What would your impression of your patient be if you noticed alternating large and small beats on your arterial line tracing or pleth wave on the SPO2? In this blog, we'll evaluate this waveform to see if there is any useful information to glean from this simple assessment.
Let's start with the idea of a metronome swinging from side to side, and see how this relates to Pulsus Alternans! (a mEnAcInG 👻 mEtRoNommmee!)
A Metronome with Two Tones
Imagine a metronome that makes a loud sound when it swings to one side, and a very quiet sound when it swings to the other. Metronomes and meant to keep moving back and forth so the musician can keep in beat, so it would continuously go:
TICK...
tock...
TICK...
tock...
And in case you just really need to hear this happening:
As you've probably noticed in the graphics and video so far, you can think of Pulsus Alternans in this way - the patient is alternating between strong and weak heartbeats:
Strong beat.
weak beat.
Strong beat.
weak beat.
Pulsus Alternans is a difference in systolic blood pressure with every other beat, so it can be found in any way that you measure blood pressure (some ways are just much easier than others). You may be able to palpate the difference in pressure or hear it while you're taking a blood pressure, but the two most likely ways you're going to notice Pulsus Alternans are with the SPO2 pleth wave and the arterial line tracing. (1)
Here's a monitor that shows both. Notice the alternating strong and weak beats.
( Also, what's that CVP waveform? Students who took the CVP class take a guess! 🤓 )
Now, you're probably wondering why this occurs, and why it matters. Let's take a look at the very interesting two-fold mechanism of Pulsus Alternans, and then we'll discuss why it's important.
Swing and Metal Mechanisms
Remember the Frank-Starling curve? It essentially shows us how with the right amount of preload (blood returning to the heart), we can get an optimized stroke volume from the ventricles. However, overfilling the ventricles will lead to decreased stroke volume due to the ventricular muscle stretching beyond its strongest posture.
🟢 The green is the ascending portion. This is the volume-responsive area. The very top of the green, right before it turns yellow, would be about the most optimum position for contraction.
🟡 As we continue, we hit the plateau phase in yellow. In this portion, the patient is volume tolerant. Adding or removing volume at this point doesn't really make a difference if you're staying in the yellow.
🔴 Finally, we hit the descending portion. In this portion, the ventricle is stretched too far, and the stroke volume is actually falling.
Typically, we imagine a patient moving through these phases very slowly. Perhaps only moving from one portion of the curve to another when we infuse or transfuse volume, or the patient loses fluid in some way. However, in Pulsus Alternans they're moving from one part of the curve to another part with every other beat. (2)
How is this happening so fast?
As I said before, there are two theorized mechanisms that cause this.
Alternating points on the Frank-Starling curve.
Utilizing more or less calcium.
I'll attempt to explain the Frank-Starling curve part first, followed by the calcium aspect. Even though I'm separating these mechanisms for the purpose of explaining them, they're likely inseparable and possess commensurate significance.
Swing
Here's an animation that probably does a better job explaining this than I can write out.
However, I'll still give it a shot and try to provide a little more detail.
1. The ventricle starts in an over-distended state on the descending portion of the Frank-Starling curve.
2. There's a pretty small amount of preload after this small contraction because there was not a large pressure gradient built up.
3. However, that reduced diastolic filling was enough to maintain the ventricle on a better portion of the Frank-Starling curve.
4. A stronger systole occurs due to both the position on the curve and utilizing more calcium.
5. (Which is really phase 1 again). After that strong systole, a large pressure gradient is created, and a significant amount of preload enters the ventricles, overdistention occurs.
Here are those same points on the curve with arrow tracings:
Metal
As far as calcium goes, we're alternating between using all of the calcium, and most of the calcium. Myocytes that are ischemic or diseased will take longer to repolarize. This means that every other beat will use either only healthy (the faster to repolarize), or healthy and diseased (if the diseased ones are ready).
Strong beat: (Healthy myocytes 💪) + (Diseased myocytes 🤕)
Weak beat: (Healthy myocytes 💪)
In the picture below, you can see how the healthy myocytes (🟩 green line) occur every beat, because they're able to repolarize normally and shift calcium rapidly. However, the diseased myocytes (🟦 blue line) take longer to repolarize, so they're added to the healthy myocytes only every other beat. (The diseased myocytes cannot be stimulated by the next beat after they've depolarized because they're in their absolute refractory period.) (2)
A Sick Left Heart
Pulsus Alternans signifies a failing left heart. When you see this presentation, it warrants that the patient be evaluated for cardiomyopathy and cardiogenic shock. The patient may need their end-diastolic volume reduced by vasodilation or diuresis, the heart may need inotropic support (or both).
"Left ventricular alternans occur in the setting of severe left ventricular dysfunction. This includes cardiomyopathy, aortic stenosis, and coronary artery disease." (2)
Conclusion
While Pulsus Alternans isn't exactly common, it doesn't take any extra effort to notice. Once your brain is primed to notice alternating systolic pressure differences (regardless of the method), you've developed a valuable passive assessment tool for assessing sick cardiac patients.
Thanks for reading!
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References:
1. Allareddy, V., Grundstad, M. L., & Badheka, A. (2017). Pulsus alternans: a visual clue to a grave disorder!. BMJ case reports, 2017, bcr2017222242. https://doi.org/10.1136/bcr-2017-222242
2. Henery D, Tummala R. Pulsus Alternans. [Updated 2022 Aug 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK557642/
3. Parmley, W. W., Tomoda, H., Fujimura, S., & Matloff, J. M. (1972). Relation between pulsus alternans and transient occlusion of the left anterior descending coronary artery. Cardiovascular research, 6(6), 709–715. https://doi.org/10.1093/cvr/6.6.709
4. Steven McGee, 2018.Evidence-Based Physical Diagnosis (Fourth Edition), https://doi.org/10.1016/B978-0-323-39276-1.00015-9.