Ann Thorac Surg 2004;78:1426-1432
© 2004 The Society of Thoracic Surgeons
Original article: cardiovascular
Intraaortic Balloon Pumping Improves Hemodynamics and Right Ventricular Efficiency in Acute Ischemic Right Ventricular Failure
Dag Nordhaug, MDa,b,*,
Tor Steensrud, MDa,b,
Stig Muller, MDa,b,
Kjell Vidar Husnes, MDb,
Truls Myrmel, MD, PhDa
a Department of Cardiothoracic and Vascular Surgery, University Hospital North Norway, Tromsø, Norway
b Surgical Research Laboratory, University of Tromsø, Tromsø, Norway
Accepted for publication December 10, 2003.
* Address reprint requests to Dr Nordhaug, Department of Cardiothoracic and Vascular Surgery, University Hospital North Norway, PO Box 102, N-9038 Tromsø, Norway
dagn{at}fagmed.uit.no
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Abstract
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BACKGROUND: Left ventricular unloading has a potentially deleterious effect in right ventricular failure as a result of altered septal interplay. However, a positive effect of an intraaortic balloon pump during right ventricular failure has been suggested. We investigated the impact of intraaortic balloon pumping on hemodynamics and both left and right ventricular function in an experimental model of isolated right ventricular failure.
METHODS: Sixteen anesthetized pigs (25 to 34 kg) were used in an in vivo model. Pressure-conductance catheters assessed right and left ventricular pressure-volume relationships. Acute right ventricular failure was induced by right coronary microembolization, and led to severely impaired right ventricular function, reduced cardiac output and arterial pressure, and an increased pulmonary vascular resistance and pulmonary arterial elastance. Animals were then randomized to balloon pump or control groups and evaluated with respect to hemodynamics and ventricular function after 1 hour.
RESULTS: Intraaortic balloon pumping did not alter right or left ventricular contractility. However, balloon pump–treated animals had significantly improved cardiac output (+18% ± 18% versus –6% ± 7%; p = 0.003) and mean arterial pressure (+36% ± 30% versus –7% ± 14%; p = 0.004) compared with controls. Animals in the balloon pump group had lower pulmonary vascular resistance (795 ± 63 versus 912 ± 259 dynes · sec · cm–5; p < 0.01) and pulmonary arterial elastance (1.14 ± 0.20 versus 1.69 ± 0.65 mm Hg/mL; p < 0.01), and increased stroke volume (22.3 ± 4.7 versus 17.9 ± 4.7 mL; p = 0.016). Right ventricular efficiency was also improved in the balloon pump group (stroke work per pressure-volume area = 0.60 ± 0.14 versus 0.41 ± 0.12; p < 0.01).
CONCLUSIONS: Intraaortic balloon pump support does not alter right or left ventricular function in acute right ventricular failure. However, arterial pressure, cardiac output, and right ventricular efficiency are improved, possibly because of a balloon pump–induced reduction in pulmonary arterial resistance.
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Introduction
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Right ventricular (RV) failure is a common clinical problem, complicating approximately half of all inferior wall infarctions [1]. The syndrome ranges from mild reversible ischemic dysfunction to fulminate cardiogenic shock and is associated with considerable morbidity and mortality [1]. Right ventricular failure also represents a particular challenge in cardiac surgery as it is often encountered after cardiac transplantation [2], inadequate use of retrograde cardioplegia [3], and during circulatory support using left ventricular (LV) mechanical assist systems [4]. Even after routine coronary revascularization, RV contractility is depressed [5]. In a report from Davila-Roman and associates [6], 23% of patients with postoperative low-output syndrome had isolated RV failure, and an additional 25% had notable RV failure with a concomitant LV dysfunction. Thus, RV failure is probably an important contributor to the low-output syndrome often seen after cardiac surgery.
The RV and LV are closely connected anatomically and physiologically. The two chambers share the common interventricular septum and muscle fibers in the anterior walls. Thus, pressure on one side of the septum may affect pressure development in the other ventricle [7]. Adequate pumping of the RV seems to depend on sufficient pressure generation in the left chamber, especially during RV dysfunction [8, 9]. Therefore, it is not surprising that several studies find impaired function of the RV during LV unloading with a mechanical pump [4, 10]. During use of an LV assist device, 20% to 30% of patients experience an acute right-sided heart failure [7].
Mechanical support with an intraaortic balloon pump (IABP) has been shown to improve LV function in acute and chronic LV failure [11]. The mechanism behind this effect is not entirely clear, but LV unloading by reducing afterload seems to be important [12]. To what extent the pressure alterations in the left chamber during IABP affect RV function have previously not been investigated. Inasmuch as pressure generation is reduced in the LV during IABP, one can imagine an effect similar to the one seen during LV assist device use. However, two reports indicate a positive effect of IABP during RV failure [13, 14], but these reports deal with only a few patients, and do not use state-of-the-art indices of LV and RV function. The patients in both these papers may have had significant LV failure, and the improvement in hemodynamics reported could result from the primary effect of IABP on LV function. Intraaortic balloon pump also had a positive effect on RV function in a model of RV pressure overload [15]. However, this study did not clarify that RV dysfunction was present and did not assess RV function using state-of-the-art load-independent indices. A few experimental data also indicate a positive effect of IABP on RV function [16, 17]. However, these studies are incomplete with regard to details allowing adequate evaluation, and since these works were published, better methods for assessing ventricular function have been developed.
From the present knowledge, we cannot determine whether IABP benefits the circulation during isolated RV failure. Therefore, the aim of our study was to investigate the impact of IABP on LV and RV function as well as general hemodynamics in an experimental model of isolated acute RV failure.
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Material and Methods
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Animals and Surgical Preparation
The experimental protocol was approved by the local steering committee of the Norwegian Animal Experiments Authority. All animals received humane care in accordance with the Guide for the Care and Use of Laboratory Animals (National Institutes of Health publication 85-23, revised 1996).
Sixteen domestic pigs of either sex (25 to 34 kg) were fasted overnight with free access to water. On the day of the experiment, the animals were premedicated with intramuscular ketamine (20 mg/kg, Warner Lambert Nordic, Stockholm, Sweden) and atropine (1 mg, Nycomed Pharma, Oslo, Norway). Anesthesia was induced by intravenous pentobarbital sodium (10 mg/kg, Nycomed Pharma) and fentanyl (0.01 mg/kg, Pharmlink, Stockholm, Sweden), and was maintained throughout the experiment with continuous infusion of pentobarbital sodium (4.0 mg · kg–1 · h–1), fentanyl (0.02 mg · kg–1 · h–1), and midazolam (0.3 mg · kg–1 · h–1; Alpharma, Oslo, Norway). Animals underwent tracheostomy, and were intubated and ventilated with 60% oxygen. The internal jugular veins were catheterized for infusions and measurement of central venous pressure. The bladder was drained through a cystostomy. A 25-mL 9.5F sheathless IABP catheter (Datascope Medical LTD, Fairfield, NJ) was placed just distal to the left subclavian artery in the descending thoracic aorta from the left femoral artery. Correct placement was confirmed by fluoroscopy. Mean arterial pressure (MAP) was measured continuously through the pressure lumen of the IABP catheter. After sternotomy, transit time flow probes (CardioMed CM-4000, Medi-Stim AS, Horten, Norway) were placed on the three main coronary arteries and on the pulmonary trunk for determination of coronary flow and cardiac output (CO). A balloon (Sorin Biomedical, CA) was introduced in the inferior caval vein for preload reduction. A combined pressure-conductance catheter (7F, 12 electrodes; Sentron, Leiden, the Netherlands) was inserted into the LV through the left carotid artery. An identical catheter was placed in the RV cavity through the main pulmonary artery. Correct placement of the conductance catheters was confirmed by fluoroscopy and by evaluation of individual conductance segments. Finally, a catheter was inserted into the pulmonary trunk for measurement of pulmonary artery pressure. After surgery, the animals received 150 mg of amiodarone (Sanofi Winthrop, Sponga, Sweden) to prevent arrhythmias, 20 mg/kg hexamethonium chloride (Sigma Chemical Co, St. Louis, MO) to avoid reflex influences on hemodynamics, and 2,500 IU of heparin. Heparin injection was repeated once during the experiment. The animals were stabilized for 30 minutes before baseline measurements.
Experimental Protocol
Right ventricular and LV pressure-conductance recordings were first performed during steady-state uninfluenced preload to assess stroke work (SW), RV and LV pressure-volume (PV) relationships, CO, MAP, and mean pulmonary arterial pressure. To assess RV and LV contractility, PV data derived from both conductance catheters were recorded during transient (12 to 15 seconds) preload reduction. The slope of the SW–end-diastolic volume relationship (preload recruitable SW) was used as the main index of contractility [18]. After these baseline measurements, acute ischemic RV failure was induced by repeated injections of 5-mg boluses of 50-µm polystyrene microspheres (NEM-005; NEN Lifescience Products, Boston, MA) in the right coronary artery until CO was reduced by approximately 35% and MAP was less than 70 mm Hg. A new set of measurements 30 minutes after the last microembolization confirmed the presence of stable RV failure and cardiogenic shock. Animals were then randomized to receive either IABP (Datascope system 98e, electrocardiogram-controlled, 1:1 modus, maximum augmentation) or no treatment. Pigs randomized to IABP first underwent 15 seconds of continuous PV sampling during which IABP was turned from on to standby modus. The first and last 5 seconds of this file were then analyzed and compared to assess the immediate hemodynamic effects of IABP. Continuous balloon pumping was then initiated. All measurements were repeated 60 minutes later to evaluate the effect of IABP over longer term. One hour of IABP has previously been shown to induce significant changes in hemodynamics during RV failure [14].
At the end of the experiment, the animals were sacrificed by intracardiac injection of potassium chloride and infusion of high-dose pentobarbital.
Analysis
The conductance catheter technique has been described previously [19]. Right ventricular and LV pressure and conductance signals were processed using a conductance conditioner (Leycom, Sigma 5DF, Cardiodynamics, the Netherlands) and displayed on a computer using the software Conduct PC, CPC version 3.15 (Leycom). The slope factor 
was calculated from the ratio between conductance and transit time–derived COs. Parallel conductance was estimated by injection of 10% saline solution in the left jugular vein with simultaneous RV and LV PV sampling. This saline dilution technique has been described previously [19].
Stroke work was calculated by integration of the PV loop. Total mechanical work was evaluated as the total pressure-volume area (PVA), that is SW plus potential energy [20]. See Figure 1. Pressure-volume area was calculated as follows:
where SW is calculated from integrated PV data; ESP and ESV are end-systolic pressure and volume, respectively; V0 is the extrapolated x-intercept of the linearly fitted end-systolic PV relationship; and EDP is end-diastolic pressure. The results were converted to joules per beat by multiplying by 0.000133 J/(mm Hg x mL). Ventricular efficiency was evaluated as work efficiency, SW/PVA.
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Fig 1. Pressure-volume area or total mechanical work. The area bounded by the loop conforms to stroke work (SW), and the area bounded by the end-systolic and end-diastolic pressure-volume relationship (ESPVR and EDPVR, respectively) is potential energy (PE). Total mechanical work is the sum of stroke work and potential energy. (V0 = x-axis intercept of linear end-systolic pressure-volume relationship.)
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Arterial elastance was calculated as end-systolic pressure divided by stroke volume. Pulmonary vascular resistance (PVR) in dyne · sec · cm–5 was calculated as PVR = (MPAP/CO) x 80, where MPAP is mean pulmonary arterial pressure.
Statistics
Linear and exponential relationships were estimated by least-squares fit regression using a spreadsheet (Excel 2000; Microsoft Corp, Redmond, WA). All data were analyzed in a statistical software package (SPSS 10.0, SPSS Inc, Chicago, IL). To assess the impact of microembolization, Student's t test for paired data was used. Instant effects of IABP were also evaluated by Student's t test for paired data with IABP on and off. Effect of IABP after 60 minutes was evaluated by two-way analysis of variance (time and group). All values are given as mean ± standard deviation. Significance is reported at 5% level.
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Results
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Microembolization
The effects of microembolization in all animals are shown in Table 1. There was a significant deterioration of CO and MAP. Right ventricular systolic and diastolic performance was severely impaired. Left ventricular performance was only minimally altered when evaluated by the same variables. Right coronary microembolization was associated with a significant increase in PVR and pulmonary arterial elastance (PAE). Furthermore, there was a slight reduction of RV efficiency (SW/PVA). Right coronary flow decreased significantly after microembolization.
Immediate Effects of Intraaortic Balloon Pump
Results of PV sampling while turning on and off the IABP are shown in Figure 2 (n = 8, IABP group). The increase in stroke volume and CO of the LV was paralleled by a modest increase in the same indices derived from the RV. As expected, the decrease in systemic arterial elastance dominated the acute effects of IABP, and was followed by a reduction of LV end-systolic pressure. A similar phenomenon was seen in the pulmonary vasculature, with a slight but statistically significant reduction of PAE. Except for a small decrease in LV end-systolic volume (27.3 ± 10.1 to 25.7 ± 10.5 mL; p = 0.02), there were no significant alterations in LV or RV end-diastolic volume or end-systolic volume.
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Fig 2. Percent change by intraaortic balloon pump (IABP) when hyperacute effects were assessed by turning intraaortic balloon pump from on to standby during continuous pressure-volume sampling. Data are given for both right and left ventricle. *p < 0.05 by intraaortic balloon pump when evaluated by Student's t test for paired data (intraaortic balloon pump on and off). (AE = arterial elastance in systemic and pulmonary vasculature; CO = right and left ventricular output; dPdtmax and dPdtmin = derivative of pressure increase and decay, respectively; ESP = end-systolic pressure; SV = stroke volume.)
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Intraaortic balloon pump group versus controls after 1 hour
The impact of 1 hour of IABP is depicted in Figure 3. Intraaortic balloon pump–treated animals had significantly improved MAP and CO. A decreased PVR and PAE were seen in IABP-treated animals compared with controls. This was associated with a significant increase in stroke volume of the RV of IABP-treated pigs. Tables 2 and 3 show the impact of IABP on RV and LV contractility, respectively. As shown, there were no alterations in RV systolic or diastolic function by IABP. Figure 4 shows RV SW, potential energy, and total mechanical work for controls and IABP group. Intraaortic balloon pump–treated animals had significantly improved RV efficiency measured as the ratio SW/PVA. Also, as shown in Table 2, there was a tendency toward increased coronary flow in the IABP group, but this did not reach statistical significance.
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Fig 3. Impact of 60 minutes of intraaortic balloon pump (IABP). P values denote difference between controls and intraaortic balloon pump–treated animals assessed by two-way analysis of variance. (CO = cardiac output; MAP = mean arterial pressure; PAE = pulmonary arterial elastance; PVR = pulmonary vascular resistance; SV right = right ventricular stroke volume.)
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Fig 4. Right ventricular (RV) work in controls and intraaortic balloon pump (IABP)-treated animals. There was no difference in total mechanical work (stroke work [SW] + potential energy [PE]). However, stroke work was significantly augmented in intraaortic balloon pump–treated animals, rendering efficiency (stroke work divided by total mechanical work) significantly improved in the intraaortic balloon pump group.
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Comment
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The main findings in our study were (1) IABP resulted in a substantially improved CO and MAP in cardiogenic shock caused by isolated ischemic RV failure; (2) IABP-treated animals with acute RV failure displayed decreased PVR and PAE and improved RV stroke volume and work efficiency (SW/PVA); (3) these positive effects were not associated with improved RV or LV contractility; and (4) the increase in right coronary artery flow was numerically substantial, but was not statistically significant.
Ischemic Right Ventricular Failure
The conductance catheter technique has previously been successfully used to assess RV function, and preload recruitable SW has been shown to detect alterations in RV contractile state [5, 21]. In our model, microembolization led to severely depressed RV systolic and diastolic function without altering LV function. Even though some parts of the LV may be perfused by the right coronary artery and some microembolization could occur in the LV myocardium, this was not evident from indices of LV mechanical function. The cardiogenic shock reported in this study was therefore the result of an isolated acute RV failure. In addition to impaired RV systolic and diastolic function, right coronary microembolization resulted in increased RV afterload measured by PVR and PAE. The mechanisms behind the pulmonary vasoconstriction were not investigated further, but analysis of this phenomenon is useful for discussion of the subsequent effect of the IABP. Because of the autonomic blockade, we can exclude sympathetic stimulation as a mechanism. Furthermore, the respirator settings were kept constant, and there were no signs of hypoxia on blood gas analysis, excluding hypoxic vasoconstriction as a cause. Interestingly, as shown in Table 1, microembolization decreased LV end-diastolic pressure, indicating that the increase in PVR was not secondary to impaired LV function. The vasoconstriction probably was a physiologic response to the decreased RV output involving, eg, altered endothelin, angiotensin, and thromboxanes or altered pulmonary vascular nitric oxide production. Importantly, the increase in afterload was associated with a deterioration of RV work efficiency (SW/PVA). This indicates that, with respect to efficiency, the failing RV behaves equivalently to the acutely failing LV, in which altered relationship between ventricular contractility and arterial elastance is a main contributor to ventricular inefficiency [22].
Effect of Intraaortic Balloon Pump in Right Ventricular Failure
In LV failure, the main effect of IABP is an afterload reduction with subsequently improved LV ejection and decreased oxygen consumption [12, 23]. Although improved coronary perfusion often is claimed to be an important factor in the positive effect on LV function, this is still controversial and is probably only important when coronary perfusion is reduced because of stenoses [23]. In previous studies investigating the effect of IABP in RV failure, a positive effect on the total circulatory setting has been observed. Improved RV and LV function secondary to improved coronary perfusion has been suggested as the cause of this positive effect, but this has not been proven [14, 15].
In our investigation, animals in the IABP group had a higher average right coronary flow, but this did not reach the 5% statistical significance level (p = 0.078). However, IABP did significantly improve the pressure in the aortic root and thus coronary perfusion pressure. Therefore, we believe that there may be a positive effect of IABP on coronary flow, particularly in this model with obstructed coronary perfusion as a result of microembolization.
We evaluated RV and LV function by several indices derived from PV analysis. Although IABP-treated animals displayed a slightly improved maximum rate of increase of LV pressure, an increase in LV contractile function was not evident from analysis of the more load-insensitive index preload recruitable SW. Importantly, RV contractile function was not altered at all by IABP treatment. All indices describing both systolic and diastolic RV function were unaltered by IABP. This indicated that improved coronary perfusion or not, alteration in ventricular function is not the cause of the improved hemodynamics observed in IABP-treated animals.
After microembolization, the reduction in RV systolic and diastolic function was paralleled by an increase in RV afterload measured by PAE and PVR. After randomization, the ventriculoarterial mismatch continued to increase in control animals. However, in IABP-treated animals, we observed a reversion of PAE and PVR toward normal. This was paralleled by an increased stroke volume and output from the RV. The LV volume analysis showed that filling of the LV was increased, and CO was augmented. Although LV afterload measured by systemic arterial elastance also was reduced in IABP-treated animals, this isolated effect would not be adequate to improve hemodynamics if LV filling was not improved.
The main contributor to the positive effect of IABP thus seems to be improved RV emptying secondary to decreased RV afterload, again leading to improved LV filling and output. The mechanism behind this reduction of PAE and PVR by IABP could be purely mechanical, ie, related to PV effects in the pulmonary circulation secondary to the IABP effects on the left side of the circulation. Previous studies have indicated that IABP may provide a slight reduction in LV end-diastolic volume and end-diastolic pressure [24]. However, in our study IABP led to increased end-diastolic volume whereas end-diastolic pressure was unaltered, implying improved LV diastolic compliance in IABP-treated animals. Nevertheless, because LV end-diastolic pressure was unaffected, it is difficult to envision altered LV preload as a background for reduced RV afterload. In theory, the changes could also be mediated by alterations in vasoactive substances in the pulmonary circulation. However, a similar although less pronounced finding was observed as a hyperacute effect when performing file sampling while simultaneously turning the IABP on and off. Owing to the hyperacute nature of these measurements, the reduced afterload is probably related to pure PV alterations affecting pulmonary afterload. Nevertheless, inasmuch as assessments of vasoactive substances (eg, by receptor inhibition) were not performed in this study, it is too early to definitely establish the mechanism behind this effect. This is indeed puzzling and clearly warrants further studies of the mechanical and biochemical alterations occurring in the pulmonary vascular bed during IABP.
Limitations of the Study
Results from a study using right coronary microembolization in open-chest pigs cannot readily be extrapolated to the clinical setting of acute ischemic RV failure in humans. However, microembolization is receiving increasing attention as an entity in acute coronary syndromes and in heart failure after coronary interventions [25]. In closed-chest humans, PV relationships may be different, with different responses to IABP. Also, in clinical settings, RV failure often occurs together with LV failure. However, the effect of IABP in cardiogenic shock dominated by LV failure has already been proven. In a mixed RV-LV failure, the positive impact of IABP would be even more pronounced than reported by us for an isolated RV failure. Investigating the effect of IABP in pure RV failure therefore demonstrates the least effect that can be expected in cardiogenic shock with a component of RV failure. The main limitation of the study is that from the present data we have not been able to decipher the exact mechanism by which the IABP reduces PVR and PAE and thereby increases RV performance.
Conclusions
We conclude that IABP is an effective treatment option in acute cardiogenic shock caused by RV failure. The mechanism behind this positive effect of IABP seems to be reduction of RV afterload, with subsequently improved coupling between the ventricle and arterial system, resulting in improved RV output and efficiency.
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Acknowledgments
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This study was supported with a grant from the Norwegian Research Council and the Norwegian Council of Cardiovascular Diseases. We are indebted to the skillful technical assistance of Hanne Maehre, Jon K. Jensen, Hege Hagerup, Ellinor Hareide, and Ernst-Rolf Albrigtsen.
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Abstract
Introduction
