| Echocardiography of Ventricular Septum and Left Ventricular Posterior Wall, in Volume- or Pressure-Overload-Related Heart Defects |
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A number of patients with manifest heart disease verified by auscultation, phonocardiography, angiography and heart catheterisation were examined. The goal was to use echocardiography in order to compare the variation of outer ventricular contour and of endothelial surfaces of the ventricular septum with that in healthy subjects.
Six patients were selected among a number of patients examined in the Department of Clinical Physiology at Södersjukhuset, Stockholm, Sweden. These patients had extreme volume- or pressure-overload-related heart defects: three had isolated Atrial Septum Defect (ASD), one had Mitral valve Stenosis (MS), one had Mitral valve Insufficiency (MI) and one had Aortic valve Insufficiency (AI). Another patient with ventricular premature beats, was also selected.
Echocardiography M-mode registration was carried out, as described in Chapter 3.
The series of events (a-k) was the same as in studies of healthy subjects.
Points of dissection of the corresponding event lines with curve 1 and 4 were also determined. It should be noted that the examination with the diseased patients were carried out in 1981 and 1982. At that time, determination of Atrio Ventricular (AV)-plane movement was not considered to be of major comparative interest, and measurements corresponding to those in points M2, M3 and M4 (Fig. 3-6A-E), were therefore not included.
The M-mode images were recorded and reconstructed in the same way as the M-mode image in Fig. 3-1A , Fig. 3-1B , Fig. 3-1C. Each defect, except for atrial septal defect, is represented by one patient.
Fig. 6-1A , 6-1B depicts one authentic and one reconstructed M-mode registration of an atrial septum defect (ASD).
Event c was absent at Ventricular Septum (VS). This should be due to that, the VS at the closing of the mitral valve is moving rapidly in the direction of Right Ventricle (RV).
A new event line (c") can be drawn through a point at which septal movement towards RV suddenly ceases, probably due to the closing of the tricuspid valve.
Another new event line, l, which sometimes is also seen in healthy people as a "ringing" phenomenon of the ventricular septum, is marked. It is caused by the dynamic influx forces. It is prominent and was therefore marked as a specific event.
The M-mode images show the VS bulging into Left Ventricle (LV) from event i through b. At the ventricular depolarisation, and even before the closing of the mitral valve, the ventricular septum rapidly adopts its predetermined systolic shape. Fig. 6-2A , Fig. 6-2B displays diastolic and systolic two-dimensional images from the same patient. VS is seen to have lost its convex shape towards RV in diastole (Fig. 6-2A).
Fig. 6-2A and Fig. 6-2B put
together as a small animation
When the AV-plane in the normal heart is drawn towards the apex in ventricular systole, the atriums is filled. Left atrial pressure will normally be somewhat higher than pressure in the right atrium. This makes the VS bulge towards RV also during diastole.
With an ASD, this balance is disturbed. Blood ejected from RV into the pulmonary circulation will pass through LA and the ASD, into the expanding RA. The AV-plane is travelling around 25% further in the RV than in the LV. Therefore the moment of inertia of the blood influx in diastole will be greater at RV than at LV; pressure equilibration between the ventricles will take place by deflection of VS towards LV early on in diastole. Communication between the atria will have a pressure-equalising effect.
In the preceding chapters, it has been shown that the outer heart contour in a healthy person changes very little during the cardiac cycle. ASD and other vitia reported below, display the same kind of LV posterior wall displacement as is seen in healthy subjects. As explained earlier, the observed displacement of 5-6 mm must be exaggerated, due to the curved form of the posterior wall segment in question (Fig. 3-10).
Look at the motion of VS in M-mode registration (Fig. 6-1A , Fig. 6-1B) and the two-dimensional images in Fig. 6-2A , Fig. 6-2B. That demonstrate unambiguously, that there are no substantial elastic forces working in diastole, to keep its form convex with respect to RV.
Increased volume work and, in the present case, also increased pressure work (because of pulmonary hypertension), causes a delay of RV systole. This is reflected in M-mode registration by VS being forced into LV at event i. It causes the mitral valve (which normally opens immediately after the aortic valve closes) to remain closed until RV pressure and volume transmitted by VS is withdrawn. Now the forces affecting the AV-plane of the left atrium, can complete the filling of LV.
A prolonged RV ejection period, coupled with a volume-delimiting VS movement towards LV, causes "excess" muscle length in short and long axis direction. That permitting the part of the AV-plane attached to VS to bulge upwards. This deformation increases the end-systolic residual volumes on both RV and LV.
Before RV pressure has decreased enough to allow the tricuspid valve and the mitral valve to open (by pressure transmission to LV in this situation) something happens; the increase of residual volumes, which for the LV are compensated for by the overriding VS, prevents the myocardium from moving upwards along the pericardial-epicardial interface. That is due to the close connection of LV-wall and VS (V will be affected, see Chapter 11).
The ventricular septum does not show a prominent fast diminution phase in diastole. That must be caused by the absence of a pressure gradient between the right and left side of the heart. The result is excess VS myocardial tissue of high plasticity.
Proof of this high compliance is provided by EC analysis in event l. It is also provided by VS taking up its systolic form already in pre-systole by a rapid movement (even before the closing of the mitral valve).
The above observations demonstrate that the ventricular septum influences the pressure-volume relationship between LV and RV.
The gripping heart pumping mode causes blood to pass via the ASD, as long as the pressure in the pulmonary vein surpasses pressure in the superior and inferior venae cava. Moreover, as long as the LV is working at higher systolic pressures than the RV, a paradoxical movement of VS in systole [179] imparts a greater ejection fraction to RV, and a reduced one to LV.
Fig 6-4A , 6-4B shows an authentic and a reconstructed M-mode registration of a severe mitral stenosis (MS).
The patient had a complete atrio-ventricular block. Therefore event a has to be substituted by a ", which dissects VS and the posterior wall just before ventricular depolarisation becomes effective. (In a healthy person this should occur between events b and c.)
In end-systole and at the onset of diastole, the kinetic energy built up during systole begins to push the AV-plane upward and to replace the volume freed by reduction of wall thickness. At RV, the upward forces can act unrestrained. At LV, this upward force is hindered by stenosis of the mitral valve. The sudden restriction to flow is sometimes audible as an opening snap.
MS reduces LV dynamic forces relative to those effective at RV, and forces VS into LV, making event i very distinct.
The bulging of the ventricular septum towards LV also effects blood in LV. In combination with the blood entering through the stenosis, that pushes the left part of the AV-plane upwards, as shown by the area between event h and j. (In this sequence the walls are getting thinner.)
The return of the posterior wall to end-diastolic thickness, begins at the point of intersection for event l.
The pressure of the pulmonary circulation, normally suffices to build up a pressure gradient necessary for the return of VS to its normal pre-systolic form; this is in contrast to the ASD case, and this function depends on the severity of the stenosis and the length of diastole.
Simultaneously, a gradual thinning of the ventricular septum is observed (Fig. 6-4A , Fig. 6-4B) between events l and a", which was not seen in the ASD ( Fig. 6-1A , Fig. 6-1B). The posterior wall does not show any movement during these events.
If the length of diastole does not suffice for the return of VS to its normal pre-systolic form (either because of extra-systolic beats or elevated heart rate), following happens; the ventricular septum will act in the manner of a membrane pump driven by the excess pressure in LV, generating an increased stroke volume in RV. The stroke volume of LV will be correspondingly reduced.
By this mechanism, the power resources of LV may drive RV, as long as RV walls and adjacent tissues are coping with the increased strain. Pressure and flow in pulmonary circulation will increase and be transmitted to the mitral stenosis, whereby flow through it will in turn increase, until VS reaches its pre-systolic "neutral" form. It is evident that this action of VS will provide for pulmonary hypertension and pulmonary edema at higher pulse rates.
Detection by echocardiography of paradoxical VS motion in patients with MS has been reported [172, 178].
Fig. 6-5A , 6-5B shows an authentic and a reconstructed M-mode registration of severe mitral insufficiency (MI).
In MI, the left atrium is filled both from the pulmonary veins and through the leaking mitral valve, when the AV-plane moves toward the apex during systole. The need for the flow-levelling effect of the pulmonary veins is thereby reduced. The left atrium and pulmonary veins encounter increased filling pressure, deflecting the inter-atrial septum as observed by oesophageal EC [114]. This static pressure may surpass the dynamic forces generated by the AV-plane in ventricular systole.
The ventricular septum is the part of LV that in the relaxation phase in early diastole has the weakest back-up of all LV wall structures. VS is thus rapidly dilated and pushed towards RV (event k).
With the onset of ventricular systole, LV adopts its circular form (in the plane perpendicular to the major LV axis), as shown by event f in the M-mode image. The result is a contribution to LV stroke volume (and a corresponding decrease in RV stroke volume).
MS entails large variations in filling pressure in LA, depending on heart rate and the movement of the AV-plane in ventricular systole.
MI though, results in a more constant filling pressure, rather independent of heart rate as long as there is no acute heart failure. Atrial contraction, which adds to ventricular filling by raising the AV-plane, may disguise incipient MI until eventually atrial fibrillation sets in.
Echocardiography is not considered particularly useful in the assessment of rheumatic mitral regurgitation [41]. Left atrial overload affecting (among other things) the inter-atrial septum, has caused MI severity-assessment to be concentrated upon deflection of the atrial walls [51].
Fig. 6-6A , 6-6B shows an authentic and reconstituted M-mode registration of a severe aortic insufficiency (AI). The configuration change of VS (from diastole to systole) is best described by sector scans ( Fig. 6-7A , Fig. 6-7B).
Fig. 6-7A and Fig. 6-7B put
together as a small animation
When the endothelial surface of the septum at RV was kept under observation from event f onward, it was found that during diastole VS increasingly bulged into RV while simultaneously thinning. No concurrent change of the outer contour of the radially shrinking posterior wall was observed.
It is apparent from this behaviour, that even in a static pressure situation, the valve plane will move away from the apex without the outer contour of the ventricles changing.
But there will nevertheless be a marked change in the shape of VS.
Events a, b and c could not be identified (no ECG was recorded in this case).
A vigorous septal movement began at event d, lasting until event f. This mode of movement in systole, and its attenuation in diastole, must be the result of the aortic insufficiency with its inherent increase in LV diastolic pressure. The septum thereby imparts an extra strike volume increment to LV, and correspondingly reduces systolic output of RV.
An increase in heart rate should not only reduce the effect of this insufficiency, but also increase RV stroke volume.
The effect on VS of premature beats in an otherwise healthy person, causing considerable distress, is shown in Fig. 6-8.
The ventricular septum has not become depolarised i.e., stabilised, before other parts of LV begin to contract. VS moves in the direction of the right ventricle and thins out, while the posterior wall exhibits normal behaviour.
One would expect the movement of the ventricular septum to depend on the site at which the premature beat arises, and on its timing relative to a normal depolarisation [44, 132, 133]. It may therefore have an impact on the stroke volume of both RV and LV.
There are two conceivable situations in the present case. In the first one, deflection of VS into RV transmits force and volume from LV to RV, increasing RV stroke volume. In the other one, a premature ventricular beat causes a sluggish septal movement in apical direction and a poorly stabilised AV-plane, which results in reduced stroke volume.
Possibly it is the sudden perturbation of circulatory equilibrium, that is felt in the form of immediate discomfort.
Fig. 6-9 displays a schematic summing-up of the movement of the endothelial septum surface at RV, curve 4, in the heart defects described above. This movement is compared with that of a healthy person (Fig. 3-2), marked in Fig. 6-9 with a dotted line. The cardiac cycle in Fig. 6-9 was divided into five phases:
No corresponding summing-up for epicardial movement mode (curve 1) in the various defects was made, since it does not deviate from that of a healthy person.
The modes of motion found in the above cases of severe heart defects, are in agreement with the theory; when the ventricles are pumping at essentially constant outer form, VS in diastole adopts the form and position according to the prevailing pressure gradient between the ventricles.
In systole, VS strives to adopt its position as part of the circular LV wall, that is, its predetermined systolic position. If the diastolic and the systolic positions of the septum are not identical, the septum will behave like the membrane in a membrane pump, and add to the stroke volume on the side opposite that to which it had moved in diastole.
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