Pulsus Paradoxus

Kussmaul described the “paradoxen puls” in 1873 (though Wilhelm Griesinger may have discovered it in 1854) as a paradox because the pulse was no longer palpable during inspiration though he could demonstrate regular cardiac contractions.

Most references define pulsus paradoxus (PP) as positive if >10 mmHg, which obviates that there is some change with inspiration and venous return that leads to a milder change normally (~6 mmHg). It is the exaggeration of this normal response that is pathologic.

E.I. Curtis et al. found that PP > 12 mmHg had a +LR 5.9 and -LR 0.03 for cardiac tamponade when the reference standard was a ≥ 20% increase in cardiac output after pericardiocentesis [1]. This also suggests a PP predicts who will respond to pericardiocentesis.

It should be noted that there are conditions that should be considered when interpreting PP, shown in Table 1.

Table 1. Conditions that Affect Pulsus Paradoxus

Conditions that can increase the PP [2,3] Conditions that mask a PP [2]
Severe obstructive pulmonary disease
Hypotension (acute or chronic)
Congestive heart failure
Pericardial adhesions
Mitral stenosis
Aortic regurgitation
Massive pulmonary embolism
Atrial septal defects
Severe hypovolemic shock
Tense ascites

The Stanford 25 has a great video on how to perform PP (below) as well as more medical history on PP and tamponade.

Pulse Oximetry for PP

PP has been shown to correlate with severity of airway obstruction, as measured by FEV1 and PEFR [4]. Knowing this, investigators have utilized the oximeter tracings as a surrogate for traditional PP estimation in patients with obstruction.

In one small study of 26 patients with airway obstruction, a respiratory waveform variation (RWV) >6 mm correlated to a PP > 10 mmHg (R2 = 0.88) with a PPV of 94% and NPV 100% for PP [5].

In a pediatric study of 36 patients with acute asthma, PP was directly measured with the oximeter and compared to the traditional measurement with a BP cuff and auscultation (PPausc).

The cuff was inflated until no signal was noted on the oximeter, deflated until only intermittent pulsations were recorded (in expiration, Pex) and then deflated until continuous pulsations were noted (inspiration and expiration, Pin), the difference being the so called PPpleth (plethysmographic waveform, Pex – Pin). The correlation in asthamtics was moderate (R2 = 0.76, P<.01), and there was only a mean difference of 0.6 mmHg between the measurement methods (PPausc vs. PPpleth) [6].  

We demonstrate this method here {link}. Note: use of oximetry has not been validated in tamponade.

  1. EI Curtiss, et al. Pulsus paradoxus: definition and relation to the severity of cardiac tamponade. Am Heart J. 1988 Feb;115(2):391-8.
  2. DH Spodick DH. Acute cardiac tamponade. N Engl J Med. 2003 Aug 14;349(7):684-90.
  3. Spodick DH. Pericarditis, pericardial effusion, cardiac tamponade, and constriction. Crit Care Clin. 1989 Jul;5(3):455-76.
  4. GK Knowles, TJ Clark. Pulsus paradoxus as a valuable sign indicating severity of asthma. Lancet. 1973 Dec 15;2(7842):1356-9.
  5. TV Hartert, AP Wheeler, JR Sheller. Use of pulse oximetry to recognize severity of airflow obstruction in obstructive airway disease: correlation with pulsus paradoxus. Chest. 1999 Feb;115(2):475-81.
  6. JA Clark, et al. Comparison of traditional and plethysmographic methods for measuring pulsus paradoxus. Arch Pediatr Adolesc Med. 2004 Jan;158(1):48-51.