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Ann Thorac Surg 2005;79:872-880
© 2005 The Society of Thoracic Surgeons
a Department of Cardiac Surgery, San Raffaele University Hospital, Milan, Italy
b Department of Intensive Care, Leiden University Medical Center, Leiden, The Netherlands
c Arrow International, Reading, Pennsylvania
Accepted for publication July 29, 2004.
* Address reprint requests to Dr Schreuder, Department of Cardiac Surgery, San Raffaele University Hospital, Via Olgettina 60, 20132 Milan, Italy; (E-mail: schreuder{at}libero.it).
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Abstract |
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METHODS: In 15 patients, LV pressure-volume relations and LV dyssynchrony were measured by conductance volume catheter. Properly timed IABP was evaluated at a 1:1 assist ratio within a 10 seconds time-span. Premature IAB inflation and late IAB deflation were evaluated at a 1:4 assist ratio.
RESULTS: Properly timed 1:1 IABP acutely decreased LV end-systolic volume by 6.1% (p < 0.0001) and LV end-systolic pressure by 17.5% (p < 0.0001) due to decreased aortic impedance. Stroke volume (SV) increased by 14% (p < 0.0001), which correlated markedly with a decrease of LV mechanical dyssynchrony (p < 0.0001). The largest SV increases occurred in patients with lowest contractile state. Premature IAB inflation decreased SV by 20% (p < 0.0001) due to abrupt increase of LV afterload during late ejection. Late IAB deflation increased SV and stroke work by 18% (p < 0.0001) and 16% (p < 0.01) respectively, due to increased afterload during early ejection and decreased afterload during late ejection.
CONCLUSIONS: Left ventricular performance during IABP is causally related to changes in LV afterload, and the timing of these changes in relation to contraction or relaxation phases, to LV mechanical dyssynchrony and to contractile state.
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Introduction |
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| Dr Schreuder, Mr Bovelander and Ms Hanlon disclose that they have a financial relationship with Arrow International; Dr Schreuder also has a financial relationship with CD Leycom.
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Intraaortic balloon counterpulsation (IABP) to support cardiac function has been well documented during the last three decades [1–7]. Primary effects of properly timed IABP are diastolic aortic pressure augmentation and left ventricular (LV) afterload reduction by decreasing impedance to LV ejection [3, 4]. LV volume and LV end-diastolic pressure (EDP) have been demonstrated toSee page 1017 decrease in patients treated with IABP, whereas cardiac output, ejection fraction (EF), and coronary flow may increase [2–6]. However, arrhythmic episodes often result in incorrect IABP timing decreasing its efficacy [7]. Premature IAB inflation may increase aortic impedance and therefore LV afterload late in the ejection phase, whereas late IAB deflation may increase afterload during early ejection. Acute load increases applied during contraction or relaxation in heart muscle preparations or in intact animal ventricles induced increases or decreases in ejection phase duration, respectively [8–11]. Moreover, altered loading conditions may result in dyssynchronous relaxation of the LV [11, 12]. Myocardial relaxation is known to be sensitive to afterload and to LV dyssynchrony in patients with dilated cardiomyopathy [13]. LV mechanical dyssynchrony in these patients decreased due to reduction in wall stress induced by interventions such as vasodilators, cardiomyoplasty, or LV ventricular reduction surgery [13–16]. Recently we demonstrated a close relationship between cardiac performance and intraventricular mechanical dyssynchrony in patients undergoing LV restoration by the Dor procedure [16]. Hence we hypothesized that IABP timing in patients with low EF may considerably influence cardiac performance by acute afterload changes and concomitant changes in LV mechanical dyssynchrony. Effects of IABP on LV performance and LV mechanical dyssynchrony were analyzed beat-to-beat from the pressure-volume plane during conventionally timed IABP, premature IAB inflation and late IAB deflation, using the conductance volume catheter technique [14–23]. The beat-to-beat measurements were performed within a time span of 10 seconds after an IABP change to exclude cardiovascular compensatory reflexes and or metabolic effects from possible increases in coronary flow [4]. Beat-to-beat changes of cardiac performance with IABP may then be primarily attributed to acute changes in aortic impedance.
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Patients and Methods |
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The study protocol was approved by the local ethics committee and written informed patient consent was obtained.
Instrumentation
All patients received high dose opioid anesthesia. Five patients belonging to NYHA class III-IV received small steady-state dosages of inotropics (dobutamine < 5 u · kg–1 · min–1).
The IAB catheters (Narrowflex; Arrow International, Reading, PA) were positioned under transesophageal echo control in the descending thoracic aorta at 2-cm distal to the left subclavian artery. Thermodilution catheters (Edwards Lifesciences, Inc., Irvine, CA) were inserted into the pulmonary artery and micromanometer-conductance catheters (F7; CD Leycom, Zoetermeer, The Netherlands) into the LV through a pulmonary vein.
The cardiac function analyzer (Leycom CFL512; CD Leycom) uses a conductance catheter to measure ventricular volumes at a dual-field excitation mode [17, 21]. The method is based on measuring time-varying electrical conductance of 5 to 7 ventricular blood segments, delineated by selected catheter electrodes. Correct positioning of the conductance catheter was verified by transesophageal echocardiography and by inspection of the segmental conductance signals. The feasibility of the conductance catheter method to measure real-time ventricular volume has been demonstrated in animal and clinical studies [14–23]. Reproducibility of conductance catheter measurements was demonstrated in patients undergoing cardiac surgery [19]. Beat-to-beat stroke volume changes were validated by pulse contour analysis [20]. Time-varying segmental conductance reflects time-varying segmental LV volume as obtained and validated by cine-angiography in canine hearts [21].
Parallel conductance was assessed by injection of 10 ml hypertonic saline (6%) into the pulmonary artery [17]. Effective conductance stroke volume (SV) was defined as difference between conductance volumes at the times of +dP/dtmax and –dP/dtmax, which largely eliminates contribution of possible regurgitant flows. Absolute LV volumes were calculated by matching effective conductance SV with simultaneously measured thermodilution SV and by subtracting parallel conductance from total conductance volume.
Mechanical Ventricular Dyssynchrony
Ventricular dyssynchrony assessment from segmental LV volume signals has been previously described for cine-angiography and the conductance catheter [14, 23, 24]. The conductance catheter measures volume segments located perpendicular to the long heart-axis. A volume segment was defined dyssynchronous when the volume change in that segment was in opposite direction (dyskinetic) or showed no change (akinetic) compared to total LV volume change. Segmental dyssynchrony was quantified by percent time a segment was dyssynchronous in relation to total volume change, total dyssynchrony was the average of segmental dyssynchrony in all segments [14, 23]. Systolic dyssynchrony was calculated from R-wave to –dP/dtmax and diastolic dyssynchrony from –dP/dtmax to R-wave.
Data Analysis
Electrocardiogram (ECG), LV pressure, aortic pressure and volume signals were digitized at a sampling rate of 250 Hz. The following variables were calculated: Tau, index of LV pressure relaxation, defined as time required from LV pressure at –dP/dtmax to be reduced by half [25]; peak ejection rate calculated as maximal –dV/dt; End-systolic elastance (Ees), representing a load independent index of contractile state, was determined from unassisted beats and first 8 seconds of IABP (Fig 1); Ees1 included last unassisted beat (arrow) and first 3 assisted beats; Ees2 included last unassisted beat and three latest assisted beats prior to10 seconds after IABP initiation.
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Measurement Protocol
Effects of properly timed IABP (inflation at the dicrotic notch, deflation inducing end-diastolic aortic pressure decrease) were measured during 15 seconds ventilatory stop, the first 5 seconds without IABP followed by assist at a 1:1 ratio (Fig 1). All measurements were made under steady state conditions.
Premature IAB inflation was set 130 to190ms before the dicrotic notch to produce an abrupt afterload increase in the second part of the ejection phase (Fig 2 [A, b]).
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Results |
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Hemodynamic Response to Premature IAB Inflation
The adverse effects of premature inflation are illustrated in Figure 2A. Abrupt increases in LV afterload late in LV ejection, as a result from increased aortic impedance, induced premature closure of the aortic valve and impaired LV ejection. Table 2 provides average data, before premature inflation (a), during premature IAB inflation applied at 130 to 190 ms before the dicrotic notch (b), and after IAB assist (c). LVESP, or end-systolic afterload, increased (p < 0.0001) during premature IAB inflation by a mean of 14 mm Hg. SV decreased (p < 0.0001) by 20%, ranging from –6% to –55%, with concomitant increase in LVESV (p < 0.0001). Stroke work decreased by a mean of 25% (p < 0.002). Tau increased by 44% (p < 0.0001), indicating deterioration of LV relaxation. The 16% mean increase (p < 0.05) in SV in the postassisted beat compared with the preassisted beat did not compensate for the 20% SV decrease of the preceding beat.
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Comment |
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Premature IAB inflation acutely impaired LV ejection due to abrupt afterload increase during late ejection, increasing systolic dyssynchrony, and Tau impairing myocardial relaxation. Late IAB deflation induced a dual effect, afterload increase during early ejection and decrease in late ejection, combined these increased SV and improved LV relaxation, but at increased SW.
Hemodynamics Conventionally Timed IABP
Short-term effectiveness of IABP was demonstrated by Nichols and colleagues [3], using multigated cardiac blood pool imaging. Cardiac output increased by 10%, 10 minutes after initiation of IABP. Our study shows in all patients, despite the heterogeneous population, beat-to-beat SV increases due to decreases in LVESV, preceding decreases in LVEDV and LVEDP. Similar changes were observed in animals with heart failure using LV pressure-volume loops [5]. Beat-to-beat improvement of cardiac performance with IABP, as demonstrated by Cheung and coworkers [4] and confirmed in the present study, may be primarily attributed to acute decreases in aortic impedance reducing LV afterload, because cardiovascular compensatory reflexes and metabolic effects from possible increases in coronary flow can be excluded within the measurement time of 10 seconds.
The decreases in LVESV and LVESP determine the end-systolic elastance (Ees) as slope of the end-systolic P-V relationship, which implies that the lower the slope the larger the decrease in LVESV. The inverse correlation between Ees and SV indicates that patients with the lowest contractile state will show the largest increases in SV with IABP (Fig 4B). The significant nonlinear convex Ees (Fig 1, Table 1) is related to low contractile state as was demonstrated by Burkhoff and associates [26] in animal studies.
Decreases in wall motion abnormalities have been demonstrated 10 minutes after IABP initiation [3]. Dyssynchrony of wall motion reduces mechanical efficiency of ventricular ejection by inducing premature onset and impaired relaxation [10]. LV mechanical dyssynchrony, as demonstrated in patients with dilated cardiomyopathy and LBBB using tagged MRI, was shown to be a key predictor for multi site pacing efficacy [27]. Patients with dilated cardiomyopathy and marked LV dyssynchrony showed decreases in LV mechanical dyssynchrony by wall stress reduction following vasodilator administration, cardiomyoplasty or LV reduction surgery [13–16]. The acute decreases in both systolic and diastolic dyssynchrony with IABP point to a similar mechanism, based on decreases in impedance reducing LV afterload with concomitant decreases in LVESV and preload, improving LV mechanical efficiency. Reductions in LV total dyssynchrony showed a strong inverse correlation with increases in SV induced by IABP assist at 1:1 (Fig 4A). The largest increases in SV with IABP result from largest decreases in LVESV combined with smallest decreases in LVEDV. Therefore increases in SV with conventional IABP are causally related to decreases in LV afterload, preload, contractile state and concomitant changes in total LV mechanical dyssynchrony.
Premature IAB Inflation-Late IAB Deflation
The present study shows that abrupt increases in aortic impedance, and therefore in LV afterload, imposed during late ejection result in shortened ejection phases, as was demonstrated in isolated cardiac muscle experiments and in vivo animal experiments [8–11]. Premature IAB inflation performed 130 to 190 ms before the dicrotic notch resulted in increased LVESP, Tau, and decreased SV. These findings agree with the animal study by Zile and Gaasch [9] where IAB inflation was applied 80 ms before the dicrotic notch. Factors such as IAB positioning and pulse-wave velocity from IAB to LV can explain differences in timing between man and animal results and the variance observed in the current patient population. The pulse-wave velocity will also vary with changes in cardiac output or aortic compliance. IAB inflation performed in animals 20 ms before the dicrotic notch revealed no change in contraction duration while early relaxation rate increased [9]. In the present study we observed that premature IAB inflation applied less than 50 ms before the dicrotic notch did not change SV. The significant increase in systolic dyssynchrony during premature IAB inflation is analogous to increase in dyssynchronous relaxation due to altered loading conditions, as described in animal studies by Gaasch and associates [11] and Schafer and colleagues [12].
Conventional IAB deflation should produce a clear reduction in end-diastolic aortic pressure. However, Kern and coworkers [28] demonstrated in a clinical IABP study that IAB deflation might be performed later in diastole without adverse hemodynamic effects. Our study shows that incidental late IAB deflation at a 1:4 assist ratio may result in immediate increases in SV, although at increased SW. Animal experiments showed that afterload increase applied during early ejection prolongs ejection phase duration similar to a decrease in afterload applied in late ejection [8–10]. Initial afterload increase in early ejection and decrease in late ejection due to late IAB deflation may explain the relatively large mean SV increase of 18% SV in a single IABP assisted beat (Fig 2 [B, c]).
Late IAB deflation induced a significantly higher SW in two ways, by increasing PLV in early ejection and by increased SV. Possible beneficial effects of late IAB deflation applied at a 1:1 ratio should be investigated in specific patient conditions. On the other hand, incidental late deflation which may occur during IABP due to arrhythmia should have no detrimental effects on cardiac performance.
The marked beat-to-beat SV alterations due to afterload changes applied at different times in the cardiac cycle with premature inflation or late deflation markedly correlated with systolic dyssynchrony changes (Fig 4C). Brutsaert's hypothesis that LV mechanical dyssynchrony or nonuniformity may act as a modulator of cardiac performance together with heart rate, contractile state, preload and afterload may therefore be applicable in heart failure patients [29]. In a previous study we demonstrated a direct relationship between increases in contractile state (Ees) and decreases in intraventricular dyssynchrony in patients undergoing LV restoration by the Dor procedure [16].
Limitations of the Study
We analyzed acute hemodynamic effects occurring within 10 seconds after initiation of IABP in heart failure patients with open chest under general anesthesia. Longer-term analysis may show differences due to metabolic effects by possible increases in coronary flow and or resulting from compensatory cardiovascular reflexes. NYHA class III-IV patients received small constant dosages of inotropic agents which may have changed their contractile state and the magnitude of the responses to IABP.
The applied LV mechanical dyssynchrony analysis is not discriminative between slow paradoxical wall motions as known from LV aneurysms or fast wall motions known from dilated cardiomyopathy or left bundle branch block [14, 16, 23, 27]. We assume that, mechanistically, both will have similar effects on LV performance.
The population we studied included patients with ischemic heart disease and mitral valve dysfunction, and did not include all potential IABP indications.
Conclusions
Precisely timed IABP in heart failure patients is highly effective in generating beat-to-beat improvements in systolic and diastolic LV performance as demonstrated by beat-to-beat increases in SV and decreases in LV afterload, LVESV, preload and LV mechanical dyssynchrony. These beat-to-beat improvements are due to decreases in aortic impedance, were generally established within four beats after IABP initiation, because metabolic effects due to possible changes in coronary flow and cardiovascular compensatory reflexes may be excluded in this time frame. Decreases in LVESV and LVESP delineated the ESPVR and its slope, the Ees, implying that the largest SV increases occur in patients with lowest contractile state.
Premature IAB inflation markedly impaired LV ejection and relaxation by afterload increase and concomitant LV mechanical dyssynchrony increase during the second part of the ejection phase, indicating that premature IAB inflation, as may occur during arrhythmia, may have detrimental effects on cardiac performance in heart failure patients. Late IAB deflation resulted in increased SV and increased SW by afterload increase during early ejection and afterload decrease in late ejection, indicating that incidental late IAB deflation will not negatively affect cardiac performance.
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Acknowledgments |
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