Jump to content
2019 Nursing Salary Survey Read more... ×
usernamee usernamee (New Member) New Member

Atrial kick and A-flutter

CCU   (429 Views 14 Comments)
225 Visitors; 2 Posts
If you find this topic helpful leave a comment.
advertisement

Hey all,

I am currently taking a dysrhythmia interpretation and management course so this this is all very new to me, forgive me if this sounds too "newbie-ish."

My understanding is that the atrial kick occurs with atrial systole, supplying the ventricles with that last 20-30% of blood before ventricular systole, and that with atrial flutter, this is lost.  I'm confused as to why this would be lost as the atria are still contracting.  Is it because it is not as much of a coordinated contraction since it is the atrial tissue generating the impulse rather than the SA node, and therefore is not traveling through the normal conduction pathway? I do understand why atrial kick is lost with a-fib, since the atria are not really contracting fully and more so just quivering, but this is not the case with a-flutter so I'm a bit lost.

Looking at an ECG strip with a-flutter, do the flutter waves not signal that the atria are depolarizing just like the P waves do? I'm not quite making the connection as to why this would not also contribute an atrial kick, especially if the ventricular rate is normal and the atria are able to contract a few times before ventricular systole.

Thanks so much in advance!

Edited by usernamee

Share this post


Link to post
Share on other sites

In a flutter the usual atrial conduction system of depolarization isn't being used so atrial contraction isn't as efficient so there is less ventricular filling that if there were NSR. It is still "better" than a fib in terms of filling. But filling isn't the only issue with these problems. Intra-atrial thrombi can form and embolize causing PE and/or stroke.

Share this post


Link to post
Share on other sites

With AFlutter, while the atria do contract, they're contracting at a rate that doesn't allow for complete filling. This means each contraction won't be as efficient as it could be and therefore the atrial kick isn't as good as it could be. End result is that the cardiac output isn't as good as it could be when the heart's in NSR. As a reminder, the atrial kick is entirely lost when the heart's in AFib... which AFlutter isn't. 

Also as a reminder, AFlutter is expressed as a ratio of atrial to ventricular beats, and there's never a 1:1 ratio with AFlutter. So if the ventricular rate is 70, with a 2:1, the atrial rate is 140. 3:1 has an atrial rate of 210. 4:1 means those atria are attempting to run at 280. The atrial kick is pretty much non-existent by that point...

Share this post


Link to post
Share on other sites

Normal sinus rhythm = a p wave with every QRS and T wave - every single beat. 

Both Afib and Aflutter lack a p-wave. Remember that only Sinus Rhythms (examples: Sinus Brady, Normal Sinus Rhythm, and Sinus Tachycardia) have P waves. If Sinus is not in the name there is no p-wave and proper conduction is not occurring. Atrial Flutter and Atrial Fibrillation do not have "Sinus" in the name as there is not proper conduction occurring in either of these two rhythms. They are both inefficient. Both lack good forward blood flow through the heart (atrial kick) and both can lead to consequences to the body.  A fib is just a little bit worse. 

This is simplified explanation but I hope that it helps

As for identifying on tele: both are irregular (the distance between each QRS can vary). Atrial Flutter as a "saw tooth appearance." It looks "prettier" than Atrial Fibrillation 

link to tele examples: 

http://www.theblondepharmacist.com/blog/2014/10/11/atrial-fibrillation-and-anticoagulation

Edited by BeatsPerMinute

Share this post


Link to post
Share on other sites
23 minutes ago, BeatsPerMinute said:

Normal sinus rhythm = a p wave with every QRS and T wave - every single beat. 

Both Afib and Aflutter lack a p-wave. Remember that only Sinus Rhythms (examples: Sinus Brady, Normal Sinus Rhythm, and Sinus Tachycardia) have P waves. If Sinus is not in the name there is no p-wave and proper conduction is not occurring. Atrial Flutter and Atrial Fibrillation do not have "Sinus" in the name as there is not proper conduction occurring in either of these two rhythms. They are both inefficient. Both lack good forward blood flow through the heart (atrial kick) and both can lead to consequences to the body.  A fib is just a little bit worse. 

This is simplified explanation but I hope that it helps

As for identifying on tele: both are irregular (the distance between each QRS can vary). Atrial Flutter as a "saw tooth appearance." It looks "prettier" than Atrial Fibrillation 

link to tele examples: 

http://www.theblondepharmacist.com/blog/2014/10/11/atrial-fibrillation-and-anticoagulation

If both are inefficient( and that is true), how is it that most patients with chronic a flutter or a fib have normal cardiac outputs at varying levels of activity?

Share this post


Link to post
Share on other sites

The body can adapt, and the ability to compensate varies greatly from person to person. A younger individual with no prior personal or familial past medical history of Afib/Aflutter will not struggle as much as the older patient who smoked for 30+ years and has both a personal and familial medical history of obstructive sleep apnea, hypertension, hyperlipidemia, pulmonary hypertension, congestive heart failure, stroke, congenital conditions / heart anomalies, diabetic, etc.. (sometimes they have all of the above and more).

For example: I have had patient recently who were diagnosed with Atrial Fibrillation (he was a 30-something year old, non-smoking, athletic male) and his cardiac output was better than the 70-something year old female diagnosed with Atrial Flutter, who was bed bound, and had an extensive past medical history of various cardiac and pulmonary conditions. 

It just depends. There are usually more factors involved when talking about Afib/Aflutter and the effect of cardiac output on the individual. 

Edited by BeatsPerMinute

Share this post


Link to post
Share on other sites
advertisement
16 minutes ago, BeatsPerMinute said:

The body can adapt, and the ability to compensate varies greatly from person to person. A younger individual with no prior personal or familial past medical history of Afib/Aflutter will not struggle as much as the older patient who smoked for 30+ years and has both a personal and familial medical history of obstructive sleep apnea, hypertension, hyperlipidemia, pulmonary hypertension, congestive heart failure, stroke, congenital conditions / heart anomalies, diabetic, etc.. (sometimes they have all of the above and more).

For example: I have had patient recently who were diagnosed with Atrial Fibrillation (he was a 30-something year old, non-smoking, athletic male) and his cardiac output was better than the 70-something year old female diagnosed with Atrial Flutter, who was bed bound, and had an extensive past medical history of various cardiac and pulmonary conditions. 

It just depends. There are usually more factors involved when talking about Afib/Aflutter and the effect of cardiac output on the individual. 

Eh...not what I was looking for...there is a more specific answer than the 'body can adapt'....and it's true for anyone with atrial disease....

Share this post


Link to post
Share on other sites

Hm, I see. It is difficult for me to explain concisely and via online messaging (I teach better while drawing and pointing to pictures / videos). I also tend to pull a lot of information from experience. I am going to recommend youtube videos for more specific explanations on how it works - I learn a lot from viewing these myself - as they walk you through the pathophysiology of these things with images to complement their explanations. 

Share this post


Link to post
Share on other sites

So what I was going for was that CO is maintained by fluid retention as a result of a fall in renal perfusion which increases atrial and ventricular filling and the secretion of BNP and ANP. The major physiological effects of ANP and BNP are vasodilation, natriuresis, and inhibition of the renin-angiotensin-aldosterone (RAA) and the sympathetic nervous systems; all of which are supposed to suppress the progression of heart failure in situations like a flutter and a fib.

In these ways, cardiac output is maintained. This is destined to fail if not medically intervened on, but it's how it's done physiologically.

Share this post


Link to post
Share on other sites
11 hours ago, offlabel said:

So what I was going for was that CO is maintained by fluid retention as a result of a fall in renal perfusion which increases atrial and ventricular filling and the secretion of BNP and ANP. The major physiological effects of ANP and BNP are vasodilation, natriuresis, and inhibition of the renin-angiotensin-aldosterone (RAA) and the sympathetic nervous systems; all of which are supposed to suppress the progression of heart failure in situations like a flutter and a fib.

In these ways, cardiac output is maintained. This is destined to fail if not medically intervened on, but it's how it's done physiologically.

What?  Fall in renal pressure leads to increased cardiac filling?  Did you miss a step there?  Doesn't decreased pressure, less sodium going past MD cells and JG apparatus lead to renin and aldosterone production? Wouldn't ANP and BNP decrease filling pressures and therefore reduce SV/CO?  

Edited by murseman24

Share this post


Link to post
Share on other sites

A fall in renal perfusion (fall in CO) causes a fall in sodium and water retention, right? That results in volume retention which acts to overcome the impediment to right heart return, or the right atrial pressure. ANP and BNP, as I noted in my post,  act to counter act that fluid retention and inhibit systems which increase vasomotor tone. But it isn't a 1:1 relationship. Fluid retention even in the presence of the ANP activity pushes volume through the heart in a compensatory mechanism that maintains cardiac output. It works the same way with any congestive heart failure scenario.

If this is confusing, look at some material dealing with "mean systemic filling pressure/venous return". 

Share this post


Link to post
Share on other sites
1 hour ago, offlabel said:

A fall in renal perfusion (fall in CO) causes a fall in sodium and water retention, right? That results in volume retention which acts to overcome the impediment to right heart return, or the right atrial pressure. ANP and BNP, as I noted in my post,  act to counter act that fluid retention and inhibit systems which increase vasomotor tone. But it isn't a 1:1 relationship. Fluid retention even in the presence of the ANP activity pushes volume through the heart in a compensatory mechanism that maintains cardiac output. It works the same way with any congestive heart failure scenario.

If this is confusing, look at some material dealing with "mean systemic filling pressure/venous return". 

Apologies....in the first sentence, "retention" should read "excretion". My bad...sorry for the confusion...

Share this post


Link to post
Share on other sites
×