"You ever find pulsus paradoxus on anyone?"
For those who are foggy on what pulsus paradoxus is, it's when your blood pressure goes down more than it should during inspiration. It's called pulsus paradoxus because Kussmaul (who first reported it in the year 1872) could not feel a pulse at the same time that he could clearly hear one by auscultation - the finding was a paradox.
The first time I ever read about this was in paramedic school. I had a difficult time imagining how you would realistically assess this because it seemed like a cumbersome assessment to perform, and it relies on you being able to auscultate very reliable Korotkoff sounds. As a student, I was thinking... I can barely hear regular blood pressure on patients, let alone assess for pulsus paradoxus. So, I asked around.
Me: "Hey, you ever find pulsus paradoxus on someone?"
Usual response: 'Is that the one with the breathing thing?'
I quickly came to realize this was one of those imaginary assessments that we do like actually catching acute JVD, hearing "muffled heart tones", or manually counting respirations 🤥 (okay... that last one actually is very useful).
Years later, pulsus paradoxus came up again in a critical care textbook, but this time in a different context - invasive blood pressure (arterial line) monitoring. In this new context of critical care transport, there was no auscultation required because you can simply view it on the arterial line pressure tracing. This was perfect because nothing extra was needed to assess for pulsus paradoxus, you just had to glance at the monitor. The pleth wave of the SPO2 might also be used as a qualitative measure of pulsus paradoxus. Krishnan (2020) evaluated this in pediatrics with moderate to severe asthma.
Also, "In 1873 the German physician Adolf Kussmaul described pulsus paradoxus in three patients when he noted their pulse disappeared completely during inspiration while their heartbeat remained regular." (Stanford Medicine 25, n.d.). That makes a few ways to perhaps notice this exaggerated blood pressure drop during inspiration:
Manual palpation of the pulse (pretty subjective)
SPO2 Pleth Wave (might as well take a look)
Blood Pressure Cuff (I seriously doubt anyone is doing this)
Arterial Line (perfect!)
Realizing that pulsus paradoxus is something we can just look at a screen and see makes it a little more interesting, and possibly useful.
The picture notes that the usual diagnostic criteria are a peak systolic pressure difference of >10 mmHg.
Negative pressure breathing: According to Van Dam (2022), As we inhale, intrapleural pressure drops; there is a decrease in intrathoracic pressure that promotes venous blood flow into the chest increasing right heart filling. However, this does not equate to an increased filling of the left heart during inspiration. This is because as we inhale, our lungs expand and pull radial traction on the pulmonary vasculature increasing its capacitance, momentarily holding blood in the chest, and decreasing blood flow to the left heart, decreasing pre-load and consequently cardiac output. The opposite occurs during exhalation, thus systolic pressure normally decreases during inspiration and increases during exhalation.
Essentially, during inhalation, the right heart expands and applies pressure to the left heart in the process. Also, the blood flow from the pulmonary veins slows due to their temporarily increased capacitance. This decreases left ventricular stroke volume and therefore lowers cardiac output and systolic blood pressure.
The same idea in graph form:
Image retrieved from: https://erj.ersjournals.com/content/42/6/1696
Positive pressure breathing (Reverse Pulsus Paradoxus): If you understand the mechanism above, it's easy to see how positive pressure ventilation would change this process. The lungs will compress the vena cava, resulting in a backup of blood that is waiting to enter the right ventricle as soon as the positive pressure breath leaves the lungs.
During the time that the positive pressure is in the chest, it's reducing preload to the right heart, and then that low preload ends up in the left ventricle a little later during exhalation, reducing its stroke volume (and therefore the cardiac output to the arterial system).
That delayed transit from the right heart to the left heart can be a little difficult to imagine. Here's an animation that shows how positive pressure ventilation (PPV) reduces the right heart preload, and then that reduced blood volume ends up in the left heart, reducing stroke volume and cardiac output to the rest of the body (resulting in a dip on the arterial waveform.
Here are a couple more images that show the arterial line tracing in reverse pulsus paradoxus:
Image retrieved from: https://pubs.asahq.org/anesthesiology/article/103/2/419/9237/Changes-in-Arterial-Pressure-during-Mechanical
Image retrieved from: https://derangedphysiology.com/main/required-reading/cardiac-arrest-and-resuscitation/Chapter%20221/cardiac-tamponade
By the way, this image is from one of my favorite websites - Deranged Physiology. You should check it out!
All of this boils down to the patient having large variations in peak systolic pressures, or pulse pressures (however you want to think about it). Nickson (2020) has a great list of things that are associated with pathological systolic pressure variations:
Dynamic hyperinflation [air trapping]
Raised intrathoracic pressure [large tidal volumes]
Raised intra-abdominal pressure
I found this graph by Dr. Yan Yu to be very useful in following the mechanics of pulsus paradoxus back to its cause if you care to get into the details. Even though this graph represents a spontaneously breathing patient, a little bit of imagination can get you to see how the same issues would be exacerbated in positive pressure ventilation (reverse pulsus paradoxus).
To massively oversimplify this, you can pretty much have a problem with the following:
Too much pressure in the chest (positive or negative pressure breathing)
A heart that can't expand
Obstruction/narrowing of the vena cava and/or pulmonary arteries
Not so imaginary after all...
Turns out that (reverse) pulsus paradoxus isn't some imaginary assessment tool, but rather a physiologic state gone awry. Even if you don't have an arterial line tracing, you still might be able to qualitatively appreciate it through something like transient losses of a radial pulse, or large variations on an SPO2 pleth waveform. While it obviously isn't a silver bullet for diagnosing anyone's pathological state, it seems to point you in the direction of a few specific disease processes mentioned above (none of which were benign).
The next time you're monitoring an arteria line waveform, give it some closer examination and see if you can spot some systolic blood pressure variations - it might give you some of the answers you're looking for!
Thanks for reading!
Peer Review by Tyler Christifulli
As Sam candidly mentions in the blog, this always seemed like some textbook finding that wouldn't be applicable to practice. In my opinion, what makes this blog particularly important is the physiological understanding that is required to make sense of why this occurs - which Sam illustrates perfectly.
If you are like me, you probably want to go grab an ultrasound probe and see how much your RV expands during inspiration. The problem is this, during rest, the inspiratory swings are very minor and even the typical "50%" collapsibility of the IVC during inspiration is underwhelming in a rest state.
There is likely a linear correlation between RV expansion and the degree in the negative thoracic pressures reached during inspiration in a spontaneous breathing patient. This makes sense as to why decreased RV output or size correlates to a plethoric IVC. The RV can only hold so much during that inspiratory swing before it leads to a drop in left ventricular end-diastolic volumes from ventricular interdependence.
The references and images in the blog would be a great piece for students to learn the effect respiratory dynamics have on hemodynamics.
Be sure to check out Studio as well!
Frédéric Michard; Changes in Arterial Pressure during Mechanical Ventilation. Anesthesiology 2005; 103:419–428 doi: https://doi.org/10.1097/00000542-200508000-00026
G Krishnan S, Wong HC, Ganapathy S, et al
Oximetry-detected pulsus paradoxus predicts for severity in pediatric asthma
Archives of Disease in Childhood 2020;105:533-538.
Nickson, C. (2020, November 3). Systolic pressure variation. Life in the Fast Lane • LITFL. Retrieved from https://litfl.com/systolic-pressure-variation/
Preiseman. (2005). Predicting fluid responsiveness in patients undergoing cardiac surgery: functional hemodynamic parameters including the Respiratory Systolic Variation Test and static preload indicators. Retrieved from https://www.bjanaesthesia.org/article/S0007-0912(17)35027-4/fulltext#%20
Stanford Medicine 25. (n.d.). Understanding pulsus paradoxus. Stanford Medicine 25. Retrieved from https://stanfordmedicine25.stanford.edu/blog/archive/2013/Do-you-know-how-to-measure-pulsus-paradoxus.html
Van Dam MN, Fitzgerald BM. Pulsus Paradoxus. [Updated 2022 May 1]. 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482292/
Walker CM, Chung JH, Reddy GP. "Septal bounce". (2012) Journal of thoracic imaging. 27 (1): W1. doi:10.1097/RTI.0b013e31823fdfbd - Pubmed