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The history of pulsus paradoxus: from Kussmaul 1873 to a continuous signal

Medically reviewed by Gregory R. Mason, MD · Pulmonary & Critical Care

Published June 5, 2026 · Last reviewed June 2026 · 8 min read

Pulsus paradoxus is more than 150 years old as a named sign. Adolf Kussmaul described it in 1873, and for most of the time since, clinicians have read it the same way: by hand, with a cuff and a careful ear. This piece traces where the sign came from, why the bedside method stayed so stable for so long, and what a continuous reading of the same signal adds.

In short: the German physician Adolf Kussmaul named pulsus paradoxus in 1873, after observing a wrist pulse that faded during inspiration while the heartbeat carried on. The paradoxical pulse had been noticed earlier, by Richard Lower in the 1600s, but Kussmaul gave it the name and the bedside description still taught today. For about a century the only practical way to measure it was a manual blood-pressure cuff, which makes it operator-dependent and gives a single snapshot. What has changed is not the physiology but access to the signal: the same breath-linked variation can now be read continuously from the pulse-oximeter waveform. PulSentry is investigational and is not a diagnosis.

Who first described pulsus paradoxus, and why "paradoxical"?

The name belongs to Adolf Kussmaul, a German internist who lived from 1822 to 1902 and whose name is attached to several careful clinical observations, including Kussmaul breathing and Kussmaul's sign (Breathnach and Westphal, 2003). According to PubMed, his historical record is well documented across biographical reviews of his work (Young et al., 2012; Breathnach and Westphal, 2003).

The phenomenon itself predates the name. Historical accounts credit Richard Lower with observing the paradoxical pulse, and with elucidating the physiology of cardiac tamponade, as early as 1669, more than two centuries before Kussmaul coined the term (Meyer et al., 2008; Young et al., 2012). Kussmaul's contribution was to describe it precisely, name it, and tie it to a recognizable clinical picture, which is why his name endured while earlier observations did not become standard teaching.

The word "paradoxical" is the part that trips people up, and it is worth unpacking, because it does not mean the underlying change is abnormal in itself.

What did Adolf Kussmaul observe in 1873?

In 1873, Kussmaul identified pulsus paradoxus as a clinical hallmark of what we now recognize as constrictive and tamponade physiology (Meyer et al., 2008; Bilchick and Wise, 2002). What he noticed at the bedside was specific: the pulse felt at the wrist weakened, or seemed to disappear entirely, during inspiration, even as the heartbeat heard over the chest kept going without interruption.

That mismatch is the "paradox." The radial pulse and the audible heartbeat appeared to disagree with each other: one faded with the breath while the other did not. The label has stuck for 150 years even though, by modern understanding, the respiratory swing in blood pressure is itself a normal feature of the circulation. Pulsus paradoxus is an exaggeration of that normal swing, conventionally defined as an inspiratory fall in systolic pressure of more than 10 mmHg, rather than something that appears out of nowhere (Bilchick and Wise, 2002). Kussmaul described the appearance; the precise numeric definition came later, once blood pressure could be measured at the bedside at all.

It is also worth noting what this article does not try to do. It describes the sign, the breath-linked variation in the pulse, not the detailed chain of respiratory and hemodynamic events behind it. The history of the observation is interesting on its own terms; the underlying mechanism is a separate subject covered carefully elsewhere in the clinical literature.

How has the bedside measurement stayed the same for 150 years?

Here is the striking part of the story. The way a clinician measures pulsus paradoxus at the bedside has barely changed since the blood-pressure cuff became common in the early twentieth century. The classic method works like this:

That maneuver would be recognizable to a physician from a century ago. Reviews of the sign continue to describe this auscultatory, cuff-based technique as the standard noninvasive way to measure it, alongside a discussion of its sensitivity and specificity and the role of echocardiography in confirming tamponade (Mooser, Regamey, Stauffer, 1994). The sign is also one of several physical findings, with Kussmaul's sign and the pericardial knock, that clinicians still look for when constrictive or tamponade physiology is suspected (Marnejon, Kassis, Gemmel, 2008).

The persistence of the method is not a failure of imagination. It is that, for most of those 150 years, the cuff and the stethoscope were genuinely the best practical tools available at the bedside.

Why did pulsus paradoxus never become a continuous, monitored vital sign?

Heart rate, blood pressure, temperature, oxygen saturation: these became routine monitored vital signs because someone built an instrument that could read them automatically and repeatedly. Pulsus paradoxus never made that jump, and the reasons are practical rather than mysterious.

So the sign stayed exactly what Kussmaul left it: a valuable bedside observation that a clinician performs by hand, interpreted in clinical context. What was missing was a noninvasive instrument that could read the same signal on its own, over time, without a person at the bedside for every measurement.

What did pulse oximetry change about access to the signal?

The pulse oximeter is now one of the most widespread sensors in medicine. Beyond the oxygen saturation number, it produces a photoplethysmography (PPG) waveform: a continuous trace of the pulse. Crucially, that waveform is modulated by breathing, and investigators have long studied how to read respiratory information out of it.

This opened a different path to pulsus paradoxus. Instead of a clinician cycling a cuff, the breath-linked variation in the pulse could in principle be read from a waveform the oximeter already generates. Early clinical work pursued exactly this. Researchers compared pulsus paradoxus measured from the plethysmographic waveform against the traditional cuff method, and developed continuous, automated measures of the sign, particularly in acute asthma, where large intrathoracic pressure swings make pulsus paradoxus a useful marker of severity (Clark et al., 2004; Rayner et al., 2006).

The shift is best understood as a change in access, not in the underlying biology. The signal Kussmaul saw fade at the wrist is present in the pulse-oximeter waveform too. What pulse oximetry added was a noninvasive, already-deployed way to observe that signal without an invasive line or a dedicated examiner for every reading.

How does a continuous PPG-derived signal extend the classic bedside finding?

This is where the 150-year arc reaches the present. A continuous reading of the PPG waveform does not replace Kussmaul's observation; it extends it along the one axis the bedside method could never cover well: time.

PulSentry computes a power spectral density of the PPG signal and reads two peaks from it, one at the cardiac frequency and one at the respiratory frequency. The ratio of the respiratory peak to the cardiac peak is the pulsus index, a continuous number that rises and falls with the same breath-linked variation in the pulse that pulsus paradoxus describes. When breathing has little effect on the pulse, the respiratory peak is small and the index is low; when the pulse develops a pronounced breath-linked variation, the respiratory peak grows and the index rises. For a fuller side-by-side comparison, see From cuff to spectrum: the pulsus index vs bedside pulsus paradoxus.

The practical difference is coverage. A cuff measurement is a high-effort snapshot; a continuous index is a low-effort trend that can run in the background. That matters because a developing hemodynamic problem tends to show up as a persistent change, not a single spike, and a clinician cannot stand at the bedside cycling a cuff every few minutes for a day. PulSentry is built around persistence: it looks for the breath-linked variation that stays elevated over time, which is also why its output is meant to prompt a closer look rather than to stand in for clinical judgment.

What the history does and does not tell us about detection

The history is encouraging, but it should be read with care, and a few boundaries are worth stating plainly.

There is also early research interest in what the respiratory component of the PPG signal might reveal about breathlessness more broadly. That work is research-stage only. It is not a product claim, not a diagnosis, and not a cleared indication.

The throughline is simple. Kussmaul named a sign that a skilled clinician could read by hand. A century and a half later, the same breath-linked signal can be followed continuously from a sensor that is already on the patient. To start with the sign itself, see our pillar, What is pulsus paradoxus? A clinician's guide. To understand the waveform the index is computed from, see Pulse oximetry 101: what the number and the waveform mean. A plain-language version of these ideas for patients and families lives in the patient and family guide.

PulSentry is investigational and not FDA cleared; it supports, it does not replace, clinical judgment. This article is educational and describes a physiologic sign, its history, and the signal PulSentry analyzes; it is not medical advice and is not a description of a diagnosis. Clinical and historical statements cited here come from the referenced literature and should be interpreted in context.

Frequently asked questions

Who discovered pulsus paradoxus and when?

The German physician Adolf Kussmaul named pulsus paradoxus in 1873, describing a pulse at the wrist that weakened or disappeared during inspiration even while heart sounds continued. The underlying paradoxical pulse had been observed earlier by clinicians including Richard Lower in the 1600s, but Kussmaul gave it the name and the careful bedside description still taught today.

Why is it called paradoxical if the change is normal physiology?

Kussmaul called it paradoxical because the radial pulse seemed to vanish on inspiration while the heartbeat, heard at the chest, kept going: pulse and heartbeat appeared to disagree. The respiratory swing in blood pressure itself is normal; pulsus paradoxus is simply an exaggeration of it, generally defined as an inspiratory drop in systolic pressure greater than 10 mmHg.

Why has measuring pulsus paradoxus stayed a manual bedside skill for so long?

For over a century the only practical tool was a blood-pressure cuff, lowered slowly while the examiner listened for the gap between the first intermittent and the first continuous Korotkoff sounds. The method is operator-dependent, gives a single snapshot, and is hard to repeat over hours or days. That is why pulsus paradoxus, despite being investigational, is now of interest as a continuous signal read from the pulse-oximeter waveform rather than a one-time manual estimate.

See the signal in action

Explore the interactive pulse-and-spectrum playground and the before/after gallery on the main site.

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References & further reading

  1. Bilchick KC, Wise RA. Paradoxical physical findings described by Kussmaul: pulsus paradoxus and Kussmaul's sign. The Lancet. 2002;359(9321):1940-1942. doi:10.1016/S0140-6736(02)08763-9.
  2. Meyer P, Keller PF, Spodick DH. Empress Sissi and cardiac tamponade: an historical perspective. The American Journal of Cardiology. 2008;102(9):1278-1280. doi:10.1016/j.amjcard.2008.06.057.
  3. Young P, Finn BC, Bruetman JE, Buzzi A, Zylberman M. The outstanding achievements of Adolf Kussmaul. Revista Médica de Chile. 2012;140(4):538-544. doi:10.4067/S0034-98872012000400018.
  4. Breathnach CS, Westphal W. Adolf Kussmaul (1822-1902): from youth to maturity under the influence of Virchow. Journal of Medical Biography. 2003;11(1):55-61. doi:10.1177/096777200301100114.
  5. Marnejon T, Kassis H, Gemmel D. The constricted heart. Postgraduate Medicine. 2008;120(1):8-10. doi:10.3810/pgm.2008.04.1754.
  6. Mooser V, Regamey C, Stauffer JC. Paradoxical pulse. Schweizerische Rundschau für Medizin Praxis. 1994;83(6):158-162. PMID:8128126.
  7. Clark JA, Lieh-Lai M, Thomas R, Raghavan K, Sarnaik AP. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Archives of Pediatrics & Adolescent Medicine. 2004;158(1):48-51. doi:10.1001/archpedi.158.1.48.
  8. Rayner J, Trespalacios F, Machan J, et al. Continuous noninvasive measurement of pulsus paradoxus complements medical decision making in assessment of acute asthma severity. Chest. 2006;130(3):754-765. doi:10.1378/chest.130.3.754.
  9. Source attribution: article metadata retrieved from PubMed.
  10. Related: What is pulsus paradoxus? A clinician's guide · From cuff to spectrum: the pulsus index vs bedside pulsus paradoxus · Pulse oximetry 101: what the number and the waveform mean.