| Ralph Shabetai, MD |
Nov 5, 1996 |
Systemic arterial pressure measured via an intraarterial cannula normally falls as much as 10 mmHg during inspiration, but this decline is not palpable at the peripheral pulses and is usually not appreciated. Moderate and severe cardiac tamponade induce hemodynamic changes that enhance the inspiratory fall in blood pressure. This exaggerated fall in systemic blood pressure during inspiration constitutes pulsus paradoxus or Kussmaul's sign (show figure 1).
Although Kussmaul named this phenomenon pulsus paradoxus [1], the paradox to which he referred was that the pulse was intermittently irregular while precordial activity was regular. The name is somewhat misleading, however, since the direction of change is similar to normal and is therefore not paradoxic.
MEASUREMENT OF PULSUS PARADOXUS ！ Severe pulsus paradoxus can easily be palpated in the radial, brachial, or femoral pulses as a weakening or disappearance of the pulse during inspiration (which is usually best observed by watching the rise and fall of the abdomen). An important clinical skill is the ability to estimate the severity of pulsus paradoxus at the bedside, which can be best appreciated as follows:
• With a sphygmomanometer, the blood pressure is measured in the standard fashion except that the cuff is deflated more slowly than usual. During deflation, the first Korotkoff sound is audible only during expiration, but with further deflation additional Korotkoff sounds are clearly heard throughout the respiratory cycle. The difference between the systolic pressure at which the first beats are heard and the pressure at which all beats are heard is the size of the pulsus.
Change in pulsus severity is a useful parameter to monitor when following a patient with tamponade both before and/or after pericardial fluid drainage. Since the depth of respiration influences the severity of pulsus, the patient should not be instructed to breathe deeply during this evaluation. As a result, any spontaneous change in respiration between observations must be taken into account when interpreting the result of pericardial fluid drainage.
PATHOPHYSIOLOGY ！ Several complex mechanisms are responsible for the development of pulsus paradoxus in cardiac tamponade. Although the details are beyond the scope of this card [2], pulsus paradoxus in tamponade largely results from the inability to prevent the normal increase in systemic venous return with inspiration (show figure 2).
With tamponade, in which there is a virtually inextensible pericardium, the expansion of the right heart volume due to increased inspiratory venous return results in two major sequential effects:
• The right ventricular transmural chamber diastolic pressure (diastolic chamber pressure minus pericardial pressure) falls to almost zero. As a result, the lateral wall of the right ventricle cannot expand outward as it is forced against the pericardial fluid, and the increased right ventricular volume leads to bulging of the septum toward the left ventricle (show echocardiogram 1).
• Bulging of the septum toward the left ventricle results in decreased left ventricular volume [2].
In normal subjects, the inspiratory increase in systemic venous return stretches all the walls of the right ventricle with much less effect upon the volume of the contiguous left ventricle. Total heart volume is minimally affected by respiration in patients with tamponade and in normals.
Pulsus paradoxus can be thought of as a direct result of competition between the left and right sides of the heart for "lebensraum" in a strictly fixed pericardial space [3]. This is a situation brought about by powerful enhancement of ventricular interaction [4] and by equalization of the diastolic compliance of the two ventricles [5]. The latter is a consequence of equilibration of left and right ventricular diastolic pressures, both being equal to the elevated pericardial pressure.
A number of other mechanisms make less important contributions to the pulsus paradoxus of cardiac tamponade [2]:
• Pericardial and pleural pressure normally fall by precisely the same amount with inspiration; in tamponade, however, the pericardial pressure declines slightly less than does pleural pressure. As a result, pressure in the pulmonary veins (which are intrapleural but extrapericardial) declines more than left heart pressure, which results in impaired left heart filling due to the smaller filling pressure gradient [6]. Blood therefore pools in the lungs during inspiration. With the decreased cardiac output that occurs when tamponade is severe, the volume pooled in the lungs constitutes a larger proportion of the stroke volume. Left ventricular stroke volume therefore declines with inspiration.
• Transit time in the lung normally causes the inspiratory increase in right ventricular stroke volume to be delayed until the subsequent expiration. In tamponade, this effect is also exaggerated because stroke volume is low.
• Since the inspiratory fall in thoracic pressure is transmitted to the aorta, inspiration can be construed as a mechanism whereby left ventricular afterload is increased [7].
In summary, the interaction of multiple forces results in the inspiratory fall in systemic arterial pressure that we call pulsus paradoxus. Competition for room in the abnormally fixed pericardial space, however, is by far the principal mechanism.
The preceding discussion has emphasized that pulsus paradoxus represents in part an inspiratory decline in stroke volume. Pulse pressure also varies directly with stroke volume. Therefore it should come as no surprise that pulsus paradoxus, when measured via an intraarterial cannula, appears as a decline in both systolic and pulse pressures; the change in arterial diastolic pressure is minimal.
ABSENT PULSUS PARADOXUS IN TAMPONADE ！ Pulsus paradoxus does not occur despite the presence of tamponade if the diastolic compliance of the two ventricles is unequal or if one or the other side of the heart fills via a shunt or valvular leak.
The most frequent clinical reason for absence of pulsus paradoxus in tamponade is coexisting disease that elevates left ventricular diastolic pressure. The following clinical example illustrates why this may occur:
• A patient with chronic renal disease with left ventricular dysfunction has a left ventricular pressure of 200/25 mmHg and develops tamponade. The pericardial pressure is 15 mmHg, which causes the right atrial pressure to also rise to 15 mmHg. However, the common right atrial and pericardial pressures are still 10 mmHg lower than the ventricular diastolic pressure. As a result, left ventricular diastolic compliance is lower than the right, which prevents the bulging of the septum into the left ventricle that is required for pulsus to occur.
Less frequently, absent pulsus arises in right ventricular failure because pericardial and left ventricular diastolic pressures are allowed to equilibrate at a lower pressure than right ventricular diastolic pressure in this setting. By comparison, atrial septal defect and aortic regurgitation prevent pulsus paradoxus by a different mechanism. In the former, the right heart fills via systemic venous return (which varies with respiration) and via the shunt (which is independent of pressure fluctuations in the thorax) [8]. In the latter, the aortic regurgitant volume is unchanged with respiration. As a result, tamponade does not result in pulsus since a significant increase in inspiratory right heart filling (the other essential prerequisite for pulsus paradoxus in tamponade) does not occur in either of these conditions.
PULSUS PARADOXUS WITHOUT TAMPONADE ！ The most frequent cause of pulsus paradoxus without pericardial effusion is chronic obstructive airways disease, a setting in which the respiratory variation of intrathoracic pressure can be greatly amplified [9]. Normally, thoracic pressure is atmospheric at end-expiration and approximately two to five mmHg below atmospheric at peak inspiration. With chronic lung disease or during an attack of asthma, alterations in thoracic pressure may be as much as 40 mmHg. Pulsus paradoxus is then detected when these pressure swings are transmitted to the aorta. In this setting, the diastolic pressure falls to the same extent as the systolic pressure and stroke volume is invariant.
In other cases of chronic lung disease and in some cases of pulmonary embolism [10], pulsus paradoxus develops, affecting the systolic but not diastolic arterial pressure (show echocardiogram 2).
In these cases, investigation using Doppler measurements has shown true respiratory variation in left and right ventricular stroke volume, comparable to that seen in cardiac tamponade.
Hypovolemic shock can also be a cause of pulsus paradoxus [11]. The suggested explanation in this setting is that pooling in the lung during inspiration accounts for a large proportion of the greatly reduced cardiac output. In tamponade, by comparison, inspiratory pooling of blood in the lungs is only a minor contributor to pulsus paradoxus.
PULSUS PARADOXUS AND CONSTRICTIVE PERICARDITIS ！ Pulsus paradoxus is uncommon in constrictive pericarditis (except in the case of effusive constrictive pericarditis). (See "Hemodynamics in constrictive and effusive constrictive pericarditis versus restrictive cardiomyopathy"). A pulsus is uncommon in this setting even though a pronounced inspiratory decline in the velocity of mitral inflow and an increase in tricuspid inflow is a characteristic Doppler finding. The reason for this apparent discrepancy is not universally agreed upon, but this author believes it is because constrictive pericarditis totally prevents transmission of the inspiratory fall in thoracic pressure into the right atrium, thereby preventing inspiration from increasing venous return.
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 appear in pericardial effusion when the effusion is considered hemodynamically insignificant and long before evidence of tamponade is present [12].