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Direct and series transmission of left atrial pressure perturbations to the pulmonary artery: a study using wave-intensity analysis

¹Departments of Medicine, Anaesthesia, and Physiology and Biophysics, Cardiovascular Research Group, University of Calgary, Calgary, Alberta, Canada T2N 4N1; and ²Department of Bioengineering, Imperial College, London, United Kingdom SW7 2BX

Submitted 24 June 2002 ; accepted in final form 1 September 2003

	ABSTRACT

TOP ABSTRACT METHODS RESULTS DISCUSSION REFERENCES

 
Pressure waves are thought to travel from the left atrium (LA) to the pulmonary artery (PA) only retrogradely, via the vasculature. In seven anesthetized open-chest dogs, a balloon was placed in the LA, which was rapidly inflated and deflated during diastole, early systole, and late systole. High-fidelity pressures were measured within and around the heart. Measurements were made at low volume [LoV; left ventricular end-diastolic pressure (LVEDP) = 5–9 mmHg], high volume (HiV; LVEDP = 16–19 mmHg), and HiV with the pericardium removed. Wave-intensity analysis demonstrated that, except during late systole, balloon inflation created forward-going PA compression waves that were transmitted directly through the heart without measurable delay; backward PA compression waves were transmitted in-series through the pulmonary vasculature and arrived after delays of 90 ± 3 ms (HiV) and 103 ± 5 ms (LoV; P < 0.05). Direct transmission was greater during diastole, and both direct and series transmission increased with volume loading. Pressure waves from the LA arrive in the PA by two distinct routes: rapidly and directly through the heart and delayed and in-series through the pulmonary vasculature.

lung; arteries; hemodynamics; wave transmission

Most commonly, pulsatile arterial phenomena have been characterized using Fourier analysis where the observed wave-forms are decomposed into sinusoidal wave trains, and the results are expressed as amplitude and phase as a function of frequency (16, 17). This frequency-domain analysis has provided much information. However, wave-intensity analysis where the observed waveforms are decomposed into a succession of infinitesimal wave fronts that are described by their amplitude and time (13, 19) allows the interaction of forward- and backward-going waves and their relation to primary hemodynamic parameters (pressure, flow, etc.) to be studied directly. This method utilizes changes in pressure and velocity to evaluate the direction, intensity, and type of waves and has been used recently to study the systemic (18), pulmonary (8, 11, 22), and coronary circulations (23).

The purpose of this investigation was to evaluate the transmission of disturbances from the LA to the proximal PA. Our hypothesis was that an abrupt increase in P_LA would cause a backward-going wave through the pulmonary vasculature, which would impede the flow of the blood from the right ventricle (RV). However, our results have indicated that waves are transmitted from the LA to the PA via two distinctly separate routes: direct transmission through the heart as well as "in-series" transmission through the pulmonary vasculature.

	METHODS

TOP ABSTRACT METHODS RESULTS DISCUSSION REFERENCES

 
Animal preparation. Seven dogs (20–27 kg; either sex) were anesthetized with 30 µg·kg^–1·h^–1 of fentanyl citrate while ventilated with a 2:1 nitrous oxide-to-oxygen mixture using a constant-volume respirator set to deliver a tidal volume of 15 ml·kg^–1·min^–1 (model 607, Harvard Apparatus, Natick, MA). Temperature was maintained at 37°C by a circulating-water warming blanket. A midline sternotomy was performed with the dog in the supine position. The pericardium was opened sufficiently to instrument the heart. Superior vena cava (SVC), RV, and left ventricular (LV) pressures (P_SVC, P_RV, and P_LV, respectively) were measured using 8-Fr micromanometer-tipped catheters with reference lumens (model PC-480, Millar Instruments, Houston, TX) introduced through branches of the external jugular vein and a carotid artery. PA and LA pressures (P_PA and P_LA) were measured using 3-Fr micromanometer-tipped catheters (model SPR-524, Millar) introduced retrogradely through small pulmonary arterial and venous branches. Aortic pressure was measured using an 8-F liquid-filled catheter introduced through a femoral artery, which was attached to a transducer (model P23 ID, Statham-Gould). Pulmonary capillary wedge (PCW) pressure (P_PCW) was measured using a 3-Fr fluid-filled catheter introduced from a small arterial lobar branch; P_PCW tracings were time adjusted to correct for transmission delay through the catheter. Pericardial pressure (P_Per) was measured using a flat liquid-containing balloon loosely sutured to the epicardium over the mid-right ventricular free wall (21); P_Per was also time adjusted. RV free wall segment length was measured using ultrasonic crystals (Sonometrics, London, Ontario, Canada). PA flow was measured using an ultrasonic flowmeter (Transonic Systems, Ithaca, NY) and converted to velocity (U_PA) using the value of PA cross-sectional area estimated from the size of flow probe. A special-order 35-ml spherical balloon was inserted into the LA through the appendage and inflated using an aortic counter-pulsation pump (Datascope, Paramus, NJ). The balloon was not inflated until required. The heart was repositioned within the pericardial sac, the margins of which were loosely reapproximated. A large-bore catheter in the external jugular vein was used to infuse a 2% albumin-saline solution or remove blood for adjustment of the intravascular volume. A single ECG limb lead was also recorded. Conditioned signals (model VR16, Electronics for Medicine/Honeywell, Pleasantville, NY) were recorded by means of a computer using data-acquisition software (Sonometrics). The analog signals were passed through anti-aliasing, low-pass filters with a cutoff frequency of 100 Hz and were then sampled at a frequency of 200 Hz. The digitized data were subsequently analyzed with specialized software (CVSOFT, Odessa Computer Systems, Calgary, Alberta, Canada) developed in the laboratory.

All animal experiments conformed to the "Guiding Principles for Research Involving Animals and Human Beings" of the American Physiological Society.

Calibration. The micromanometer in the PA was referenced to the fluid-referenced micromanometer in the RV during systole. The micromanometer in the LA was referenced to the fluid-referenced micromanometer in the LV during diastole. The pericardial balloon was calibrated at the beginning and rechecked at the end of the experiment. The method for calibration of the pericardial balloon has been previously described (9).

Experimental protocol. Three distinct loading conditions were defined using LV end-diastolic pressure (LVEDP) and RV segment length: 1) low volume (LoV), defined as LVEDP 5–9 mmHg; 2) high volume (HiV), defined as LVEDP 16–19 mmHg; and 3) high volume with the pericardium removed (HiV_Per–). With respect to the last condition, after the pericardium had been opened widely and the heart was suspended in a pericardial cradle, blood volume was adjusted so that the end-diastolic length of the RV segment was equal to that during HiV. All hemodynamic measurements were obtained with the respirator stopped in the end-expiratory position for not more than 20 s. After the respirator had been turned off, several beats were initially recorded without any intervention (control beats) before the LA balloon was inflated once and then rapidly deflated (duration of inflation cycle, 100 ± 20 ms) at a specified time during the cardiac cycle (balloon beat) (see Fig. 1). Approximately 10–12 control beats were allowed between balloon inflations. The designated inflation-deflation times were 1) diastole, 2) early systole, and 3) late systole. Diastolic balloon inflations were initiated during middiastole, early-systolic inflations just after the onset of the P_PA upstroke, and late-systolic inflations during the decline in P_PA. The protocol for each balloon inflation time was repeated for each loading condition (LoV, HiV, HiV_Per–).

View larger version (17K): [in this window] [in a new window]   Fig. 1. Example of left ventricular (LV), left atrial (LA), right ventricular (RV), and pulmonary arterial (PA) pressure measurements for a control beat (left) and an early-systolic balloon inflation/deflation beat (right). Notice the simultaneous increment in pressure in each measurement produced by balloon inflation.

Data analysis. For each intervention, one control beat and its subsequent balloon inflation/deflation beat were analyzed. Pressure changes (P) were determined as the peak difference in pressure obtained by subtracting the control-beat pressure from that of the inflation/deflation beat. P was expressed in absolute (mmHg) and relative (as a % of P_LA) terms. Time delays were determined by the difference between the onset of the P_LA and the onset of P at the site being evaluated. Onset was defined as the intersection of the linear projections of the baseline and the initial portion of the rising P. Because the rise in P was commonly rapid, this determination of the onset of arterial systole was generally simple and unambiguous.

Wave-intensity analysis (19) was used to evaluate the direction, intensity, and type of waves (see Fig. 2). As indicated above, the direction of the wave was defined in terms of the direction of PA blood flow such that the waves that emanated from the RV were defined as forward going and those from the pulmonary vasculature were defined as backward going. The intensities of the forward-going (dI_W+) and backward-going waves (dI_W–) were calculated as

(1)

(2)

where is the density of blood, c is the wave speed, dP is the measured difference in PA pressure during a sampling interval, and dU is the measured difference in velocity during the same sampling interval. Note that dI_W+ > 0 and dI_W– < 0.

View larger version (17K): [in this window] [in a new window]   Fig. 2. Example of wave-intensity analysis of proximal PA hemodynamics; a normal cardiac cycle without inflation of the LA balloon. A: pressure and velocity waveforms. B: intensities of the forward-going (dIW+) and backward-going (dIW–) waves. C: dP+ and dP–, respectively, indicate whether the forward-going or backward-going waves (B) were compression (c) or expansion (e) waves. See text for details.

The pressure differences across the forward- and backward-going wavefronts were calculated as

(3)

(4)

where + and – again refer to the forward and backward waves. A wave can be one of two types, either compression or expansion, depending on the sign of dP₊ and dP_–. A wave producing a positive pressure difference is a compression wave, and one producing a negative pressure difference is an expansion wave. Thus the four possibilities are forward compression, forward expansion, backward compression, and backward expansion waves.

In the case of a forward-going wave, a compression wave is associated with an increase in pressure and an increase in velocity, and an expansion wave is associated with a decrease in pressure and a decrease in velocity. In the case of a backward wave, a compression wave is associated with an increase in pressure and a decrease in velocity, and an expansion wave is associated with a decrease in pressure and an increase in velocity.

The value used for c was calculated from the ratio of dP/dU during early systole when pressure and velocity were both increasing, a time when wave reflections were unlikely to be present (4, 12, 16, 17). These values were not different from wave-speed estimations calculated from characteristic impedance (3, 4, 17).

Statistical analysis. Data recorded at different inflation/deflation times and loading conditions were compared using a two-tailed paired Student's t-test where P < 0.05 was considered significant. Regressions through data points were compared by evaluating the confidence intervals of the slopes. Results are expressed as means ± SE, except where indicated.

	RESULTS

TOP ABSTRACT METHODS RESULTS DISCUSSION REFERENCES

 
Baseline hemodynamic data are presented in Table 1. Figure 3A depicts the P_LA, P_PCW, P_PA, P_SVC, P_RV, P_Per, and P_LV waveforms from a typical control and early systolic inflation/deflation beat, superimposed on each other. There were marked balloon-induced pressure changes within and around the heart as indicated by the differences between the control and inflation/deflation beats. By subtracting the pressure during the control cycle from that during the cycle with the balloon inflation, the balloon-induced pressure change became more clear. These differences (Ps) are shown in Fig. 3B. The magnitude of the balloon-induced perturbation in the LA was 11 mmHg at HiV. Pressure changes within and around the heart ranged from 2 to 5 mmHg, as shown in Table 2 for each inflation/deflation period and loading condition.

View larger version (24K): [in this window] [in a new window]   Fig. 3. Example of pressure and pressure change (P) waveforms from an early-systolic balloon inflation/deflation and its preceding control beat. A: balloon inflation/deflation pressure waveforms (solid lines) and the preceding control waveforms (dashed lines) superimposed on each other. B: their differences. In B, delay = 0 represents the onset of the pressure increase in the LA. To facilitate temporal comparisons, the 1st vertical dotted line marks peak PLA, the 2nd line marks peak PPCW, and the 3rd dotted line marks peak PPA (due to series transmission). Thus the interval between the latter lines, t, reflects the time required for series transmission through the pulmonary arterial vasculature. SVC, superior vena caval; PCW, pulmonary capillary wedge position; Per, pericardial. Other abbreviations are as in Fig. 1.

In the PA, the effects of inflation/deflation of the LA balloon were most easily seen during diastole when potentially confounding cardiac effects were relatively few. Figure 4 shows the differences in the pressures between the inflation/deflation beat and the preceding control beat in the LA and in the pulmonary capillary wedge position (P_LA and P_PCW; Fig. 4A), in P_PA (Fig. 4B) and U_PA (Fig. 4C), and forward and backward wave intensities (dI_W±; Fig. 4D). During systole, the differences between the control and inflation/deflation beats were negligible. During diastole, inconsistent with the hypothesis that LA disturbances are transmitted only by retrograde transmission through the pulmonary microcirculation, wave-intensity analysis revealed an immediate forward compression wave associated with the forward acceleration of blood in the PA. After a delay of 30 ms, this was followed by a backward expansion wave. Because it was an expansion wave, it could not be the result of retrograde transmission of the compression wave generated in the LA but was likely the result of a reflection of the preceding forward compression wave. This reflection of a compression wave as an expansion wave, corresponding to a negative reflection coefficient, is consistent with our previous observations of wave propagation in the normal pulmonary circulation (11). The next wave was a forward expansion wave caused by the deflation of the balloon and transmitted, like the earlier compression wave, directly through the heart from the LA to the RV. Finally, after a delay of 100 ms, we see a backward compression wave that decelerated flow. As discussed below, we cannot be completely definitive about the origin of this wave. It is consistent with the anticipated backward compression wave transmitted from the LA through the pulmonary microcirculation and detected when it arrived at the PCW recording site several milliseconds earlier. However, it may have been augmented by the negative reflection of the previous forward expansion wave. To recapitulate, diastolic inflation and deflation of the LA balloon generated forward waves that were rapidly and directly transmitted into the PA. After delays of 30 ms, negative reflections of these forward waves were seen. Approximately 100 ms after the inflation of the balloon, a backward compression wave was seen that corresponded to the series transmission through the pulmonary microcirculation.

View larger version (16K): [in this window] [in a new window]   Fig. 4. Example of proximal PA wave-intensity analysis with diastolic LA balloon inflation/deflation demonstrating direct and series transmission. A: pressure changes in the LA and wedge position caused by balloon inflation/deflation. B: the associated changes in PPA. C: the associated changes in PA velocity (UPA). D: changes in intensity of forward (dIW+) and backward (dIW–) waves. In B–D, data from the control beat are indicated by dashed lines and those from the inflation/deflation beat by solid lines. Direct transmission caused a forward compression wave followed by a backward expansion wave and a forward expansion wave associated with balloon deflation. Series transmission led to a demonstrable backward compression wave.

In Fig. 5, we see the effect of inflation/deflation during early systole, shown in the same format as Fig. 4. During early systole, there was a forward compression wave in the control beat generated by the contraction of the RV (the dashed line in Fig. 5D). During the inflation/deflation beat this forward compression wave was augmented by a forward compression wave generated by the inflation of the balloon (note the change in the wave-intensity scale between Figs. 4D and 5D). This augmentation followed almost immediately after the increase in LA pressure, as seen from the LA pressure difference in Fig. 5A. The first significant backward wave was again an expansion wave, corresponding to the negative reflection of the initial forward compression wave (11). The following forward expansion wave during the inflation/deflation beat (absent in the control beat) corresponded to the decrease in pressure in the LA (due to the deflation of the balloon), being directly transmitted through the heart to the RV. Finally, after a delay of 70 ms from the start of inflation of the balloon, a backward compression wave was observed (probably due both to reflection and to series transmission through the microcirculation).

View larger version (17K): [in this window] [in a new window]   Fig. 5. Example of proximal PA wave-intensity analysis with early-systolic LA balloon inflation/deflation demonstrating direct and series transmission, shown in the format of Fig. 4. [In this figure and in others, note the negatively reflected backward waves, e.g., the expansion wave, which follow incident forward waves, e.g., the compression wave, by 40 ms, consistent with our observations of negative reflection in the PA (1).] The first vertical dotted line (peak PLA) pertains to direct transmission, which causes an augmented forward compression wave followed by a reflected backward expansion wave and a forward expansion wave associated with balloon deflation (D). The second vertical dotted line (peak PPCW) pertains to series transmission through the pulmonary vasculature, which causes a backward compression wave (D).

The results when the balloon was inflated and deflated during late systole are shown in Fig. 6. During late systole, the directly transmitted, forward-going waves arrived when P_PA was decreasing. This was evidenced by the small but distinct rise in P_PA and interruption of the decline in U_PA. The interruption in the decline of P_PA and U_PA did not result in a measurable forward compression wave as expected; however, the accelerated decline in P_PA and U_PA resulting from balloon deflation was marked by a significant forward expansion wave. Later, when the flow out of the RV was rapidly decreasing, the series-transmitted backward compression wave arrived in the PA (possibly augmented by negative reflection of the previous forward expansion wave). This backward compression wave caused P_PA to increase abruptly and U_PA to decrease further. This backward compression wave was immediately followed by an equally prominent forward compression wave. These compression waves (backward followed by forward) were seen in both the control and inflation/deflation beats; they were much smaller in the control beat, however. We speculate that the backward compression wave may have been positively reflected from the closed pulmonic valve as a forward compression wave. Then this forward compression wave may have been negatively reflected back from the pulmonary vasculature as a backward expansion wave (7). Each of the waves (forward expansion, backward compression, forward compression, and backward expansion) was present in the control beat; however, balloon inflation enhanced each of them considerably.

View larger version (16K): [in this window] [in a new window]   Fig. 6. Example of a proximal PA wave-intensity analysis with a late-systolic LA balloon inflation/deflation demonstrating direct and series transmission, shown in the format of Fig. 4. Direct transmission caused an augmented forward expansion followed by a backward compression wave. Series transmission through the pulmonary vasculature enhanced the backward compression wave associated with valve closure, which was followed by a forward compression wave (reflected off the closed pulmonic valve) and a backward expansion wave.

Direct transmission. There were no measurable delays in the direct transmission of pressure to measuring sites within and around the heart when the pericardium was intact (LoV and HiV) with the exception of P_Per at LoV during late systole (10 ± 3 ms), when the heart was smallest. After the pericardium was removed (HiV_Per–), transmission time to the PA was 13 ± 8 ms during early systole and 8 ± 4 ms during late systole, while transmission to the RV during late systole was 8 ± 5 ms. Transmission from the LA to the SVC showed a delay in the transmission at LoV and HiV_Per– during each balloon inflation. The SVC delay at LoV and HiV_Per–, respectively, were 16 ± 4 and 14 ± 7 ms in early systole, 27 ± 6 and 4 ± 2 ms in late systole, and 6 ± 5 and 22 ± 8 ms in diastole.

The least-attenuated (direct) transmission of pressure through the heart occurred during diastole, when the ventricles more completely filled the pericardial sac and were more compliant (see Fig. 7). Figure 8A depicts P_RV (as a % of P_LA), plotted against its corresponding P_Per values. The slopes of the lines through the values obtained during systole and diastole are different (P < 0.0001). The y-intercepts of these regressions, however, are not different. These results for direct transmission to the RV were similar to those to other areas within and around the heart.

View larger version (18K): [in this window] [in a new window]   Fig. 7. Magnitude of transmission during early systole (A), late systole (B), and diastole (C). (These experiments were performed at high volume.) The original signal, the normalized change in pressure in the LA (100%), is shown by the open bars. Gray bars show direct transmission effects. Solid bars at right show series transmission effects. The magnitude of direct transmission was greatest during diastole and smallest during late systole. The magnitude of series transmission did not vary significantly among the 3 inflation times. Pi, change in pressure at the site indicated. *Early-systolic values different from late-systolic values (P < 0.05). Systolic values different from diastolic values (P < 0.05).

View larger version (18K): [in this window] [in a new window]   Fig. 8. Direct (A) and series (B) pressure transmission. A: the relationship between normalized pressure transmission to the RV and pericardial pressure (PPer). Pericardium-removed data are plotted as PPer = 0 mmHg. The relationship during diastole is much steeper than during systole, indicating greater transmission during diastole. B: the relationship between the normalized series pressure transmission to the PA (PPA series) to the instantaneous value of PPA. Analysis of the y-intercepts did not reveal a statistically significant difference between systole and diastole.

Series transmission. Series transmission of pressure perturbations through the pulmonary vasculature required 97 ± 9 ms; there were no statistically significant differences during the cardiac cycle. As shown in Fig. 8B, transmission increased with volume loading (i.e., it was dependent on P_PA). Although transmission during diastole tended to be greater than during systole, statistical analysis of the y-intercepts did not demonstrate a difference (P = 0.7). There was no effect of the presence of the pericardium.

	DISCUSSION

TOP ABSTRACT METHODS RESULTS DISCUSSION REFERENCES

 
Traditionally, arterial pressure and flow have been analyzed using impedance analysis, a Fourier transform-based method that considers the measured pressure and flow waveforms to be the summation of sinusoidal wave trains at the fundamental and harmonic frequencies. Impedance analysis is expressed in terms of frequency and phase, and it is therefore difficult, or impossible, to relate the results to temporal events in the measured signals. Wave-intensity analysis is a relatively new method of analyzing arterial hemodynamics that considers the observed waveforms to be the summation of successive, infinitesimal wavefronts. Because it retains temporal information, it can be used to study the timing of discrete waves, such as those generated by the inflation/deflation of the balloon in the LA in this study. Furthermore, wave-intensity analysis provides a convenient way to separate the waveforms into the forward and backward waves that combine to produce the measured pressure and velocity in the artery. We recognize that, although we have used wave-intensity analysis to separate the forward and backward pressure and velocity waveforms, this separation could also have been done using Fourier techniques and the characteristic impedance. We believe, however, that there are distinct advantages in using wave-intensity analysis, particularly because it provides a convenient way to determine both the direction and the timing of individual waves such as those produced by the inflation and deflation of the balloon.

The major finding from this study is that pressure perturbations originating in the LA are transmitted to the proximal PA via two distinctly different routes. LA balloon inflation caused a compression wave, which was transmitted directly through the heart and, except for late systole, was detected in the PA as a forward-going compression wave. The compression wave caused by balloon inflation was also transmitted backward through the pulmonary vasculature in a series fashion and was detected in the PCW position as a distinct increase in pressure. Balloon deflation caused an expansion wave, which was transmitted similarly. The magnitude of direct transmission was dependent on P_Per with a different dependency during systole and diastole. The magnitude of series transmission was dependent on P_PA but was not dependent on the time of inflation.

Direct transmission. Direct transmission of the compression wave caused by inflation/deflation during diastole and early systole caused a forward compression wave in the PA indicated by the increase in P_PA and U_PA. During late systole, its only effect was to interrupt the decline in P_PA and U_PA. During diastole, direct transmission of the expansion wave caused by balloon deflation caused a forward expansion wave in the PA, which caused P_PA and U_PA to decrease and, during late systole, to decrease more rapidly (i.e., it accelerated the decreases in P_PA and U_PA that were already declining).

Direct wave transmission through the heart from the LA to the RV was greatest during diastole and least during systole (Fig. 8A). During both diastole and systole, transmission was dependent on P_Per. During diastole, the data suggest that, at P_Per 30 mmHg, transmission would have been 80% (i.e., P_RV 0.8·P_LA). By comparison, during systole at P_Per 30 mmHg, transmission would have been 30%.

We can only speculate why transmission was dependent on P_Per and why it was so much greater during diastole. The effect of the pericardium on the compliance of the system would seem to be critical. When the pericardium is closed and P_Per elevated, the heart and the pericardium constitute a composite shell, the pericardium being stiffer than the ventricles. The higher the P_Per, the less compliant the system, because the pericardial stress-strain curve is markedly nonlinear (14). In the absence of the pericardium, the overall compliance of the whole system is increased and Fig. 8A shows that transmission is minimal. According to wave-intensity theory, the power carried by a wave (i.e., the net wave intensity) equals dPdU,dU being related to V and, therefore, compliance (V/P). Then, assuming that the waves generated in the LA are of constant intensity, dP (P_RV) should be inversely related to compliance and directly related to P_Per. Despite the fact that each cardiac chamber has its own compliance, the effect of P_Per on each would be qualitatively similar. With respect to the fact that transmission is less during systole but still dependent on P_Per, the ventricles are stiffer during systole and, so, the effect of increasing P_Per would be smaller.

Series transmission. We recorded P_PCW by ligating a small branch of the pulmonary artery and inserting a catheter antero-gradely. Thus the increase in P_PCW that we observed documented series transmission unequivocally. After the increase in P_PCW, 100 ms after the beginning of LA balloon inflation, a backward compression wave was observed in the proximal PA. It is likely that this backward compression wave was composed of two distinct waves: a backward compression wave transmitted in-series through the pulmonary microvasculature and a backward compression wave generated by the negative reflection (11) of the preceding forward expansion wave. Because these two waves would have occurred almost simultaneously, we are unable to discriminate one from the other or to assess their individual contributions to the observed composite backward compression wave. The presence of two such waves might have introduced some temporal variability in the beginning and the end of the composite backward compression wave.

Series transmission was dependent on P_PA but, despite the apparent trend favoring diastolic transmission, analysis of the y-intercepts did not reveal a statistically significant difference between systole and diastole (Fig. 8B). Series transmission was dependent on P_PA, likely because vascular compliance decreased as pressure increased (2, 6).

Limitations. There are some limitations to wave-intensity analysis. As indicated several times above, it cannot distinguish between two different simultaneous waves of the same direction and type (e.g., a PA backward-going compression wave due to series transmission and one due to the negative reflection of an earlier forward expansion wave). Also, as is evident from the equations given, separating forward from backward waves depends on a correct determination of wave speed, c. In general, the shape and timing of separated waves are not substantially changed by small variations in wave speed and their magnitudes, only slightly more so. In this study, we determined wave speed by the ratio of dP/dU as well as from characteristic impedance, which agreed.

Clinical implications. Our observations do not serve to greatly augment our understanding of the stiff LA syndrome, a syndrome in which, in the absence of mitral regurgitation, patients have reduced LA compliance accompanied by large V waves (i.e., the late-systolic peak in atrial pressure due to venous filling while the atrioventricular valve remains closed) and increased pulmonary systolic pressures (15, 20). This syndrome has been thought to increase the load on the RV, thus requiring more energy to propel the blood through the pulmonary vasculature (15), as some patients have gone on to develop right-heart failure (6, 15). In dogs with normally compliant LAs, we created artificial, relatively small and short-lasting V waves early and late during systole by suddenly filling the LA by inflation of the counter-pulsation balloon. If the LA had been less compliant, the direct transmission might have been less, consistent with our suggested explanation for the reduced direct transmission during systole (Fig. 8A). With respect to timing, perhaps neither our early- nor late-systolic inflations was optimal, one being slightly too early and the other too late with respect to the pathophysiological V wave. Our data do suggest that the effect of an LA V wave on RV afterload might be measurable. We found that direct transmission to the PA or RV was 25%. Thus the direct transmission of a 20-mmHg V wave (6, 20) might increase RV afterload by as much as 5 mmHg. (In principle, rapid and direct transmission might have been augmented by delayed, in-series transmission, as well.) The physiological significance of such an increase in RV afterload remains to be determined, and it is likely that the most important explanation for increased PA pressure in this syndrome is the substantial increase in back pressure, per se.

Our study may be more significant with respect to the mechanism of the Bernheim syndrome, which Wood (24) defined as a conspicuous a wave in the jugular venous pulse in patients with LV dysfunction. Although it had been ascribed to distortion of the RV cavity by an impinging hypertrophic LV, Henein et al. (10) concluded that there need not be any obstruction and that the dominant jugular a wave might be due to shared interatrial myocardial fibers and a form of atrial interaction. In addition, Goldstein et al. (7) showed that increased RA contraction was manifest by an increased LA a wave and x descent. It seems entirely possible that these observations might be explained by direct transmission (note that, during diastole, the simultaneous change in SVC pressure was >60% of the change in LA pressure; Table 2 and Fig. 7).

In conclusion, in addition to a retrograde series transmission through the vasculature, pressure disturbances in the LA are very rapidly transmitted directly through the heart.

	ACKNOWLEDGMENTS

 
We acknowledge the excellent technical support provided by C. Meek, G. Groves and R. Sas and the statistical advice of Dr. R. Brant of the Centre for the Advancement of Health. The late S. Wolvek of Datascope specially fabricated the counter pulsation balloon.

GRANTS

E. H. Hollander held a Studentship from the Heart and Stroke Foundation of Canada (Ottawa), and J. V. Tyberg is a Heritage Scientist of the Alberta Heritage Foundation for Medical Research (Edmonton). The study was supported by a grant-in-aid from the Heart and Stroke Foundation of Alberta (Calgary) to J. V. Tyberg.

	FOOTNOTES

 

Address for reprint requests and other correspondence: J. V. Tyberg, Depts. of Medicine and of Physiology and Biophysics, 3330 Hospital Dr. NW, Calgary, Alberta, Canada T2N 4N1 (E-mail: jtyberg{at}ucalgary.ca).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

	REFERENCES

TOP ABSTRACT METHODS RESULTS DISCUSSION REFERENCES

 

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