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Ann Thorac Surg 1996;61:888-894
© 1996 The Society of Thoracic Surgeons
Departments of Thoracic and Cardiovascular Surgery and Cardiology, Loyola University Medical Center, Maywood, Illinois
Accepted for publication November 9, 1995.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. To characterize the effects of IABC on arterial input impedance, impedance measurements were obtained using aortic annulus Doppler flow and pressure from the aortic balloon catheter. Impedance spectra were compared between the cardiac cycles preceding and following the cycle with IABC in 25 patients.
Results. Intraaortic balloon counterpulsation increased stroke volume (23%; p = 0.001), reduced myocardial oxygen demand (11%; p = 0.02), and decreased the aortic pressure at the onset of systole (16%; p = 0.001). There was also a decrease in systemic vascular resistance (24%; p = 0.001), characteristic arterial impedance (21%; p = 0.002), and pulse wave reflection (20%; p = 0.006). Linear regression analysis showed that an increase in stroke volume was predicted only by the decrease in systemic vascular resistance (r = -0.81; p = 0.001).
Conclusions. The reduction in systemic vascular resistance appeared to be the major mechanism by which IABC improved cardiac pumping efficiency. This effect may result from the passive distention of the peripheral vascular bed due to the propagation of the balloon-augmented diastolic pressure through the arterial system.
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Introduction |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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The most widely used circulatory assist device is the intraaortic balloon pump. This device supports the left ventricle by introducing external energy into the vascular systems. The left ventricle perceives the added energy as a change in its external load or afterload. In its simplest form, external afterload is thought to be the pressure in the aorta that the ventricle must overcome to eject blood. It is generally accepted that systolic unloading is the most important effect of intraaortic balloon counterpulsation (IABC) in patients with impaired cardiac performance [1–3]. Because the left ventricle pumps pulsatile flow into a viscoelastic arterial system, a more accurate index of external afterload is obtained by the measurement of arterial input impedance. Analysis of arterial input impedance allows an estimation of both steady (peripheral resistance) and pulsatile afterload. Pulsatile load includes characteristic impedance and pulse wave reflection [4, 5]. Previous clinical studies have measured several hemodynamic parameters during IABC; this study examined the effects of IABC on arterial impedance. Because IABC produces an artificial rise in diastolic pressure, impedance spectra will be distorted if they encompass the period of balloon augmentation. To circumvent this limitation, IABC was on every third cardiac cycle in the present study and impedance spectra were generated for the cardiac cycles preceding and following the cycle with diastolic pressure augmentation (Fig 1
). Comparison of the impedance spectra between these two beats allowed a precise quantitative description of the effects of IABC on arterial impedance.
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Material and Methods |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Real-Time Hemodynamic Data Acquisition
When a patient in sinus rhythm had a cardiac index greater than 2.0 L•min-1•m-2, IABC was placed in a 1:3 mode and the central hemodynamic measurements were performed. After heart rate and blood pressure stabilized, a two-dimensional echocardiogram was obtained for determining the aortic diameter in the parasternal long-axis view with the subject in the supine position. The apical four-chamber view was used for measuring aortic blood flow velocity with the sample volume located at the level of aortic leaflets [6, 7] using a 2.5-MHz pulsed-wave Doppler transducer (Hewlett Packard, Andover, MA). Central aortic pressure was obtained from the tip of the intraaortic balloon catheter. The catheter-tip pressure was electronically calibrated before the study in each patient. Damped natural frequency and damping coefficient of the pressure measuring system including the catheter and transducer (Abbott, North City, IL) were 14.8 Hz and 0.226, respectively. The output signal of the central aortic pressure was connected to and further amplified through a physiologic module (model 77020 CV; Hewlett Packard). The real-time graphic display of the analog signals including aortic Doppler echocardiography, central aortic pressure, and electrocardiography was viewed on a monitor (100 mm/s) and recorded on video tape for off-line computer-aided analysis. All pressure and flow data were collected in less than 60 seconds.
Data Processing and Analysis
The aortic diameter was measured from the leading edge of the anterior to the leading edge of the posterior echo at the annulus of the aortic root in a parasternal long-axis view [6, 7]. Instantaneous volume flow was obtained as the product of the Doppler time-velocity integral and aortic annular cross-sectional area. Hard copies were obtained from selected video images for digitization. All pressure and flow recordings obtained during the end of expiration were digitized at 5-millisecond intervals using a digitizing pad (Summa Sketch II; Summagraphics, Bristol, CT) interfaced with a personal computer (EVERX 486/33). The aortic pressure wave was digitized by aligning the foot of the pressure wave to the onset of aortic flow to correct the phase shift that resulted from the measurements of pressure and flow waves at different locations [6, 8]. The aortic Doppler flow and pressure waveforms were digitized before and after the cycle that had IABC. The unassisted and assisted beats were defined as the cardiac cycle before and after the balloon-augmented cycle, respectively (see Fig 1
). The digitized data were averaged for five consecutive balloon-augmented cycles. To eliminate a potential interobserver variability of the echocardiographic variables, echocardiograms of all patients were obtained by a single echo technician and analyzed by a single investigator (S.Y.K.) throughout the entire study.
Characterization of Pulsatile Afterload and Impedance Spectra
The digitized pressure and flow wave recordings were averaged and Fourier analysis was performed for constructing the impedance spectrum. The arterial input impedance spectrum was derived as the impedance modulus (Zn) and impedance phase (
n). The impedance modulus is the ratio of the respective pressure modulus to flow modulus (Qn) of the nth harmonic (n = number of harmonics), and the impedance phase is the difference between pressure and flow phase angle [5]. The zero-order term of the impedance spectrum is the total systemic vascular resistance (SVR). Characteristic impedance, an index of aortic stiffness, was the average impedance modulus between 2 and 12 Hz [4, 5]. An index of peripheral pressure, pulse wave reflection, was obtained from the ratio of backward pressure amplitude to forward pressure amplitude [9].
Left Ventricular Function and Hydraulic Pumping Energy Cost
Myocardial oxygen consumption was estimated by the calculation of the tension-time index (TTI). The ratio of TTI over the diastolic pressure-time index was used to evaluate myocardial oxygen demand and supply [10]. The TTI and diastolic pressure-time index were obtained from the measurements of the area under the systolic and the diastolic portion of the aortic pressure curve, respectively. The mean and pulsatile components of the left ventricular power were assessed by the calculation of potential hydraulic work per unit time performed by the left ventricle on the systemic circulation. Pulsatile power (Wo) was calculated from the following formula [11]: Wo = 0.5 x 
Qn2 Zn cos(n). Mean power was calculated as the product of mean aortic pressure and flow, and total power was the sum of mean and pulsatile power. The ratio of pulsatile to total power was used as an index of the vascular efficiency of power transfer [11]. The cardiac pumping energy cost was evaluated by the left ventricular energy expenditure for any given stroke volume (SV) [3, 8]: TTI/SV.
Statistics
Student's paired t test was used to compare hemodynamic changes within individuals. Linear regression analysis was performed to determine the relationship between changes in the different variables. A p value less than 0.05 was considered statistically significant. Data are presented as mean ± standard deviation.
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Results |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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. A representative example of the input impedance spectra is shown in Figure 2. Intraaortic balloon counterpulsation decreased aortic pressure at the peak of systole, aortic pressure at the onset of systole (SBPo), and aortic mean blood pressure by 10% (p = 0.004), 16% (p = 0.001), and 13% (p = 0.009), respectively. Intraaortic balloon counterpulsation increased SV by 23% (p = 0.001) and decreased cardiac energy consumption (TTI) by 11% (p = 0.02). Total SVR, characteristic impedance, and pressure pulse wave reflection were decreased by 24% (p = 0.001), 21% (p = 0.002), and 20% (p = 0.006), respectively. The relative increase in SV was significantly and inversely correlated (r = -0.81; p = 0.0001) to the relative change in SVR (Fig 3). However, no significant correlation was found between the relative change in SV and the relative change in aortic pressure at the peak of systole (r = -0.12; p = 0.562), SBPo (r = -0.22; p = 0.298), characteristic impedance (r = -0.19; p = 0.368), and pulse wave reflection (r = -0.14; p = 0.508). Intraaortic balloon counterpulsation increased mean and total left ventricular hydraulic power by 13% (p = 0.006) and 10% (p = 0.007), respectively, and decreased the ratio of pulsatile to total power by 9% (p = 0.007).
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). There was no significant correlation between the change in TTI/SV and the change in either the aortic pressure at the onset of systole (r = 0.14; p = 0.499) or characteristic impedance (r = 0.13; p = 0.525) or peripheral pressure pulse wave reflection (r = 0.16; p = 0.447). As shown in Figure 4, the change in the energetic cost, however, was highly dependent on the change in the total SVR (r = 0.9; p = 0.001).
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Comment |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Several studies demonstrated that Doppler estimates of cardiac output had a close relationship with invasively measured cardiac output [6, 7]. In addition, agreement between the aortic pulsed Doppler waveform and invasively obtained aortic flow velocity contour by electromagnetic flow meter was verified in humans [13].
Because the pressure and flow waves were recorded at different locations, the resulting phase shift was corrected in this study to the onset of the flow for impedance determination. Damped natural frequency of the pressure measurement system was 14.8 Hz, which was determined in our laboratory. Impedance variables were calculated up to 12 Hz; thus, the frequency response of pressure recording system does not represent an important limitation. Furthermore, the goal of this study was to determine the change in impedance between the unassisted and the assisted cardiac beats; therefore, absolute errors in the measurement of pressure and flow would be less important.
Vascular Properties and Impedance Data
The results of this study show that IABC significantly decreased both steady (SVR) and pulsatile (characteristic impedance and pulse wave reflection) vascular loads. Although the magnitude of the relative decrease in these three impedance variables was similar, the absolute magnitude of the decrease in SVR was substantially greater than the decrease in both characteristic impedance and pulse wave reflection. The linear relationship between the relative decrease in SVR and the relative increase in SV suggests that IABC primarily increases cardiac output through a decrease in SVR (see Fig 3). Previous studies [1–3] have suggested that IABC increases SV through a reduction in SBPo. Although a significant decrease in SBPo was observed in the present study, there was no significant correlation between the increase in SV and the decrease in SBPo. Thus, it would appear that the change in aortic pressure, per se, is not the major mechanism by which IABC unloads the left ventricle. Presumably the significant reductions of SBPo and peak systolic blood pressure and mean blood pressure are a manifestation of the increased distal runoff of blood due to a decrease in SVR. Although it is possible that IABC improved ventricular performance by increasing preload or contractility, changes in these parameters have been shown not to influence arterial impedance [4].
In contrast to the results presented here, IABC did not decrease systemic vascular resistance significantly in previous clinical studies [14, 15]. The discrepancy in results may be due to the selection of cardiac beats for calculating SVR. When IABC occurs every cardiac cycle, SVR may be artificially elevated due to the balloon-induced augmentation of diastolic pressure. The ability of balloon augmentation to elevate SVR was documented in the present study. The SVR of the augmented beats (1,461 ± 388 dynes•s•cm-5) was significantly greater than the SVR of the preceding unassisted beats (1,157 ± 290 dynes•s•cm-5; p = 0.0001). The increase in SVR was due to an elevation of mean arterial pressure because cardiac output of the augmented beats (102 ± 25 mL/s) was not different from the output of the unassisted beats (102 ± 22 mL/s). These observations indicate that the direct effects of IABC on arterial impedance must be evaluated by comparing the beats preceding and following the beat with balloon augmentation.
Studies in experimental animals have shown that IABC increases the activation of arterial baroreceptors resulting in a reflex decrease in SVR [3, 16, 17]. It is unlikely that enhanced baroreceptor activity was important in the present study because there was no difference in the R-R interval between the unassisted (733 ± 155 ms) and the assisted beats (738 ± 163 ms). Furthermore it is unlikely that there was sufficient time between the rise in diastolic pressure during balloon augmentation and the next ventricular contraction for a baroreceptor-mediated change in SVR [18].
Although the precise mechanism for the reduction in SVR is unknown, a pressure-induced passive vascular distention in the arterial system is a potential mechanism. Balloon augmentation introduces a large pulsation of pressure and flow into the arterial system. This pulsatile energy is transmitted longitudinally in the arterial system and increases the distal flow of arterial blood [5, 9]. This pulsatile energy transmission during the diastole in the augmented beat may effectively open more distal vessels [19, 20], thereby transiently reducing the peripheral vascular resistance.
The compliance in large arteries depends on transmural distending pressure: the lower the pressure, the higher the compliance [21]. Studies in a canine model reported that the dependence of characteristic impedance of arteries showed little variation over a mean arterial pressure range of 80 to 150 mm Hg [22]. However, in this study, the value of mean arterial pressure was 78 mm Hg in the unassisted and 68 mm Hg in the assisted beats. Therefore, the observed decrease in characteristic impedance in the assisted beats could be a simple consequence of reduction of the transmural distending pressure.
Because pulse wave reflection is thought to result from local vascular impedance mismatch either in resistance or in compliance [5], the reduced vascular resistance may have been responsible for the decrease in peripheral pressure pulse wave reflection.
In contrast to reductions in vascular impedances, IABC produced a significant increase in hydraulic power. The left ventricular hydraulic power depends not only on the ability of the left ventricle to do external work, but also on the properties of the arterial tree into which blood is ejected: power = flow2 x impedance. Mean power is mainly dissipated in moving blood through the resistive arterioles, whereas pulsatile power is dissipated in arterial pulsation, and depends primarily on the elasticity of the aorta [4, 11]. In the present study, a significant increase in mean power is attributed to a large increase in SV in the assisted beat. The increase in SV would be expected to increase pulsatile power as well. However, a substantial decrease in characteristic impedance may have offset the expected increase in pulsatile power. The increase in mean power with no change in pulsatile power was responsible for the decrease in the pulsatile component of total power from 21% to 18%. The decrease in this ratio suggests an increase in the vascular power transfer efficiency.
Cardiac Energetic Cost as an IABC Performance Index
The most direct indicator of energy expenditure by the heart is oxygen consumption, which was estimated by TTI in the present study. One of the direct indicators of the useful external energy supplied to the circulatory system is SV. Therefore the relationship between these two indicators can be a useful index of cardiac mechanical efficiency. In the present study this relation was expressed as cardiac energetic cost (TTI/SV). Intraaortic balloon counterpulsation decreased cardiac energetic cost by 27%. Figure 4 shows a significant correlation between the change in cardiac energetic cost and the relative decrease in SVR. Because there was no correlation between the change in either pulsatile afterloads (characteristic impedance and pulse wave reflection) or aortic pressure at the onset systole and the change in TTI/SV, it would appear that improved cardiac efficiency results mainly from decreasing the steady component of vascular afterload, ie, SVR.
Limitations
The hemodynamic effects of IABC depend on a wide variety of variables including size of the balloon, ratio of balloon size to aortic size [15], duration of IABC support, and other variables that were not controlled in the present study. The pharmacotherapy (intravenous vasodilators, inotropes) was a potentially confounding but unavoidable variable. To minimize the variation among patients, we compared the hemodynamic and impedance variables between the unassisted and the assisted beats in each patient.
It is conceivable that afterload reduction due to balloon augmentation may have lasted more than one cardiac cycle and have influenced hemodynamic variables in the unassisted beats. The observation that the SV of the augmented beats was the same as SV in the unassisted beats suggests that the salutary effects of balloon augmentation did not extend beyond the assisted beat.
Conclusion
Intraaortic balloon counterpulsation adds external energy into the vascular system. The present study shows that the effect of the augmented energy is manifested by an increase in SV with the reduced myocardial oxygen demand and the decreases in both steady and pulsatile afterload. The reduction in SVR appears to be the major mechanism by which IABC increases cardiac output and improves cardiac efficiency. The passive distention of peripheral vascular bed due to the diastolic augmented pressure propagation is considered as a potential explanation for the decrease in SVR. The change in SV and total SVR of a patient can be easily and accurately determined using aortic Doppler ultrasound and indwelling balloon tip pressure measurements. These measurements can be useful indices for evaluating the clinical course of the performance state of IABC.
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Acknowledgments |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Footnotes |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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