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Department of Thoracic and Cardiovascular Surgery, University Hospital of Tromsø, N-9038 Tromsø, Norway
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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In the "virtual work model," left
ventricular total mechanical energy (TME) is linearly related to
myocardial oxygen consumption (M
O2). This relationship
(MO2-TME) is supposedly
independent of inotropic stimulation, vascular loading, and heart rate
variations. We reexamined the effect of inotropic stimulation
(dopamine) on the metabolic to mechanical energy transfer in nine
open-chest anesthetized pigs. Left ventricular mechanical energy was
calculated using TME (mean ejection pressure × end-diastolic
volume + stroke work), TMEW
(end-diastolic volume reduced by unstressed ventricular volume), and
the pressure-volume area (PVA). A highly linear relationship between
MO2 and mechanical energy
was found for all three indexes during control and dopamine runs
(r = 0.87-0.99). The slopes were unaltered by dopamine. y-Axis
intercepts were (control vs. dopamine) as follows (in
J · beat
1 · 100 mg1; means ± SD): TME,
0.36 ± 0.12 vs. 0.61 ± 0.30 (P < 0.02); TMEW, 0.43 ± 0.16 vs. 0.72 ± 0.32 (P < 0.02); and
PVA, 0.34 ± 0.13 vs. 0.60 ± 0.30 (P < 0.02). We conclude that the
virtual work model is dependent on inotropic stimulation and that new
insight into myocardial chemomechanical coupling is not added by this concept.
left ventricle; myocardial oxygen consumption; myocardial energetics; pressure-volume area; total mechanical energy
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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THE LEFT VENTRICULAR (LV) pressure-volume area (PVA),
defined by Suga (34), has been found to have a linear relationship to
myocardial oxygen consumption
(MO2). Total PVA is
described in the pressure-volume (PV) diagram as the area bounded by
the end-systolic and end-diastolic PV relations (ESPVR and EDPVR) and
the systolic PV trajectory. The total area consists of two smaller
areas: one surrounded by the PV loop (external work or stroke work) and
one limited by ESPVR and EDPVR and the diastolic PV trajectory (elastic
potential energy). Attempts to find thermodynamic grounds to justify
the use of PVA have been largely unsuccessful (3, 10), and the
subcellular processes corresponding to different parts of the areas are
largely unknown (7). On the other hand, a series of experiments have
related the y-axis intercept of the linear MO2-PVA relationship
to energy used for basal metabolism and excitation-contraction coupling
(PVA-independent MO2) (27, 37). An inotropy-induced increase in the PVA-independent
MO2 has been shown to
represent an increased energy demand for excitation-contraction coupling and has been termed the "oxygen-wasting" effect of
inotropic stimulation (35).
Elbeery et al. (12) and Lucke et al. (21) have recently introduced the "virtual work model," using a new index of LV total mechanical energy (TME) as an alternative to the PVA concept. TME was defined as
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(1) |
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(2) |
O2. TME was also found to be
unaltered by preload, afterload, and heart rate. Importantly, inotropic
stimulation with calcium (12) or ouabain (21) did not alter the
slope or y-axis intercept of the
MO2-TME relationship in their
experiments. The authors (12, 21) thus suggested that the concept of
oxygen waste related to inotropy has been based on incorrect indexes of
mechanoenergetic relationships. If this is correct, we need to alter
our conception that inotropic drugs unfavorably change myocardial
energy transfer efficiency.
The aim of the present study was to reexamine the reported independence
of the MO2-TME relationship
to inotropic stimulation, utilizing dopamine as an inotrope and the
MO2-PVA relationship as a
reference. Additionally, as illustrated in Fig.
1, we explored to what extent oxygen waste
of inotropy is concealed by the simplification of the TME equation from
Eq. 1 to Eq. 2, because LV unloaded volume (V0 and
VW) has been found to increase
during dobutamine infusion (17, 19, 23, 31).
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MATERIALS AND METHODS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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The experimental protocol was approved by the local steering committee of the Norwegian Experimental Animal Board and was registered by the board. All studies were conducted in compliance with institutional animal care guidelines, the National Institute of Health's Guide for the Care and Use of Laboratory Animals [DHHS Publication No. (NIH) 85-23, Revised 1985], and the "Guiding Principles in the Care and Use of Animals" of the American Physiological Society.
Experimental Preparation
Nine pigs (Norwegian landswine) (25-31 kg, either sex) were fasted overnight with free access to water. The pigs were premedicated with an intramuscular injection of ketamine (20 mg/kg) and atropine (1 mg). An initial bolus of pentobarbital sodium (10 mg/kg) and Fentanyl (0.01 mg/kg) was then given intravenously. The pigs were tracheostomized and intubated. Ventilation was maintained with an air-oxygen mixture (FIO2 = 50) on a volume-controlled respirator (Servo 900, Elema-Schönander, Stockholm, Sweden). Tidal volume was adjusted according to arterial blood gas samples (PCO2 4.0-5.0 kPa) (BGM, Allied Instrumentation Laboratory). Anesthesia was maintained with continuous intravenous infusions of pentobarbital sodium (4 mg · kg1 · min1),
fentanyl (0.05 mg · kg1 · min1),
and midazolam (0.3 mg · kg1 · min1) via the left
external jugular vein. Mean arterial pressure (MAP) was measured in the
thoracic descending aorta, with the catheter inserted from the left
femoral artery. A short catheter for arterial blood samples and
measurements of arterial blood resistivity (
) was advanced to the
abdominal aorta via the right femoral artery. Central
venous pressure was recorded in the right atrium with a catheter
inserted via the right external jugular vein. After sternotomy, the
left hemiazygos vein was ligated at its passage through the
pericardium. Transit time ultrasonic flow probes (CardioMed) were
placed on the main stem of the left coronary artery and on the trunk of
the pulmonary artery. Heparin sodium (5,000 IU) was administered
intravenously and repeated once during dopamine infusion. The coronary
sinus was catheterized with a stiff catheter through the left thoracic
wall and into the sinus via the ligated left hemiazygos vein. A 7-Fr
balloon catheter (Sorin Biomedical) was advanced to the proximal part
of the inferior vena cava via the right femoral vein. Proper
positioning of the catheter was verified by rapidly inflating the
balloon, resulting in an immediate fall in cardiac output (CO) and MAP.
A 6-Fr, 12-electrode, dual-field, pigtail combined
conductance catheter, giving both pressure and volume signals (Millar
Instruments), was positioned in the left ventricle via the left common
carotid artery. The proper position of the conductance catheter was
verified digitally by palpating the pigtail in the apex of the heart.
Blood volume was maintained by intravenous infusion of 0.9% NaCl
enriched with glucose at 1.25 g/l. Infusion rate was initially set to
15 ml · kg1 · h1
and was adjusted to keep central venous pressure constant throughout the protocol (range 2-5 mmHg) and diuresis above 1 ml · kg1 · h1.
The bladder was catheterized via a suprapubic midline incision. By the
end of the experimental protocol, anesthesia was terminated with
infusion of large doses of pentobarbital sodium, fentanyl, and
midazolam. Animals were then killed with an intraventricular injection
of 10 ml (1 mmol/ml) potassium chloride.
Experimental Protocol
The protocol consisted of two time periods: the control and dopamine runs. After instrumentation, the pigs were stabilized for 15 min. At the start of each run, arterial blood samples for Hb, O2 saturation, and assessment
were drawn. Parallel volume (Vp)
assessments, representing nonblood conductance, were done by injecting
a 3-ml bolus of 10% NaCl into the pulmonary artery (2). During every
PV measurement, the respirator was disconnected for 10 s to avoid the
respiratory influence on hemodynamics. Five to eight data acquisitions,
including MO2 and PV data,
were recorded simultaneously during each run. Recordings started at uninfluenced preload, and subsequent recordings were done during steps
of preload reduction (MAP decrement in steps of 5-10 mmHg) using
the caval balloon catheter. Sixty to ninety seconds were needed to
reach a desired steady-state MAP level, which was held for 10-15 s
before the start of sampling. PV data were then recorded over a period
of 10 s, while simultaneously coronary sinus blood for
O2 saturation measurement was
drawn and coronary blood flow was assessed. The half-time of coronary
flow adaptation to decreased perfusion pressure is ~5 s (9). After
the start of continuous dopamine infusion, and stabilization for a
minimum of 15 min, the measurements during the dopamine time period
were performed identically. The dopamine infusion was given using a
syringe pump (Therumo STC 521, Vingmed, Horten, Norway) at 5-10
µg · kg1 · min1.
Doses were adjusted to give an increased MAP of at least 20 mmHg.
Data Acquisition
The microtip pressure part of the combined conductance catheter was connected to a pressure-transducer control unit (Millar TC-510, Millar Instruments) and relayed via a signal amplifier (Gould) to the conductance conditioner (Leycom Sigma 5 DF, Cardiodynamics). The conductance catheter part of the catheter was directly connected to the Sigma 5 DF. Calibration of the pressure signals was done in vitro before insertion of the catheter, using the standardized 0- and 100-mmHg signals from the Millar TC-510 and the calibration program in the conductance calibration software (CPCcal, Cardiodynamics). The sampling rate of the conductance and pressure signals was set to 250 Hz. On-line real-time displays of segmental volumes were then inspected to find the combination of segments giving maximal total volume, as well as excluding segments lying outside of the left ventricle. Factors of were determined once per control and dopamine runs by drawing
arterial blood, using an air-tight syringe cuvette designed for the
Sigma 5 DF. The correct placement of the flow probes was evaluated
directly by inspecting the waveform of the flow signal and using the
on-screen strength-of-signal display in the flow computer (CardioMed
CM-4000, Cardiomed). Hb O2
saturation was measured using a hemoximeter (OSM2 Hemoximeter, Radiometer, Copenhagen, Denmark). Calibration of the hemoximeter was
done before each experiment. Hb was analyzed from EDTA-blood on a cell
analyzer (CA 460, Medonic).
Calculations
Conductance-catheter signals. The conductance-catheter method has been extensively described earlier with respect to technical and methodological aspects (2, 19), accuracy (1), and limitations (5). We used the dual-field technique (33). The conversion of conductance to volume is calculated by the formula
![V(<IT>t</IT>) = (1/&agr;) × (<IT>L</IT><SUP>2</SUP>/&rgr;) × [<IT>G</IT>(<IT>t</IT>) − <IT>G</IT><SUB>p</SUB>]](/content/vol276/issue4/fulltext/H1339/img003.gif)
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(3) |
is the slope factor, relating
conductance volumes to an independent method, e.g., ultrasonic flow
probes or temperature dilution technique;
L is the interelectrode distance; is the blood resistivity;
G(t) is the summed
segmental conductances; and
Gp is the total
parallel conductance (2, 19). We adjusted our volume signals for and parallel conductance but did not use the gain correction factor
(), because we were interested in relative volume changes only, not
the absolute volumes.
PV relationships. Calculations were done using the analysis software of the Conduct-PC package (CPCW version V3.15, Cardiodynamics). The Vp for control runs and dopamine runs was determined using consecutive beats in the ventricular phase of the 10% NaCl bolus wash-through (from baseline to maximal end-diastolic volume). The selection of the correct Vp was then based on a mean of sets from a minimum of four beats. The theoretical background for Vp calculations was described previously (2). The same Vp value was used in all different preload states in the control condition, and a new Vp value was used in the dopamine series. The heart cycle was defined to start at the peak of the R wave in the QRS complex, corresponding to end diastole. End systole is calculated as proposed by Sagawa (30). PV data were then calculated automatically by the software, after inspection of each file for proper electrocardiogram marking and exclusion of extrasystoles.
MO2 and mechanical
energy.
MO2 (J/beat) was calculated
as
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(4) |
1)
and TMEW
(VED reduced by
VW) were then calculated
according to Eqs. 2 and 1, respectively. PVA (in
mmHg · ml · beat1)
was calculated as (39)
![PVA = SW + [P<SUB>ES</SUB> × (V<SUB>ES</SUB> − V<SUB>0</SUB>)/2]](/content/vol276/issue4/fulltext/H1339/img006.gif)
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![− [P<SUB>ED</SUB> × (V<SUB>ED</SUB> − V<SUB>0</SUB>)/4]](/content/vol276/issue4/fulltext/H1339/img007.gif)
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(5) |
4
J · ml1 · mmHg1.
The calculated MO2, TME,
TMEW, and PVA data were normalized to 100 g of LV wall wet weight, where LV wall wet weight was calculated as 3.3 g LV wall wet wt/kg total pig wt, originating from swine of the
Yorkshire strain (24).
Contractility. We utilized two indexes reflecting LV contractility, the slope (PRSWI) of the linear SW-VED relationships (preload recruitable SW) (13) and the slope (EES) of the ESPVR (35). It is reported that over a wide range of loading conditions the PRSWI seems to be more stable than the EES (38). In this study, we chose the PRSWI as the key index of LV contractility. The points used for estimation of both PRSWI and EES are values set from each steady-state preload reduction, during each of the control and dopamine runs.
Statistics
Each experiment served as its own control. No time controls were performed. Experiments were included only if the slope of the SW-VED relationship (PRSWI) was significantly increased by dopamine on an individual basis [significant interaction at P < 0.05 by analysis of covariance (ANCOVA), see below]. The effect of dopamine on general variables was examined by a paired t-test. Least-squares linear regression lines were calculated using MO2 as the dependent
variable and TME, TMEW, or PVA as
independent variables. The effect of dopamine on slopes and
y-axis intercepts was examined by a
paired t-test, in accordance with Goto
et al. (14). A further assessment of the overall effect of increased inotropy was also done by an ANCOVA on the pools of
MO2 to TME, TMEW, and PVA data using the
regression (20)
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(6) |
0-3 are the different
coefficients estimated by the analysis,
X is the independent variable,
D is a dummy variable (0 if control, 1 if dopamine), and X × D is the interaction (i.e., probability of intersecting lines). Backward stepwise elimination of
products from Eq. 6 was done if
0-3 had a probability of
P > 0.1. By elimination of
interaction (omitting
3 · X · D), ANCOVA was performed with equal mean of
X and equal slopes assumed (20).
Values are reported as means ± SD. Significance was generally accepted at P < 0.05. Calculations
and statistics were performed using a spread sheet (Microsoft
Excel 5.0) and a statistical package (SPSS 8.0.0).
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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Figure 2 shows an example of averaged PV
loops from each step of caval occlusions during control and dopamine
runs. Table 1 presents hemodynamic data at
the start of the control and dopamine runs. Table
2 presents mechanical indexes. Dopamine
increased HR, CO, afterload (MAP, MEP,
PES), left coronary artery flow, MO2, and contractility
(PRSWI, dP/dtmax,
and EES). No
significant alterations of the ventricular volumes
(VES/ED) were found (Table 1).
The x-intercepts of both the ESPVR
(V0) and
SW-VED
(VW) relationships were shifted
to the right during dopamine infusion (Table 2). Arteriovenous oxygen
saturation difference was 69 ± 12% at the start of the control
runs and 73 ± 13% at the start of the dopamine runs
(P < 0.05, paired
t-test). Calculated LV wall wet weight was 95 ± 9 g (range 83-106 g).
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Linear regression equations between
MO2 and mechanical energy
indexes of all experiments are presented in Table
3. The means of the slopes showed no
significant difference between control and dopamine runs using TME,
TMEW, or PVA as the independent
variable. Mean y-axis intercepts were
significantly increased during the dopamine runs for all mechanical
energy indexes used. The magnitude of
y-axis intercept elevation during
dopamine infusion was greater if
VW was included in the calculation
of TME (in
J · beat1 · 100 g1:
TMEW, 0.30 ± 0.25; TME, 0.24 ± 0.25; P < 0.05, paired
t-test). The PVA-independent
MO2 increment was 0.26 ± 0.25 J · beat1 · 100 g1. The statistical
differences presented in Table 3 were confirmed by ANCOVA on the pools
of MO2 to mechanical energy
data (data presented in Fig. 3). In these
regressions, the probabilities of interaction were as follows: TME,
P = 0.51;
TMEW,
P = 0.42; PVA,
P = 0.74. After one-step backward
elimination of interaction, the increases in
y-axis intercepts of dopamine infusion
were as follows (in
J · beat1 · 100 g1):
TMEW, 0.31 ± 0.15; TME, 0.23 ± 0.15 (both P < 0.001, ANCOVA). The corresponding increment in PVA-independent
MO2 was 0.30 ± 0.15 J · beat1 · 100 g1
(P < 0.001).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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This study demonstrates the oxygen-wasting effect of inotropic
stimulation, as has been shown in a number of previous mechanoenergetic studies (6, 11, 14, 35). Our novel data show that such an inefficient
mechanoenergetic relationship can be found also when the TME of the
virtual work model (12) is used. In accordance with the original study
presenting the virtual work model, we found a highly linear correlation
in the MO2-TME relationship. Contrary to Elbeery et al. (12), our results show that oxygen waste of
inotropy is a general phenomenon, a finding unrelated to type of index
used to describe myocardial energy transfer (i.e., PVA, TME, and
TMEW). Finally, the virtual work
model was not found superior to the PVA concept as reported by Elbeery
et al. (12).
When discussing their results, Lucke et al. (21) and Elbeery et al.
(12) suggest that an oxygen-wasting effect of inotropic stimulation is
a phenomenon confined to isolated heart preparations. The relatively
increased myocardial oxygen consumption during inotropic stimulation in
these heart models could be caused by a mismatch between coronary flow
and mechanical energy consumption. However, the present in situ study
demonstrates an inotropy-related increase in both oxygen extraction and
coronary flow, giving a significant oxygen waste, revealed in an
increased MO2-to-TME ratio.
Nozawa et al. (26) have also shown that dobutamine infusion causes an
oxygen-wasting effect using the PVA concept in a conscious dog model.
These studies therefore contradict the suggestion that oxygen wasting
is a phenomenon restricted to isolated heart preparations.
Elbeery et al. (12) also proposed that oxygen waste was an apparent effect due to inotropy-induced dynamic creep in isolated hearts, or a leftward shift of the intercept (VW) of the SW-VED relationship on the x-axis. This could falsely suggest a relatively increased oxygen consumption compared with mechanical energy output. This is opposed to a series of experiments in intact animals (19, 23, 31) and in humans (17) that has shown a rightward shift of the unloaded volume (VW) after inotropic stimulation. In the present study, VW as well as V0 from the ESPVR was shifted to the right during inotropic stimulation. When VW was excluded from the TME calculation, this caused an underestimation, but not a total elimination, of the calculated oxygen waste. Consequently, our study does not support the presumption that VW can be excluded from the TME calculation.
When PVA is calculated, the V0 is
derived from a linear ESPVR by definition (35). As in the present
study, a negative estimate of V0
is often reported. Theoretically,
V0 represents the volume at which
the ventricle generates no pressure, but a negative
V0 obviously has no physiological
meaning (18). A possible explanation for the negative
V0 could be that the ESPVR is load
dependent and might be curvilinear outside the registered load levels
(18, 35, 38). Additionally, conductance volumetry in general gives a
somewhat lower EES and therefore
potentially contributes to the negative
V0 (19). Whether dopamine
increases the nonlinearity of the ESPVR outside our loading levels, and
thus influences the PVA calculations, is uncertain. This represents a
limitation of the PVA model and the study design. However, the
MO2-PVA relationship, and its
response to dobutamine, has been shown earlier to be similar whether
the ESPVR is assumed to be linear or nonlinear (26).
The virtual work model has been criticized by Hata et al. (16). Their
main objection has been apparently missing and incorrect steps in the
mathematical deductions of hemodynamic indexes from total heat
production. The present study does not address these deductions. In our
study both TME and TMEW were
correlated to PVA with a coefficient of 0.99 (P < 0.01, n = 116). Thus the virtual work model
differs only from the PVA model on a factorial level. Indexes based on
tension development or pressure work will incorporate the main
energy-consuming process in the myocardium, and close correlations to
MO2 will therefore be found.
Whether new indexes, such as the virtual work model, improve on
describing the true thermodynamic processes in the heart is still
uncertain (10).
Relationships between MO2 and
mechanical energy are, to date, best documented empirically and
theoretically in the time-varying elastance model (PVA) (35). The
advantage of the model lies in the possibility of dividing total
MO2 into
MO2 related to external work
and unloaded metabolism (y-intercept) (35). Unloaded metabolism represents the oxygen consumption in a contracting ventricle doing no external work and is subdivided into energy for
excitation-contraction coupling and basal metabolism
(MO2 of cardiac arrest). In
this model, the mechanism for the oxygen-wasting effect of increased
inotropy has been extensively examined in a series of experiments by
Suga (35) and Nozawa et al. (27). These studies conclude that the
inotropy-induced increase in y-axis intercept with no alteration in the slope of the
MO2-PVA relationship represents increased energy related to excitation-contraction coupling.
Recent studies using both catecholamines and a new class of calcium
sensitizers with no calcium-increasing effects (15, 25) support such a
mechanism for inotropy-induced oxygen wasting.
The increase in oxygen consumption during inotropic stimulation was
well documented in the late 1960s and early 1970s, as reviewed by
Braunwald (4). Increased MO2
during norepinephrine (32), digitalis glycosides (8), glucagon (22),
and calcium (32) infusions has been studied thoroughly using the
velocity of contraction and tension-time index (TTI) models. On the
other hand, Rooke and Feigl (29) found inotropy-induced oxygen wasting using the pressure-rate product and TTI, but not when using an empirical equation that also included stroke volume and external work
(pressure-work index; PWI). However, the PWI is limited by its
dependence on time-varying loading conditions and the lack of
ventricular volume measurements. Suga et al. (36) similarly varied
stroke volume as well as ventricular volume and pressures, finding no
alteration in the MO2-PVA
relationships during these variations but still an oxygen-wasting
effect of catecholamines (36).
The present study is the first to examine the effect of catecholamines
in the virtual work model. It is not entirely clear that catecholamine
and noncatecholamine inotropes affect the TME-relationship identically.
However, the mechanoenergetic inefficiency caused by increased inotropy
in the virtual work model should probably not be conveyed only to
catecholamines, because oxygen waste of inotropy has been shown both
for calcium (28) and ouabain (40) in the
MO2-PVA model.
In conclusion, the present study shows that an oxygen-wasting effect of inotropic stimulation can be found using the virtual work model for left ventricular chemomechanical relationships. Thus the virtual work model has not added insight into understanding myocardial chemomechanical coupling above and beyond the PVA relationship. Simplifications to avoid assessment of the unloaded volume during mechanoenergetic calculations can potentially give misleading results.
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ACKNOWLEDGEMENTS |
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Expert feedback was kindly given by Prof. Eivind S. P. Myhre, Dept. of Medical Physiology, University of Tromsø, and Dept. of Internal Medicine, University Hospital of Tromsø, Norway. Statistical advice was given by Associate Professor Ingard Holme, Institute of Community Medicine, University of Tromsø, Norway.
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FOOTNOTES |
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This work was supported in part by grants from the Norwegian Council on Cardiovascular Diseases, the Norwegian Research Council, and the Odd Berg Research Fund, Norway.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: C. Korvald, Dept. of Thoracic and Cardiovascular Surgery, University Hospital of Tromsø, N-9038 Tromsø Norway (E-mail: korvald{at}fagmed.uit.no).
Received 13 April 1998; accepted in final form 29 December 1998.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES
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