Venous Pulse Contour in Constrictive Pericarditis

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Elevated venous pressure with the sharpy descent and deep "y trough' in constrictive pericarditis has been known as the diastolic collapse of Friedreich for more than a century (20). However, atypical cases, some with rapidly evolving "constrictive pericarditis," have been described, which show only a dominant x' descent despite high venous pressure (16,53). As expected in these patients, the RV early diastolic pressure was quite high, with very little pressure difference between the right atrium and the right ventricle at the time of tricuspid valve opening to account for the lack of a good y descent. This would be almost a hemodynamic imitation of tamponade to the extent that the restriction to ventricular filling also involved the early rapid filling phase.

Such a high elevation of early diastolic RV pressures in the absence of true extrinsic compression as in tamponade would imply poor systolic emptying of the right ventricle and decreased right ventricular systolic function (Figs. 4, 5, 16, and 17). Rarely such a situation could occur in severe cardiomyopathy. Such patients have poor x' descent.

Ischaemic Cardiomyopathy

Fig. 26. Simultaneous recordings of electrocardiogram (ECG), jugular venous pulse (JVP), and phonocardiogram (Phono) in a patient with ischemic cardiomyopathy. The right ventricle (RV) is spared and the right heart function is normal, as evidenced by the good X descent in the JVP. (Reproduced with kind permission from ref. 47.)

Fig. 26. Simultaneous recordings of electrocardiogram (ECG), jugular venous pulse (JVP), and phonocardiogram (Phono) in a patient with ischemic cardiomyopathy. The right ventricle (RV) is spared and the right heart function is normal, as evidenced by the good X descent in the JVP. (Reproduced with kind permission from ref. 47.)

In fact, in patients with severe cardiomyopathy, preservation of a good X descent would imply an ischemic etiology involving predominantly the left ventricle (Fig. 26).

Venous Pulse Contour in Severe Heart Failure

Patients with severe cardiac failure and poor RV systolic function will have high jugular venous pressure as a result of elevated pre-a wave and v wave pressures. The latter will be further raised in the jugulars secondary to high venous tone caused by the co-existent sympathetic stimulation (19). The X descent will be poor or lost. This may be aggravated by tricuspid regurgitation that may develop as a result of right ventricular dilatation. Atrial fibrillation may set in due to atrial overdistension. This will further diminish the x' descent as a result of the loss of the Starling effect. If early diastolic pressure in the RV falls to close to zero, as it should normally, then the y descent will be either dominant or the only descent noted (Fig. 6).

If the early diastolic RV pressures were also elevated during the rapid filling phase, as may happen in severely compromised RV with very poor compliance, then the y descent may be also poor even though the v wave pressure is elevated because of very little gradient of pressure between the atrium and the ventricle. The overall effect could be such that one would have high jugular pressure with poor descents.

Venous Pulse Contours in RV Infarction

RV infarction may complicate acute infero-posterior infarction, particularly when there is acute occlusion of a dominant right coronary artery in its proximal segment close to its origin. The RV, because of its thin walls and lower systolic pressure, has favorable systolic tension, which imposes less demands on oxygen compared to the left ventricle. If the hemodynamic failure is not severe with marked persistent hypotension and shock, the RV might recover most of its function. Nevertheless, during the acute phase, the ischemic dysfunction will alter both its diastolic compliance and systolic function. The extent ofthe functional derangement will depend on the acuteness and the extent of the ischemic insult. The latter may be modified by the severity and the chro-nicity of the underlying coronary atherosclerotic disease as well as the development of coronary collaterals. The hemodynamic compromise may be further complicated by disturbance in the sinoatrial (S-A) node and A-V nodal function caused by ischemia. The S-A nodal artery is often the first branch of the right coronary artery. The A-V nodal branch, however, arises further down where the right coronary artery takes the u-bend past the crux. The resulting arrhythmic disturbance may manifest as failure of sinus mechanism with development ofjunctional rhythms, first, second, or higher degrees of S-A and/or A-V block. If the right atrial branches, which arise from the proximal segment of the right coronary artery, are involved in the acute occlusion, it may cause atrial infarct, compromise the right atrial function, and may result in atrial arrhythmias such as atrial fibrillation.

In addition, the LV infero-posterior walls are often invariably the site of infarction and in severe cases often involve the posterior part of the interventricular septum. Acute RV dilatation might be accompanied by paradoxical septal motion. During diastole, the interventricular septum might encroach on the left side, restricting its filling, and during systole bulge towards the RV and move thus paradoxically. Acute and abrupt RV as well as the LV posterior wall dilatation might also cause intrapericardial pressures to rise. The pericardial constraint might further impair both RV and LV compliance and filling. Both the posterior septal infarct and pericardial constraint would be contributing to the paradoxical septal motion noted in severe cases.

When RV systolic dysfunction is significant, the x' descent will be diminished or absent. If the arterial supply to the right atrium is not compromised, there could be augmented and forceful contraction ofthe right atrium to support RV filling. Strong atrial contraction and the accompanying good atrial relaxation would cause the a wave and the x descent to be prominent. The latter also would help to accelerate venous inflow. The altered diastolic function and decreased compliance of the RV will lead to elevation of thepre-a wave pressure. This will raise the right atrial a wave and v wave pressures and consequently the mean right atrial pressure. The raised right atrial pressures will be reflected in the jugulars as well. As long as the RV diastolic dysfunction is not severe enough to raise the early diastolic pressure in the RV, the raised v wave will be accompanied by an exaggerated y descent. Therefore, the jugulars in these patients would show a diminished or absent x' descent with a dominant or single y descent. If the x descent is exaggerated because of forceful right atrial contraction and relaxation in the presence of normal PR interval, it would be indistinguishable from the x' descent at the bedside. This might actually cause the double descents with equal x andy. Sometimes the RV annular dilatation with or without right ventricular papillary muscle dysfunction could lead to tricuspid regurgitation of variable degree, raising further the right atrial v wave pressure.

When the diastolic dysfunction is severe, even the early diastolic pressure in the RV might become raised, blunting they descent despite elevated v wave pressures. Such a profound elevation in the RV filling pressures is often indicative of severe RV infarction. This means that RV diastolic filling is compromised even in the early rapid filling phase. This of course is a hemodynamic imitator of cardiac pre-tamponade-like state with total diastolic restriction. This situation might be accompanied by RV dilatation as well as LV posterior wall dilatation. The pericardial constraint will lead to very high right atrial and jugular venous pressures. The blood can enter the tight space only when the blood can leave the space, namely during systole. In these patients one would see very little descent in the highly elevated venous column at the bedside. With recording of right atrial pressure, one may actually show some drop in the intra-atrial pressure during systole.

Looking for "w" and "m" patterns of waveforms described by some authors in relation to the right atrial pressure recordings, in the jugulars at the bedside will not be a fruitful exercise. In this context, because they also attribute the mechanism of the normal x' descent to the fall in intrapericardial pressure due to ventricular systolic emptying, a comment again on the mechanism of the normal x' descent needs to be made prevent confusion. The normal xX descent is essentially due to the descent of the base and not because of drop in intrapericardial pressure caused by ventricular systole. On the two-dimensional echocardiographic images, one can see the atrial area and consequently the volume expand with each systole as the contracting right and the left ventricles pull on the tricuspid and the mitral annulus, respectively (see Normal Subject image file in Jugular Venous Pulse, Normal on the Companion CD). Furthermore, the right atrial and therefore the jugular x' descent is selectively diminished gradually and eventually lost in chronic pulmonary hypertensive patients when RV failure sets in. In these patients, left atrial recording will confirm the presence of the normal left atrial pressure pulse contour with preserved x' descent. This disparity between the two sides should not be there if fall in the intra-pericardial pressure because of ventricular systole is the mechanism ofthe x' descent. Similarly, one can observe in patients with severe LV dysfunction with preserved right ventricular function, the x' descent will be preserved until pulmonary hypertension develops and begins to alter RV function. Intrapericardial pressure will play an important part when the pericardial space is compromised as in cardiac tamponade or situations that mimic the hemodynamics of cardiac tamponade with impediment to filling throughout diastole. This could arise in severely dilated hearts with failure and severely elevated filling pressures, rare patients with constrictive pericarditis, and some patients with severe RV infarction and shock.

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