A very brief introduction to atrial fibrillation and atrial flutter. The concepts of rhythm control and rate control are introduced. The role of digoxin as an agent for rate control is explained.
In the previous videos we discussed that digoxin has got two important effects firstly and has got a positive inotropic effect on the heart which makes it useful in the management of heart failure with reduced ejection fraction we also discussed that digoxin has got a vago magnetic effect on the av nod and therefore is useful in the management of such conditions
As atrial fibrillation and atrial flutter now it’s worth investing some time into developing at least a rudimentary understanding on atrial fibrillation and atrial flutter as this would help us to get a better appreciation of how digoxin is useful in the management of these entities now atrial fibrillation and natal flutter are conditions where the atrial rates
Are very high pathologically high for example in atrial fibrillation the atrial rates can vary from 300 to 600 impulses per minute while in atrial flutter the atria rates may vary from 250 to 350 impulses per minute now there is only one electrical window by which impulses are conducted from the atria down to the ventricles and this is the atrial ventricular nod
Now when the atrial rates become excessive the av knot prevents many atrial impulses from passing down to the ventricles and thank god that it does because if the ventricles were allowed to beat that these excessive rates they would not get time to relax and if the ventricles do not relax they do not fill with blood if they don’t fill with blood they’re not going
To eject any blood and therefore the cardiac output would fall sharply vital organs would be acutely deprived of oxygen and blood and this would cause multi organ failure of course we discussed that this doesn’t often happen because the av not prevents many impulses from reaching the ventricles the manner in which the av not conducts impulses from the atria to
The ventricles varies in atrial flutter and atrial fibrillation and these differences may be due to the differences in the pathophysiology of these entities now in atrial flutter abnormal impulses are generated in the atria but in general these impulses stimulate the atria in a fixed and predictable manner on the other hand an atrial fibrillation there is nothing
Fixed and predictable here there is completely uncoordinated atrial activation completely unpredictable highly chaotic they actual rates in atrial flutter varies from 250 to 350 impulses per minute while an atrial fibrillation it varies from 300 to 600 impulses per minute but as we discussed the av not prevents many of these impulses from being conducted down to
The ventricles now in atrial flutter because the impulses are generated or rather because the impulses stimulate the atria in a fixed and predictable manner it may so happen that the av not begins conducting impulses from the atria to the ventricles in a fixed conduction ratio most commonly the conduction ratio is a two ways to 1 ratio this would simply mean that
If the atria were to beat at a rate of say 300 impulses per minute the ventricle would beat at a rate of 150 impulses of beats per minute so for every 2 atrial beats the ventricle would beat only once so that’s what we mean by a 2 is to 1 conduction ratio on the other hand in atrial fibrillation such conduction ratios never occur the ventricular rate varies from
100 to 160 beats per minute in a ttle flutter we often encounter situations where the atrial and ventricular rhythms are regular such a condition never arises in atrial fibrillation in fact the hallmark of atrial fibrillation is an irregularly irregular pulse now it may come as a surprise to the beginner but the cornerstone of the treatment for both atrial flutter
And fibrillation involve antithrombotic therapy in the form of antiplatelet and anticoagulant drugs now this actually isn’t very surprising because if we were to recall the atrial rates in atrial flutter and fibrillation in atrial flutter it varies from 250 to 350 impulses per minute and in atrial fibrillation the atrial rate can go up to 600 beats per minute now at
These fast and furious rates the atria failed to contract effectively rather we we come across futile fibrillate ory movements quivering movements now these sort of movements are not sufficient to effectively pump the blood forcefully into the ventricles the result is stasis of blood within the atria now if we are familiar with the virtue triad we would be familiar
With those conditions that predispose a patient to the development of a pro thrombotic state these include endothelial injury hyper coagulated blood and altered blood flow by altered blood flow we mean either stasis or turbulence of blood flow as we just saw atrial flutter and fibrillation predisposed the patient to stasis of blood in the atria and for predispose
The patient to a prothrombotic state this explains why antithrombotic therapy is a very important component in the treatment of atrial flutter and atrial fibrillation we now come to the concept of rate control now both atrial flutter and atrial fibrillation are cardiac arrhythmias and therefore it is logical that rhythm control with anti-arrhythmic drugs should
Be beneficial in both these conditions indeed rhythm control is an important strategy that may be pursued in some patients however adopting a rhythm control strategy is not suitable for many patients and hence in such subset of patients a rate control strategies preferred over a rhythm control strategy now in the rape control strategy drugs are administered which
Makes it more difficult for impulses to pass from the atria down to the ventricles these drugs are called negative draw mo tropic drugs drama tropi refers to conduction velocity by making it more difficult for impulses to pass from the atria down to the ventricles we achieve a better control of the ventricular rate and it’s important to remember that ventricular
Rate is the heart rate by achieving better control over the heart rate we reduce symptoms and increase the efficiency of the heart as a pump right so in rate control strategy we administer negative drama tropic drugs this ensures that the ventricular rate or the heart rate is kept within normal limits symptoms reduce and carry efficiency increases but it is extremely
Important to remember that rate lowering agents have little to no effect on the rhythm of the heart in other words the atria will continue to flutter or fibrillate as the case may be right so irrespective whether rhythm control or a rate control strategies adopted daily antithrombotic therapy is required to prevent thromboembolic events okay so long-term management
Of atrial fibrillation and even atrial flutter involves the use of antithrombotic agents rhythm control using anti-arrhythmic drugs and rate control the drugs most commonly used for rate control include beta blockers the non dihydropyridine calcium channel blockers namely diltiazem and vera panel cardiac glycosides like digoxin and amiodarone now if we were to look
At these drugs which are used for rhythm control beta blockers are class to antiarrhythmic drugs the non dihydropyridine calcium channel blockers are class four anti-arrhythmic drugs digoxin comes under the so called unclassifiable anti-arrhythmic drugs and amiodarone comes under class three anti-arrhythmic drugs so all these drugs which are used for rate control
Are in fact anti-arrhythmic drugs but it’s important to note that when these drugs are given for rate control they have very little effect on the rhythm of the heart a main purpose of using these drugs is to control the rate the first-line agents used for rate control include the beta blockers and the calcium channel blockers verapamil and diltiazem but there are
Situations where vera pamela and diltiazem are not at all preferred and the most important example for this would be heart failure with reduced a judge infraction so if there is a patient with atrial fibrillation of flutter with coexisting heart failure the use of digoxin becomes appropriate it’s worth noting that the johnson adequately controls the heart rate at
Rest but the ability of digoxin to control ventricular rate during exercise is quite limited when combined with beta blockers however the combination becomes more effective in controlling the ventricular rate even during exercise it’s worth noting that in patients without systolic heart failure the use of digoxin for rate control may not be such a good idea also
In patients with a vague atonic form of paroxysmal atrial fibrillation digoxin use may be associated with worse outcomes so these are two situations in which the dachshund may not be such a good idea right when talking about the dose of the jaques in atrial fibrillation it’s worth talking about the concept of loading dose when a constant dose of a drug is given it
Would take four to five half-lives for the drug to reach the desired plasma concentration in the case of digoxin the half-life is 36 hours which would mean that it would take seven to ten days for the desired concentration decide plasma concentration to be reached this may be too long a period especially when we consider the treatment of atrial fibrillation so in
Such situations we may administer a loading dose so what exactly is a loading dose this involves a series of doses given at the onset of therapy with the aim or intention of achieving the target concentration much more rapidly the use of loading dose of the jaxen is recommended in the treatment of af atrial fibrillation right so if we were to use the iv route the
Loading dose of digoxin in atrial fibrillation would be 0.25 milligrams every two hours until a total dose of one milligram is achieved the maintenance dose would be 0.125 to 0.25 milligrams per day if we were to give the johnson by the oral route the loading dose would be up to one point two five milligrams over a pill 24 hours and this total dose may be divided
Over three to four divided doses the maintenance dose would be 0.125 to 0.25 milligrams per day now even when administered in such a manner the onset of digoxin would require more than an hour and it would take up to six hours for the for the action to peak therefore digoxin may not be an optimal agent when rapid rate control is desired right so if we were to
Compare the efficacy of rate control for atrial flutter and atrial fibrillation we would see that rate control is more challenging in atrial flutter by comparison there is much more easy to achieve in atrial fibrillation and this is why the role of digoxin in atrial flutter x is extremely limited but if there is a patient with atrial fibrillation with coexisting
Heart failure with reduced ejection fraction digoxin may have a much larger role to play finally digoxin is commonly initiated and maintained at a dose of 0.125 to 0.25 milligrams per oral daily there is no need for using loading doses of digoxin in heart failure
Transcribed from video
Digoxin in Atrial Fibrillation and Atrial Flutter By Counterpharmacology