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European Journal of Heart Failure 2008 10(5):467-474; doi:10.1016/j.ejheart.2008.03.012
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© 2008 European Society of Cardiology

Haemodynamics and left ventricular function in heart failure patients: Comparison of awake versus intra-operative conditions

Ellen A. ten Brinkea, Robert J. Klautzb, Sven A. Tulnera, Frank H. Engbersc, Harriette F. Verweya, Douwe E. Atsmaa, Martin J. Schalija, Ernst E. van der Walla, Jeroen J. Baxa, Hein Putterd, Robert A. Dionb and Paul Steendijka,*

a Department of Cardiology of the Leiden University Medical Center The Netherlands
b Department of Cardiothoracic Surgery of the Leiden University Medical Center The Netherlands
c Department of Anesthesiology of the Leiden University Medical Center The Netherlands
d Department of Medical Statistics of the Leiden University Medical Center The Netherlands

* Corresponding author. Department of Cardiology, Leiden University Medical Center, PObox 9600, 2300RC, Leiden, The Netherlands. Tel.: +31 71 526.2020; fax: +31 71 526.6809. E-mail addresses: p.steendijk{at}lumc.nl (P. Steendijk).


   Abstract
Top
 Abstract
1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 
Background: Heart failure patients are increasingly subjected to surgery. Left ventricular (LV) function is generally assessed in awake patients, but intra-operative LV function is not well studied.

Aim: To investigate the relation between LV function indices obtained in the catheterization laboratory and those obtained intra-operatively.

Methods: We enrolled 11 patients with heart failure (NYHA III–IV) scheduled for surgical interventions. LV function was assessed by pressure–volume loops (conductance catheter) during diagnostic catheterizations and intra-operatively under anaesthetized conditions.

Results: Compared to awake conditions, cardiac output was unchanged intra-operatively but ejection fraction was significantly reduced (–16%) due to increased end-diastolic volume (+13%). Systolic and diastolic LV pressure and afterload (EA) dropped significantly (–32%, –22%, –35%, respectively). LV systolic function assessed by dP/dtMAX and the end-systolic pressure–volume relation (EES) was significantly reduced (–34%, –35%). LV diastolic stiffness was reduced (–44%). Ventricular–arterial coupling (EA/EES) was maintained.

Conclusion: Intra-operative cardiac output was unchanged compared to awake conditions due to a balance between reduced systolic and improved diastolic function. Ventricular–arterial coupling was maintained by a reduced afterload. Presumably, systolic function and afterload were reduced by anaesthesia, whereas diastolic function improved after pericardectomy. These findings provide insight into the combined effects of anaesthesia, thoracotomy and pericardectomy, and help to interpret LV function measurements in intra-operative conditions.

Key Words: Heart failure • Haemodynamics • Left ventricular function • Pressure–volume relations • Intra-operative conditions

Received September 27, 2007; Revised February 27, 2008; Accepted March 27, 2008


   1. Introduction
Top
 Abstract
 1. Introduction
2. Methods
 3. Results
 4. Discussion
 References
 
Chronic heart failure is one of the major healthcare problems in the Western world. Despite optimal medical treatment, the 1- and 5-year survival rates for heart failure patients with NYHA III-IV are about 70% and 45%, respectively [1,2]. Heart transplantation remains the most effective surgical therapy, with a 1- and 5-year survival of approximately 90% and 75%, but it is hindered by donor shortage and its limited applicability [3]. Given the limitations of medical therapy and heart transplantation, several alternative surgical therapies for end-stage heart failure have been adopted recently, such as surgical ventricular restoration (SVR) by means of an endoventricular circular patch plasty (Dor procedure) and restrictive mitral annuloplasty (RMA) [4,5].

Selection of patients eligible for heart failure surgery importantly depends on baseline haemodynamics and left ventricular (LV) function. These assessments are typically obtained during diagnostic procedures in awake patients and, by definition, are not indicative of haemodynamics and LV function during surgery. In this study, we therefore compared haemodynamics and LV function indices obtained in the catheterization laboratory in the awake patient with those obtained in the operating room under anaesthetized, open-chest, open-pericardium conditions, just before the start of cardiopulmonary bypass.

The main aim of the study was to determine the effect of these intra-operative conditions on haemodynamics and LV function in heart failure patients. This should help to improve the interpretation of intra-operative LV function measurements and, ultimately, could be relevant for operative risk assessment and for future optimization of anaesthetic/operative procedures in these high-risk patients.

Haemodynamics and cardiac performance are dependent on intrinsic myocardial function, loading conditions and chronotropy which all may change substantially in the anaesthetized, open-chest, open-pericardium condition. Therefore we assessed LV function at multiple fixed (paced) heart rates by pressure-volume loop analysis using the conductance catheter methodology. The advantage of this approach is the ability to derive relative load-independent indices which directly reflect intrinsic myocardial function.


   2. Methods
Top
 Abstract
 1. Introduction
 2. Methods
3. Results
 4. Discussion
 References
 
The study protocol was approved by our local Ethics Committee, and all patients gave written informed consent.

2.1. Patients
The study group consisted of 11 patients with NYHA class III-IV heart failure despite optimal medical treatment, who were scheduled for RMA and/or SVR. In accordance with the heart failure program at our institution, all patients with ischaemic or non-ischaemic dilated cardiomyopathy and persistent NYHA class III-IV despite optimal medical treatment are routinely considered for surgical treatment. Heart failure patients with a large anteroseptal aneurysm are indicated for SVR, whereas moderate to severe mitral regurgitation is considered an indication for RMA. Additional coronary artery bypass grafting (CABG) is performed when indicated. Heart failure symptoms were assessed using the NYHA classification. Quality of Life score was determined using the Minnesota Living with Heart Failure questionnaire with the highest score reflecting the worst quality of life [6]. Exercise tolerance was evaluated using the 6-minute hall-walk tests. The severity of mitral regurgitation was graded semi-quantitatively from colour-flow Doppler in the conventional parasternal long-axis and apical 4-chamber images (Table 1).


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  		Table 1 Baseline patient characteristics, medication, and surgical interventions

 
In all patients, complete pressure-volume data (see below) were acquired in awake conditions in the catheterization laboratory. The second set of measurements was obtained during anaesthesia in the operating room directly after median sternotomy and opening of the pericardium, before start of cardiopulmonary bypass and cardiac surgery (intra-operative condition). All patients subsequently underwent normothermic heart operations as scheduled with intermittent antegrade warm, oxygenated blood cardioplegia.

2.2. Anaesthesia
Baseline measurements were obtained in awake patients during diagnostic catheterization under local anaesthesia only. Patients received 5 mg diazepam as pre-medication. The patients were scheduled for the surgical procedure which was performed on average 1 month later.

Two hours prior to surgery the patients received 2 mg of lorazepam as sublingual pre-medication. Subsequently, all patients received total intravenous anaesthesia with target-controlled infusion of propofol, remifentanil and sufentanil. Hypnotic state was monitored with a Bispectral Index Monitor (Aspect Medical Systems, Newton, Mass). A single dose of pancuronium bromide (0.1 mg/kg) was given to facilitate intubation. During the operation, the propofol concentration was adjusted between 1.5 and 2.0 µg/mL to maintain a Bispectral Index value of less than 60. Remifentanil was titrated between 5 and 10 ng/mL in response tot the patient's haemodynamic reaction to surgical stimuli. Sufentanil was initiated at a targeted concentration of 0.1 ng/mL after the start of the operation to allow smooth transition of the patient's analgesic state from the operating room to the intensive care unit (ICU). All patients were ventilated with an oxygen/air mixture (fraction of inspired oxygen, 40%) at a ventilation rate of 12-15 breaths/min, and tidal volume was adjusted to maintain PaCO2 between 4.5 and 5.5 kPa (34-41 mmHg). In the pre-bypass condition we aimed to limit the volume load to avoid unnecessary haemodilution. Typically a loading dose of 500 mL hydroxyethyl starch solution (Voluven) was used followed by saline drip to maintain adequate pressures. No additional inotropes or vasoconstrictors were used pre-bypass. We anticipated that some patients would need inotropic support. Therefore, to avoid bias we decided to provide the same (low dose) support in all patients. Inotropic support was started directly after induction of anaesthesia, with a low loading dose of 0.25 mg/kg enoximone in 10 min, and thereafter we provided continuous infusion at a rate of 0.50 µg.kg–1.min–1 which was maintained during the whole operation.

2.3. Instrumentation
Pressure-volume loops were obtained using a 7 F integrated pressure-conductance catheter (CD-Leycom, Zoetermeer, The Netherlands) incorporating a solid-state pressure sensor and 12 electrodes with an interelectrode spacing of 10 mm. A pigtail facilitated placement through the aortic valve and positioning within the LV apex. The catheter was connected to a Leycom Cardiac Function Lab signal processor (CD-Leycom). The conductance signals were calibrated by thermodilution and hypertonic saline dilution as previously described [7]. During measurements in the catheterization laboratory (awake condition), the conductance catheter was placed in the LV via the femoral artery. Further instrumentation included placement of a Swan-Ganz thermodilution catheter and a temporary pacing lead positioned in the right atrium, introduced via the femoral veins. In the operating room (intra-operative condition), the conductance catheter was introduced via a sheath in the ascending aorta [7], a thermal filament catheter was placed with its tip in the pulmonary artery via the right internal jugular vein for semi continuous thermodilution cardiac output measurements (Edwards Life Sciences, Uden, The Netherlands), and epicardial pacing wires were placed on the right atrium. A multiplane TEE probe was inserted to monitor cardiac function and facilitate positioning of the conductance catheter intra-operatively. Positioning was aimed at locating the pigtail in the apex and locating the most proximal electrodes just above the aortic valve.

2.4. Study protocol
The study protocols during catheterization and during surgery involved measurements at paced heart rates of 80, 100 and 120 bpm. Pressure-volume loops were acquired consecutively, approximately 60 s after switching to a higher rate. Steady-state periods of at least 10 s were selected for offline analysis.

2.5. Pressure-volume analysis
Cardiac function and haemodynamics were derived from steady-state pressure-volume loops at each pacing rate. LV function was quantified by cardiac output and stroke volume, end-diastolic and end-systolic volume, LV ejection fraction, end-systolic and end-diastolic pressure, and maximal and minimal rate of LV pressure change (dP/dtMAX, –dP/dtMIN). Furthermore, the time constant of relaxation (Tau) was determined with phase-plot analysis and stroke work was calculated as the area of the pressure-volume loop. Effective arterial elastance (EA) was calculated as end-systolic pressure divided by stroke volume. The end-systolic pressure-volume relationship (ESPVR) and the end-diastolic pressure-volume relationship (EDPVR) were determined by single-beat analysis as described in more detail below. The ESPVR was represented by its slope, end-systolic elastance (EES), and its position at a fixed pressure level of 100 mmHg (ESV100) [8]. The EDPVR was quantified by its slope EED. In addition we determined the stiffness constant KED using an exponential curve fit: EDP=CED.exp(KED.EDV).

2.6. Single-beat analysis
The ESPVR was determined by single-beat analysis using a modification of the method originally described by Takeuchi et al. [9]. Briefly, peak systolic LV pressure for an isovolumic (non-ejecting) contraction (PISO) at the existing end-diastolic volume was estimated by fitting a 5th-order polynomial to the pressure curve, excluding all data points between the moments of maximal and minimal dP/dt. The calculated ‘isovolumic’ pressure-volume point was connected with the actual end-systolic pressure-volume point to define the ESPVR as illustrated in Fig. 1. The EDPVR was derived from a fit to the filling phase trajectory of the pressure-volume loop including all data points between the moments of minimal pressure and maximal volume (see Fig. 1).


Figure 01
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  		Fig. 1 Single-beat estimation of the end-systolic and end-diastolic pressure-volume relationships (ESPVR and EDPVR). PISO is the estimated peak isovolumic LV pressure.

 
2.7. Statistical analysis
We used a linear mixed-effects model to account for multiple and repeated measurements on each patient. In this model, patients were included as random effects and conditions (awake, intra-operative), pacing (80, 100 and 120 bpm), and their interaction as fixed effects. Data are presented as mean±SD. A probability value <0.05 was considered statistically significant.


   3. Results
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
4. Discussion
 References
 
Eleven heart failure patients (mean age 62±12 years) with complete pressure-volume loop studies were analyzed. Baseline patient characteristics and surgical procedures are shown in Table 1. All patients had moderate to severe heart failure with a mean NYHA class of 3.18±0.40. Four patients were scheduled for RMA, 1 patient for SVR, and 6 patients for a combined RMA-SVR procedure.

Haemodynamics and LV function data in awake and intra-operative conditions are summarized in Table 2. The statistical model tested differences between, condition (awake vs. intra-operative), effect of heart rate (pacing), and the interaction between condition and pacing. If the latter was significant it indicated that the effect of pacing was different between conditions (or that the effect of conditions depended on the pacing rate).


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  		Table 2 Haemodynamics and LV function in awake and intra-operative conditions

 
Compared to the awake condition, cardiac output was unchanged intra-operatively. However, systolic function was significantly depressed. This was reflected by a significantly (p<0.006) reduced ejection fraction (at 80 bpm: from 48±17 to 40±14%) and a significantly (p<0.001) reduced dP/dtMAX (1224±292 to 813±157 mmHg/s). Moreover, load-independent systolic function was significantly reduced as indicated by a decreased slope and rightward shift of the ESPVR: EES decreased from 1.09±0.37 mmHg/mL to 0.71±0.28 mmHg/mL (p<0.001) and ESV100 increased from 87±45 to 162±103 mL (p<0.001). Diastolic function, however, was improved which was reflected by a significantly (p=0.011) reduced end-diastolic pressure (EDP: 15.5±7.6 to 12.1±5.9 mmHg) while end-diastolic volume showed a small but significant (p=0.048) increase (EDV: 183±56 to 207±100 mL. This clearly indicated a reduced diastolic stiffness (i.e. improved compliance) as also directly shown by EED which decreased significantly (p=0.007) from 0.16±0.13 to 0.09±0.07 mmHg/mL and by the diastolic stiffness constant KED which decreased from 0.020±0.021 to 0.010±0.008/mL p=0.005). Relaxation time constant Tau remained unchanged when comparing awake to intra-operative conditions.

In addition to these effects on ventricular function, the intra-operative condition was associated with a significant reduction in afterload as quantified by the effective arterial elastance: EA reduced from 2.23±0.72 to 1.45±0.46 mmHg/mL (p=0.002). The combined reduction in systolic function and afterload resulted in a significantly lower systolic pressure: ESP reduced from 124±33 to 84±17 mmHg (p<0.001). The simultaneous decrease in EES and EA resulted in an almost unchanged ventricular-arterial coupling: EES/EA was 2.30±1.14 in the awake condition and 2.21±0.60 intra-operatively.

In the normal heart, increased heart rate improves cardiac output, and systolic and diastolic function. The heart failure patients in our study, however, did not show positive effects of increased heart rate: in the awake condition the increase in cardiac output was limited (4.87±1.18 to 5.84±1.80 L/min) and did not reach statistical significance. Systolic and diastolic indices did not show positive effects of pacing. The interaction effect was not significant for any index, indicating that the intra-operative condition did not alter heart rate dependency.


   4. Discussion
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
References
 
Heart failure patients who are being considered for surgical interventions generally undergo diagnostic procedures which include assessment of haemodynamics and ventricular function. However, how such measurements obtained in the awake patient relate to ventricular function in the anaesthetized, open-chest, open-pericardium condition in the operating room is not well known. In the present study, we assessed LV function by pressure-volume loops in both conditions: our results indicate that compared to the awake condition, the intra-operative condition was associated with a significant reduction in systolic function and afterload, and an improvement in diastolic function, whereas ventricular-arterial coupling and cardiac output were largely maintained. The chronotropic responses in these heart failure patients were very limited and were unaltered intra-operatively. Presumably, the reduced systolic function reflects the negative inotropic effects of the anaesthesia applied during surgery. The finding that not only were ejection fraction and dP/dtMAX decreased, but also that the load-independent indices derived from the ESPVR were depressed, confirms direct negative myocardial effects.

In our study we used total intravenous anaesthesia with target-controlled infusion of propofol, remifentanil and sufentanil. The rationale for the combination of the longer acting opioid sufentanil with the ultra-short acting opioid remifentanil is to allow smooth transition from the operating theatre to the ICU. The selected dose of sufentanil is of a magnitude that will provide basic analgesia (estimated plasma concentration 0.1 ng/ml) while still allowing spontaneous respiration. The major opioid effect intra-operatively is provided by remifentanil, of which the short time of onset allows for precise titration against surgical stimulus. The use of propofol in high-risk patients is debated; however, the effect of propofol on the heart is highly concentration dependent. Target-controlled infusion, as used in the current study allows the patient to be rendered unconscious at very low dose propofol. A long period of experience with this technique exists in our department with good results even with high-risk patients. Thus, although low dose propofol is often considered to be an anaesthetic agent with few or no negative inotropic effects, recent studies have shown reduced LV function by tissue-Doppler markers, suggesting a negative myocardial effect [10]. In contrast, a recent study by Lecomte et al. [11] in isolated rabbit hearts showed that neither remifentanil nor sufentanil induced significant myocardial effects. Very similar findings were reported by Ogletree et al. [12] for failing human heart muscle, indicating that remifentanil does not directly modify either inotropic or lusitropic properties of the myocardium. These results are also consistent with the data on isolated human right atria [13]. Thus, the negative inotropic effects found in our study were most likely mainly due to propofol. Moreover, Kanaya et al. [14] recently reported that the inhibitory effects of propofol are temperature dependent and more pronounced during normothermic conditions, as used in our study, than during hypothermia. With regard to enoximone, we used a low loading dose of 0.25 mg/kg in 10 min, and thereafter we provided continuous infusion at a rate of 0.50 {varepsilon}g/kg/min. Phosphodiesterase III inhibitors are reported to have combined positive inotropic, lusitropic and vasodilator effects [15]. At this relatively low dose, enoximone presumably has only limited effects on systolic function, but by inhibiting the breakdown of cAMP it potentiates the action of adrenergic agents enabling adequate inotropic support at lower catecholamine levels. Although positive lusitropic effects of enoximone have been shown previously, a recent study in surgical patients using a pre-emptive bolus of 0.35 mg/kg, similar to that in our study, failed to show effects on diastolic function, but systemic vascular resistance was significantly decreased by >20% [16]. Thus, in our study the use of enoximone presumably partly explained the reduced afterload, but contributed only slightly to the improved diastolic function. If anything, the observed decrease in systolic function might have been more pronounced in the absence of enoximone. We quantified afterload by the effective arterial elastance EA. This parameter incorporates both steady and pulsatile components of the arterial load, and previous studies have shown that it is very useful to assess arterial load and ventricular-arterial interaction. EA was calculated as LV end-systolic pressure divided by stroke volume, which has been shown to be closely correlated with the values obtained from more complicated Windkessel models [17]. The intra-operative reduction in afterload in the present study is fully in line with the reported vasodilatory effects of all three applied anaesthetic agents (propofol, remifentanil and sufentanil) and that of enoximone. Propofol dilates blood vessels by inducing NO-synthesis, blocking calcium channels, and activating protein kinase C and reduced afterload has been shown in patients with normal and depressed LV function and in numerous experimental studies [18]. Systemic arterial vasodilation has also been reported for both remifentanil [19] and for sufentanil [20].

The ratio of arterial and ventricular elastance EA/EES describes the coupling between the ventricle and the arterial system. Theoretically, the heart delivers maximal stroke work when EA/EES=1, whereas optimal efficiency (stroke work divided by oxygen consumption) is obtained when EA/EES=0.5 [21,22]. In a group of patients with normal LV function, EA/EES was reported to be ~0.7 [23], in line with earlier studies showing a ratio of ~0.5 in patients with ejection fraction >60%, ~1 for patients with slightly depressed ejection fraction (40%-60%) and EA/EES>2 in patients with ejection fraction <40% [24]. In our study, EA/EES was 2.30 in the awake condition which reflects a poor coupling resulting from a relatively low ventricular elastance combined with a relatively high arterial elastance, as would be expected in patients with heart failure. Interestingly, the reduced ventricular elastance during surgery was matched with a simultaneous reduction in arterial elastance, leaving EA/EES almost unaltered. Thus, the intra-operative conditions were not associated with altered ventricular-arterial coupling.

Diastolic function improved significantly in the intra-operative condition. It should be noted that this effect was demonstrated not only by a reduced end-diastolic pressure, but also by a downward shift of the EDPVR and a reduced diastolic stiffness constant and thus the improvement cannot be explained merely by altered loading conditions. We speculate that this effect was due to the pericardectomy. In patients with dilated heart failure the relatively non-distensible pericardium may affect diastolic compliance and hamper filling even in resting conditions and thus pericardectomy may relieve the pericardial constraint and acutely improve diastolic function [25,26]. To our knowledge, our study is the first to directly show this effect with invasive measurements in heart failure patients. Our findings are consistent with previous experimental studies showing a downward shift of the EDPVR and increased diastolic volume and decreased diastolic pressure after pericardectomy in dogs with ischaemic LV dysfunction [26] and in dogs in which pericardial constraint was induced by right ventricular dilatation [27]. Although passive diastolic function was improved, the relaxation time constant Tau was unchanged and –dP/dtMIN was reduced. However, these two parameters reflect the early, active phase of relaxation and, although often referred to as diastolic parameters, they are strongly dependent on systolic function and the preceding ejection [28].

We also tested the effects of increased heart rate on the various indices. In the healthy heart, a frequency increase up to 180 bpm enhances contractility and lusitropy and results in a gradual increase in cardiac output. The molecular basis for the positive force-frequency relation or the Bowditch effect is that the repetitive calcium entry results in an accumulation of cytosolic calcium leading to increased contractile force, while at the same time calcium re-uptake in the sarcoplasmic reticulum is stimulated enabling more rapid relaxation. However, consistent with previous results [29,30], the failing hearts in the present study showed diminished chronotropic responses reflecting exhausted LV functional reserve capacity, which importantly explains the limited functional and exercise capacity of these patients. The pressure-volume loops in Fig. 2 show that stroke volume gradually decreased with incremental heart rates, whereas in the normal heart stroke volume is maintained or even increased at higher heart rates. This effect was due to an increase in end-systolic volume reflecting reduced systolic function consistent with the rightward shift of the ESPVR indicated by ESV100, although the latter effects did not reach statistical significance. Intra-operatively the effects of pacing were very similar as indicated by the lack of any interactive effects.


Figure 02
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  		Fig. 2 Schematic pressure-volume loops (based on mean end-diastolic and end-systolic pressures and volumes) at awake (catheterization laboratory) and intra-operative conditions: Effect of heart rate (pacing).

 
4.1. Study limitations
The number of patients included in the present study was relatively small; however, by comparing two conditions, each patient served as their own control, which greatly improves statistical power. Moreover, we used invasive pressure-volume measurements which are generally regarded as highly accurate and the gold standard for LV function assessments.

We used single-beat approaches to estimate ESPVR and EDPVR rather than multiple beats at different loading conditions. Although load interventions by caval vein balloon occlusions are certainly feasible [31], we decided not to apply this, to avoid an additional venous access in the catheterization laboratory. The current approach also limited the length of our protocol, which included registration of pressure-volume loops at incremental pacing rates in patients with severe heart failure. Previous studies have shown good agreement between single-beat and multiple-beat analysis of pressure-volume relations [9,32]. Furthermore, since we used the same approach in both conditions, we do not expect that this methodology affected our findings.

This study was performed in heart failure patients undergoing cardiac surgery, therefore extrapolation to heart failure patients undergoing non-cardiac surgery should be done with caution because although anaesthetic conditions may be similar, the different surgical conditions may have an effect.

4.2. Conclusion
We compared haemodynamics and LV function in heart failure patients in intra-operative and awake conditions. Cardiac output was unchanged due to a balance between reduced systolic and improved diastolic function, ventricular-arterial coupling was maintained by a reduced effective arterial elastance. Presumably, reduced systolic function and afterload were mainly due to anaesthesia, whereas the improved diastolic function resulted from pericardectomy. Chronotropic responses were limited and not different between conditions. These findings provide insight into the effects of widely used anaesthetic agents and intra-operative conditions on LV function, and help to interpret intra-operative LV function measurements. Ultimately, these findings might be relevant for operative risk assessment and optimization of anaesthetic/operative procedures in high-risk heart failure patients.


   References
Top
 Abstract
 1. Introduction
 2. Methods
 3. Results
 4. Discussion
 References
 

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