Experimental myocardial preservation study of adding perfluorochemicals (FC43) in lidocaine cardioplegia.

OBJECTIVE: Lidocaine exhibits a cardioplegic action via acute inhibition of sodium influx into the myocardial cells. In terms of the cardiac function and calcium dynamics in the myocardial cells, we investigated the myocardial protective effect of addition of FC43 of Perfluorochemicals, which has an excellent oxygen transport function to meet the myocardial oxygen demand, on lidocaine-induced cardioplegia. METHODS: Isolated rat hearts were perfused with Langendorff mode and were divided to three experimental groups. During of preservation, these hearts were perfused continuously with the next three solution, potassium chloride was added to Krebs-Henseleit bicarbonate buffer to make potassium concentration of 20 mM in the first group (Group A), 2 mM lidocaine was added to Krebs-Henseleit bicarbonate buffer in the second group (Group B), and 2 mM lidocaine and 20% FC43 were added to Krebs-Henseleit bicarbonate buffer in the third group (Group C). After 60 minutes of continuous perfusion, the cardiac function and the intracellular calcium concentration in Groups A and B during cardioplegia were measured. Furthermore, after 360 minutes of continuous coronary perfusion, the cardiac function were measured in Group B and Group C. RESULTS AND CONCLUSIONS: Lidocaine cardioplegia showed a good recovery of cardiac function, because lidocaine induced prompt cardiac arrest by blocking sodium influx and inhibited the intracellular calcium overload by the following inhibition of sodium-calcium channels. Moreover, our results suggested that combining Perfluorochemicals with lidocaine produced a more effective myocardial-preservation that meets the myocardial oxygen demand during long-term cardiac arrest.     

Electrolyte versus Blood Cardioplegia: Randomized Clinical and Myocardial Ultrastructural Study

In 40 consecutive patients undergoing coronary artery bypass, one of two solutions for cardioplegia, each containing 30 mEq/L of K⁺ was used randomly. The groups were comparable except for intramyocardial temperature. With electrolyte solution (Group A), it was 16.5° ± 0.34°C, while with blood from the pump-oxygenator (Group B) it was 20.3° ± 0.41°C (p < 0.001). After bypass left atrial pressure (LAP) was 11.9 ± 0.67 torr in Group A and 8.1 ± 0.49 torr in Group B (p < 0.001). CPK-MB was elevated in 45% of Group A patients versus 15% in Group B (p < 0.05). No patient died. Two myocardial infarctions occurred in Group A and one in Group B. Stereological morphometric electron microscopy was performed on biopsy specimens taken from the left ventricle (1) before perfusion, (2) after cardioplegia, and (3) 30 minutes after reperfusion. Group A showed marked intracellular edema, mitochondrial swelling, pronounced depletion of glycogen stores, and focal myofibrillary disorganization. Group B showed near normal myocardial ultrastructure with increased glycogen stores and minimal mitochondrial swelling. Morphometric analysis revealed a statistically significant increase in the degree of mitochondrial swelling (51%) in Group A compared with Group B after reperfusion (p < 0.001). Thus, blood K⁺ cardioplegia resulted in better preservation of myocardial ultrastructure, lower ventricular filling pressure, and lesser CPK-MB release compared with this particular electrolyte cardioplegia.     

Avoidance of Profound Hypothermia During Initial Reperfusion Improves the Functional Recovery of Hearts Donated After Circulatory Death

The resuscitation of hearts donated after circulatory death (DCD) is gaining widespread interest; however, the method of initial reperfusion (IR) that optimizes functional recovery has not been elucidated. We sought to determine the impact of IR temperature on the recovery of myocardial function during ex vivo heart perfusion (EVHP). Eighteen pigs were anesthetized, mechanical ventilation was discontinued, and cardiac arrest ensued. A 15‐min standoff period was observed and then hearts were reperfused for 3 min at three different temperatures (5°C; N = 6, 25°C; N = 5, and 35°C; N = 7) with a normokalemic adenosine–lidocaine crystalloid cardioplegia. Hearts then underwent normothermic EVHP for 6 h during which time myocardial function was assessed in a working mode. We found that IR coronary blood flow differed among treatment groups (5°C = 483 ± 53, 25°C = 722 ± 60, 35°C = 906 ± 36 mL/min, p < 0.01). During subsequent EVHP, less myocardial injury (troponin I: 5°C = 91 ± 6, 25°C = 64 ± 16, 35°C = 57 ± 7 pg/mL/g, p = 0.04) and greater preservation of endothelial cell integrity (electron microscopy injury score: 5°C = 3.2 ± 0.5, 25°C = 1.8 ± 0.2, 35°C = 1.7 ± 0.3, p = 0.01) were evident in hearts initially reperfused at warmer temperatures. IR under profoundly hypothermic conditions impaired the recovery of myocardial function (cardiac index: 5°C = 3.9 ± 0.8, 25°C = 6.2 ± 0.4, 35°C = 6.5 ± 0.6 mL/minute/g, p = 0.03) during EVHP. We conclude that the avoidance of profound hypothermia during IR minimizes injury and improves the functional recovery of DCD hearts.     

Effect of delayed induction of postischemic hypothermia on spinal cord damage induced by transient ischemic insult in rabbits

Objective: This study was performed to determine the effect of delayed induction of mild hypothermia after transient spinal cord ischemia in rabbits. Methods: Abdominal aortic occlusion was performed for 15 minutes to induce spinal cord ischemia at a rectal temperature of 37.3±0.3°C. Four groups of rabbits were investigated: Group 1 (n=8) was subjected to ischemia and reperfused at the same temperature for 7 hours; Group 2 (n=8) was subjected to ischemia and reperfused at the same temperature for 1 hour, followed by 6 hours of systemic hypothermia (32.5±0.5°C); Group 3 (n=8) was subjected to ischemia, reperfusion at the same temperature for 3 hours and then 6 hours of systemic hypothermia (32.5±0.5°C); and Group 4 (n=8) comprised non-ischemic controls. Neurological status of all rabbits in Groups 1– 3 was recorded and animals were sacrificed 1 week after ischemic injury. Spinal cord sections were examined microscopically to determine the extent of ischemic neuronal damage. Results: Mean modified Tarlov’s score at 1 week after ischemic insult was 0.5±0.8 in Group 1, compared to 4.3±1.5 in Group 2 and 2.9±1.8 in Group 3. Mean total number of surviving neurons within examined sections of spinal cord was significantly greater for Groups 2 and 3 compared with Group 1 (Group 1, 81±66.1; Group 2, 293.4±110.9; Group 3,227.1± 105.5; p<0.001). Conclusions: Delayed postischemic hypothermia induced within 3 hours after reperfusion significantly reduces ischemia-induced spinal cord neuronal damage in rabbits.     

I. Development of an In Vitro Model of Myocardial Cooling: A Study of the Effect of Cardiac Size on Cooling Rate

A physical model for the study of local cardiac hypothermia was developed using excised animal hearts. The validity of the model was established by showing close similarity between cooling curves of dog hearts in vivo and in the model. The model was then used to compare the cooling rates of three groups of excised hearts using cold saline irrigation. Groups 1, 2, and 3 had mean left ventricular weights of 166, 379, and 1,429 gm, respectively, and mean left ventricular wall thicknesses of 1.5, 2.0, and 3.1 cm, respectively. For the same 10°C temperature fall, Group 1 took 25 ± 2.8 minutes, Group 2 took 54 ± 9.2 minutes, and Group 3 took 117 ± 21 minutes. To avoid slow cooling and consequent ischemic damage in the hypertrophic ventricle, it may be desirable to initiate cooling using coronary perfusion with cold blood or cold cardioplegic solutions.     

Cold Blood–Diltiazem Cardioplegia

The calcium channel blocker, diltiazem, has been studied in the same model used for evaluation of cold blood–potassium cardioplegia. Six dogs (Group 1) had one hour of myocardial ischemia with topical ice (myocardial temperature, 7° ± 2°C) after coronary perfusion with 200 ml of cold blood (5° ± 1°C) containing diltiazem, 400 μg per kilogram of body weight. Seven dogs (Group 2) had two hours of ischemia after perfusion with 200 ml of cold blood containing 200 μg/kg and reperfusion every 30 minutes with 100 ml of cold blood and diltiazem, 100 μg/kg. Baseline studies were repeated after rewarming and 40 minutes of reperfusion. No inotropic agents or calcium were used.Heart rate, peak systolic pressure, velocity of the contractile element, peak + rate of rise of left ventricular pressure (dP/dt), peak ? dP/dt, dP/dt over common peak isovolumic pressure, left ventricular compliance and stiffness, and heart water were unchanged in Group 1. In Group 2, heart rate slowed (p < 0.025) and compliance decreased (p < 0.02). In both groups, coronary vascular resistance declined (p < 0.001) and recovery of adenosine triphosphate (p < 0.001), adenosine diphosphate (p < 0.025), and the adenosine pool (p < 0.001) was impaired. Ultrastructure was well preserved, but myofibrillar lesions were noted in Group 2.Diltiazem cardioplegia was associated with good functional recovery, but there was impairment of high-energy phosphate metabolism.     

Comparison of Roller Pump versus Pressurized Bag Administration of Potassium Cardioplegic Solution

We sought to determine the relative efficacy of administering cardioplegia by the pressurized bag versus roller pump technique. Fourteen dogs were placed on cardiopulmonary bypass at 30°C and subjected to 2 hours of cardioplegic arrest. Group 1 (7 dogs) was administered cardioplegic solution from a plastic bag under pressure into the ascending aorta every 20 minutes for the 2-hour period, and Group 2 (7 dogs) was given cardioplegia by means of a roller pump.Myocardial temperature decreased in Group 1 to 13.4°C following administration of the cardioplegic solution, and to 13.1°C in Group 2 (not significant). These temperatures were reached in 3.0 minutes in Group 1 and 1.9 minutes in Group 2 (p < 0.03). Aortic root pressures during cardioplegic infusion were 31 ± 2 mm Hg in Group 1 versus 46 ± 2 mm Hg in Group 2 (p < 0.01). No significant differences between groups were noted in myocardial distribution of cardioplegia, myocardial blood flow or metabolism, or left ventricular hemodynamics.We conclude that both methods of administering cardioplegia lowered myocardial temperature adequately and protected the myocardium for a period of 2 hours in these normal hearts. The roller pump method facilitated faster cooling and produced significantly higher aortic perfusion pressures, however, which may be important in hearts with coronary stenosis.     

Effects of varied cardioplegic perfusion pressure on myocardial preservation with critical coronary stenosis

Inadequate delivery of cardioplegic solution distal to coronary artery stenosis may result in increased injury during ischemic arrest. This study was performed to determine the effects of cardioplegic perfusion pressure on cardioplegia delivery and myocardial preservation in hearts with critical coronary artery stenosis. Twenty dogs underwent 90 minutes of cold potassium cardioplegic arrest with partial occlusion of the circumflex coronary artery. Group 1 received cardioplegia at 50 mm Hg pressure, Group 2 at 90 mm Hg pressure, and Group 3 at 130 mm Hg pressure. It was found that cooling rates were 5.4 degrees, 9.1 degrees, and 18.2 degrees C per minute in the nonischemic area (p = 0.004) and 2.0 degrees, 4.5 degrees, and 7.9 degrees C in the ischemic area (p = 0.008) in Groups 1, 2, and 3, respectively. Total of cardioplegic solution flows were 86, 188, and 262 ml per minute per 100 gm in Groups 1, 2, and 3, respectively (p = 0.001). However, flow did not differ significantly between groups in the ischemic area. Rate of rise of left ventricular (LV) pressure decreased significantly in Groups 1 and 2 but not in Group 3 (p = 0.002). Other measured variables did not differ significantly between groups, although LV function curves showed less deterioration in the high-pressure groups. It is concluded that higher cardioplegic perfusion pressure resulted in more rapid cooling in normal and ischemic areas and slightly better preservation of ventricular function as measured by some indexes. However, preservation was generally good for each of the pressures for up to 90 minutes of ischemia when the septum was consistently cooled to 10 degrees C.     

Mechanism of defective oxygen extraction following global ischemia

Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O₂E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O₂ delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O₂. Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O₂E determinations, myocardial O₂ (P_mO₂) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O₂E was depressed in Group I (70 ± 5% of control) and Group II (70 ± 4% of control) but was unaltered in Group III (105 ± 8% of control). This impairment of O₂E was not associated with increased A-V shunting. P_mO₂ was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O₂E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O₂E, therefore, must be an impaired capacity for utilization of delivered O₂ at the cellular level.     

The Protective Effect of St. Thomas Cardioplegia Enriched With Zacopride on the Isolated Rat Heart

The activation of the heart inward rectifier potassium channel (I_K1) can reduce the injury of myocardial cells by shortening the action potential duration and reducing intracellular calcium overload. Zacopride is a selective I_K1 agonist and suppresses triggered arrhythmias in rat hearts. This investigation studied the effects of St. Thomas (ST) cardioplegia enriched with Zacopride on the isolated rat heart model. Sprague‐Dawley rat hearts were harvested and perfused for 20 minutes with 37°C Krebs‐Henseleit (KH) buffer followed by 15 minute perfusion with 4°C calcium‐free KH buffer in the Control group (Con, n = 8), ST cardioplegia in the ST group (ST, n = 8) and ST cardioplegia with Zacopride in the STZ group (STZ, n = 8). After 45 minutes of arresting, all hearts were reperfused with 37°C KH buffer for 60 minutes. Hearts in the STZ group arrested faster than the Con and ST groups (9.25 ± 2.38 s vs. 72.25 ± 8.1 s, 12.75 ± 2.87 s). The recovery of the left ventricular developed pressure, ± dP/dtmax, heart rate, and coronary flow in the STZ group is significantly better than the other two groups during reperfusion. Compared with the Con and ST groups, the STZ group showed significant decreases in the maximum carciac troponin I level (P < 0.05) and the infarct size (P < 0.05). The superoxide dismutase level in the STZ group increased during the first 20 minutes of reperfusion (P < 0.05). ST cardioplegia enriched with Zacopride has beneficial effects against ischemia‐reperfusion injury in this isolated rat heart model.     

Advantages of potassium cardioplegia and perfusion hypothermia in left ventricular hypertrophy.

An attempt was made to determine the effect of hypothermic potassium cardioplegia (35 mEq of potassium chloride) on the hypertrophic ventricle. Puppies with induced left ventricular hypertrophy were divided into four groups and studied after one hour on global ischemia. Myocardial adenosine triphosphate (ATP) was best preserved in the hypothermically perfused groups and correlated well with measurements of coronary sinus creatine phosphokinase (CPK). In Groups 1 and 2 (anoxic arrest at 37 degrees C and KC1 perfusion at 37 degrees C), CPK at 30 minutes of reperfusion was 1,031 and 198 IU, respectively, compared to 35 IU in Group 3 (KC1 perfusion at 4 degrees C) and 44 IU in Group 4 (Ringer's lactate at 4 degrees C). Myocardial injury was milder in Groups 3 and 4 regardless of whether potassium chloride was added. It is apparent that hypothermic perfusion of a hypertrophic ventricle was the major factor in myocardial preservation, as determined by myocardial ATP and coronary sinus CPK.     

The significance of multidose cardioplegia and hypothermia in myocardial preservation during ischemic arrest

A standard experimental protocol was developed to explore the optimal technique for myocardial preservation during 120 minutes of ischemic arrest followed by 30 minutes of reperfusion. Eight different experimental groups were evaluated with the use of an in vivo pig heart preparation. The parameters measured included myocardial contractility and compliance, myocardial blood flow, and endocardial/epicardial blood flow ratio. Myocardial preservation was inadequate after hypothermic arrest alone, cardioplegic arrest alone (at normothermia), and single-dose cardioplegia plus hypothermia. Adequate myocardial preservation was found only after hypothermia and multidose cardioplegia with either potassium (35 mEq. per liter) or magnesium-procaine solutions. Continuous cardioplegia and hypothermia, while providing a moderate degree of myocardial preservation, was not as satisfactory as multidose cardioplegia and hypothermia. No difference in myocardial preservation was apparent when potassium-induced cardioplegia was compared with magnesium-procaine-induced cardioplegia.     

The significant role of membrane stabilization in hypothermic cardioplegic cardiac preservation in a canine experimental model

Isolated mongrel hearts were preserved for 6 h at 5°C followed by normothermic reperfusion for 2 h. The dogs were divided into three groups; K ⁺-cardioplegic solution alone, group C, n =7; K ⁺-cardioplegic solution with lidocaine 200 mg/l, group L, n = 7; and K ⁺-cardioplegic solution with betamethasone 250 mg/l and lidocaine 200 mg/l, group B + L, n = 7. Ventricular fibrillation occurred early during reperfusion in all dogs in group C, in one of seven in group L, and in two of seven dogs in group B + L. The serum MB fraction of creatinine kinase (MB-CK), mitochondrial aspartate aminotransferase (m-AAT) and calcium overload were suppressed to a greater extent in both groups L and B + L during reperfusion compared to group C. Myocardial ATP, total adenine nucleotide, and creatine phosphate did not differ between the three groups at the end of reperfusion. Myocardial ADP and AMP declined significantly during reperfusion in group C, however, they remained unchanged in group B + L and increased in group L which showed significantly higher levels compared to group C. Left ventricular functional recovery during reperfusion was consistently better in both group L and B + L compared to group C. These results suggested that membrane stabilization prevents myocardial damage from hypothermia and cardioplegia and provides better myocardial viability and functional recovery in donor heart preservation.     

The Safety of Simultaneous Arterial and Coronary Sinus Perfusion: Experimental Background and Initial Clinical Results

Concern over myocardial damage from simultaneous arterial (antegrade) and coronary sinus (retrograde) perfusion has led to alternating between these delivery routes to maximize their individual benefits. Based upon predominant retrograde drainage via Thebesian veins, this study: (1) confirms experimentally the safety of simultaneous arterial and coronary sinus perfusion; and (2) reports initial clinical application of this combined strategy in 155 consecutive patients. Experimental: Five mini-pigs (25 to 30 kg) underwent 1 hour of aortic clamping with simultaneous aortic and coronary sinus perfusion at 200 mUmin with normal blood (37°C) before and after 30 minutes of perfusion with either warm (37°C) or cold (4°C) blood cardioplegia. Coronary sinus pressure was always less than 30 mmHg. There was no right or left ventricular edema, lactate production, or lipid peroxidation as transmyocardial and myocardial conjugated dienes were unaltered, and postbypass recovered left ventricular end-systolic elastance (conductance catheter) and preload recruitable stroke work Index 101%± 3% and 109%± 90%, respectively. Clinical: Simultaneous arteriaVcoronary sinus perfusion was used in 155 consecutive high risk patients (New York Heart Association Class III to IV) undergoing isolated coronary artery bypass grafting (CABG) (n = 109) and CABG + valve replacementlrepair or aneurysm (n = 46). Included were 16 patients in cardiogenic shock and 24 undergoing reoperation. Mean aortic clamping time averaged 90 ± 4 minutes (range 30 to 207), with 3.5 ± 0.1 grafts per patient; all anastomoses were performed with the aorta clamped. Cold intermittent blood cardioplegia was used for distal anastomoses and valve implantationhepair in 123 patients, and warm continuous blood cardioplegia was used in 32 patients. Following a warm cardioplegic reperfusate, all patients received warm non-cardioplegic blood perfusion simultaneously via grafts and coronary sinus. Coronary sinus pressure was always less than 40 mmHg. Of 18 patients requiring postoperative mechanical circulatory support (IABP), 16 had IABP placed preoperatively for cardiogenic shock. There were three postoperative myocardial infarctions (2%), and six patients died (3.9% mortality). Conclusion: These experimental and clinical findings overcome perceived concerns about myocardial damage from simultaneous arterial and coronary sinus perfusion, and suggest this approach may add to the armamentarium of cardioprotective strategies. (J Card Surg 1994;9:15–25)     

Warm heart surgery in cold haemagglutinin disease

Continuous warm retrograde blood cardioplegia and systemic normothermia are a promising method for heart surgery in patients with cold autoimmune disorders in order to avoid the adverse effects of both systemic and coronary hypothermia during cardiac arrest and cardiopulmonary bypass. A 59-year-old white man with cold haemagglutinin disease who underwent coronary surgery using continuous retrograde normothermic blood cardioplegia and systemic normothermia is reported.     

Intramyocardial pH during Elective Arrest of the Heart: Relative Effects of Hypothermia versus Potassium Cardioplegia on Anaerobic Metabolism

Using an intramyocardial pH needle probe (21 gauge) to monitor myocardial metabolism during ischemia, we determined the effect of potassium cardioplegia at both moderate and deep hypothermia. Five groups of 5 dogs each were placed on cardiopulmonary bypass and the pH probe was inserted approximately 10 mm into the left ventricular free wall. Cardiac ischemia was achieved by cross-clamping the ascending aorta at 37°C (Group 1), 27°C (Group 2), or 17°C (Group 3). In the remaining two groups, aortic cross-clamping was followed by the infusion of 600 to 800 ml of potassium cardioplegic solution adjusted to cardiac temperatures of 27°C (Group 4) or 17°C (Group 5). In each group, myocardial temperature was maintained constant, electrical and mechanical activity observed, and pH recorded until a plateau was reached or for 3 hours.Our results show a progressive and significant decrease in the metabolic rate with reduction in temperature over the 37° to 17°C range. By abolishing contractile activity, potassium cardioplegia markedly reduces the rate of hydrogen ion accumulation at 27 °C, but at 17 °C the additive effect of cardioplegia is much less pronounced. These observations support the principle of reducing contractile activity to a minimum during elective arrest of the heart but indicate that potassium cardioplegia does little to further reduce the rate of anaerobic metabolism, as shown by the measurement of intramyocardial pH, under conditions of deep hypothermia.     

Modifications of techniques and early results of pulmonary thromboendarterectomy for chronic pulmonary embolism

In 1980 we described bilateral pulmonary thromboendarterectomy with median sternotomy, cardiopulmonary bypass, deep hypothermia, and circulatory arrest for the relief of pulmonary hypertension caused by chronic pulmonary embolism. In our subsequent experience, which totals 41 patients, we have identified three groups of patients characterized by differences of intraoperative management. In Group A (N = 16) myocardial protection consisted of single-dose crystalloid cardioplegia followed by pericardial irrigation with cold saline. Extrapericardial dissection of the pulmonary arteries was performed. Group B (N = 7) was treated the same as Group A except for the substitution of saline slush contained in a laparotomy pad for iced saline. In Group C (N = 18) myocardial protection was single-dose blood cardioplegia followed by the application of a specially designed cooling jacket to the right and left ventricles. Another modification was that of intrapericardial dissection of the pulmonary arteries with extension of the dissection into the hilar tissues without entrance into the pleural spaces. The hospital mortalities of Groups A, B, and C were 18.7%, 14.3%, and 5.5%, respectively (not statistically significant differences). However, other statistically significant differences (p less than 0.05) among the groups were observed: Phrenic nerve paresis occurred in five of seven (71%) Group B patients but in no Group A or C patients; Group B patients required ventilatory support for 32.2 days compared with 8.4 days for Group A and 6.2 days for Group C; time in the intensive care unit was 36 days for Group B patients versus 13 for Group A and 10.3 for Group C; pulmonary vascular resistance decreased 59% (649 versus 259) intraoperatively in 13 patients in Group C. We believe simultaneous bilateral pulmonary thromboendarterectomy with median sternotomy, cardiopulmonary bypass, deep hypothermia with circulatory arrest, and the modified methods of myocardial preservation and dissection represent current optimal surgical management of this problem.     

A comparative study of experimental models for cardiac preservation through orthotopic transplantation

Various kinds of models for canine heart preservation were evaluated through orthotopic transplantation. Following warm ischemic (WIT) and preservation times (PT), donor hearts were orthotopically transplanted to recipients and observed for 2 hours. The study was divided into four groups. A heart-lung preparation (Group A) was preserved by coronary perfusion with diluted blood for an hour following 15-minute WIT in A-1 (n = 33), and 2 hours following 30-minute WIT in A-2 (n = 19). Following 30-minute WIT, the heart (Group B) was preserved for an hour by coronary perfusion with diluted blood in B-1 (n = 20), a modified Krebs solution in B-2 (n = 14), and a EL-solution in B-2 (n = 14). Following 30-minute WIT, the heart (Group C) was preserved for 2 hours by a Langendorff's model with coronary perfusion using perfluorochemical in C-1 (n = 5) and Hydroxyethyl starch in C-2 (n = 1). In Group D, electromechanical arrest of the heart and coronary vascular washout were performed in D-1 (n = 8) with K+ cardioplegia, D-2 (n = 8) with K+-verapamil cardioplegia, and D-3 (n = 5) with Collins M-verapamil cardioplegia. The heart was then removed and suspended in the same solution. The graft was preserved at 4 degrees C for 6 hours in D-1 and D-2, and 24 hours in D-3. Fourty-eight % in A-1 and 26% in A-2 were successfully transplanted.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparison of three haemodynamic monitoring methods in comatose post cardiac arrest patients*

Objectives. Haemodynamic monitoring during post arrest care is important to optimise treatment. We compared stroke volume measured by minimally-invasive monitoring devices with or without thermodilution calibration, and transthoracic echocardiography (TTE), and hypothesised that thermodilution calibration would give stroke volume index (SVI) more in agreement with TTE during targeted temperature management (TTM). Design. Comatose out-of-hospital cardiac arrest survivors receiving TTM (33 °C for 24 hrs) underwent haemodynamic monitoring with arterial pulse contour analyses with (PiCCO2®) and without (FloTrac^®/Vigileo^® monitor^®) transpulmonary thermodilution calibration. Haemodynamic parameters were collected simultaneously every fourth hour during TTM (hypothermia) and (normothermia). SVI was measured with TTE during hypothermia and normothermia. Bland-Altman analyses were used for determination of SVI bias (±1SD). Results. Twenty-six patients were included, of whom 77% had initial shockable rhythm and 52% discharged with good outcome. SVI (bias ±2SD) between PiCCO (after thermodilution calibration) vs FloTrac/Vigileo, TTE vs FloTrac/Vigileo and TTE vs PiCCO were 1.4 (±25.8), ?1.9 (±19.8), 0.06 (±18.5) ml/m2 during hypothermia and 9.7 (±23.9), 1.0 (±17.4), ?7.2 (±12.8) ml/m2 during normothermia. Continuous SVI measurements between PiCCO and FloTrac/Vigileo during hypothermia at reduced SVI (<35 ml/m2) revealed low bias and relatively narrow limits of agreement (0.5 ± 10.2 ml/m2). Conclusion. We found low bias, but relatively wide limits of agreement in SV with PiCCO, FloTrac/Vigileo and TTE during TTM treatment. The methods are not interchangeable. Precision was not improved by transpulmonary thermodilution calibration during hypothermia.     

Lung perfusion during cardiac surgery with cardiopulmonary bypass: is it necessary?

Thirty-two pigs were randomized into group I (aortic cross clamping, antegrade cardioplegia, moderate hypothermia) and group II (normothermia, beating empty heart). Groups were subdivided into subgroups A, B and C, receiving no lung perfusion, perfusion with arterial blood and perfusion with venous blood. Swan-Ganz catheter was used to take mean pulmonary artery pressure which would be used as lung perfusion pressure. Cardiopulmonary bypass (CPB) was established through cannulating aorta and double venae cavae, mechanical ventilation was interrupted and lung perfusion was carried out for 30 min. Blood samples and pulmonary specimens were withdrawn pre- and postoperatively for gasometrical, histological and genic analyses. Postoperative comparison revealed that pulmonary vascular resistance was lower in IC than IA (P=0.01) and it was lower in IIC than IIA (P=0.005). Subgroup IIB had increasing venous oxygen tension (P=0.01) as well as arterial and venous oxygen saturation (P=0.01) compared to IIA. Arterial oxygen saturation was decreased in IIC vs. IIA (P=0.006). Histological differences were observed between subgroups A and B as well as A and C (P=0.003). Lung perfusion during CPB may improve pulmonary hemodynamic performance, optimize gas exchange and maintain cellular integrity.