The Pre-brief
Subtle, clinical exam findings can often provide great insight into complex cardiopulmonary interactions that occur in the setting of acute, life-threatening illness. Pulsus paradoxus is an exaggerated fall in systolic blood pressure by 10 mmHg or more during inspiration; its discovery may have serious implications with regards to the clinical status of our patients.
Historical Background
There exists an abundance of paradoxes in modern medicine, many of which helped us elucidate the nature of physiological processes occurring at baseline states, as well as in the setting of disease. In 1873, the German physician, Adolf Kussmaul, also famously known for coining the expression “Kussmaul breathing” in diabetic ketoacidosis, made note of a paradoxical pulse during his examination of three patients diagnosed with constrictive pericarditis. The paradox itself was a naturally occurring phenomenon by which the peripheral arterial pulses would either diminish or disappear completely at intervals consistent with inspiration despite the presence of a regular, continuously beating heart. He would proceed to name this finding “Pulsus Paradoxus” and its discovery would dramatically influence our understanding of cardiopulmonary interactions and how they are affected by certain disease states.
Consider the following…
You admit a young male with pleuritic chest pain to the ICU for hemodynamic monitoring after discovering a moderately sized pericardial effusion on point of care ultrasound. Shortly after placing an indwelling arterial catheter, the following pattern is observed:
The key findings in the arterial tracing shown above are the observation of arterial pulsations with diminishing amplitude that correspond with the inspiratory phase of the patient’s respiratory cycle; this is characteristic of pulsus paradoxus, a clinical finding that is defined by an exaggerated drop in systolic blood pressure of 10 mmHg or more during inspiration. The utility of this finding does not lie in its diagnostic value as it is rather non-specific, and most often made incidentally; however, its identification may either indicate the presence of a serious physiological disturbance, or worse, act as an ominous sign for a life-threatening emergency. In the context of the above clinical scenario, this finding heralds the presence of Cardiac Tamponade.
Connecting the Dots
As our understanding of this phenomenon evolved, so too has our ability to associate its finding with clinical diagnosis and severity of illness in our patients. Making these connections requires an understanding of some basic physiology, thus, we begin with a brief overview of normal cardiopulmonary interactions that take place during the respiratory cycle.
During inspiration pleural pressure falls creating a pressure gradient that favors enhanced systemic venous return to the right heart. Pooling of blood in the pulmonary circulation reduces both venous return to the left heart and consequently, LV Preload. At the other end, there is a concomitant rise in LV transmural pressure imposing a state of preload-dependency as the LV must now generate a much higher pressure to contend with this increase in afterload. Therefore, under normal conditions it is not unusual to observe a decrease in systolic blood pressure during inspiration; however, certain disease states alter these normal physiological interactions and a more precipitous, exaggerated fall in systolic blood pressure may result.
Cardiac Tamponade:
As fluid accumulates in the pericardial space, the intrapericardial pressure rises. At variable thresholds, this pressure imposes a significant barrier that limits the ability of the RV to expand and accommodate the increased systemic venous return that normally occurs during inspiration. To compensate, the interventricular septum shifts further into the left ventricular cavity, resulting in compression and impaired LV diastolic filling, reduced LV preload and ultimately, reduced LV stroke volume. In this setting, pulsus paradoxus is a dangerous finding that signifies the development of an overwhelming pressure exerted on the ventricular chambers by the pericardium and should influence clinical decision-making towards the consideration of emergency interventions such as pericardiocentesis or a pericardial window.
Acute Pulmonary Embolism:
The presence of thrombi in the pulmonary circulation creates pulmonary hypertension, the afterload against which the RV must contend with in order to maintain stroke volume. Depending on the degree of thrombi and the patient’s pre-existing cardiopulmonary status, the RV may be less tolerable to increases in afterload and RV dysfunction may quickly ensue. RV dysfunction leads to increased pooling of blood during inspiration and progressive shifting of the interventricular septum into the LV causing compression during diastole. The development of pulsus paradoxus may be a sign of progressive RV dysfunction due to an overwhelming burden imposed by pulmonary emboli and should prompt consideration for lytic therapy.
Asthma Exacerbation:
As the severity of airflow obstruction increases, progressive lung hyperinflation may follow. It is also not uncommon to observe large variations in intrapleural pressures with a tendency towards much more negative intrapleural pressures during inspiration that significantly increase systemic venous return to the right heart. Lung Hyperinflation along with ventilation-perfusion mismatching in poorly ventilated alveoli substantially increase RV afterload and eventually may lead to RV dysfunction. The combination of significantly enhanced venous return and increased venous pooling in the RV results in compression of the LV during diastole, reduced LV filling and consequently, stroke volume. It is noteworthy to mention that although the appearance of pulsus paradoxus may clinically correlate with the severity of airflow obstruction, its disappearance may not necessarily be indicative of clinical improvement and the patient should be evaluated for muscle fatigue.
Measurement of Pulsus Paradoxus
Arterial Waveform Analysis: By far the simplest, most convenient method of observation. Invasive hemodynamic monitoring with an indwelling arterial line will show variability in the arterial pulsatile waveform with reduced amplitude during inspiration.
Pulse Oximetry: In certain conditions, reduced amplitude of the pulse oximetry waveform may be observed during inspiration.
Manual Cuff Sphygmomanometry: Requires multiple steps:
- The cuff is initially inflated until the disappearance of Korotkoff sounds are noted.
- The cuff is then slowly deflated until the reappearance of Korotkoff sounds during expiration only. This pressure is recorded.
- The cuff is then further deflated until Korotkoff sounds are heard during both inspiration and expiration. This pressure is recorded.
- The difference between both pressures is calculated, a difference exceeding 10 mmHg is confirmatory for pulsus paradoxus.
*It is essential to ensure a normal breathing pattern to avoid an inaccurate measurement*
Pulse Palpation: In severe cases, it may be possible to palpate a diminished or absent radial pulse during inspiration.
Reverse Pulsus Paradoxus
This is a phenomenon resulting from the reversal of cardiopulmonary interactions that occur during the respiratory cycle in patients receiving positive pressure ventilation. During inspiration, pleural pressure rises causing a reduction in systemic venous return to the right heart. In addition, venous return to the left heart is enhanced while transmural pressure is reduced with a concomitant reduction in LV afterload. The result is an increase in LV stroke volume and systolic blood pressure during inspiration, and a reduction during expiration. This may be observed in conditions such as hypertrophic cardiomyopathy, severe heart failure, and severe hypovolemia. In hypotensive patients, it is often referred to as “Pulse Pressure Variation” a dynamic variable which is used to predict fluid responsiveness in mechanically vented patients.
The Debrief
Pulsus paradoxus should not be used primarily for diagnostics; it is non-specific. However, when discovered it should be viewed as a warning sign for the presence of a serious physiological disturbance that should be investigated further.
References
- Marik PE, Cavallazzi R, Vasu T, Hirani A. Dynamic changes in arterial waveform derived variables and fluid responsiveness in mechanically ventilated patients: a systematic review of the literature. Crit Care Med. 2009 Sep;37(9):2642-7. doi: 10.1097/CCM.0b013e3181a590da. PMID: 19602972.
- Wong FW. Pulsus paradoxus in ventilated and non-ventilated patients. Dynamics. 2007 Fall;18(3):16-8. PMID: 17879762.
- Massumi RA, Mason DT, Vera Z, Zelis R, Otero J, Amsterdam EA. Reversed pulsus paradoxus. N Engl J Med. 1973 Dec 13;289(24):1272-5. PMID: 4584188.
- Rick JJ, Burke SS. Respirator paradox. South Med J. 1978 Nov;71(11):1376-8, 1382. PMID: 362537.
- Hamzaoui O, Monnet X, Teboul JL. Pulsus paradoxus. Eur. Respir. J. 2013 Dec;42(6):1696-705. PMID: 23222878.
- Perel A. The value of dynamic preload variables during spontaneous ventilation. Curr Opin Crit Care. 2017 Aug;23(4):310-317. PMID: 28614095.
[…] what happens if a large pericardial effusion is present, and how tamponade physiology can occur. This is the video I was referring to that illustrates these concepts well and demonstrates how a pulsus paradoxus […]