta blocker or DM acutely beside those options that may also be used in heart failure preserve or mid-range EF now I will finish with a summary idea regarding aib and heart failure after you treat heart failure decompensation and for all the reasons I described earlier it's important to eventually establish and maintain sinus rhythm in heart failure patients particularly after acute therapy and after heart failure becomes compensated this is where you will have a higher chance of sustaining the sinus rhythm and a higher likelihood of benefiting from sinus rhythm as I have shown in this figure and that is why Trials of a fib ablation in harf with reduced F have consistently shown an F of 10 to 30% after ablation mainly in persistent a but also in parisal a with high burden even in patients who aib is rate controll those two trials here have shown a reduction of mortality with aib ablation and those two here have shown a dramatic Improvement of EF with aib ablation and this benefit of sinus rhythm likely extrapolates to heart failure with preser thef this is B on the Cabana trial of aib ablation the heart failure with preserve F sub study Which derived a more dramatic benefit than non-heart failure patients and this is also based on East aib net 4 trial heart failure substudy where Rhythm control mostly with drugs improved outcome compared to rate control more so in the heart failure patient the absolute benefit was doubled in the heart failure patient Rhythm control even with with drugs even in heart failure with preserve F but the best data is in heart failure with reduc f ablation but probably benefit also with rhythm control with drugs probably also in heart failure with PVF