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Ann Thorac Surg 1999;68:454-459
© 1999 The Society of Thoracic Surgeons

Original Articles

Warm or cold continuous blood cardioplegia provides similar myocardial protection

Anders B. Ericsson, MDa, Shigeto Takeshima, MDa, Jarle Vaage, MD, PhDa

a Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden

Address reprint requests to Dr Ericsson, Department of Thoracic Surgery, Karolinska Hospital, S-171 76, Stockholm, Sweden


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 References
 
Background. This study was performed to investigate the effect of temperature of blood cardioplegia on the recovery of postischemic cardiac function.

Methods. Pigs on cardiopulmonary bypass were subjected to global ischemia (30 minutes), followed by cold (n = 10) or warm (n = 11) continuous antegrade blood cardioplegia (45 minutes) delivered at 55–60 mm Hg.

Results. Global left ventricular function, evaluated by preload recruitable stroke work, decreased with cold cardioplegia from 91 (85–103) [mean (quartile interval)], at baseline, to 73 (55–87) erg x 103/mL postbypass (p = 0.03), but was unchanged after warm cardioplegia; 110 (80–132) to 109 (71–175) erg x 103/mL (p > 0.5). However, the difference between treatment effects was not significant (p = 0.25). Diastolic function, evaluated by end-diastolic pressure-volume relation, deteriorated without any difference between groups. Mean cardioplegic flow was similar between groups. Coronary vascular resistance increased at constant rate during warm cardioplegic delivery, but remained unchanged with cold cardioplegia (p = 0.001 between regression coefficients).

Conclusions. No significant difference was found in postischemic functional recovery comparing cold and warm continuous blood cardioplegia. Cold cardioplegia is therefore preferred due to added safety of hypothermia.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 References
 
The concept of warm aerobic arrest has gained much attention since its introduction in 1989 [1]. By avoiding ischemia and hypothermia, it has a potential for preservation of mitochondrial, membrane, and enzymatic function, with a possible improvement in postoperative outcome, especially in patients with limited cardiac reserve and after long cross-clamp times [2]. Despite the theoretical advantages using warm continuous blood cardioplegia, results diverge when compared with cold blood cardioplegic techniques. With warm cardioplegia, both good [3–5] and detrimental cardiac effects are shown [6–9]. Also systemic effects, such as increased risk for neurologic events and low systemic vascular resistance, are reported [10, 11].

The arrested, normothermic heart requires 90% less oxygen than does the normal working heart. Still, a warm heart requires more oxygen than a cold one (1.1 vs 0.135 mL O2/min/100 g myocardium, at 37°C and 11°C, respectively) [12]. This difference, although small, represents an increased demand on myocardial oxygen supply, and as a consequence maybe a larger susceptibility for inhomogeneity in cardioplegic distribution. Cardioplegic delivery to myocardium beyond proximal occlusions is not optimal [13], and hypoperfusion of the right ventricle has been demonstrated using retrograde cardioplegia [14]. Even in absence of coronary artery obstructions, antegrade perfusion to the cardioplegic heart is not homogeneous with subendocardial layers being more vulnerable [15]. Also, cardioplegic flow and pressure may then, in the warm heart, be of more critical importance, and pump accidents may be fatal due to decreased time margins. Ischemic damage may further result when warm "continuous" cardioplegia is temporarily interrupted, as done by many to better visualize the operating field [16].

These remarks may have important implications for the use of warm heart surgery, and we hypothesize that parts of the observed advantages with warm continuous cardioplegia are attributed to the continuous perfusion per se, rather than to favorable metabolic effects of normothermia. In addition, even with continuous cardioplegia, hypothermia may still be an important adjunct to myocardial protection. Hence, the purpose of this study was to isolate and investigate the impact of cardioplegic temperature on postbypass functional recovery, keeping parameters as cardioplegic flow, pressure, and route of administration similar between groups. We used a pig model with 30 minutes of global ischemia, followed by "resuscitation" for 45 minutes with continuous cold or warm antegrade blood cardioplegia.


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 References
 
All animals received humane care in compliance with the guidelines from the U.S. National Institutes of Health (NIH) regulating the care and use of laboratory animals (NIH publication no. 86-23, revised 1985). The study was approved by the Ethics Committee for Animal Research at Karolinska Institutet (Stockholm, Sweden).

Anesthesia and surgical procedure
Pigs with a body weight of 44 (40–48) kg [mean (interquartile interval)] were premedicated with intramuscular ketamine hydrochloride (20 mg/kg) and atropine sulfate (0.5 mg). Anesthesia was induced with intravenous sodium pentobarbital (15 mg/kg) and maintained by a cocktail (0.35 mL/kg/h) containing 2 mg fentanyl citrate, 25 mg midazolam, and 24 mg pancuronium bromide in a volume of 57 mL. The infusion was preceded by a bolus of 0.15 mL/kg. The pigs were intubated and ventilated with a mixture of oxygen and N2O using a volume-cycled ventilator (Engström 300; Datex-Engstöm AB, Bromma, Sweden).

Catheters were inserted into the right femoral artery and vein for drug and fluid administration, blood sampling, and pressure monitoring. A catheter and a temperature probe were surgically introduced into the urinary bladder. An electrocardiogram was recorded by surface electrodes. A catheter was placed in the pulmonary artery for pressure monitoring and injections of hypertonic saline for parallel conductance calibrations.

The pericardium was opened after median sternotomy. A 5 F transducer-tipped pressure catheter (Mikro-Tip; Millar Instruments Inc, Houston, TX) and a 7 F, 12-pole conductance catheter (Cordis; Webster, Baldwin Park, CA) with 9- or 7-mm spacing between the electrodes, depending on heart size, were introduced into the left ventricle through a stab wound in the apex. The tip of the conductance catheter was brought through the aortic valve. A proper position of the catheter was confirmed before each set of measurements by visual inspection of the individual segmental volume signals.

After heparinization (activated clotting time > 480 seconds), the brachiocephalic artery was cannulated for cardiopulmonary bypass (CPB) with a 22 F arterial cannula. Venous return was through a 32 F two-stage cannula in the right atrium. CPB was initiated with a flow of 75 to 90 mL/kg per minute using a roller pump (7400; Sarns Inc/3M Health Care, Ann Arbor, MI) and a membrane oxygenator (Maxima; Medtronic Blood System, Anaheim, CA) primed with Ringer’s acetate solution. The left ventricle was vented by a 16 F catheter introduced through the left atrial appendage and connected to the venous line for passive drainage. A cardioplegia cannula was inserted into the aortic root with a side branch for pressure monitoring. Cardioplegic flow was continuously measured by an ultrasound transit-time flow meter (HT207; Transonic Systems Inc, Ithaca, NY) with a flow probe on the cardioplegia tubing.

Data acquisition
Hemodynamic and mechanical data were acquired during disconnection of the ventilation in end-expiration to minimize the effects of intrathoracic pressure variations. Mechanical data were acquired during variable loaded beats by occluding the inferior vena cava for 10 to 15 seconds. Every measurement was repeated at least twice.

The conductance catheter was connected to a Leycom Sigma-5 signal-conditioner processor (CardioDynamics BV, Zoetermeer, the Netherlands). The volume and pressure signal were processed (Conductance-PC software; CardioDynamics BV), and the left ventricular pressure-volume loops were displayed on-line and stored on the computer hard disk. The volume signal was corrected for parallel conductance and the blood resistivity. The principle and technique for volume measurement have previously been presented in detail [17].

Data were acquired with an IBM-compatible computer with an analog-to-digital (AD) converter board (DAS-1601; Keithley Data Acquisition, Taunton, MA) at a sampling frequency of 200 Hz. The time-varying conductance G(t) from five intraventricular segments of the conductance catheter was recorded and summarized in the Leycom Sigma-5 giving the time-varying volume [V(t)] by the formula:

where {alpha} is a slope factor giving the relation between the "true" and the measured volume and was approximated to 0.6 [18]. L is the distance between the electrodes on the catheter and {sigma} is the resistivity of the blood, which was measured in a cuvette before each set of volume recordings. Gp, the parallel conductance from structures surrounding the left ventricle, was calculated by a bolus injection of 4 mL hypertonic (10%) saline solution into the pulmonary artery. This was repeated at least twice before every set of measurement.

Data analysis and calculations
Hemodynamics
End-diastole was defined as the lower right hand corner of the pressure-volume loop. Left ventricular end-diastolic pressure (EDP) and volume (EDV) were measured. Stroke work (SW) was calculated as the area within the pressure-volume loop, and the coronary vascular resistance was calculated as the cardioplegic perfusion pressure, measured in the aortic root, divided by the cardioplegic flow.

Mechanical data
Global left ventricular function was quantitated by the regression coefficient (MW) of the preload recruitable stroke work relation (PRSW), and by V0, its x-axis (volume) intercept by the equation [19]:

Left ventricular diastolic function was quantitated by the stiffness constant (ß), by the formula:

Diastolic function could also be quantitated by the regression coefficient (Eed) of the linear end-diastolic pressure-volume relation (EDPVR) by the equation:

Vd is the x-axis intercept.

Experimental protocol
Pigs were randomized to cold (n = 12; 6–7°C) or warm (n = 13; 34–35°C) continuous antegrade blood cardioplegia. Baseline hemodynamic and mechanical data were recorded followed by cannulation and start of totally vented CBP. The aorta was clamped and the hearts fibrillated if still beating 5 minutes after cross-clamping. After 30 minutes of normothermic global ischemia, continuous cold or warm antegrade blood cardioplegia was delivered during 45 minutes. An initial dose of 500 mL high-potassium cardioplegia was given, followed by a low-potassium solution (Table 1). Cardioplegic flow was continuously adjusted to maintain an aortic root pressure of 55 to 60 mm Hg and flow was recorded after 5, 15, 25, 35, and 45 minutes. High-potassium cardioplegia was reintroduced if needed to sustain a totally arrested heart. In the cold group, body temperature was allowed to drift, but in no animal below 29°C. In the warm group, it was maintained at 33–37°C. After stopping cardioplegic perfusion, the aorta was unclamped and rewarming begun. The left ventricular vent was discontinued after another 30 minutes. Starting at 45 minutes after unclamping, the CBP flow was gradually decreased during 15 minutes followed by immediate decannulation. No inotropic support was ever used. After 90 minutes of reperfusion, hemodynamic and mechanical data were acquired. At the end of the experiment, the pig was given a lethal intravenous injection of pentobarbital and potassium.


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  		Table 1. Content of Cardioplegic Solution Mixed 1:4 With Blood

 
Statistical analysis
Data are reported as mean and quartile interval, except when otherwise stated. In analyzing coronary vascular resistance, a 95% confidence interval (95% CI) for the regression coefficient, based on individual slopes, is given. A paired t test was used for within-group comparisons and an unpaired t test between groups (Statistica; StatSoft, Inc, Tulsa, OK).


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 References
 
Two pigs in the cold group were weaned from CPB, but died before postbypass measurement. One died of ventricular fibrillation and one of pulmonary hypertension with subsequent arrhythmias. In the warm group, two pigs could not be weaned from CPB and died of cardiac failure. These subjects were excluded, leaving 10 pigs in the cold and 11 in the warm group for final analysis.

Cardioplegia and coronary vascular resistance
Total mean cardioplegic flow was similar with cold and warm cardioplegia: 143 (104–174) and 137 (124–155) mL/min, respectively. Flow after 5 minutes was 154 (114–189) and 182 (160–198) mL/min in the cold and warm group, respectively (p = 0.14). With warm cardioplegia, mean coronary vascular resistance increased constantly during the 45 minutes of cardioplegic delivery, with a rate of 6.0 (95% CI; 3.4 to 8.5) mm Hg x 10-3/mL, but was unchanged with cold cardioplegia; 0.9 (95% CI; -0.4 to 2.2); (p = 0.001 between regression coefficients) (Fig 1).



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  		Fig 1. Coronary vascular resistance (CVR) during infusion of continuous cold or warm blood cardioplegia after 30 minutes of global ischemia. Data are presented as mean + SEM. For p values, see text.

 
Hemodynamics
There was no difference in hemodynamics between groups (Table 2). However, the decline in ejection fraction was significant in the warm, but not in the cold group, and mean arterial pressure declined in the cold, but not in the warm group.


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  		Table 2. Hemodynamic Data

 
Global and diastolic left ventricular function
The decline in PRSW, as an index of left ventricular contractility, was not significantly different between cold and warm cardioplegia (p = 0.25) (Table 3 and Fig 2). Also, the difference in recovery of PRSW was not significant [81% (68%–84%) vs 99% (70%–120%) of baseline with cold and warm cardioplegia, respectively] (p = 0.19). The EDPVR increased after cardioplegia in both groups and the stiffness constant (ß) increased in the warm group, indicating deterioration in diastolic function (Table 3). However, no difference between treatments was found in EDPVR or ß.


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  		Table 3. Mechanical Data

 


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  		Fig 2. Box plots of the difference between baseline (pre) and postbypass (post) preload recruitable stroke work (PRSW), when global ischemia was followed by cold or warm continuous blood cardioplegia (p = 0.25). The box represents the quartile interval, the point the median, and the whiskers show the range of data.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
References
 
This study was designed to specifically isolate the effect of cardioplegic temperature on the recovery of postbypass left ventricular function. The present model mimics the use of continuous blood cardioplegia as resuscitation of the already ischemic and metabolically compromised myocardium. Theoretically, warm blood cardioplegia may in this situation have particular metabolic advantages. Using this model with unprotected ischemia, the myocardium is maximally challenged, and by several hours shortens the length of cardioplegia and time on CPB necessary to obtain a significant postcardioplegic dysfunction. Thus, the animals are kept in better conditions for hemodynamic studies. A model of global and not regional ischemia was used to avoid any negative bias to the warm group due to a supposed greater vulnerability for nonhomogeneous cardioplegic distribution. This was also the reason for choosing antegrade and not retrograde perfusion. Global ischemia made it possible to use the relatively load-insensitive PRSW as an index of ventricular contractility. The global myocardium will in this study functionally represent a region exposed to a sudden coronary occlusion in the clinical situation.

Although no statistical difference was found between treatments, the decline of PRSW in the cold group was significant, but not in the warm group (Table 3). As in many animal studies of this type, the statistical power is low, with the risk of committing a type II error. This was a result of the large variability in postoperative outcome in the warm group and a small numerical difference between the groups (Fig 2). With a ß error of 0.10, a calculated study group of 58 animals in each group might have shown a difference with p < 0.05 if the values for recovery and variability of PRSW had remained unaffected. However, we do not know the clinical significance of this difference (81% vs 99% recovery), and the larger variability in global cardiac function after warm cardioplegia may have clinical implications. The reduction in the more load-sensitive index ejection fraction was on the other side less pronounced with cold compared with warm cardioplegia, and there was no tendency towards a difference between groups in diastolic function.

Our results indicate that in the optimally perfused and vented cardioplegic heart, the temperature of the perfusate may be of minor importance for the recovery of left ventricular function. Continuous cardioplegic perfusion may be of greater importance, and responsible for positive clinical effects otherwise attributed to the warm temperature. Theoretical advantages using warm cardioplegia may be minimized by an inability to provide aerobic metabolism in all regions of the myocardium. Besides a larger vulnerability to inhomogeneous cardioplegic distribution, the warm heart may also be more susceptible to insufficient flow and edema formation [6, 8, 9, 15, 20].

With warm cardioplegia, a constant increase in coronary vascular resistance during the 45 minutes of delivery was observed, but with cold cardioplegia, coronary resistance remained unchanged. This may be explained by an increasing endothelial dysfunction or perivascular edema in conjunction with warm continuous cardioplegia. An increased vascular resistance may decrease the homogeneity in the distribution of warm cardioplegic solution, thus increasing the risk for ischemic injury. An increase in coronary vascular resistance during aortic reperfusion has earlier been shown by Digerness and associates [21]. In that study, cold, crystalloid cardioplegia was used, followed by controlled aortic root reperfusion with warm, hyperkalemic blood for 3 to 5 minutes and then normokalemic blood. However, at the beginning of cardioplegic perfusion, vascular resistance tended in our study to be greater in the cold group. This is consistent with a larger resistance during cold compared with warm intermittent cardioplegia, as shown by others [22].

Continuous cold blood cardioplegia has never been widely used among cardiac surgeons because of the inconvenience of a continuous perfusion without any evident advantages over intermittent cold techniques. However, already in 1981, Bomfim and colleagues [23] compared continuous cold antegrade and single-dose blood cardioplegia during aortic surgery. They showed a decrease in lactate release and a normal lactate extraction 30 minutes after declamping with continuous cardioplegia. Creatine kinase (CK)-MB and myoglobin release was significantly lower in the continuous group, and myocardial adenosine triphosphate (ATP) and creatine phosphate (CP) decreased less. Khuri and associates [24] reported no change in myocardial pH during aortic clamping with continuous cold blood cardioplegia, but a decline with multidose perfusion. However, pH equalized during aortic reperfusion, and the clinical outcome was similar between groups. Recently, Louagie and associates [25] reported that continuous retrograde cold blood cardioplegia results in better left and right ventricular stroke work index during the first 20 hours after coronary artery bypass grafting compared with historical controls using intermittent ante- or retrograde cold blood cardioplegia.

The only study besides ours, isolating and investigating the effect of cardioplegic temperature per se on myocardial recovery, is a study by Bufkin and colleagues [7]. After left anterior descending artery occlusion, antegrade cardioplegic induction was followed by continuous retrograde cardioplegia at 18°C, 28°C, or 37°C. After 90 minutes of reperfusion, PRSW was higher in the 18°C and 28°C groups than in the 37°C group. However, both the regional ischemia and the retrograde cardioplegic delivery may have contributed to the worse outcome in the 37°C group. In our study, the cold perfusate had the temperature of 6–7°C, which is the standard temperature for intermittent cold blood cardioplegia at our clinic. Several investigators have shown good results with tepid cardioplegia [7, 26], and this may perhaps combine some advantages of aerobic metabolism with safety aspects and myocardial protection using hypothermia.

In summary, when comparing cold and warm continuous blood cardioplegia, we did not observe any difference in postbypass recovery of global or diastolic left ventricular function. Our findings indicate that warm (34°C) cardioplegic perfusion has no advantage over cold (6°C) perfusion when used continuously. Unless warm cardioplegia is proven to be better, cold cardioplegia is advocated because hypothermia provides less vulnerability to inadequate cardioplegic distribution and flow, leaving the surgeon with a larger safety margin.


   Acknowledgments
 
This study was supported by grants from the Swedish Heart Lung Foundation, the Swedish Medial Research Council (grant no. 11235), Karolinska Institutet, and the Karolinska Hospital. The assistance by chief perfusionist Ove Johansson, and the perfusionist team of the Department of Thoracic Surgery, Karolinska Hospital, is gratefully acknowledged.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 References
 

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Accepted for publication May 14, 1999.




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