Pls HELP!! Confused, Am I understanding this right?

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    Ok, So I am doing my prep work for my pt tomorrow. I am in second semester and we just started learning cardiac last week. I am trying to understand A-Fib. This is my understanding from all my research:

    A-Fib causes rapid disorganized, uncoordinated contractions of the atrial musculature. It's usually associated with other things like CAD, HTN, hyperthyroidism, all of which my pt has.
    So this is where I am getting confused. When I visually think about what the heart is doing and when I think about what my prof was saying in class, I picture the the atrium on top beating faster then the ventricle on the bottom. Then I read my med-surg book and it says: "Atrial rate is 300-600, Ventricular rate is usually 120-200 in untreated A-fib" ok makes sense. BUT THEN it says: "A rapid ventricular response reduces the time for ventricular filling, resulting in a smaller stroke volume" So now I'm confused. Am I reading this wrong (I do that) A-fib is the atrial rate increased correct not the ventricular? So is this saying that the ventricle tries to speed up to keep up with the atrial rate? I do understand the smaller stroke volume part. I'm just looking for clarification if someone could please

    I hope I explained my confusion properly lol.
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    Yes, you are right. A-fib is a problem with the SA node being dysfunctional, so the electrical impulse doesn't begin there...it begins somewhere else, causing the atria to contract. The AV node is still functioning, so the ventricles think they need to keep up with the workload. Sometimes the heart rate is normal, though. Sometimes it's not.
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    Loved the heartbeat dance! Made me laugh!
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    The atria aren't so much contracting as quivering, and the ventricle actually fills more or less passively. Therefore because the ventricular rate is irregularly irregular, by definition, each beat has an irregular amount of blood to pump out, so the pulse quality varies beat-to-beat too. If the ventricles contract irregularly, for example, two beats are close together, then a pause, a beat, another beat, then three fast ones, all eight of those beats will have different amounts of time for filling and thus different amounts of blood to pump out, resulting in a different systolic pressure for each one. This is, in part, why automatic BP cuffs are useless in afib. You need practiced human ears to see what the real BP is.

    Ventricular rate in afib is never regular. The impulses getting through the AV node are not always effective and they sure as heck aren't regular.
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    Quote from GrnTea
    The atria aren't so much contracting as quivering, and the ventricle actually fills more or less passively. Therefore because the ventricular rate is irregularly irregular, by definition, each beat has an irregular amount of blood to pump out, so the pulse quality varies beat-to-beat too. If the ventricles contract irregularly, for example, two beats are close together, then a pause, a beat, another beat, then three fast ones, all eight of those beats will have different amounts of time for filling and thus different amounts of blood to pump out, resulting in a different systolic pressure for each one. This is, in part, why automatic BP cuffs are useless in afib. You need practiced human ears to see what the real BP is.

    Ventricular rate in afib is never regular. The impulses getting through the AV node are not always effective and they sure as heck aren't regular.
    Last semester I had a pt with A-fib and and we did a apical/radial rate and it was off of course by a bit, but it was interesting to listen to it. I will say, yesterday was a doozy of a day and a bit scary i might add!!! i made it through though. I was having trouble listening to heart sounds and I was disappointed I didn't get the help I asked for from my instructor in differentiating between sounds, so I would know. I was listening to the Apical HR but I was hearing popping sounds too? idk I had another student listen, she heard the same thing! Anyways thank you everyone for your help
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    Popping sounds might have been from the lungs. Or was it with every ventricular contraction? Does the patient have a really old valve replacement (they click)? Or a calcified valve? See if you can find a hint in the physician's admitting physical.
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    I combed page by page through my pt chart, all it has is the admitting dx of a-fib and the coexisting dx are CVA, HTN, coronary artery disease, CHF, hypothyroidism oh and previous MI! But nowhere in the chart is there anything about surgeries. It could of been lung sounds. The pt was moaning a lot and the breath sounds were loud. I'm just use to hearing "effective" sounds and I can usually seperate the heart from the lungs, but it was hard this time. I just don't feel like my clinical instructor is willing to help me, she is new to teaching and I just have a HUGE vib she doesn't like me.
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    If you pass a cup under water for 10 seconds, will you get more water than if you pass the same cup under the faucet for 5 seconds? Yes. Your filling time will determine your stroke volume. So if your heart is beating faster, the time the cup (ventricle) is under the faucet (tricuspid or bicuspid valve) is shortened, making the amount of blood in the ventricle significantly less.

    Don't forget about the quivering of the atrium, the patient is at risk of stroke because of not moving the blood efficiently, and should be placed on blood thinners.
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    Congrats on digging deep to make sure you have a clearer understanding of this important concept. Remember how cardiac valves actually operate. AV valves are passive.... the automatically open when the ventricles are relaxed, and close when the ventricles begin to contract and pull on papillary muscles to hold them shut. Keep this image in mind.

    I re-read the PPs comments to make sure that I am not repeating this - In a perfectly synched heart, the AV valves open passively (higher pressure from Atria pushes them open & ventricle is relaxed) as the atria begin to 'tighten up'... the atrial blood drains into the ventricles (which are relaxed at that point). Then, the atria actually contract & 'push' the remaining atrial blood into the ventricles just before ventricles begin to contract and pull the valves closed. This is called atrial kick & it adds ~ 30% to the ventricular volume.

    So, if the atria are not in synch... due to any one of a number of atrial problems, including afib or PACs, the atrial kick is lost. So, right off the bat, the ventricles are only 70% filled when they begin to contract - so the cardiac output is decreased by at least 30%. Interestingly enough, many patients with atrial arrhythmias don't feel anything different when PACs or a-fib happens.... instead, they feel the next 'normal' beat because that ejection volume is so much bigger... and describe it as a palpitation.

    Since the atria are never really able to empty themselves in a-fib and PACs (because they are trying to eject against a closed AV valve) some blood just sits around and this gives rise to the potential formation of clots.

    A deeper understanding of the underlying physiology is what separates the expert clinician from his/her peers.....
    GrnTea likes this.


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