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Anesth Analg 2002;94:1421-1426
© 2002 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

Propofol Alters Left Atrial Function Evaluated with Pressure-Volume Relations In Vivo

Franz Kehl, MD, Tobias T. Kress, Boris Mraovic, MD, Douglas A. Hettrick, PhD, Judy R. Kersten, MD, David C. Warltier, MD PhD, and Paul S. Pagel, MD PhD

Departments of Anesthesiology, Medicine (Division of Cardiovascular Diseases), and Pharmacology and Toxicology, Medical College of Wisconsin and the Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee, Wisconsin; and Arrhythmia Management Research, Medtronic, Inc, Minneapolis, Minnesota.

Address all correspondence and reprint requests to Paul S. Pagel, MD, PhD, Medical College of Wisconsin, MEB-M4280, 8701 Watertown Plank Rd, Milwaukee, Wisconsin 53226. Address e-mail to pspagel{at}mcw.edu


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
The effects of IV anesthetics on left atrial (LA) function in vivo are unknown. We tested the hypothesis that propofol alters LA mechanics evaluated with pressure-volume relations in barbiturate-anesthetized dogs (n = 9) instrumented for measurement of aortic, LA, and left ventricular (LV) pressures (micromanometers) and LA volume (epicardial orthogonal sonomicrometers). LA myocardial contractility (Ees) and dynamic chamber stiffness were assessed with end-systolic and end-reservoir pressure-volume relations, respectively. Relaxation was determined from the slope of LA pressure decline after contraction corrected for peak LA pressure. LA stroke work and reservoir function were assessed by A and V loop area, respectively, from the steady-state pressure-volume diagram. LA-LV coupling was determined by the ratio of Ees to LV elastance. Dogs received propofol (5, 10, 20, or 40 mg · kg-1 · h-1) in a random manner, and LA function was determined after a 15-min equilibration at each dose. Propofol decreased heart rate, mean arterial blood pressure, and the maximal rate of increase of LV pressure. Propofol caused dose-related reductions in Ees, dynamic chamber stiffness, and Ees/LV elastance. An increase in V loop area and declines in LA stroke work, emptying fraction, and the active LA contribution to LV filling also occurred. Relaxation was unchanged. The results indicate that propofol depresses LA myocardial contractility, reduces dynamic chamber stiffness, maintains reservoir function, and impairs LA-LV coupling but does not alter LA relaxation in vivo.

IMPLICATIONS: Propofol depresses contractile function of left atrial (LA) myocardium, impairs mechanical matching between the LA and the left ventricular (LV), and reduces the active LA contribution to LV filling in vivo. Compensatory decreases in chamber stiffness contribute to relative maintenance of LA reservoir function during the administration of propofol.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
The effects of propofol on systemic hemodynamics (1,2), left ventricular (LV) systolic (3) and diastolic (4) function, LV-arterial coupling (5), and afterload mechanics (6) have been previously described, but the actions of this IV anesthetic on left atrial (LA) function in vivo are unknown. The LA serves as a contractile chamber, a reservoir for pulmonary venous blood during LV contraction and relaxation when the mitral valve is closed, and a conduit that passively transfers its contents to the LV during rapid filling and diastasis. These actions play a critical role in determining stroke volume and cardiac output. Depression of LA function by IV anesthetics such as propofol may represent an important mechanism by which these anesthetics affect cardiovascular performance. Propofol may produce direct negative inotropic effects in LA myocardium in vitro (7,8), but the actions of this anesthetic on LA contractility in vivo have not been quantified using heart rate- and load-independent indices of contractile state. The effects of propofol on LA relaxation, LA dynamic chamber stiffness, LA reservoir function, and the mechanical coupling between the LA and LV are also unknown. Thus, we examined the actions of propofol on LA function using invasively derived pressure-volume relations in barbiturate-anesthetized dogs. We tested the hypothesis that propofol alters active and passive LA mechanical properties and adversely affects LA-LV coupling in the intact canine heart.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
All experimental procedures and protocols used in this investigation were reviewed and approved by the Animal Care and Use Committee of the Medical College of Wisconsin in Milwaukee. All conformed to the Guiding Principles in the Care and Use of Animals of the American Physiological Society and the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health (Revised, 1996).

The experimental preparation used in the current investigation has been previously described (9). Briefly, mongrel dogs (n = 9) of either sex weighing between 25 and 30 kg were fasted overnight and anesthetized with sodium barbital (200 mg/kg) and sodium pentobarbital (25 mg/kg). Fluid deficits were replaced before experimentation with 500 mL of 0.9% saline, which was continued at 3 mL · kg-1 · h-1 for the duration of each experiment. After endotracheal intubation, the lungs of each dog were ventilated using positive pressure with oxygen. Arterial blood carbon dioxide tensions and acid-base status were maintained within a physiological range by adjustment of tidal volume and respiratory rate. Temperature was maintained with a heating blanket. A 7F dual micromanometer-tipped catheter was inserted into the aorta and LV through the left carotid artery for measurement of arterial and LV pressures and the maximal rate of increase of LV pressure (+dP/dtmax). The femoral artery and vein were cannulated for the withdrawal of arterial blood samples and fluid or drug administration, respectively. A thoracotomy was performed in the left fifth intercostal space. A 7F micromanometer-tipped catheter was inserted into the LA through the left upper pulmonary vein for measurement of continuous LA pressure. Two pairs of ultrasonic segment length transducers (5 MHz) were sewn to the anterior and posterior walls (long axis [LAX]) and medial and lateral walls (short axis [SAX]) of the LA (9,10). Hemodynamics were continuously monitored on a polygraph and digitized using a computer interfaced with an analog-to-digital converter.

LA pressure-volume diagrams used to assess LA function were recorded during steady-state hemodynamic conditions at end-expiration after instrumentation had been completed. LA volume (VLA) was determined from the LAX (anterior-posterior) and SAX (medial-lateral) dimensions using the equation: VLA = ({pi}/6)x(LAX)x(SAX)2 (9,10). LA end-diastolic volume and end-systolic volume (Ves) were defined at 10 ms before the peak of the LA pressure a wave and at maximum LA elastance (11), respectively. LA stroke volume and emptying fraction were calculated using standard equations (9). Total LA reservoir volume was determined as the difference between maximal LA volume (Vmax) and Ves. LA A and V diagram areas were measured using planimetry (9). A LA relaxation constant (RLA) was quantified as the slope of LA pressure decay after atrial contraction corrected for peak LA pressure (12). A series of differentially loaded LA pressure-volume diagrams (Fig. 1) were obtained at end-expiration by increasing LV and LA afterload with an IV bolus of phenylephrine (200 µg) (9). LA myocardial contractility was evaluated using time-varying elastance (9,11). Using linear regression analysis, the LA end-systolic pressure (Pes) and Ves of each LA pressure-volume diagram were fit to the equation: Pes = Ees x(Ves-V0s), where V0s is the volume intercept of the relation. LA end-reservoir dynamic chamber stiffness (Eer) was also calculated from this series of pressure-volume diagrams using the equation: pressure corresponding to each Pmax = Eer x(Vmax-V0r), where V0r is the volume intercept of the relation (9,13). Effective LV elastance (ELV) was determined as the ratio of Pes to LA stroke volume (13), and LA-LV coupling was calculated as the ratio of Ees to ELV.



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  		Figure 1. Continuous left atrial (LA) pressure, LA short and long axis dimensions (SAX and LAX, respectively), LA volume (VLA), aortic blood pressure, and left ventricular (LV) pressure wave forms (top) and corresponding LA pressure-volume diagrams (bottom) resulting from the IV administration of phenylephrine (200 µg) in a typical experiment.

 
Baseline systemic hemodynamics and LA pressure-volume diagrams were recorded under control conditions 60 min after instrumentation was completed. Dogs randomly received propofol (5, 10, 20, and 40 mg · kg-1 · h-1). Hemodynamics were recorded and LA pressure-volume diagrams were obtained using the techniques described above after 15 min of equilibration at each dose. Additional IV fluids (0.9% saline) were administered as required during propofol infusions to maintain constant LV preload because propofol dilates venous capacitance vessels and reduces venous return in the intact cardiovascular system (14). At the end of each experiment, the heart was electrically fibrillated, and the positions of all catheters, micromanometers, and ultrasonic crystals were confirmed.

Statistical analysis of data before and during the administration of propofol was performed using repeated-measures analysis of variance followed by Student’s t-test with Bonferroni correction for multiplicity. Linear regression analyses were used to determine the slopes (Ees and Eer) and volume intercepts (V0s and V0r) of the LA end-systolic and end-reservoir pressure-volume relationships used to determine LA myocardial contractility and dynamic chamber stiffness, respectively. Changes between interventions were considered statistically significant when P < 0.05. All data are expressed as mean ± SEM.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The hemodynamic effects of propofol are summarized in Table 1. Propofol caused significant (P < 0.05) decreases in heart rate, mean arterial and LV systolic blood pressures, rate-pressure product, and LV +dP/dtmax. Increases in LV end-diastolic, LA end-systolic, and LA mean pressures and Ves were also observed during the administration of the largest dose of propofol. The LA end-diastolic volume and Vmax, V0s, and V0r were unchanged. Decreases in stroke work (A loop area) and emptying fraction also occurred. Propofol produced dose-related reductions in Ees (3.3 ± 0.5 mm Hg/mL during baseline to 2.3 ± 0.4 mm Hg/mL during the 40 mg · kg-1 · h-1 dose; r2 >= 0.97) and Eer (2.0 ± 0.3 mm Hg/mL during baseline to 1.4 ± 0.2 mm Hg/mL during the 40 mg · kg-1 · h-1 dose; r2 >= 0.97) consistent with depression of LA myocardial contractility and reduced dynamic chamber stiffness, respectively (Fig. 2). The RLA remained unchanged (Table 1). An increase in V loop area was observed during the administration of the largest dose of propofol. Total reservoir volume was unchanged. A decline in the active LA contribution to LV filling occurred (77% ± 7% during baseline to 49% ± 7% during the 40 mg · kg-1 · h-1 dose; Fig. 2). Propofol caused a dose-related decrease in Ees/ELV (1.14 ± 0.24 during baseline to 0.53 ± 0.15 at the largest dose; Fig. 2), indicating impairment of mechanical coupling between the LA and LV.


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  		Table 1. Hemodynamic Effects of Propofol
 


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  		Figure 2. Histograms depicting the slope (left atrial [LA] elastance [Ees]; top left panel) of the LA end-systolic pressure-volume relation, the slope (LA end-reservoir dynamic chamber stiffness [Eer]; top right panel) of the LA end-reservoir pressure-volume relation, LA-left ventricular (LV) coupling (Ees/LV elastance [ELV]; bottom left panel), and the ratio of the LA A loop area to total pressure-volume diagram area (A/A + V; bottom right panel) under baseline conditions (C) and during the administration of propofol (5, 10, 20, or 40 mg · kg-1 · h-1). *Significantly (P < 0.05) different from baseline.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Propofol depresses the contractile function of isolated atrial myocardium obtained from guinea pigs (7) and humans (8) at concentrations larger than those typically achieved during IV infusions in a clinical setting. These findings are similar to those observed in normal ventricular myocardium in vitro (15,16), in situ (17), and in vivo (3,5). The negative inotropic actions of propofol in ventricular myocardium have been attributed to inhibition of Ca2+ current (18,19) and L-type Ca2+ channel function (20), and it seems likely that similar mechanisms are responsible for depression of contractility in atrial myocardium. This investigation is the first to quantify the effects of propofol on LA myocardial contractility in vivo using invasively derived pressure-volume analysis. The results indicate that propofol reduces LA contractile function to approximately 68% of control during the administration of the 40 mg · kg-1 · h-1 dose. The magnitude of this negative inotropic effect in LA myocardium was nearly identical to the degree of LV contractile depression (approximately 65% of control) produced by the 40 mg · kg-1 · h-1 dose of propofol as quantified with both end-systolic pressure-volume relations and preload recruitable stroke work in a very similar canine model (5) and LV +dP/dtmax in this investigation. As a result of these propofol-induced reductions in LA contractility, decreases in the ratio of LA to LV elastance (Ees/ELV) were observed as consistent with impaired mechanical matching between these elastic chambers. The material properties of LV myocardium are the primary determinant of LA afterload in the absence of mitral valve disease. We (4), and others (21), have previously demonstrated that propofol does not affect indices of LV isovolumic relaxation and compliance, even at concentrations that far exceed those required for clinical anesthesia, despite producing concomitant modest negative inotropic effects. Thus, the impairment of LA-LV coupling observed during the administration of propofol most likely resulted from the depression of LA contractile function and not because of LV diastolic dysfunction.

The current results indicate that propofol affects LA passive filling and emptying properties during the maintenance of relatively constant LA pressure and volume. The V component of the steady-state LA pressure-volume diagram is an index of reservoir function (22) that denotes the passive elastic energy stored during the reservoir phase (12). LA relaxation (12) and compliance (10,23), the extent of cardiac base descent during LV contraction (24), and the transmission of right ventricular systolic pressure through the pulmonary veins (25) are the major factors that determine reservoir function. This elastic energy accumulated during the reservoir phase is subsequently returned during the conduit phase after the opening of the mitral valve and is a major determinant of LV stroke volume (23). An increase in V loop area occurred during the administration of the 40 mg · kg-1 · h-1 doses of propofol, and total LA reservoir volume remained unchanged. These findings suggest that LA reservoir function is maintained during propofol anesthesia. This preservation of reservoir function may partially compensate for reductions in the active contribution of LA contraction to LV filling and serves to maintain stroke volume (5).

Eer decreased during the administration of propofol despite modest increases in LA pressure, suggesting that LA compliance is improved by this IV drug. The preservation of reservoir function that occurred during the administration of propofol was probably related to these decreases in Eer because decreases in LV systolic function (e.g., LV +dP/dtmax) were observed that would be expected to reduce reservoir function (12). A delay in LA relaxation has also been shown to contribute to a reduction in reservoir function (12), but RLA was unchanged during the administration of propofol in this investigation. The latter data support previous observations that indicate that this drug does not alter LV relaxation (4,21), even at concentrations that far exceed those required for clinical anesthesia.

The present results should be interpreted within the constraints of several possible limitations. Prolate ellipsoid geometry was used to model VLA using epicardial orthogonal sonomicrometry. Alterations in VLA are precisely determined using this geometric model (10,26), and absolute VLA measured with a water displacement-cast technique also correlates closely with VLA calculated with this method (27). Pressure-volume analysis of LA function does not strictly quantify retrograde pulmonary venous blood flow during LA contraction, but this retrograde flow is relatively small in the normal LA. An increase in LA pressure produced by an IV bolus of phenylephrine was used to generate the LA pressure-volume diagrams for the determination of Ees and Eer. We chose to increase LA pressure and volume because of the normal low operating range of these variables in the LA in vivo, and we have previously demonstrated that this method causes a more gradual increase in LA pressure than aortic constriction (9). An identical dose of phenylephrine was used to produce increases in LA pressure of similar magnitude during each experimental intervention. Residual circulating phenylephrine probably did not substantially affect the current results because hemodynamics were allowed to return to steady-state conditions before any subsequent interventions were undertaken. Propofol also caused similar cardiovascular effects in this as well as our previous study in barbiturate-anesthetized dogs (5).

The linearity and relative load-independence of the LA end-systolic pressure-volume relationship used to determine LA myocardial contractility have been demonstrated in the isolated heart (11) but have not been extensively characterized in the intact heart (26). However, Ees was calculated within the usual operating range of LA pressure and volume in which the LA end-systolic pressure-volume relation has been previously validated (11,26). Decreases in heart rate produced by propofol may have contributed to reductions in Ees or altered other indices of LA function. However, the LA end-systolic pressure-volume relation reflects alterations in LA myocardial contractility independent of changes in heart rate in the isolated, ejecting canine LA (11). Decreases in mean arterial and LV systolic blood pressures occurred during the administration of propofol, but it is also unlikely that these systemic hemodynamic effects contributed to the decreases in Ees because this index accurately quantifies alterations in LA myocardial contractility independent of loading conditions. It also appears unlikely that changes in hemodynamics affected the determination of Eer because preload was intentionally maintained by the administration of saline, and the LA remains isolated from its afterload system (i.e., the LV and arterial circulation) during the reservoir phase because the mitral valve is closed during this period. The 20 and 40 mg · kg-1 · h-1 doses of propofol have been demonstrated to produce plasma concentrations between 2 and 13 µg/mL in dogs (28) that may correlate with clinically relevant concentrations in humans. Nevertheless, plasma concentrations of propofol were not specifically measured in this investigation, and comparison of the effects of propofol on systemic hemodynamics and LA function between barbiturate-anesthetized, open-chest dogs and humans should be approached with caution. In addition, the larger doses of propofol may have produced plasma concentrations that exceeded those observed during maintenance anesthesia in humans. Acute surgical instrumentation causes LV systolic and diastolic dysfunction (29), and the current results should be interpreted with this limitation in mind as well. The presence of baseline sodium barbital and pentobarbital also produced myocardial depression in which the actions of propofol on LA function were further magnified compared with findings in the conscious state.

In summary, the current results indicate that propofol alters LA active and passive mechanical function evaluated using invasively derived pressure-volume relations. Propofol reduced LA myocardial contractility, decreased the active LA contribution to LV filling, and impaired LA-LV coupling in vivo. However, decreases in dynamic chamber stiffness and preservation of LA relaxation contributed to relative maintenance of LA reservoir function during the administration of propofol. Thus, the effects of propofol on LA function and its contribution to cardiac performance are complex. Propofol attenuates LA contractile properties but preserves passive mechanical behavior, partially compensating for these detrimental effects.


   Acknowledgments
 
Supported, in part, by National Institutes of Health grants HL-03690 (to Dr. Kersten), HL-63705 (to Dr. Kersten), HL-54820 (to Dr. Warltier), GM-08377 (to Dr. Warltier), and AA-12331 (to Dr. Pagel) from the United States Public Health Service, Bethesda, Maryland.

The authors thank John P. Tessmer, BS, and David A. Schwabe, BSEE, for technical assistance.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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Accepted for publication January 16, 2002.





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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press