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Pulsus paradoxus in pericardial disease

Pulsus paradoxus in pericardial disease
Literature review current through: Jan 2024.
This topic last updated: Jan 08, 2024.

INTRODUCTION — Systemic blood pressure is not constant but varies slightly from heart beat to heart beat and between inspiration and expiration. Normally, the systolic blood pressure decreases by less than 10 mmHg during inspiration, but a decline of this magnitude is not detectable on examination of the peripheral pulse. Moderate to severe cardiac tamponade, and occasionally constrictive pericarditis, induce hemodynamic changes that enhance the inspiratory fall in systolic blood pressure. This exaggerated drop in systemic blood pressure during inspiration is termed pulsus paradoxus (waveform 1 and waveform 2).

Although Kussmaul named this phenomenon pulsus paradoxus, the paradox to which he referred was not the change in blood pressure but rather that the pulse palpated on examination is of variable strength, while precordial activity is regular [1]. The name is somewhat misleading, since the direction of systolic blood pressure change is the same as in normal subjects (albeit more exaggerated in pathologic instances) and is therefore not paradoxical.

Pulsus paradoxus will be discussed here, including its proper measurement, pathophysiology, and clinical conditions in which it may be present. Specific clinical conditions in which pulsus paradoxus may be present are discussed in greater detail separately. (See "Cardiac tamponade" and "Constrictive pericarditis: Diagnostic evaluation".)

PATHOPHYSIOLOGY OF PULSUS PARADOXUS IN CARDIAC TAMPONADE — Pulsus paradoxus can be thought of as a direct result of competition (ie, enhanced chamber interaction) between the right and left sides of the heart for limited space; for the right heart to fill more, the left heart must fill less. The interaction of multiple forces results in the excessive inspiratory fall in systemic blood pressure, but enhanced chamber interaction, especially in cardiac tamponade, is by far the principal mechanism.

Although enhanced chamber interaction is the most important mechanism, several other complex mechanisms contribute [2].

Under normal conditions, inspiration increases systemic venous return and right heart volumes increase; the free wall of the right ventricle expands into the unoccupied pericardial space with little impact on left heart volume.

In cardiac tamponade, when the pressure within the pericardium increases markedly, the effective compliance of all chambers becomes that of the tightly-stretched pericardium [3]. This is the reason for equalization of diastolic pressures in right- and left-sided cardiac chambers during pericardial tamponade (all being equal to intrapericardial pressure) [4,5]. As a result, the increase in right heart filling that occurs during inspiration can only be accommodated by a bowing of the interventricular septum toward the left. This leads to a reduction in left ventricular diastolic volume, a lower stroke volume, and a consequent decrease in systolic pressure during inspiration (waveform 2 and waveform 3) [2].

Pericardial and pleural pressure normally fall by approximately the same amount with inspiration; in constrictive pericarditis, however, the thickened pericardium may prevent the normal inspiratory decrease in pleural pressure from being transmitted to the cardiac chambers [6]. As a result, the inspiratory fall in left-sided filling pressure is absent or blunted. Thus, pressure in the pulmonary veins, which are intrapleural but extrapericardial, declines more than left ventricular diastolic pressure, decreasing the normal pressure gradient for left ventricular filling (waveform 4). This also contributes to left ventricular volume being smaller during inspiration than expiration [7]. As a result, right ventricular stroke volume exceeds that of the left ventricle during inspiration. The opposite events occur during expiration, and the net effect is that pulmonary and systemic arterial pressures increase and decrease with respiration 180 degrees out of phase with one another.

Since the left and right heart chambers are arranged in series, the inspiratory increase in right ventricular stroke volume eventually leads to increased left heart filling. Because of the transit time through the pulmonary circulation, this may lead to augmented left atrial filling during the following expiration, contributing to the difference in systolic pressure between inspiration and expiration. In cardiac tamponade and in some patients with constrictive pericarditis, when stroke volume is low, the increase in left heart filling is relatively exaggerated. The magnitude of this effect is influenced by both heart rate and respiratory rate. In addition, pulmonary venous pressure exceeds pericardial (and therefore left atrial) pressure during expiration, increasing expiratory left-sided filling and contributing to the respirophasic systolic pressure differential [3].

Another effect of inspiration is to augment the left ventricular transmural pressure (the sum of intracavitary pressure and negative intrathoracic pressure transmitted to the ventricle), which serves to increase left ventricular wall stress and afterload [8]. This factor, which contributes to the inspiratory drop in aortic systolic pressure, is not unique to cardiac pathology, and is more pronounced when the negative inspiratory force is elevated, as occurs in asthma, obesity, obstructive sleep apnea, and chronic pulmonary disease. (See 'Pulsus paradoxus without pericardial pathology' below.)

MEASUREMENT OF PULSUS PARADOXUS — For patients without an indwelling arterial catheter, pulsus paradoxus must be measured by the clinician using a manually-operated sphygmomanometer; an automated blood pressure machine can not accurately measure pulsus paradoxus. Alternatively, in patients with continuous invasive arterial blood pressure monitoring, pulsus paradoxus can be measured directly from the invasive blood pressure recordings.

To measure pulsus paradoxus, a manually-operated sphygmomanometer is employed for blood pressure measurement in the standard fashion except that the cuff is deflated more slowly than usual. During deflation, the first Korotkoff sounds are audible with heart beats occurring only during expiration. With further cuff deflation, Korotkoff sounds become audible on all heart beats throughout the respiratory cycle. The difference between the systolic pressure at which the first Korotkoff sounds are heard during expiration and the pressure at which they are heard throughout the respiratory cycle quantifies pulsus paradoxus. Pulsus paradoxus can also be quantified by an invasive arterial measurement and may also be observed by respirophasic variation of the pulse oximetry waveform (waveform 1). Pulsus paradoxus primarily reflects the inspiratory decline in left ventricular stroke volume. Thus, when measured via an intra-arterial cannula, pulsus paradoxus appears as a decline in both systolic and pulse pressures; the change in diastolic pressure is minimal.

Severe pulsus paradoxus, variably defined as >10 to 20 mmHg, can be palpated in the radial, brachial, or femoral pulses as a weakening or disappearance of the pulse during inspiration (which is best observed by watching or palpating the rise and fall of the chest). However, in most patients pulsus paradoxus is not as severe and is most readily identified while measuring the blood pressure. It may be necessary to have the patient breathe slowly and deeply throughout the entire examination to elucidate this finding when pulsus paradoxus is not severe.

Since the depth of respiration influences the severity of pulsus, the patient should not be instructed to change his/her breathing pattern during this evaluation (ie, to breathe deeply in the middle of the examination); any spontaneous change in respiration between observations must be taken into account. The magnitude of respiratory effort-related changes may be exaggerated in patients with obesity and those with pulmonary disease.

CLINICAL PRESENTATION OF PATIENTS WITH PULSUS PARADOXUS — Pulsus paradoxus can be seen in a variety of clinical settings (table 1), most commonly cardiac in origin (eg, cardiac tamponade, constrictive pericarditis, etc) but also in a variety of noncardiac conditions (eg, asthma and chronic obstructive pulmonary disease, obstructive sleep apnea, pulmonary embolism, etc). However, the change in pulsus paradoxus severity is a useful parameter to monitor when following a patient with cardiac tamponade before, during, and after pericardial fluid drainage. Monitoring this parameter is also useful when following a patient with pericardial effusion.

Pulsus paradoxus in cardiac tamponade — Estimates of the incidence of pulsus paradoxus in cardiac tamponade vary widely, with reports ranging from 12 to 75 percent of cases [9]. Among patients with pericardial effusion, the sensitivity of pulsus paradoxus for cardiac tamponade exceeds 80 percent and is higher than any other single physical finding [10]. The presence of a pulsus paradoxus greater than 10 mmHg increases the likelihood of tamponade by 3.3-fold, while its absence greatly lowers but does not completely eliminate the possibility of cardiac tamponade [11]. Pulsus paradoxus is typically absent in low pressure (occult) or regional tamponade. (See "Cardiac tamponade".)

Pulsus paradoxus often precedes severe hemodynamic deterioration. Therefore, nearly all patients with cardiac tamponade who have pulsus paradoxus should be evaluated for urgent or emergent pericardial fluid drainage. (See "Pericardial effusion: Approach to management", section on 'Indications for pericardial fluid removal'.)

Cardiac tamponade without pulsus paradoxus — Cardiac tamponade can occur without the development of pulsus paradoxus in the following circumstances [3,12,13]:

Coexisting disease that significantly elevates left ventricular diastolic pressure (eg, systemic hypertension, aortic stenosis) or right ventricular diastolic pressure (eg, pulmonary hypertension with cor pulmonale).

An intracardiac shunt or significant valvular regurgitation (eg, aortic regurgitation).

Aortic dissection with resulting pericardial effusion and cardiac tamponade.

"Low pressure" tamponade, as in the presence of dehydration and hypovolemia, where a pericardial effusion that would not otherwise cause cardiac compression can affect cardiac function.

Pulsus paradoxus in constrictive pericarditis — Pulsus paradoxus is seen in approximately one-third of patients with constrictive pericarditis, even though a pronounced inspiratory decline in the velocity of mitral inflow and an increase in tricuspid inflow are characteristic Doppler findings. An exception to this occurs in the patient with suspected effusive-constrictive pericarditis, in which a significant pulsus paradoxus is far more likely to be seen. (See "Differentiating constrictive pericarditis and restrictive cardiomyopathy".)

The reason for this apparent discrepancy is not universally agreed upon, but it may be because constrictive pericarditis prevents transmission of the inspiratory fall in thoracic pressure into the right atrium, such that inspiration cannot increase venous return to the right heart to the extent seen with tamponade. On the other hand, the drop in left ventricular filling during inspiration is greater than in cardiac tamponade because the left ventricle does not see the drop in pleural pressure. The right heart increases in volume solely by ventricular interaction, occurring when the left ventricle is smaller. In cardiac tamponade, the septal bulging takes place slowly, favoring pulsus paradoxus, whereas in constriction, the septum bounces rapidly so that the change in the ratio of ventricular volumes takes place abruptly, which does not favor pulsus paradoxus.

This particular explanation implicitly suggests that the respiratory variation in ventricular inflow velocities is not an indication of similar changes in the inflow volumes. Support for this explanation comes from the observation that increased respiratory variation in transmitral and transtricuspid blood flow velocities occur in pericardial effusion when the effusion is considered hemodynamically insignificant and long before evidence of cardiac tamponade is present [14].

Pulsus paradoxus without pericardial pathology — Pulsus paradoxus can be seen in conditions without pericardial pathology, including (table 1) [15]:

Asthma and chronic obstructive pulmonary disease

Obstructive sleep apnea

Tension pneumothorax

Pulmonary embolism

Right ventricular myocardial infarction

Bilateral pleural effusion

Restrictive cardiomyopathy

Marked obesity

Hypovolemic shock [16]

Pectus excavatum [17]

Extrinsic cardiac compression

The most frequent causes of pulsus paradoxus without pericardial disease are asthma and chronic obstructive pulmonary disease. In these conditions, the respiratory variation in intrathoracic pressure, which normally ranges from atmospheric pressure at end-expiration to 2 to 5 mmHg below atmospheric pressure at peak inspiration, is greatly amplified and may be as high as 40 mmHg [18]. When these pressure swings are transmitted to the extrathoracic aorta and downstream conduit vessels, pulsus paradoxus can be detected. The same mechanism may cause pulsus paradoxus in patients with obstructive sleep apnea or marked obesity [19,20].

Importantly, when pulsus paradoxus results from a nonpericardial source, diastolic pressure oscillates to the same extent as the systolic pressure, and pulse pressure is relatively constant. This is in contrast to pulsus paradoxus in tamponade where there is a decline in both systolic and pulse pressures, with minimal change in diastolic pressure. In rare cases of chronic lung disease or pulmonary embolism, pulsus paradoxus develops, affecting the systolic but not diastolic blood pressure, comparable to the findings in cardiac pathology [21].

SUMMARY AND RECOMMENDATIONS

Pulsus paradoxus is an exaggerated drop in systemic blood pressure of greater than 10 mmHg during inspiration. Several complex mechanisms generate pulsus paradoxus in cardiac tamponade, the most important of which is an amplified interdependence between the right and left sides of the heart inside a restricted pericardial space. In addition, pressure in the pulmonary veins, which are intrapleural but extrapericardial, declines more than left ventricular diastolic pressure, decreasing the pressure gradient for left ventricular filling. (See 'Introduction' above and 'Pathophysiology of pulsus paradoxus in cardiac tamponade' above.)

For patients without an indwelling arterial catheter, pulsus paradoxus must be measured by the clinician using a manually-operated sphygmomanometer; an automated blood pressure machine can not accurately measure pulsus paradoxus. To measure pulsus paradoxus, a manually-operated sphygmomanometer is employed for blood pressure measurement in the standard fashion, except that the cuff is deflated more slowly than usual. The difference between the systolic pressure at which the first Korotkoff sounds are heard during expiration and the pressure at which they are heard throughout the respiratory cycle quantifies pulsus paradoxus. (See 'Measurement of pulsus paradoxus' above.)

Pulsus paradoxus is most frequently seen in patients with pericardial pathology (table 1), specifically cardiac tamponade and, less commonly, constrictive pericarditis. In addition, pulsus paradoxus can also be seen in a variety of conditions without pericardial pathology, with the most frequent causes of pulsus paradoxus without pericardial effusion or cardiac tamponade being asthma and chronic obstructive pulmonary disease, conditions in which the respiratory variation in intrathoracic pressure is greatly amplified. (See 'Clinical presentation of patients with pulsus paradoxus' above.)

Pulsus paradoxus does not occur in patients with tamponade if the diastolic pressure in one of the ventricles is greater than that of the pericardial space, or if there is an intracardiac shunt or valvular leak. The most frequent situation where this occurs is with a coexisting disease that elevates either left or right ventricular diastolic pressure (eg, systemic hypertension, cor pulmonale). (See 'Cardiac tamponade without pulsus paradoxus' above.)

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