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Ann Thorac Surg 1996;61:82-87
© 1996 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Neonatal Myocardial Oxygen Consumption During Ventricular Fibrillation, Hypothermia, and Potassium Arrest

Department of Surgery, Medical College of Virginia, Richmond, Virginia

Accepted for publication August 16, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Background. Many investigators have examined oxygen consumption in adult hearts under conditions that simulate those encountered during cardiac operations and those that approximate basal metabolism. Few studies, however, have addressed this issue in neonatal myocardium.

Methods. Hearts from 3- to 9-day-old piglets were studied in a blood-perfused isolated heart preparation in working, empty beating, fibrillating, potassium chloride-arrested (at 37°C and 15°C), and hypothermic (15°C) states.

Results. Oxygen consumption (expressed in milliliters of O₂ per 100 g of ventricular tissue per minute; mean ± standard deviation) was 6.69 ± 1.91 for working hearts and fell to 3.19 ± 1.08 for empty-beating hearts, 3.72 ± 0.84 for fibrillating hearts, 1.30 ± 0.34 for potassium-arrested hearts at 37°C, 0.37 ± 0.18 for hypothermic (15°C) hearts, and 0.32 ± 0.10 for potassium-arrested hearts at 15°C. All values were significantly different except the two obtained at 15°C.

Conclusions. Vented fibrillating hearts used more oxygen than empty beating hearts. The addition of an arresting concentration of KCl did not lower oxygen consumption below that observed with hypothermia alone at 15°C. If potassium-based cardioplegia is incrementally beneficial in neonatal myocardial protection over that afforded by hypothermia alone, its effects cannot be explained by reduction in oxygen demand.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
See also page 87.

The basal oxygen consumption of adult myocardium has been determined by several investigators [1, 2], using a variety of techniques to arrest the heart. These studies have provided a basis for myocardial protective techniques that have proved useful in clinical cardiac surgery, where attempts are made to reduce the metabolic requirements of the heart to their lowest level. Similar protective strategies have been applied to corrective cardiac surgical procedures in neonates, yet their metabolic basis has not been fully evaluated in this population. Neonatal myocardium differs from adult myocardium in several important respects, including calcium regulation [3], sarcolemmal permeability to cations [4], and substrate dependence [5]. We hypothesized that oxidative requirements of neonatal cardiac tissues in the arrested state differed significantly from those observed in adult myocardium. If true, this might alter our concepts of the relative merit of contemporary myocardial protective strategies in this population.

Other conditions that relate to myocardial protection are less well studied in neonates. The diminution in basal (arrested) oxygen consumption that is achieved through myocardial cooling requires quantification in the newborn heart, as hypothermia remains one of the major myocardial preservation methods used in this group. As well, prolonged ventricular fibrillation, even in the totally vented heart, has been demonstrated to have deleterious effects on myocardial oxygen supply and demand [6]. The influence of fibrillation on metabolic demands in the neonatal heart needs to be addressed. We therefore sought to evaluate myocardial oxygen consumption (MVO₂) in intact, blood-perfused, neonatal porcine hearts in working, empty beating, fibrillating, and potassium-arrested states at normothermia and at 15°C.

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Perfusion System
Twelve newborn piglets, 3 to 9 days old (mean ± standard deviation, 5.3 ± 0.5 days) weighing between 1,200 and 2,600 grams (mean, 1,825 ± 386 g) were used in these studies. All animals received humane care in compliance with the ``Principles of Laboratory Animal Care'' formulated by the National Society for Medical Research and the ``Guide for the Care and Use of Laboratory Animals'' prepared by the Institute of Laboratory Animal Resources and published by the National Institutes of Health (NIH publication 85-23, revised 1985). Animals were anesthetized with intravenous pentobarbital (30 mg/kg) and administered intravenous heparin (400 U/kg). A tracheostomy tube (4-mm inner diameter) was rapidly inserted and the piglets were ventilated with 100% oxygen. Through a median sternotomy, the heart was excised and immersed in ice-cold heparinized saline solution to achieve immediate arrest. The ascending aorta was perfused with adult pig blood, obtained earlier from a donor animal and oxygenated with a membrane oxygenator. An overflow system regulated perfusion pressure at 50 mm Hg during stabilization. Perfusion pressure in the aortic cannula was continuously monitored. A metal cannula connected to a blood-filled reservoir 15 cm above atrial level was inserted into the left atrium via a pulmonary vein, and remaining pulmonary veins were ligated. The pulmonary artery was cannulated with a plastic cannula that directed right ventricular (RV) outflow (coronary sinus return) past a branch point, where it was exposed to the tip of a saturation catheter (Oximetrix; Abbott Critical Care Systems, Mountain View, CA). The venous blood then exited the cannula and flow was measured by timed collection. The saturation catheter connected to a computer, which provided continuous oxygen saturation readouts (Oximetrix). All venous effluent and overflow blood was filtered and returned to the oxygenator for reuse. Arterial blood samples from the aortic cannula and from the PA cannula were collected under anaerobic conditions for blood gas determinations. The perfusion system is depicted in Figure 1.

View larger version (44K): [in this window] [in a new window]   Fig 1. . Isolated heart preparation used to evaluate myocardial oxygen consumption. A heart in the working mode is shown. (L. = left; P.A. = pulmonary artery; R. = right.)

WORKING HEART.
A system based on modifications of the working isolated heart of Neely and associates [7] was used. In brief, oxygenated porcine blood was supplied via the left atrial cannula from a continuously replenished reservoir at a pressure of 15 cm H₂O. The heart was allowed to eject blood across the aortic valve, through the aortic cannula, and into an elasticity chamber. Aortic flow then passed through silicone tubing to a height of 70 cm, permitting measurement of aortic flow by timed collection. Pressure developed in the aortic cannula was monitored and recorded.

EMPTY BEATING STATE.
In this state, oxygenated blood was supplied retrograde through the aortic cannula at a constant pressure of 50 mm Hg. The left atrial cannula was clamped. A small polyethylene catheter with multiple side holes was inserted via an incision in the left atrial appendage, passed across the mitral valve, and secured in position with a ligature. This assured venting of the left ventricle (LV) by gravity drainage to a level below the heart. The vent was opened for this and all subsequent states. A stab electrode was inserted into the left ventricle and connected to an electrocardiographic transducer to record the electrocardiogram.

FIBRILLATING HEART.
The apparatus used in the empty beating state was used in an identical manner with the exception that an alternating current fibrillator was used to provide a continuous current to the heart via the electrocardiographic lead and a ground lead on the aortic cannula. The minimal current that would achieve fibrillation was applied (usually less than 1 V). As removing the stimulus often led to resumption of sinus rhythm, the stimulus was applied continuously during the measurements of this state. A perfusion pressure of 50 mm Hg was maintained. If fibrillation persisted after myocardial oxygen consumption measurements, hearts were defibrillated electrically before switching to the next state.

HYPOTHERMIA.
The empty beating configuration was used at a perfusion pressure of 50 mm Hg. Arterial blood was cooled to 15°C in the oxygenator reservoir and via a modified Buckberg-Shiley blood cardioplegia reservoir (Sorin Biomedical, Irvine, CA). The bath around the heart was also cooled by water jacketing, and a temperature probe was inserted into the apex of the LV to monitor LV temperature, which was regulated at 15° ± 0.5°C.

POTASSIUM CHLORIDE ARREST.
The empty beating configuration was used at a perfusion pressure of 50 mm Hg. Measured aliquots of potassium chloride (KCl) were added to the oxygenator reservoir until complete mechanical and electrical arrest was achieved. Measurements were made from the arrested heart at normothermia (37°C) and hypothermia (15°C) by the cooling techniques described above.

Measurement of Oxygen Consumption
Myocardial oxygen consumption was calculated as the product of arteriovenous oxygen content difference and coronary flow. Blood oxygen content was calculated from the following formula: O₂ content = [(1.39 x hemoglobin x %O₂ saturation) + (0.003 x oxygen tension)]. Hemoglobin measurements were made for each state for each heart, and oxygen tension values were measured by blood gas analysis. Arterial saturation values were assumed to be 100% as the arterial oxygen tension was never less than 190 mm Hg. Venous saturation values were measured directly from the Oximetrix saturation computer. Arterial pH was maintained in the range of 7.35 to 7.45 by the addition of sodium bicarbonate when needed, and arterial carbon dioxide tension was maintained in the range of 35 to 40 mm Hg by regulation of gas flow to the oxygenator. Under hypothermic conditions, oxygen tension values were corrected for temperature by the technique described by Hedly-Whyte and Laver [8]. Blood pH and carbon dioxide tension values were temperature-corrected using nomograms developed by Kelman and Nunn [9] to assure constant conditions during each state. At the conclusion of the experiment, the isolated heart was cleared of blood and weighed in total. Separate LV and RV portions were also weighed. The MVO₂ was divided by the sum of LV and RV weights and expressed as milliliters of oxygen per minute per 100 g of combined ventricular weight.

Statistical Analysis
Calculated oxygen consumption values were compared between conditions by a paired t test using commercially available software (SAS Institute Inc, Cary, NC).

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
The working mode could not be well established in 3 hearts, and MVO₂ data were not collected for this state in these. In 1 heart, the preparation deteriorated after only the working and empty beating states had been evaluated. Measurements of MVO₂ were not made at hypothermia in the empty beating heart in 2 other studies.

Hemodynamic measurements in the working mode are presented in Table 1. The pressures generated were greater than those measured in 4 piglets in vivo before extraction of the heart, where systolic and diastolic arterial pressures averaged 67 ± 5 and 44 ± 9 mm Hg, respectively. The isolated heart was free of any depressant effects of anesthetics and appeared to be stressed to a greater work-load than the anesthetized piglet.

As the neonatal heart is highly dependent on glucose as substrate and the preparation is typically in use for about 3 hours for each study, we measured blood glucose levels at the conclusion of 5 experiments. These values ranged from 57 to 165 mg/dL, with a mean of 94 ± 43 mg/dL. Adequate substrate appeared present throughout this experiment.

Heart weight varied from 12.2 to 22.2 g (mean, 16.8 ± 2.8 g). Chamber weights are presented in Table 2. As the right ventricle was never vented, but used to deliver coronary flow through the system, it was presumed to make a contribution to MVO₂ in all states. As a result MVO₂ values are expressed in milliliters of oxygen per minute per 100 g of combined RV and LV weight, although RV work was probably minimal.

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

Ventricular Fibrillation
The induction and maintenance of electrical ventricular fibrillation led to an increase in oxygen utilization to 3.7 mL per minute per 100 g. Although only a 15% increase from empty beating levels, this increase was observed in virtually all experiments. As a result, by paired t test, the difference was statistically significant. In contrast, work by Hottenrott and associates [10] in 1974 in adult canine hearts found that fibrillating normothermic ventricles consumed more than 50% more oxygen than empty beating hearts. In part, differences in intrinsic heart rates may explain this phenomenon. In Hottenrott and associates' study, hearts were paced at 100 beats/min to establish empty beating MVO₂ levels, whereas the hearts in the present investigation beat at a rate of approximately 160 beats/min. When this group reported a subsequent study comparing ventricular fibrillation with unpaced adult hearts beating at greater than 160 beats/min [11], the increase observed was in the order of 16%. However, other features of neonatal myocardium may contribute to the observation that ventricular fibrillation did not increase MVO₂ by the magnitude reported in adult studies. Neonatal myocardium may have less contractile elements to respond or the immature sarcoplasmic reticulum may be unable to maintain calcium mobilization. Further studies will be required to clarify this phenomenon.

Of interest, most studies in adult myocardium allow ventricular fibrillation to be maintained spontaneously after a brief electrical induction. Continuous electrical fibrillation may have different consequences on energy requirements [10]. In our study, ventricular fibrillation could not be spontaneously maintained in the perfused neonatal heart, likely due to small mass. As a result, a continuous electrical stimulus was applied. Voltages used were very low (less than 1 V), and would be insufficient in larger animals. Most hearts resumed sinus rhythm spontaneously within seconds of discontinuing the current.

Hypothermia and Potassium Arrest
This investigation examined interventions predicted to lower the metabolic rate of the heart. Production of depolarized arrest with KCl reduced MVO₂ to 1.3 mL per minute per 100 g. This represents a significant decline from empty beating levels, and is similar to levels observed in adult myocardium with potassium arrest [1]. In all studies, arrest was maintained for at least 20 minutes before measuring MVO₂ as shorter periods may lead to falsely elevated values [12].

Hypothermia to a myocardial temperature of 15°C offered the greatest reduction in MVO₂ to a level of 0.37 mL per minute per 100 g. At this temperature, no mechanical ventricular activity was observed, although atrial activity continued slowly. The addition of an arresting concentration of KCl to the perfusate did not lead to a significant change in MVO₂ at this temperature (0.32 mL per minute per 100 g). Thus, as evaluated by oxygen cost, hyperkalemic arrest appears to offer no additional protective benefits if myocardial cooling of this magnitude has been achieved.

Relationship Between Oxygen Consumption and Coronary Blood Flow
Unlike studies in adult animals on cardiopulmonary bypass [2], arteriovenous O₂ content difference showed considerably more variability between the different states in the present study (see Table 3). As a result, differences in MVO₂ were not directly related to blood flow changes. For example, coronary flow was greater under empty beating conditions compared with the working state, although MVO₂ was lower. Under hypothermic conditions, MVO₂ declined by a much greater degree than the change in blood flow. Several factors may be involved in these observations. First, autoregulatory mechanisms may be altered in the immature heart, and may be further modified in a denervated isolated heart preparation. Second, conditions such as hypothermia may affect regulatory processes in the coronary vasculature of the neonate, reducing the ability to match flow to metabolic demand. Finally, as conditions change, the distribution of coronary blood flow within the myocardial wall may vary. For example, if blood flow was preferentially shunted through regions with low oxygen extraction and low resistance, higher coronary flow values and lower arteriovenous O₂ differences would be observed. These autoregulatory issues have implications for myocardial protective strategies that use similar conditions and deserve further investigation.

Implications for Myocardial Protection
Myocardial protection remains a significant issue in neonatal cardiac surgery. Studies by Bull and associates [13] related 50% of postoperative mortality to problems of inadequate protection during operation. Furthermore, the techniques used clinically have largely been those adapted from use in adult cardiac operations: hypothermia and potassium arrest. As contemporary studies are finding more physiologic and biochemical age-related differences, the use of these techniques must be reevaluated.

The use of cardioplegia for neonatal myocardial protection is controversial and serves as an example. Baker and co-workers [14] reported that the use of St. Thomas II solution in addition to hypothermia (14°C) led to lower functional recovery after 2 to 6 hours of ischemia than the use of hypothermia alone. In contrast, Bove and colleagues [15] found that single-dose and multidose crystalloid cardioplegia with hypothermia afforded better protection against 2 hours of ischemia than hypothermia alone. Temperature, however, was 28°C in the latter study.

Our results suggest that potassium-based arrest reduces metabolic demand, and may have protective effects on the neonatal heart. However, the addition of potassium cardioplegia when myocardial temperature was 15°C did not lower oxygen demands. This provides a rationale for the differing results in the above-mentioned studies and agrees with work by Corno and associates [16], who found no difference in protection afforded by hypothermia alone and hypothermia with cardioplegia. One must note that variations in cardioplegia composition [17], frequency of administration [18], degree of hypothermia [19], or combinations of these variables [20] can influence recovery of neonatal myocardium after ischemia. As well, the age [21] and species [22] of the experimental animals can affect results, limiting the scope of many experimental investigations. Further work will be required to define the role of cardioplegia in neonatal cardiac surgery.

Study Limitations
The present study was conducted in an isolated heart preparation and carries with it problems inherent in the use of such systems. In particular, denervation of the heart may alter MVO₂ values. Drake and co-workers [23] have reported an increase in MVO₂ levels with cardiac denervation, and our study may be subject to a similar phenomenon. As well, this preparation uses oxygenated blood provided by an oxygenator. No endogenous catecholamines are present in the preparation, nor are any of the normal hepatic or renal mechanisms that regulate waste metabolites in the intact animal. One additional concern is that neonatal hearts contain a lower contractile mass per unit weight, and have a higher water content. As a result, the expression of oxygen per 100 g of wet weight may make comparisons with adult data more difficult.

This study demonstrates that MVO₂ is different under a variety of conditions. However, it cannot state whether MVO₂ is adequate for these conditions. If relative myocardial ischemia were present under any condition, coronary resistance would fall, and autoregulation would be affected. It is unknown whether this played a role under the conditions studied here as no measurements of ischemic metabolites or comparisons with baseline function were made.

In this study no measurements of MVO₂ of adult hearts were made. Ventricular geometry, wall thickness, perfusion pressure, and heart rate all differ between adult and neonatal hearts. As a result, conditions of perfusion pressure or ventricular stress normal for one age group might be very suboptimal for the other. Therefore, comparisons of metabolic rates must be qualitative at best.

These studies suggest that the relationships of MVO₂ in different states in the neonate may have some intrinsic differences to those which have been observed in studies using adult hearts. The effects of fibrillation, hypothermia, and KCl arrest may all have slightly different consequences to myocardial protective strategies in this age group. Further studies will be needed to define the specific cellular processes that contribute most to oxygen demand and coronary blood flow regulation in the neonate. This may allow the development of optimal myocardial protective strategies for the newborn.

	Acknowledgments

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
This work was supported by National Institutes of Health grant HL 26302.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 
Address reprint requests to Dr Jessen, Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Dallas, TX 75235-8879.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment Acknowledgments References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Michael E. Jessen Andrew S. Wechsler Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jessen, M. E. Articles by Wechsler, A. S. Search for Related Content PubMed PubMed Citation Articles by Jessen, M. E. Articles by Wechsler, A. S. Related Collections Related Article