Cause of hypoxia in dysrhythmias

[NYMedic828]

So my girlfriend was writing a powerpoint project for her nursing class and she wrote that atrial fibrillation results in poor blood oxygen levels.

It never really occurred to me now but other than in later stages of shock where systemic failure sets in with MOD and whatnot, is there any reason hypoxia should occur? I know cold extremities produce false readings on an O2 sat. But in non-respiratory related conditions such as afib is there any reason why a low PO2 would present early on? I suppose after a while you would get pulmonary edema...

Afib, if rapid enough is not pumping sufficient blood to the body. But that blood that makes it out is still oxygenated in the lungs, only less of it makes it way to the lungs to actually acquire oxygen. Right?

Maybe im just forgetting something at the moment... Its hot in my room going nuts lol.

 

[hibiti87]

inadequate preload directly effecting cardiac output causing hypotension and hypoxia . In my opinion cardiac related problems are always respiratory problems as well.

 

[mycrofft]

Right up my alley.

Actually many atrial fib pts have hypertension not only as a history but concurrent with the condition as well, at least until heart failure results.

The ventricles are laboring mightily (increased intrinsic ventricular rate) to make up for their "superchargers" (atria) crapping out, but blood becomes stagnant in lower extremities and must experience slowed travel through the lungs to some degree. My pulse ox is normally at about 94 even when in good health and resting/breathing deeply. It can drop farther.

And if the blood and tissues become hypoxic, what sort of effect on blood chemistry will this have? (Not to mention cell count and red cell distribution width)?:huh: ....

 

[NYMedic828]

That makes perfect sense and didn't occur to me before. If blood is slow to go out, blood is slow to come in. That blood becoming essentially static it becomes depleted of oxygen to surrounding tissues in need and eventually results in a low PO2.

Thanks

 

[mycrofft]

...and remember that blood is coming back with a lowered pH (more CO2 and lactic acid), the cell count is showing more RBC's but a normal RDW....look for swollen ankles at 3 PM and you will know where that blood is hiding, among other places.

One gets loggy towards the end of the day, but lying down for a half hour works wonders, including, I'm told, skin color.

 

[VFlutter]

Loss of atrial kick?

 

[mycrofft]

Atrial fib=NO atrial kick. I have badass ventricles though, they can do pull-ups.
Get SOB readily, do some pursed breathing, and it passes quickly. Before I was DX'ed, could push a car a little ways, take off thirty seconds, then push again, take off 30 sec....good way to wind up dead. Subject to orthostatic decomp, takes 1/2 to 1 min after standing for it to kick in.

 

[NYMedic828]

little side note to avoid making another thread.

She asked me why the heart speeds up in a-fib.

I told her that in afib the atria are constantly firing at a very rapid rate that would be far too fast for the ventricles to sustain so the AV node blocks the majority of these impulses in the interest of maintaining a stable rate.

When rapid afib occurs, the av node fails to keep all of the signals from the atrium out and they reach the ventricles resulting in a rapid heart rate unable to maintain sufficient cardiac output. Seemed accurate in my head?

I should tell her to look this stuff up! She's the nursing student im just supposed to be a lowly medic. :unsure:


Also myo, never even dawned on me that with the atria constantly firing off so fast regardless of ventricular rate you don't have an atrial kick. Cool stuff. (not so much for you though)

 

[mycrofft]

Like I tell my students, it's like a bucket brigade trying to go faster, but they can't fill their buckets that fast. Yo can get it fast, you can get it good, but not both if the atria are uncompliant.

A nursing student needs to research this stuff herself also to get the full learning benefit.

Ask her to find out why the ventricles run fast.

Also, ask her to try to imagine why the pulse will not only be irregularly irregular, but irregularly strong, with occasional very strong single pulses.

PS: "adequate output"; most of the time and at rest, it is adequate, although in the long run it will cause morphological changes to the heart. Increasing the circulatory demand results in the output becoming inadequate, if you measure adequacy by oxygenation, sensations of shortness of breath, and loss of physical energy .

 

[VFlutter]

Absence of atrial kick in atrial fibrillation can cause a reduction of stroke volume by 10-20%. In patients with an already reduced cardiac output, like CHF, it can cause them to quickly decompensate even without an increase in heart rate. Add a little RVR on top of all that and your patient will be crashing fast.

I am now going to ramble on because I am bored at work. Maybe you can impress her with random cardiac knowledge...

Atrial flutter is caused by a macro re-entry circuit in the atrium, typically right. So the electrical impulses are getting "recycled" over and over again in an endless loop inside the atrium. This occurs at a rate of around 200-400 bpm. So if there was a 1:1 conduction through the AV node the ventricles would fire at 200-400bpm. Would you be able to maintain a pressure with that HR? No, because your ventricules would not have enough time to fill during diastole. (This is why people in V Tach go pulseless; does a patient have any atrial kick in V Tach? Or better yet does a patient in A Flutter have any atrial kick?)

Since the ventricules can not beat at the same rate as the atria the AV node must block some of the incoming impulses. The ventricular rate is determined by the "AV conduction ratio". So for instance in 2:1 conduction the atrial rate is 300 and then ventricular rate is 150. So there will be two P (flutter) waves per QRS. If the conduction was 3:1 the ventricular rate would be 100 with 3 flutter waves per QRS and so on. What would happen if the sinus node was firing at an appropriate rate , lets say 60, but had a 2:1 AV conduction rate? The heart rate would be 30 with 2 p waves per QRS....what would that be? Similar concept but different mechanism.

So we have established that the AV node is the road block keeping the speeding atrial impulses under control. But what if those impluses pull a dukes of hazard and jump that road block? This is what happens with accessory pathways. The impluses bypass the AV node and conduct directly to the ventricles allowing a 1:1 conduction. So in the case of A flutter with an atrial rate of 300 the ventricular rate would be.....300 :unsure: Google 1:1 Atrial Flutter for some examples. It is a rare arrhythmia but once you see it you will never forget it.

Lastly, what drugs do we use to treat A fib/Flutter? How do they work?

This was supposed to lead into an explanation of Atrial Fibrillation but I am tired of typing on my IPad so I will add that later. Hopefully I explained stuff right

 

[NYMedic828]

What's the reasoning again that atrial flutter is usually at very regular rates of

300, 150, 100, 75.

I knew the reason and can't remember :sad:

 

[VFlutter]

What's the reasoning again that atrial flutter is usually at very regular rates of

300, 150, 100, 75.

I knew the reason and can't remember :sad:

Since it is a re-entry rhythm it is regular unlike A Fib which is a chaotic discharge of pluses due to multiple ectopic pacemakers. A flutter is a single pacemaker on repeat (think of SVT) where A Fib is like a whole bunch of pacemakers having a rave.

The rate is dependent on the degree of av block or av conduction ratio. So if its a fixed 2:1 it will be regular. But it can be a variable block

 

[NYMedic828]

Since it is a re-entry rhythm it is regular unlike A Fib which is a chaotic discharge of pluses due to multiple ectopic pacemakers. A flutter is a single pacemaker on repeat (think of SVT) where A Fib is like a whole bunch of pacemakers having a rave.

The rate is dependent on the degree of av block or av conduction ratio. So if its a fixed 2:1 it will be regular. But it can be a variable block

Lol not to sound like an arrogant prick, But i knew everything in your last two posts already.

A while back chris I believe stated in an SVT related thread that when you have an SVT at almost exactly 150bpm it's probably flutter because flutter usually presents at 300 (1:1) 150 (2:1) 100 (3:1) 75 (4:1) and there was some reason behind the regularity of those numbers across different patients.

That it I am completely imagining that ever being said.

 

[Christopher]

Lol not to sound like an arrogant prick, But i knew everything in your last two posts already.

A while back chris I believe stated in an SVT related thread that when you have an SVT at almost exactly 150bpm it's probably flutter because flutter usually presents at 300 (1:1) 150 (2:1) 100 (3:1) 75 (4:1) and there was some reason behind the regularity of those numbers across different patients.

That it I am completely imagining that ever being said.

I'm sure I said it at one time or another.

In typical flutter you get a macro-reentry circuit that for whatever reason is nearly smack dab on sending impulses to the AVN at 300 bpm. Depending on who you read, flutter waves roll into the AVN at 250-350; and the waves themselves are slower if they're medicated.

1:1 is rare outside of accessory pathways or enhanced conduction (neonates).

3:1 and 4:1 are rare outside of a patient taking medication decreasing conduction through the AVN.

2:1 conduction is the most common as the AVN is usually refractory as the 2nd wave comes by. By the time the flutter loop comes back the AVN is ready to accept another impulse. This is not a block per-se, but a physiological function of the AVN.

This is why it can get interesting if you give procainamide to flutter patients. Procainamide may slow the flutter circuit faster than it slows the AVN! The AVN will gladly send along antegrade impulses at 200-220 bpm in some patients, so if the flutter circuit slows to that range, you could get 1:1 conduction...oops.

 

[systemet]

So my girlfriend was writing a powerpoint project for her nursing class and she wrote that atrial fibrillation results in poor blood oxygen levels.

It can, but doesn't necessarily.

It never really occurred to me now but other than in later stages of shock where systemic failure sets in with MOD and whatnot, is there any reason hypoxia should occur? I know cold extremities produce false readings on an O2 sat. But in non-respiratory related conditions such as afib is there any reason why a low PO2 would present early on? I suppose after a while you would get pulmonary edema...

You're defining hypoxia as hypoxemia. Not all hypoxia involves hypoxemia. Sometimes hypoxia is classified into four forms:

(1) Hypoxic hypoxia: what you're thinking about, the pO2 is low.
(2) Hypemic hypoxia: the arterial oxygen content is decreased, but pO2 may be normal, e.g. anemia
(3) Stagnant hypoxia: blood flow is inadequate to meet oxygen demand
(4) Histotoxic hypoxia: the tissues are unable to utilise the delivered oxygen, e.g. cyanide poisoning

Hypoxia can also be regional, versus global.

 

[systemet]

What's the reasoning again that atrial flutter is usually at very regular rates of

300, 150, 100, 75.

I knew the reason and can't remember :sad:

There's a good discussion of a.flutter in general here:
http://lifeinthefastlane.com/ecg-library/atrial-flutter/

The flutter waves themselves tend to be around 300/min because the re-entry pathway in most cases is around the tricuspid isthmus and the IVC. The distance of the pathway and the conduction velocity of the myocardium result in a relatively constant time for one cycle of this re-entry circuit.

The ventricular rate depends on how fast the AV node can conduct the impulses. Most people's AV nodes aren't capable of conducting at 300/min under normal conditions, so every second beat gets blocked. [This is a protective role of the AV node -- it's the same reason a.fib doesn't become v.fib most of the time].

 

[mycrofft]

The "point of origin of atrial fib" is a good reminder of the limitations of the concept of "A Cause". The gap between knowing generally what region "it" is in, and finding the little bugger(s) to precisely ablate it/them, are two different things.

 

[NYMedic828]

The "point of origin of atrial fib" is a good reminder of the limitations of the concept of "A Cause". The gap between knowing generally what region "it" is in, and finding the little bugger(s) to precisely ablate it/them, are two different things.

Isn't ablasion of afib pretty rarely done?