| VideoWiki/Ventricular fibrillation (Tutorial) | |
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Initial author: Tanner Marshall, MS
Editor: Rishi Desai, MD, MPH, Tanner Marshall, MS
1
editVentricular refers to the bottom chambers of the heart, the right and left ventricles, as opposed to the top chambers, the right and left atria. Fibrillation means quivering from uncoordinated muscle fiber contraction. So ventricular fibrillation, or sometimes v-fib or VF, means the heart’s muscle fibers start quivering because they’re not contracting at the same time.
2
editNormally, an electrical signal spreads fast enough so that all the muscle fibers in the ventricles contract at almost the same time, which essentially looks like a single, coordinated contraction. If they don’t all contract at about the same time, not much gets accomplished. It’s kind of like a rowboat—it works best when everyone rows at the same time, right? Well with VF, all the rowers stop rowing together and just row whenever they want, and the rowboat just moves in circles, and eventually sinks.
3
editJust like the rowboat, If the heart’s not squeezing anymore, and it’s just squirming around “like a bag of worms”—which is actually used to describe what it looks like—then you can probably guess that this situation is extremely dangerous, since your body, especially your brain, isn’t getting fresh oxygen, meaning ventricular fibrillation can lead to death within minutes of onset, called sudden cardiac death.
4
editNow, the exact mechanisms leading up to VF aren’t always super clear, though, mostly because it’s hard to know what’s happening in the heart immediately before VF; most often though, the heart cells become stressed or damaged in such a way that different areas of tissue are structurally and electrically changed, and have different properties—and this known as tissue heterogeneity. When they’re homogenous, or the same, they all behave the same and can depolarize and contract at nearly the same time.
5
editWhen they have different electrical properties, they aren’t as good as working together, and are more prone to abnormal behavior and depolarizing on their own. In general, tissue heterogeneity can happen after something “stresses” the ventricular muscle, so things like certain medications, illicit drugs like methamphetamine or cocaine, electrolyte imbalances, and ischemia to the ventricular muscle.
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editWhen a group of ventricular pacemaker cells starts firing at the wrong time, if the surrounding cells have the same or nearly the same properties, that signal radiates outward at almost the same time, and the ventricles contract...and this is called a premature ventricular contraction, or PVC, which, although not the norm, is a relatively benign phenomenon and can even be seen sometimes in otherwise healthy hearts. Having more than 3 PVCs in a row, though, would be called ventricular tachycardia, and ventricular tachycardia can sometimes progress to ventricular fibrillation.
7
editIn our example, let’s say that surrounding cells have way different properties, like maybe these cells don’t conduct the signal as fast as these cells, instead of radiating outward uniformly, the wave of conduction can start to curve, and ultimately ends up literally spiraling out of control—where the wavefront circles back on itself, and initiates another depolarization. This situation is called functional reentry, and that spiral can spread and break down into other mini spirals, leading to fibrillation and the different areas of the heart depolarizing and contracting at different times.
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editAlternatively, the reentry behavior can start up because of the presence of scar tissue which can happen after a heart attack, because remember that scar tissue isn’t electrically conductive, so the signal just goes around and around the scar. In this case it’s known as anatomical reentry.
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editOne last means of inducing fibrillation is through electrocution, meaning external electrical stimulation. Here’s a normal reading of the heart’s electrical activity, an electrocardiogram or ECG, and we call these waves PQRST (and sometimes U). The QRS complex, right in the middle, corresponds to the ventricles contracting. If the heart tissue is stimulated at just the right time, during the upslope of the T wave, here—it can actually induce fibrillation.
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editRight after the ventricles contract, the cells enter into a refractory period, where they can’t be stimulated to contract again, and during the upslope of the T wave, some cells are starting to come out of refractory, so those cells might be ready to go again, whereas other cells might still be in a refractory phase.
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editSome cells therefore might contract, and some might not, and this can lead to this abnormal conduction that could lead to similar reentry phenomenon we just talked about. During VF, the whole PQRST breaks down completely, and all you see are these small “fib waves”, each one corresponding to an area of the ventricle depolarizing on its own. One of the only ways to stop fibrillation once it’s started, unless it breaks on its own, is again external electrical stimulation, or de-fibrillation. This is typically a high-energy shock that’s meant to depolarize everything at once, or at least a large enough portion of heart tissue, or a critical mass, to allow the sinus node, or the heart’s main pacemaker, to take control again. Basically we’re trying to interfere and stop all these reentry spirals at the same time, so this would be like if the captain of our rowboat got on the loudspeaker and screamed to get everyone’s attention all at once.
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editSometimes, people might be given an implantable cardioverter-defibrillator, or ICD. ICD’s are surgically implanted, and can constantly monitor a people’s ECG; if the people’s ECG suddenly breaks down into fib waves, the device recognizes it is as VF and promptly delivers a defibrillating shock. People may also be given medications following a VF event to help reduce the likelihood of episodes in the future. Although ICDs and medication can’t fix the underlying condition that ultimately leads to VF, they have been shown to be very beneficial and effective at improving survival.
References
edithttp://circ.ahajournals.org/content/112/8/1232.full
http://emedicine.medscape.com/article/761148-overview#a5