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Anesth Analg 2003;96:1274-1279
© 2003 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

The Effect of Pericardial Restraint, Atrial Pacing, and Increased Heart Rate on Left Ventricular Systolic and Diastolic Function in Patients Undergoing Cardiac Surgery

Colin F. Royse, MBBS MD, FANZCA*,{dagger}, Alistair G. Royse, MBBS MD, FRACS*,{ddagger}, Christina T. Wong*, and Paul F. Soeding, MBBS FANZCA{dagger}

*Department of Pharmacology, University of Melbourne; and Departments of {dagger}Anaesthesia and Pain Management and {ddagger}Cardiothoracic Surgery, The Royal Melbourne Hospital, Australia

Address correspondence and reprint requests to Colin Royse, MD, PO Box 1022, Research, Victoria, Australia, 3095. Address e-mail to Colin.Royse{at}mh.org.au


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Baseline measurements of systolic and diastolic function performed after the induction of anesthesia may be compared with subsequent measurements acquired under different physical conditions such as open pericardium and different heart rate or rhythm. We acquired data from 21 patients undergoing coronary artery surgery. Combined echocardiographic and pulmonary artery catheter measurements were performed before and after pericardial opening, atrial pacing at the native rate, and atrial pacing 30 bpm faster. Indices of systolic function included fractional area change, afterload corrected fractional area change, and myocardial performance index; diastolic function included mitral inflow and pulmonary vein Doppler profiles, color M-Mode Doppler flow propagation velocity, instantaneous end-diastolic stiffness, and isovolumetric relaxation time. Hemodynamic indices included cardiac index, mean arterial, right atrial, and pulmonary capillary wedge pressures, and systemic vascular resistance index. There were no changes in measurements after opening of the pericardium or with institution of atrial pacing. With increased heart rate, there were no changes in systolic function, but instantaneous end-diastolic stiffness increased. Propagation velocity showed a paradoxical improvement with increased heart rate opposite to other trends. Beat fusion occurs with increasing heart rate for mitral inflow Doppler. We recommend that serial measurements are performed at a similar heart rate.

IMPLICATIONS: Pericardial restraint or the institution of atrial pacing do not alter left ventricular function, as assessed by pulmonary artery catheter and transesophageal echocardiography measurements. Diastolic (but not systolic) measurements showed inconsistency with increased heart rate.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Assessment of left ventricular systolic and diastolic function is important in the management of patients during cardiac surgery. Current clinical measurements of systolic function include ejection phase indices of volume change such as cardiac index and ejection fraction. Diastolic function is frequently assessed using Doppler measurements of mitral and pulmonary venous inflow (1). Baseline measurements are frequently acquired during harvesting of the internal mammary artery, which usually represents a stable phase of the anesthetic. However, measurements performed after cardiopulmonary bypass are often made with different physical conditions, such as with an open pericardium, with different rhythm, such as atrial pacing, and often at increased heart rate (HR). Such conditions could independently alter left ventricular function or lead to artifact in the measurements themselves.

Although load-independent measurements derived from pressure-volume loops overcome these limitations (2), they are highly invasive and consequently are unsuitable for routine clinical use. Measurements such as Color M-Mode Doppler flow propagation velocity (Vp) (3), tissue Doppler diastolic velocities (4), myocardial performance index (5), preload-adjusted maximal power (6), and measurements reported from our research group—afterload-corrected fractional area change (FACac) (7) and instantaneous end-diastolic stiffness (IEDS) (8)—are examples of measurements demonstrated to be less sensitive to changes in loading conditions.

Our aim was to assess the effect of pericardial restraint, atrial pacing, and increased HR on left ventricular function in patients undergoing coronary artery bypass graft (CABG) surgery, with the hypothesis that these conditions do not alter function.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
After approval from the Royal Melbourne Hospital Human Ethics Committee, written informed consent was obtained from 24 patients undergoing CABG. All patients were monitored with a pulmonary artery catheter (834HF75, Baxter Healthcare Corporation, Irvine, CA) and indwelling radial artery catheter. Transesophageal echocardiography was performed using a multiplane transducer (Omniplane II transducer, Sonos 2500 or 5500 machine, Phillips Medical Systems, Andover, MA). In general, the highest frequency was used for near-field structures and lower frequencies for transgastric imaging. The probe for the Sonos 5500 allowed fusion frequencies, whereas only 5 or 6.2 MHz was available for the Sonos 2500 machines. Patients were excluded if there was more than mild aortic or mitral valve regurgitation, atrial fibrillation, or concomitant valve surgery.

Measurements were performed during left internal mammary artery harvesting with patients in sinus rhythm. The pre- and postpericardiectomy measurements were added to the trial after the first five patients, and hence, only 16 complete data sets were available for that aspect of the study. The load interventions were:

  1. Patient at level position with chest open but intact pericardium
  2. As above but with pericardium open
  3. As above but with atrial triggered pacing applied at just above the normal rate to allow atrial capture
  4. Atrial pacing but with the atrial rate 30 bpm faster

The first two measurements occurred before harvesting of the internal mammary artery. Atrial pacing wires were attached after opening the pericardium, and the last two measurements were performed during harvest of the internal mammary artery.

At each intervention, hemodynamic and echocardiography measurements were acquired and stored for offline analysis. Measurements from three consecutive cardiac cycles were analyzed by two independent observers and averaged. Blinding of transesophageal echocardiography data was partial because the hemodynamic data were recorded on the data sheet of one observer but not the other.

The following hemodynamic variables were recorded: mean arterial blood pressure (MAP; mm Hg), right atrial pressure (RAP; mm Hg), pulmonary capillary wedge pressure (PCWP; mm Hg), and HR (bpm). Thermodilution cardiac output, using 10 mL of room temperature 5% dextrose solution as the injectant, was performed in triplicate and indexed to body surface area (cardiac index [CI], L · min-1 · m2). For curves exceeding 10% difference, further measurements were made and the extremes excluded (9).

Echocardiography measurements were as follows:

  1. Color M-mode Doppler of left ventricular inflow Vp (cm/s) was obtained from the midesophageal four-chamber view by measuring the slope of the first aliasing velocity from the mitral leaflet tips to a position 4 cm into the left ventricle (4). The Nyquist limit was set to 40 cm/s and only reduced if there was absence of aliasing at this limit.
  2. Mitral inflow Doppler spectral display was obtained from the midesophageal four-chamber view with the pulsed wave Doppler sample volume placed at the apposition of the mitral leaflet tips (4,5). Measurements included peak early diastolic velocity (E; cm/s), peak late diastolic velocity or atrial contraction velocity (A; cm/s), deceleration time of the E wave (DT; ms), and duration of the A wave (M-duration; ms).
  3. Pulmonary vein Doppler spectral display was obtained with the pulsed wave Doppler sample volume positioned within the left upper pulmonary vein (where imaging was unobtainable, the right upper pulmonary vein was used) and the duration of the atrial reversal wave (P-duration; ms) measured.
  4. A cine loop of the transgastric midpapillary short axis view was obtained to determine left-ventricular end-diastolic area (EDA; cm2) and end-systolic area (ESA; cm2). The blood pool area was measured by direct planimetry (10). EDA was identified at the electrocardiograph R-wave peak and ESA at the end of the T wave (10).
  5. Continuous-wave Doppler was performed from the transgastric long-axis view to include mitral valve inflow, left ventricular outflow tract, and the aortic root. The isovolumetric contraction time (IVCT; ms), isovolumetric relaxation time (IVRT; ms), and ejection time (ET; ms) of left ventricular outflow were obtained from spectral tracings (5).

The following indices of systolic and diastolic left ventricular function were derived from data acquired above:

Systolic indices:

  1. FAC = (EDA - ESA)/EDA (7)
  2. FACac = FAC x log10([MAP - RAP]/CI) x 100 (mm Hg · L-1 · min-1 · m2) (7)
  3. Myocardial performance index = (IVCT + IVRT)/ET (5)

Diastolic indices:

  1. IEDS = 100 x (log10PCWP)/EDA (mm Hg/cm2) (8)
  2. E/A ratio of peak E and peak A velocities.
  3. P-M duration (ms) is the difference between P duration and M duration.

Patients were anesthetized with a combined regional and general anesthetic technique. An epidural catheter was inserted before surgery at T2-3 or T1-2 spinal levels. Eight to 10 mL of 0.5% ropivacaine was administered before the induction of anesthesia. Thereafter, ropivacaine 0.2% with morphine 0.02 mg/mL of morphine was infused at a rate of 5–10 mL/h and removed on the morning of the second postoperative day. General anesthesia consisted of midazolam 0.05–1 mg/kg, fentanyl 3 µg/kg, and a target-controlled infusion of propofol set for a blood concentration of 2 µg/mL (Diprifusor algorithm, AstraZeneca, North Ryde, Australia) and ceased after the last skin suture. The effects on ventricular function and hemodynamic indices has been extensively examined in a randomized, controlled trial comparing the epidural technique with a combined propofol and alfentanil anesthetic regimen (11). In brief, there were no differences in intraoperative hemodynamic or echocardiographic measurements between the two techniques with the exception of lower MAP with use of an epidural anesthetic technique. Our patient population has a frequent incidence of hypertension and diabetes, and most patients are on a combination of ß1-adrenoceptor blocking drugs and angiotensin converting enzyme inhibitors. Our practice is to continue the ß-blockers up to the time of surgery but to cease the angiotensin converting enzyme inhibitors the day before surgery.

The effects of pericardial restraint, atrial pacing, and increased HR were assessed with paired-samples t-test. Analyses were corrected for multiple hypotheses within families of end-points using the Ryan-Holm Bonferroni stepdown procedure (P') (12). Hemodynamic indices (six analyses), systolic function (three analyses), and diastolic function (four analyses) constituted the families of end-points. Raw P values are presented, and when P < 0.05, the corrected values (P') are displayed. Significance was defined as P' < 0.05. All values are expressed as mean ± SE of the mean (SEM). The statistical analyses were performed using SPSS for Windows version 11.0.0 (SPSS Inc, Chicago, IL).


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Hemodynamic instability after the induction of anesthesia lead to cancellation of the study protocol in three patients. There were 18 men and 3 women who completed the protocol, with a mean age of 64.7 ± 8.1 yr. There was a wide range of baseline systolic function, with FAC <30% in 14%, FAC 30%–40% in 19%, FAC 40%–50% in 10%, and FAC >50% in 57%. Baseline Vp data identified abnormality (Vp < 45 cm/s) in 53%. Baseline CI was <2.5 L · min-1 · m2 in 33%, and PCWP was >15 mm Hg in 38%. There were no significant changes to hemodynamic or left ventricular systolic and diastolic function after opening of the pericardium (Table 1).


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  		Table 1. The Effect of Pericardial Restraint on Left Ventricular Function
 
The institution of atrial pacing did not require a significantly increased HR for atrial capture to occur. There were no differences in any measurements of function with atrial pacing (Table 2). There was a small reduction in systemic vascular resistance index, which did not remain significant after correction for multiple hypothesis correction.


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  		Table 2. The Effect of Atrial Pacing on Left Ventricular Function
 
There were no changes in systolic function or with hemodynamic indices with increased HR (Table 3). MAP and EDA decreased, but changes became nonsignificant with multiple hypothesis correction. IEDS increased (increased left ventricular stiffness, suggestive of worsened function) significantly. Vp also increased significantly (suggestive of improved diastolic function). Analysis of the E/A, DT, and P-M duration was suggestive of impaired diastolic function. The E/A ratio and DT could not be determined if there was fusion of the E and A waves into a single wave. The incidence of this beat fusion increased with HR. Nonfused beats adequate for E/A analysis were obtainable in 100% of patients with HR <=59 bpm, 96.4% with HR 60–69 bpm, 85.2% with HR 70–79 bpm, 63.6% with HR 80–89 bpm, 12.5% with HR 90–99 bpm, and 0% with HR >=100 bpm.


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  		Table 3. The Effect of Increased Heart Rate on Left Ventricular Function
 
Interobserver differences for each echocardiography measurement performed after opening of the pericardium are shown in Table 4. The differences between observers were small, and none remained significant after correction for multiple hypotheses.


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  		Table 4. Interobserver Differences in Echocardiography Measurements
 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Our study shows that left ventricular systolic and diastolic function is not affected by pericardial restraint or the institution of atrial pacing in open chest patients undergoing cardiac surgery. With increased HR, important differences were identified in indices of diastolic function. Mitral inflow Doppler assessment of diastolic function suggested worsened diastolic function (reduced E/A ratio). IEDS suggested increased stiffness with increased HR; DT shortened, and the P-M duration decreased. All were suggestive of impaired diastolic function. However, the change in Vp suggested improvement. Because all our patients were undergoing CABG, one could expect worsened diastolic function if the ventricle became ischemic secondary to increased HR. This inconsistency in the direction of change of Vp may reflect a normal adaptation of ventricular filling to increased HR, rather than reflecting the actual state of diastolic function. The effect of increased HR may be a limitation in the use of Vp as a measurement of diastolic function.

The introduction of echocardiography has allowed sophisticated assessment of both systolic and diastolic function. In critically ill or anesthetized patients, there has been a transition from pressure-based assessment of function using pulmonary artery catheters to echocardiography-based evaluation of function, with the former being used as complementary technology to monitor trends in cardiovascular function. Echocardiography has the appeal of being relatively noninvasive, but many of the measurements are either qualitative rather than quantitative or sensitive to changes in loading conditions. For serial assessment of ventricular function, it is important to know whether changes in physical conditions can affect the measurements independent of changes in cardiac function.

Increased HR is a limiting factor in the assessment of diastolic function. Traditional assessment of function requires analysis of both mitral inflow and pulmonary venous Doppler profiles to produce a qualitative stage of function (1). Our data show that the incidence of fusion of the E and A waves increases in an exponential fashion with HR faster than 70 bpm, and with HR faster than 100 bpm, all beats were fused. Newer methods of diastolic function such as Vp or tissue Doppler (4) offer methods that may be less load-sensitive and more quantitative than mitral inflow Doppler assessment. Garcia et al. (13) found Vp to be load insensitive in animal and human models and found that Vp correlated well with the time relaxation constant. Brun et al. (3) found that flow Vp varies inversely with rate of ventricular relaxation. If ventricular relaxation is prolonged because of ischemia, the Vp should decrease. It is possible that Vp is sensitive to alteration in HR, and we recommend that it is only used for serial measurement of diastolic function if the HR are similar for each measurement period.

Measurement of diastolic function is complex because of both energy requiring and passive phases, which cannot be measured by a single index. It is likely that separate measurements of relaxation and passive filling are required to fully determine left ventricular diastolic properties. In our study, we have measured indices of early relaxation (IVRT) and end-diastole (IEDS) in addition to conventional mitral inflow Doppler variables, to better delineate aberrations of diastolic function. IEDS worsened with increased HR, consistent with reduced filling time at the same filing pressure (PCWP). If stiffness is constant, then a reduced PCWP would occur at faster HR. It is possible that myocardial ischemia was induced with this maneuver in a population with known ischemic heart disease. However, there were no changes in any measurements of systolic function with any of the interventions.

Our study is limited by the absence of load-independent reference measurements, such as those derived from pressure volume loops. However, the hemodynamic state was relatively stable during the study period, and if changes in function did occur that were missed by our measurement technology, then they were likely to be small and clinically unimportant. The time taken to acquire the measurements after each intervention was small (several minutes), but it is possible that changes in hemodynamic state or in left ventricular function could have occurred during that time. We included patients with a wide variation in systolic and diastolic function, which reduced the homogeneity of the sample, with nearly half of the study group being classed as abnormal. However, it is possible that the effect of pericardial restraint may be considerable in patients with severely dilated cardiomyopathy. The interventions did not produce a global change in hemodynamic conditions, but subtle changes in diastolic function may not be detected by pressure or thermodilution based monitoring.

Pericardial incision and atrial pacing does not alter left ventricular function in anesthetized patients undergoing cardiac surgery. With increased HR, mitral inflow Doppler is frequently uninterpretable because of fusion of the E and A waves. Color M-Mode flow Vp may be sensitive to changes in HR. We recommend that serial measurement of left ventricular function should preferably be conducted at a HR less than 70 bpm.


   Acknowledgments
 
Supported, in part, by educational grants from the Windermere Foundation, Perpetual Foundation (Arnott grant), and the Australian Society of Anesthetists.

The authors thank Dr John Ludbrook (Biomedical Statistical Consulting Service Pty. Ltd) for statistical advice and for reviewing the manuscript. We thank Karen Groves for her assistance in manuscript preparation and data management.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Rakowski H, Appleton C, Chan KL, et al. Can consensus recommendations for the measurement and reporting of diastolic dysfunction by echocardiography: from the Investigators of Consensus on Diastolic Dysfunction by Echocardiography. J Am Soc Echocardiogr 1996; 9: 736–60.[Medline]
  2. Sagawa K. The end-systolic pressure-volume relation of the ventricle: definition, modifications and clinical use. Circulation 1981; 63: 1223–7.[Free Full Text]
  3. Brun P, Tribouilloy C, Duval AM, et al. Left ventricular flow propagation during early filling is related to wall relaxation: a color M-mode Doppler analysis. J Am Coll Cardiol 1992; 20: 420–32.[Abstract]
  4. Garcia MJ, Thomas JD, Klein AL. New Doppler echocardiographic applications for the study of diastolic function. J Am Coll Cardiol 1998; 32: 865–75.[Abstract/Free Full Text]
  5. Tei C, Nishimura RA, Seward JB, Tajik AJ. Noninvasive Doppler-derived myocardial performance index: correlation with simultaneous measurements of cardiac catheterization measurements. J Am Soc Echocardiogr 1997; 10: 169–78.[Web of Science][Medline]
  6. Mandarino WA, Pinsky MR, Gorcsan J 3rd. Assessment of left ventricular contractile state by preload-adjusted maximal power using echocardiographic automated border detection. J Am Coll Cardiol 1998; 31: 861–8.[Abstract/Free Full Text]
  7. Royse CF, Royse AG. Afterload corrected fractional area change (FACac): a simple, relatively load independent measurement of left ventricular contractility in humans. Ann Thorac Cardiovasc Surg 2000; 6: 345–50.[Medline]
  8. Royse CF, Royse AG, Blake DW, Grigg LE. Instantaneous end diastolic stiffness (IEDS): a simple, load independent measurement of left ventricular diastolic function in patients undergoing cardiac surgery. Ann Thorac Cardiovasc Surg 2000; 6: 203–10.[Medline]
  9. Royse CF, Royse AG, Blake DW, Grigg LE. Measurement of cardiac output by transesophageal echocardiography: a comparison of two Doppler methods with thermodilution. Anaesth Intensive Care 1999; 27: 586–90.[Web of Science][Medline]
  10. Royse CF, Barrington MJ, Royse AG. Transesophageal echocardiography values for left ventricular end-diastolic area and pulmonary vein and mitral inflow Doppler velocities in patients undergoing coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth 2000; 14: 130–2.[Web of Science][Medline]
  11. Royse CF, Royse AG, Soeding P, et al. Prospective randomized trial of high thoracic epidural analgesia for coronary artery bypass surgery. Ann Thorac Surg 2003; 75: 93–100.[Abstract/Free Full Text]
  12. Ludbrook J. Multiple comparisons procedures updated. Clin Exp Pharmacol Physiol 1998; 25: 1032–7.[Web of Science][Medline]
  13. Garcia MJ, Smedira NG, Greenberg NL, et al. Color M-mode Doppler flow propagation velocity is a preload insensitive index of left ventricular relaxation: animal and human validation. J Am Coll Cardiol 2000; 35: 201–8.[Abstract/Free Full Text]
Accepted for publication December 19, 2002.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2003 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press