In constrictive pericarditis (CP), the thickened, dense pericardium imposes a restraint on ventricular filling. Although the typical echocardiographic features of CP in spontaneously breathing patients have been extensively described (1,2), data on the hemodynamic and echocardiographic features of CP during positive pressure mechanical ventilation are incomplete. We are reporting our intraoperative findings from a patient undergoing pericardiectomy for CP.
A 77-yr-old female presented for pericardiectomy 6 yr after mitral valve replacement. Her symptoms consisted of fatigue, two-pillow orthopnea, and shortness of breath with exertion. She had suffered from exacerbations of congestive heart failure and pulmonary edema that were unexplained until demonstration of constrictive hemodynamics at cardiac catheterization. Intraoperatively, in addition to the standard invasive hemodynamic pressure monitoring, right ventricular (RV) pressure was transduced via the infusion port of an oximetric pulmonary artery catheter (Abbott, North Chicago, IL) and transesophageal echocardiographic (TEE) examination (Hewlett-Packard, Andover, MA) was performed during mechanical ventilation before and after pericardiectomy.
The initial RV tracing demonstrated a “square root” sign with an end-diastolic pressure of 20 mm Hg, and the central venous pressure (CVP) waveform displayed “M” configuration with a plateau after the “y” descent (Fig. 1A). The TEE examination initially revealed a calcified and thickened pericardium, a normally functioning mitral valve prosthesis without mitral regurgitation or perivalvular leaks, normal left ventricular (LV) and RV systolic function and no pericardial effusion. TEE Doppler examination revealed significant respiratory variation of LV diastolic filling. A respirometer tracing was not available to depict the respiratory cycle and accurately distinguish inspiration from expiration. However, at 25 mm/s sweeping speed of the echocardiogram, the Doppler velocities were obtained for a time period exceeding one respiratory cycle as the patient was ventilated with a respiratory rate of 10 breaths/min. During mechanical respiration, the peak velocity of the early filling wave (E) of transmitral flow (TMF) varied more than 50% (from 52.9 cm/s to 34.3 cm/s, Fig. 2A), whereas the peak velocity of the diastolic filling wave (D) of pulmonary venous flow (PVF) changed more than 30% (from 90.8 cm/s to 67.7 cm/s, Fig. 2A). The pattern of LV filling was restrictive, consisting of TMF E/A ratio >1, and PVF S/D ratio <1 (Fig. 2A).
After pericardiectomy, RV end-diastolic pressure decreased to 12 mm Hg, whereas the “square root” sign and plateau disappeared from the RV and CVP tracings, respectively (Fig. 1B). The TEE examination revealed decreased respiratory variation of LV filling. During mechanical ventilation, the TMF E-wave varied only 30% (from 54.6 cm/s to 71.9 cm/s) and the PVF D-wave varied only 16% (from 69.7 cm/s to 81.1 cm/s) (Fig. 2B). Furthermore, the measured stroke volume and cardiac output increased as well (69 mL vs 43 mL prepericardiectomy, and 4.9 L/min vs 3.8 L/min prepericardiectomy, respectively).
In CP, only a small amount of blood enters the ventricles during diastole. The early increase of RV end-diastolic pressure to a value close to one-third of RV systolic pressure (3), and the subsequent plateau, during which there is no blood entering the ventricle, give the waveform a distinctive “dip and plateau,” or “square root” pattern. The CVP is usually increased, with an “M” or “W” shaped contour. The atrial waveform manifests an augmented “a” wave, reflecting enhanced atrial contraction into a “stiff” ventricle, a sharp “x” descent attributable to subsequent accelerated atrial relaxation and pericardial depressurization during ventricular emptying, and a steep “y” descent reflecting rapid, resistance-free early diastolic filling. Right and left heart chamber filling pressures are typically increased and equalized, reflecting the common constraining effects of the pericardium (4).
Doppler echocardiographic examination in CP patients breathing spontaneously reveals restrictive LV diastolic filling (5), characterized by TMF E/A ratio >1, short deceleration time of TMF E velocity (6), and PVF S/D ratio <1 (1). Additionally, the respiratory variation of TMF (6), and PVF (1) Doppler flow velocities is enhanced as compared with normal patients where PVF velocities remain constant throughout the respiratory cycle (7) and TMF E velocity does not change more than 10%–15%(2,6). In CP, the thickened pericardium shields the heart (but not the extrapericardially located pulmonary veins) from changes in intrathoracic pressure during respiration. Moreover, because the intracardiac blood volume in CP is relatively fixed, the constraint of the intrapericardial space results in exaggerated RV and LV interdependence and a reciprocal relation between the left and right heart filling. LV filling reaches a minimum value during spontaneous inspiration (4) and increases at the expense of RV filling during spontaneous expiration as the pressure gradient between the pulmonary veins and the left atrium increases (2,7).
Positive pressure ventilation decreases RV output; this may decrease LV preload and output. However, during early mechanical inspiration, LV stroke volume increases as the increased intrathoracic pressure compresses the LV and increases the pressure gradient between intra- and extrathoracic vascular beds (8). Consequently, in CP during mechanical ventilation, the entry of blood into the LV will be augmented during inspiration concurrently with a decrease in blood return into the RV. During mechanical expiration, the restoration of the previously positive intrathoracic pressure toward atmospheric pressure will favor the filling of RV at the expense of LV. The above cyclic changes during mechanical ventilation will result in a TMF-E wave much higher during mechanical inspiration. The LV filling can be also reflected by the PVF velocities. In a restrictive filling pattern, as in CP, enhanced early LV diastolic filling corresponding to TMF-E wave will be accompanied by augmented diastolic PVF (PVF-D wave) much higher than systolic PVF (PVF-S wave), resulting in a PVF S/D ratio <1. Because TMF changes are mirrored by reciprocal changes in PVF, mechanical ventilation will result in cyclic variation of PVF, as well.
The increased respiratory variation in TMF E-wave is a pathognomonic sign of CP and should be sought whenever a restrictive filling pattern of the LV is encountered in the presence of thickened pericardium, particularly in those patients with a history of previous surgery, pericarditis, or irradiation of the mediastinum (9,10). However, the presence of other disease states that are characterized by increased transvalvular flow velocity variation, such as marked obesity, chronic obstructive pulmonary disease, RV infarction, or large pulmonary emboli, should be considered (6).
Although not all patients will revert to a normal pattern of LV diastolic filling immediately after pericardiectomy (2), previous studies have shown that the respiratory variation in TMF is markedly reduced in spontaneously breathing patients (6).
Intraoperative TEE examination of LV filling dynamics (TMF and PVF) correlates with data derived from invasive hemodynamic monitoring (CVP, RV tracings) and greatly enhances management of CP patients. In CP patients who are mechanically ventilated, a rather “abnormally” high CVP value should not mandate withholding IV fluid administration, particularly in the presence of data suggesting a restrictive pattern (square root sign) or increased interventricular interdependence (exaggerated respiratory variation of TMF and PVF). After pericardiectomy, a more normalized respiratory variation in TMF and PVF should accompany disappearance of the square root sign and decrease of right heart filling pressures.
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