Release Of Aortic Cross-clamp Research Articles

Perfusion-related factors of endotoxin release during cardiopulmonary bypass.

To investigate whether the release of endotoxin during cardiopulmonary bypass (CPB) is determined by perfusion-related factors, endotoxin concentrations were determined before, during, and after CPB in 21 male patients (age range 45-75 years) undergoing elective coronary artery bypass grafting. Hemodynamic parameters and oncotic pressure were also measured. Significant increases in endotoxin concentrations were observed after the start of CPB (P < 0.005), before aortic cross-clamp release (P < 0.05), and after aortic cross-clamp release (P < 0.05). The median endotoxin concentration after cessation of CPB was 0.264 EU/ml (range < 0.036-0.480 EU/ml). Endotoxin concentrations derived from the prime solutions were not contributory. Positive correlations were found between arterial pressure after the start of CPB and the endotoxin concentration 10 min after (r = 0.58, P < 0.01) and between the duration of aortic cross-clamping and the endotoxin concentration after the cessation of CPB (r = 0.64, P < 0.005). Arterial pressure after the start of CPB, the duration of aortic cross-clamping, and decrease in oncotic pressure appeared to be independent variables in a forward variable selection model that predicted endotoxin concentrations after CPB. We conclude that in patients undergoing elective coronary artery bypass grafting, an early phase of endotoxin release during CPB could be demonstrated, and that this is due to vasoconstriction. The endotoxin concentrations after the cessation of CPB were determined by early vasoconstriction, duration of aortic cross-clamping, and hypo-oncotic hemodilution.

Contact, Coagulation and Platelet Interaction with Heparin Treated Equipment during Heart Surgery

Heparin coating of an extracorporeal device may reduce blood activation. To evaluate protein and platelet interaction with Duraflo II surface treatment of the cardiopulmonary bypass (CPB) circuit, thirty coronary artery bypass grafting patients were randomly divided into two groups (Duraflo II, n = 15 or Control, n = 15). Binding of antibodies against factor XII, antithrombin III (ATIII) and platelet receptor GpIb were significantly higher (p < 0.01) on the Duraflo II treated surface. Hageman Factor fragment (HFf or factor XIIf) activity observed in the fluid phase tended to be lower in the treated circuits, although complexes of factor XIIf-C1 inhibitor (C1INH) increased by the same extent in both groups. Thrombin was effectively bound on the Duraflo II surface while thrombin-antithrombin III formation was reduced during the first phase of CPB. As expected, this thrombin inhibiting capacity remained higher on the Duraflo II, although in the arterial line a reduction of 10% per hour was observed. This indicated loss of functional bound heparin of the Duraflo II surface. During the second phase of CPB, after release of the aortic crossclamp, factor XII and thrombin were strongly activated in both groups indicated by a sharp increase in concentrations of T/AT complex as well as FPA. Platelet numbers tended to increase more in the control group during CPB than in the Duraflo II group, likely by interaction of platelet GpIb receptors on the Duraflo II treated surface (p < 0.01). However, platelet activation assessed by beta-TG was similar in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypotension after the release of aortic cross clamp in patients undergoing open heart surgery

One hundred consecutive adult patients under-going various elective open heart surgical procedures were included in this prospective study. An indwelling radial arterial cannula was used to measure mean arterial pressure (MAP). Systemic vascular resistance (SVR) during bypass was calculated using the formula SVR=MAP×80/pump flow dynes-sec-cm−5. Patients in whom vasodilators were used during cardiopulmonary bypass were excluded. Measurements were made just before the release of aortic cross clamp when the pump flows were normal; and 1,3,5 and 10 minutes following the cross clamp release. There were 60 males and 40 females with a mean age of 29.4±13.9 years and mean weight of 46±13 Kg. The MAP fell from 65±14 to 47±15 mm Hg (p<0.00001) and the SVR fell from 1699±511 to 1163±365 dynes-sec-cm−5 (p<0.00001) one minute after the release of aortic cross clamp. There was some recovery during the subsequent period, but the change continued to remain statistically significant upto 10 minutes after the release of aortic cross clamp. MAP and SVR decreased in all except 9 and 3 patients respectively at 1 minute. The mean temperature at the time of release of aortic cross clamp was 33.7±2.7°C. There was a poor correlation between the temperature and duration of bypass and extent of decrease in MAP and/or SVR. We conclude that there is a significant decrease in MAP (27%) and SVR (31%) after the release of aortic cross clamp and it persists for 10 minutes.

The patterns and mechanics of delayed declamping hypotension in abdominal aneurysm surgery

Some degree of hypotension commonly occurs following release of aortic cross-clamping in surgery of abdominal aneurysm, but is usually not prolonged in patients with adequate volume replacement. However, we have observed that in some patients delayed declamping hypotension occurred in spite of volume replacement. In this report, we examined the physiological patterns of such hypotension and considered possible mechanisms.

Heparin-coating of extracorporea circuits reduces thrombin formation in patients undergoing cardiopulmonary bypass

This clinical study was performed to evaluate the inhibiting effects of heparin- coated extracorporeal circuits on thrombin formation during cardiopulmonary bypass (CPB). Thirty patients undergoing coronary artery bypass grafting were randomly divided into two groups with (Duraflo II, n=15) orwithout (control, n=15) the use of heparin-coated circuits. Standard systemic heparinization was performed in all the patients before CPB. The results showed that thrombin formation during the first phase of CPB was inhibited by heparin-coating identified by the significantly lower concentrations of thrombin-antithrombin III (TAT) complex formed in plasma in the Duraflo II group than in the control group (p &lt;0.05). Heparin concentrations were higher in the Duraflo II group than in the control group at the end of CPB ( p &lt;0.05). However, after release of the aortic crossclamp in the second phase of CPB, thrombin became strongly activated in both the Duraflo II and the control groups indicated by a sharp increase of TAT complex as well as fibrinopeptide A. Thus, Duraflo II heparin-coating reduces thrombin formation in the early phase of CPB, however, this beneficial effect was counteracted after aortic crossclamp release by material-independent stimuli. Therefore, adequate systemic heparinization is still required despite improved haemocompatibility of the circuits offered by heparin-coating.

Anaesthetic management for surgical correction of coarctation of aorta

In this paper we have reviewed the anaesthetic management of 57 consecutive patients who underwent surgical correction of coarctation of aorta. The patients were divided into two groups. In group I of ten patients, no volume preloading was done prior to the release of aortic cross-clamp and the declamping hypotension was managed by rapid infusion of fluids along with correction of metabolic acidosis. In group II of 47 patients, volume preloading was done along with administration of sodium bicarbonate 1 mEq/kg just prior to declamping. Statistically significant (p<0.05) decrease in the systolic and diastolic pressures were observed after declamping in group I; whereas in group II, the hypotension observed was statistically insignificant. Declamping hypotension can thus be prevented or minimised by appropriate volume preloading and correction of existing metabolic acidosis just prior to the release of aortic cross-clamp.

An improved lidocaine infusion protocol for cardiac surgical patients

A new protocol for lidocaine administration was tested to determine whether it would provide higher free and total serum lidocaine concentrations during and after weaning from cardiopulmonary bypass (CPB), without leading to accumulation toxicity, than those resulting from a conventional protocol (1.5 mg/kg loading dose bolus + 2 mg/min infusion rate). Ten elective adult cardiac surgical patients were studied. Ten seconds prior to aortic cross-clamp release (0 min), each patient received a lidocaine bolus (1.5 mg/kg) and simultaneous lidocaine infusion (5 mg/min for 1 hour, followed by 2 mg/min for 23 hours). Weaning occurred 20 to 30 minutes after cross-clamp release. Lidocaine levels were determined from arterial blood samples at 0, 10, 20, 30, and 60 minutes, and at 2, 4, and 24 hours postcross-clamp release. Compared with the conventional protocol, the new protocol showed a significant increase in mean total lidocaine concentration ( P ⪯ 0.02) at 30 and 60 minutes, and a significant increase in mean free lidocaine concentration ( P ⪯ 0.005) at 20, 30, and 60 minutes. No patient had toxic levels at 24 hours. Results of this study suggest that in patients undergoing cardiac surgery, a “5 + 2” mg/min infusion protocol is safe and superior to a conventional protocol in achieving therapeutic serum levels of free and total lidocaine.

Comparison of bretylium and lidocaine in the prevention of ventricular fibrillation after aortic cross-clamp release in coronary artery bypass surgery

The authors compared bretylium and lidocaine for reducing the incidence and persistence of ventricular fibrillation following aortic cross-clamp release performed during coronary artery bypass surgery. Thirty-three adult patients scheduled for elective bypass surgery were randomly assigned in a double-blind fashion to receive a bolus of bretylium, 10 mg/kg, lidocaine, 2 mg/kg, or saline, in equal volumes prior to the release of the aortic cross-clamp. Coronary artery bypass surgery was conducted using standard cardiopulmonary bypass (CPB) procedures with systemic cooling to 24° to 28°C. Temperature, arterial blood gases, and electrolytes were recorded. After clamp release, the first electrical rhythm was noted. Abnormal rhythms (ventricular fibrillation) were allowed to persist for 1 to 2 minutes, and if spontaneous conversion to a supraventricular rhythm did not occur, defibrillation with internal DC countershocks was applied. Patients were compared with respect to occurrence of ventricular fibrillation, need for DC countershocks, antiarrhythmic drugs, and inotropic support. There was no significant difference among the groups with respect to age, sex, preoperative medications, past medical histories, ejection fractions, average number of bypasses, cross-clamp times, or temperatures during bypass. The incidence of ventricular fibrillation after aortic cross-clamp removal was: saline 91 %, lidocaine 64% ( P < 0.01), and bretylium 36% ( P < 0.01). The number of countershocks required to defibrillate, while lower in the grotylium group, did not reach statistical significance. After cardiopulmonary bypass, cardiac output and systemic vascular resistance were comparable. Bretylium warrants further study in this setting.

Free and total lidocaine levels in cardiac surgical patients

A lidocaine bolus of 2 mg/kg has been shown to decrease the incidence of ventricular fibrillation in cardiac surgical patients during reperfusion following aortic cross-clamp release (CCR). In an effort to extend this effect into the immediate postoperative period, many centers routinely administer a prophylactic lidocaine infusion for the first 12 to 24 hours after surgery. Sequential total serum lidocaine levels were measured over 6 hours in 28 adult cardiac surgical patients without liver, kidney, or respiratory disease, and free serum lidocaine levels were measured in 15 of these patients. In addition, pharmacokinetic data were collected and analyzed in 8 of these patients. Each patient received a lidocaine bolus of 1.5 mg/kg and an infusion at 2 mg/min immediately before CCR. Serum levels were determined just before CCR, and at 10, 20, 30, 60, 120, 240, and 480 minutes after CCR. More than 50% of patients had subtherapeutic total serum lidocaine levels from 20 to 120 minutes after CCR, but free lidocaine levels remained within the therapeutic range. No patient showed malignant ventricular dysrhythmias during the study. The results suggest that (1) it may be misleading to estimate free lidocaine concentration based on total lidocaine levels; and (2) free drug is the moiety-responsible for lidocaine's antiarrhythmic effect.

Myocardial blood flow and oxygen consumption after aortic cross-clamping

The effect of four repetitive periods of 10 min global ischemia, followed by 15 min of reperfusion on myocardial blood flow and oxygen consumption at 34°C (group N) and 25°C (group H) were studied in comparison with that of 60 min continuous ischemia combined with multidose St. Thomas Cardioplegia (group C) in dogs on cardiopulmonary bypass (CPB). Two groups, in which a protocol comparable to the groups N and H, respectively, but without repetitive periods of ischemia was followed, served as control. In all groups a hyperemic response was observed after release of aortic cross-clamping (AC). Myocardial blood flow was not diminished at the end of CPB as compared to the values at the start of CPB. We conclude that the no-reflow phenomenon did not occur after these procedures of intermittent or continuous AC. Immediately following release of AC the arterial-coronary sinus difference of oxygen content reached a peak value in groups N and H indicating rapid replenishment of the low tissue oxygen content. These peak values appeared to be much smaller after cardioplegia. After 10 min of reperfusion a significant lower oxygen consumption was observed at 25°C (0.2 μmole·g −1·min −1 O 2) as compared to 34°C (1.5 μmole· g −1·min −1 O 2). This difference cannot be explained by temperature alone because oxygen consumption did not decrease below 0.5 μmole·g −1·min −1 in the control group of dogs put on CPB at 25°C. Based on the findings of myocardial blood flow and oxygen consumption the conclusion is drawn that the heart tolerates well the periods of ischemia and reperfusion, as used in the present protocols mimicking the procedures routinely applied during aorta-coronary bypass surgery.

Comparison of Bretylium and Lidocaine for the Prevention of Venticular Fibrillation After Aortic Cross-Clamp Release During Coronary Artery Bypass Surgery

Comparison of Bretylium and Lidocaine for the Prevention of Venticular Fibrillation After Aortic Cross-Clamp Release During Coronary Artery Bypass Surgery

Superoxide dismutase and hemodynamic changes following aortic crossclamp release

Release of an aortic crossclamp usually results in hypotension which is mainly due to hypovolemia from sequestration of fluid in the tissues and the release of vasoactive substances lie, bradykinin, free radicals) that increase capillary permeability. The purpose of this study was to evaluate superoxide dismutase (SOD), a free-radical scavenger, as a pharmacologic technique to prevent hemodynamic changes following aortic crossclamping and release. Fourteen mongrel dogs were studied and divided into two groups. The aorta was clamped for 60 minutes. Group A received NaHCO 3, 3.5 mEq/kg, and SOD, 15,000 U/kg; while group B received only NaHCO 3, 3.5 mEq/kg, prior to aortic crossclamp release. There was a statistically significant difference in cardiac output, systolic blood pressure, systemic and pulmonary vascular resistances, and arterial oxygen tension between the two groups following aortic crossclamp release. Cardiac output increased from 2.2 ± .05 to 2.5 ± .03 L/min ( P < .05) after declamping, and returned toward preclamping baseline values after five minutes in group A. In group B, cardiac output decreased from 2.3 ± .05 to 2.1 ± .01 ( P < .005) after declamping and remained unchanged five minutes later. No statistically significant changes in PaO 2 occurred in group A, while there was a significant decrease in PaO 2 in group B after crossclamp release. In group B, PaO 2 decreased from 95 ± 7 to 70 ± 1 mmHg ( P < .005) after crossclamp release. Bradykinin levels were almost identical in both groups studied. It is concluded that SOD significantly decreases the cardiovascular changes following aortic crossclamp release.

Rise in pulmonary arterial pressure following release of aortic crossclamp in abdominal aortic aneurysmectomy.

Rise in pulmonary arterial pressure following release of aortic crossclamp in abdominal aortic aneurysmectomy.

Verapamil Pretreatment before Aortic Cross-Clamping in Patients Undergoing Coronary Artery Bypass Graft

In 12 of 22 patients with coronary artery disease undergoing elective coronary artery bypass graft (CABG), verapamil (0.075 mg/kg body weight) pretreatment was given on initiation of cardiopulmonary bypass (CPB) before aortic cross-clamping (ACC), whereas no verapamil was used in 10 control patients. The volume of cardioplegia solution required to achieve and maintain cardiac asystole during ACC while on CPB was not significantly different in the two groups. After the release of ACC, the energy of direct current countershock required for defibrillation, the incidence of heart block, and the need for pacemaker were not significantly different. However, defibrillation was more readily achieved by a single countershock in the verapamil group than in the control group. Also, the incidence of ST segment changes after defibrillation was significantly lower in the verapamil group, suggesting that verapamil pretreatment before ACC may potentiate the myocardial preservation achieved by the cardioplegia, and hence may decrease the incidence of ischemic changes during the critical reperfusion period.

Influence of mannitol and dopamine on renal function during elective infrarenal aortic clamping in man.

The impact of elective infrarenal aortic clamping on parameters of renal function was evaluated in 27 extracellular fluid volume expanded patients. Significant transient decreases (p less than 0.05) in glomerular filtration rate were observed in all three groups either in the early or late post-clamp release period, despite maintenance of hemodynamic stability. This study documents transient decreases in glomerular filtration rate which occurred following release of the infrarenal aortic cross-clamp. No clinically important benefit from the use of mannitol and dopamine over extracellular fluid volume expansion with saline alone was demonstrated in the prevention of the changes in renal function associated with aortic cross-clamping.

Release patterns of CK-MB and mitochondrial CK following myocardial ischaemia

Following myocardial damage as in acute myocardial infarction (AMI) or open heart surgery, the tissue damage might result in a release of mitochondrial CK (CK-MIT). The presence of this CK isoenzyme in serum may be detected after Chromatographic separation of CK-activity on Sephacryl S-200. By combining Chromatographic separation of CK-MB with immunologic inhibition of CK-M, both CK-MB and CK-MIT can be estimated in serum. Using this procedure changes in enzyme activities were studied in ten patients with AMI and twelve patients subjected to open heart surgery using cardioplegia. Following AMI CK-MB peaked about 24 h after onset of ischaemic symptoms. CK-MIT increased similarly and reached a plateau after 24 h where it remained during an additional 24–36 h. At peak CK-MB concentration, the corresponding CK-MIT activity was about 22% of the CK-MB activity. Following cardiac surgery there was a rapid release of CK-MB with a peak about 5 h after release of aortic cross-clamping, and with a simultaneous CK-MIT activity amounting to 19% of the CK-MB activity. In conclusion, CK-MIT is released into serum following myocardial ischaemia. Its appearance has time characteristics similar to that of other mitochondrial enzymes. The CK-B method does not specifically determine CK-B, but non-CK-M, which in cardiac ischaemia at peak serum CK-MB concentrations includes about 20% CK-MIT.

Myocardial and non-myocardial release of myoglobin and creatine-kinase MB following cardiac operations with hypothermic potassium cardioplegia.

Serum time-activity curves for myoglobin, creatine-kinase (CK) and its isoenzyme MB were determined during and after coronary bypass surgery and aortic valve replacement. Hypothermic potassium cardioplegia was the method employed to initiate cardiac arrest. Cardiac myoglobin and CK-MB release rates were maximal 0.5 to 1.0 h post aortic cross-clamp release (PACR) with maximal concentrations at 1 and 4 h PACR respectively. The cardiac release ceased within 5 h PACR but was followed by a noncardiac release with maximal concentrations from 10 to 35 h PACR. The cardiac myoglobin release was significantly lower in the coronary bypass group, whereas no significant intergroup difference was observed for CK-MB. The cumulative CK-MB release corresponded roughly to about 5 g of myocardium.

Effect of intra-aortic balloon pumping and calcium antagonist for reducing coronary reperfusion injury.

Open heart surgery under aortic cross-clamping is often required, but coronary reperfusion injury after release of aortic cross-clamping is unavoidable irrespective of applications of various protective methods to the myocardium. The anterior descending branch of the left coronary artery of mongrel adult dogs was occluded for 2 hours and then reperfused. The protective effects of intra-aortic balloon pumping (IABP) and of a calcium antagonist "diltiazem hydrochloride" (diltiazem) on the decreased reperfusion of ischemic, border and normal areas were examined by measuring the regional myocardial blood flow (RMBF) using a radioactive microsphere method. Diltiazem could increase significantly the RMBF in the border area. IABP induced a significant increase in the RMBF of the same area more than Diltiazem, with the increase in the endocardial layer tending to be superior to that in the epicardial layer. The results suggested that diltiazem is very effective for reducing the coronary reperfusion injury. It is also suggested that IABP is even more effective than diltiazem because it increases the RMBF significantly and, moreover, has a tendency to increase the blood flow in the endocardial layer which is poor in collateral vessels and thus vulnerable to ischemia.

Myocardial protection during aortic valve replacement. effects of mannitol in the cardioplegic solution on cardiac metabolism and enzyme release.

Myocardial substrate metabolism and enzyme release following hypothermic potassium cardioplegia with and without the addition of mannitol in the cardioplegic solution were studied in two series of patients undergoing isolated aortic valve replacement. Measurements were made of PO2. O2-saturation and content, PCO2, pH, glucose, lactate, pyruvate, potassium, myoglobin, creatine kinase (CK), its isoenzyme MB and aspartate aminotransferase (ASAT) simultaneously in arterial and coronary sinus blood before cardioplegia and during the first 60 min after the release of aortic cross-clamping. In addition, myoglobin and enzymes were followed in peripheral venous blood for 72 hours after cardioplegia. Analysis of the results revealed no striking difference between the groups. Nevertheless, with the addition of mannitol, there was a slightly lower release of lactate and myoglobin probably indicating a more rapid metabolic recovery of the myocardium.

Shock Following Release of Aortic Cross-Clamping

The hypotension which follows release of the occluding aortic clamp has been noted by everyone doing surgery for abdominal aortic aneurysms. This hypotension may be only temporary or it may be sustained. Experimentally, at least, temporary hypotension occurs after release of aortic clamping of short duration, and sustained hypotension is expected only if the aorta has been occluded for an hour or more before declamping. Significant hypotension, whether temporary or sustained, is undesirable in any patient, but particularly so in those with degenerative arterial disease affecting the coronary, carotid, or cerebral arteries. Since the incidence of such disease is high in patients with aortic aneurysms1the prevention of hypotension in these cases is obviously highly desirable. Several factors probably contribute to hypotension developing after declamping the aorta. The sudden increase in the size of the vascular bed to be filled undoubtedly accounts for some decrease in arterial pressure, and