Mechanism of Abnormal JVF Patterns and Jugular Pulse Contours in Restriction to Ventricular Filling

Restriction to ventricular filling may vary in degree and may be pericardial, myocardial, or endocardial in origin. Restriction in its mild form may be apparent only at the end of diastole during the atrial contraction phase. It may involve both mid and late diastole when more severe, and when very severe it may involve almost all phases of diastole beginning with the rapid filling phase (Fig. 21).

Late Diastolic Restriction

If the restriction is limited to late diastole, the only abnormality seen in right heart hemodynamics will be elevation of right atrial a wave pressure. This will be reflected in the jugular venous pulse as a prominent a wave (Fig. 8) (see JVP Videofile 8 on the Companion CD).

Mid and Late Diastolic Restriction

When restriction to ventricular filling encroaches more and more into mid to early diastole, elevation of all RV diastolic pressures would result and lead to elevations of both mean RA and v wave pressures. The increased v wave pressure head during early diastole will lead to augmented Df (exaggerated y descent). As long as ventricular function is preserved, the increased Df will equal Sf (x' = y). In contrast, patients with myocardial dysfunction and diminished contractility will have flow patterns of Sf < Df and jugular contours ofx' < y (Figs. 4 and 5) (see JVP Videofile 4 on the Companion CD).

Fig. 21. The varying severity of restriction to diastolic ventricular filling is shown with lines to indicate the ventricular diastolic pressure elevations and their timing in diastole. In mild form, the pressure increase is during atrial contraction (AC) at end diastole (line #1). As restriction gets worse, the pre-a wave pressure starts to rise gradually and earlier and earlier in diastole. This progression is shown as four successive lines (lines #2). When severe, it may be total during mid and late diastole, restricting flow into the RV beginning with the slow filling phase (SF). There will be very rapid inflow only during early diastole or the rapid filling phase (RF) followed by a rapid rise in pressure with no further flow producing the classic dip and plateau or the square root pattern (line #3). This is typical for chronic constrictive pericarditis. If the restriction is severe and involves also the RF phase, the pressures rise quickly in the RV in early diastole limiting inflow altogether. This can occur in severe pericardial effusion leading to cardiac tamponade where the high intra-pericardial pressure will limit ventricular expansion altogether. Line #4 depicts pre-tamponade, and line #5 is full tamponade with no diastolic inflow possible. Such severe elevations in diastolic pressures may rarely also occur in severe cardiomyopathy, cardiac failure, and in some patients with severe right ventricular infarctions.

Fig. 21. The varying severity of restriction to diastolic ventricular filling is shown with lines to indicate the ventricular diastolic pressure elevations and their timing in diastole. In mild form, the pressure increase is during atrial contraction (AC) at end diastole (line #1). As restriction gets worse, the pre-a wave pressure starts to rise gradually and earlier and earlier in diastole. This progression is shown as four successive lines (lines #2). When severe, it may be total during mid and late diastole, restricting flow into the RV beginning with the slow filling phase (SF). There will be very rapid inflow only during early diastole or the rapid filling phase (RF) followed by a rapid rise in pressure with no further flow producing the classic dip and plateau or the square root pattern (line #3). This is typical for chronic constrictive pericarditis. If the restriction is severe and involves also the RF phase, the pressures rise quickly in the RV in early diastole limiting inflow altogether. This can occur in severe pericardial effusion leading to cardiac tamponade where the high intra-pericardial pressure will limit ventricular expansion altogether. Line #4 depicts pre-tamponade, and line #5 is full tamponade with no diastolic inflow possible. Such severe elevations in diastolic pressures may rarely also occur in severe cardiomyopathy, cardiac failure, and in some patients with severe right ventricular infarctions.

Total Diastolic Restriction

When restriction is severe and occurs throughout diastole as in tamponade, no inflow can occur into the atrium during this phase. This totally abolishes diastolic flow into the atrium. In cardiac tamponade, the four chambers of the heart are boxed within a pericardial sac under high fluid pressure. During diastole no new blood can enter the heart, but blood is shifted from the atrium to the ventricle with the total volume in the boxed four chambers constant. The only time new blood can enter the heart is when blood leaves this enclosed box, namely during systole. Patients with tamponade, therefore, exhibit inflow only during ventricular systole, when the ventricular sizes are the smallest, thus allowing some expansion and filling of the atria within the pericardial sac (47) (Fig. 22).

Jugular flow recordings in patients with cardiac tamponade are extremely hard to obtain because of diminished flow velocity. Thus, the only recordable forward flow would occur in systole and only during inspiration with a corresponding x' descent in the jugular pulse (40,44). Jugulars distend in tamponade and hardly show any descent. If a descent is recognizable at all it will be an x' and may be seen only during inspiration.

Fig. 22. A diagrammatic representation of the pathophysiology of the cardiac inflow and outflow in cardiac tamponade. The extracardiac pressure is so high that the heart is as if encased in a solid box at all times. The only time flow into this "box" can occur is when blood leaves the "box." This occurs during systole as blood is ejected out of the ventricles. Flow into the heart (atria) can occur only at that time (the middle diagram). In early diastole, the blood is shifted from the atria into the ventricles, but new blood cannot enter the heart. (Reproduced with kind permission from ref. 47. )

Fig. 22. A diagrammatic representation of the pathophysiology of the cardiac inflow and outflow in cardiac tamponade. The extracardiac pressure is so high that the heart is as if encased in a solid box at all times. The only time flow into this "box" can occur is when blood leaves the "box." This occurs during systole as blood is ejected out of the ventricles. Flow into the heart (atria) can occur only at that time (the middle diagram). In early diastole, the blood is shifted from the atria into the ventricles, but new blood cannot enter the heart. (Reproduced with kind permission from ref. 47. )

Usually the venous pressure is so high that the pulsation at the top of the column would be higher than the angle of the jaw. Therefore, the pulsations cannot be seen, but flow may be recorded by Doppler to show single systolic flow. In fact, the occurrence of a steep y descent in patients with pericardial effusion excludes tamponade.

If the RV filling pressures are severely elevated even in the early rapid filling phase, as might happen in rare instances of constrictive pericarditis and severe cardiomyopathy, poor diastolic inflow (and correspondingly poor y descent) will result despite high RA mean and v wave pressures for the simple reason that there is not enough pressure difference between the RA and RV during the early rapid filling phase. If this should happen in constrictive pericarditis, it would be accompanied by good Sf (and a corresponding X descent) (16), whereas in cardiomyopathy such a severe elevation of filling pressures would be associated with poor RV systolic function and therefore poor X descent.

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