On-pump beating-heart mitral valve plasty without aortic cross-clamping

Patients with ischemic cardiomyopathy often have mitral regurgitation, which should be corrected for better long-term survival. Mitral valve surgery is usually performed during cardiopulmonary bypass under the arrested heart condition. The ascending aorta is cross-clamped and the heart is arrested using a cardioplegic solution. However, because ischemic cardiomyopathy patients often have a severely atherosclerotic ascending aorta and low cardiac function, aortic cross-clamping and cardiac arrest increase the risk of postoperative thromboemboli and low cardiac output syndrome. Under the on-pump beating-heart condition, we performed mitral valve plasty concomitant with coronary artery bypass grafting, tricuspid annuloplasty, left ventricular aneurysmectomy, and the maze procedure without aortic cross-clamping for a patient with ischemic dilated cardiomyopathy and bradycardial atrial fibrillation. The patient had no postoperative complications and recovered rapidly. Thus, to prevent serious postoperative complications, on-pump beating-heart mitral valve surgery without aortic cross-clamping may be a suitable surgical option for patients with ischemic cardiomyopathy.     

Leakage test during mitral valve repair

Mitral valve repair is the preferred surgical treatment for mitral regurgitation. Cardiac surgeons must increasingly pursue high-quality mitral valve repair, which ensures excellent long-term outcomes. Intraoperative assessment of a competency of the repaired mitral valve before closure of the atrium is an important step in accomplishing successful mitral valve repair. Saline test is the most simple and popular method to evaluate the repaired valve. In addition, an “Ink test” can provide confirmation of the surface of coaptation, which is often insufficient in the assessment of saline test. There are sometimes differences between the findings of the leakage test in an arrested heart and the echocardiographic findings after surgery. Assessment of the mitral valve in an arrested heart may not accurately reflect its function in a contractile heart. Assessment of the valve on the beating heart induced by antegrade or retrograde coronary artery perfusion can provide a more physiological assessment of the repaired valve. Perfusion techniques during beating heart surgery mainly include antegrade coronary artery perfusion without aortic cross-clamping, and retrograde coronary artery perfusion via the coronary sinus with aortic cross-clamping. It is the most important point for the former approach to avoid air embolism with such precaution as CO₂ insufflation, left ventricular venting, and transesophageal echocardiography, and for the latter approach to maintain high perfusion flow rate of coronary sinus and adequate venting. Leakage test during mitral valve repair increasingly takes an important role in successful mitral valve reconstruction.     

升主动脉粥样硬化患者的冠状动脉旁路移植

目的 总结冠状动脉粥样硬化性心脏病合并升主动脉粥样硬化患者冠状动脉旁路移植手术的特点。方法 22例患者中,13例采用非体外循环、心脏不停跳下冠状动脉旁路移植术(59％);9例采用低温体外循环(41％),其中5例在深低温、低流量并间断停循环条件下不阻断升主动脉行旁路-升主动脉近端吻合。结果 20例康复出院,术后早期死亡2例;并发症有肺部感染、心绞痛、室颤、急性心肌梗死和血胸,无神经系统并发症。结论 减少术中升主动脉操作是防止升主动脉损伤和减少并发症的关键。应用带蒂动脉旁路、旁路远端序贯吻合和近端Y形吻合可避免或减少旁路-升主动脉吻合;低温体外循环加左心室引流时,可不阻断升主动脉行旁路远端吻合;深低温、低流量并间断停循环下行旁路-升主动脉吻合,可避免阻断和部分阻断升主动脉,利于控制并发症。     

Assessment of myocardial perfusion with laser Doppler flowmetry. An experimental study on porcine heart

Laser Doppler flowmetry was applied to the arrested heart of four pigs and to the fibrillating heart of three pigs during cardiopulmonary bypass. The coronary blood flow was maintained during cardiac arrest by infusion of hyperkalemic blood into the aortic root. A significant correlation (r = 0.88, n = 52, p less than 0.001) between laser Doppler signal and coronary blood flow was found during cardiac arrest. During ventricular fibrillation after release of the aortic cross-clamp there was significant correlation (0.84, n = 38, p less than 0.01) between laser Doppler signal and extracorporeal blood flow. A residual laser Doppler signal of about 60% of the maximal value was recorded even after the bypass flow was discontinued. Laser Doppler flowmetry is concluded to permit measurement of myocardial perfusion in the arrested porcine heart. Muscular activity of the heart contributes to the output signal during ventricular fibrillation.     

Left ventricular assist device insertion and open abdominal aortic aneurysm repair in same admission for an end-stage heart failure patient

Patients suffering from end-stage heart failure also suffer from multiple cardiovascular comorbidities such as abdominal aortic aneurysm (AAA). Mechanical support with left ventricular assist device with open repair of AAA repair has rarely been reported in literature. The authors describe a 60-year-old male with end-stage heart failure and a symptomatic AAA with sequential left ventricular assist device insertion and open AAA repair with aortic cross-clamping.     

Assessment of gut mucosal perfusion and colonic tissue blood flow during abdominal aortic surgery with gastric tonometry and laser Doppler flowmetry

The objective of this study was to investigate the effect of infrarenal aortic cross-clamping and unclamping on gut mucosal perfusion by gastric tonometry and on sigmoid colonic tissue blood flow by laser Doppler flowmetry during abdominal aortic surgery. This was a prospective before-and-after intervention comparison study in a university hospital of 8 male patients, aged 57-87, undergoing elective infrarenal abdominal aortic surgery. Each patient was pretreated with ranitidine. Following general anesthesia, a nasogastric tonometer was inserted into the stomach. The balloon of the tonometer was filled with 2.5 mL of normal saline for gas tension and pH analysis. This process was repeated before and after aortic cross-clamping and unclamping. Gastric mucosal pHi was calculated with the Henderson-Hasselbalch equation from the arterial Hco3- and the tonometrically measured mucosal Pco2. A laser Doppler flow probe was placed in contact with the serosa of the sigmoid colon against the mesentery after the abdomen was opened. Sigmoid colonic tissue blood flow (SCBF) was assessed by the laser Doppler flowmeter. Gastric mucosal pHi by gastric tonometry and colonic tissue blood flow by laser Doppler flowmetry were measured before and after aortic cross-clamping and unclamping. Gastric mucosal pHi decreased significantly 30 minutes after aortic cross-clamping (7.37 +/-0.07) (p < 0.01), 60 minutes after aortic cross-clamping (7.39 +/-0.08) (p < 0.05), and 30 minutes after aortic unclamping (7.37 +/-0.08) (p < 0.01), compared with pHi before aortic cross-clamping (7.50 +/-0.06). Gastric mucosal pHi increased to the original level 60 minutes after aortic unclamping (7.46 +/-0.08). Since a gastric mucosal pH above 7.35 is considered normal, these mean values of pHi were clinically insignificant. However, gastric mucosal pHi decreased below 7.32 in 5 patients during abdominal aortic surgery. Gastric mucosal pHi decreased further to 7.30 in 1 patient following aortic cross-clamping and below 7.30 in 3 patients 30 minutes after aortic unclamping. SCBF decreased significantly after aortic cross-clamping (28.1 +/-4.8 mL/min/100 g) compared with the value before aortic cross-clamping (51.9 +/-11.3 mL/min/100 g) (p < 0.01). Following aortic unclamping, SCBF returned to 41.7 +/-7.4 mL/min/100 g. It is concluded that transient episodes of significant intestinal mucosal ischemia may have been encountered occasionally in patients undergoing abdominal aortic surgery, but a sigmoid colonic tissue blood flow of 41.7 +/-7.4 mL/min/100 g was sufficient to prevent postoperative ischemic colitis regardless of whether there was ligation or no ligation of inferior mesenteric artery among the studied population since none of the patients developed clinically significant ischemic colitis.     

Correlation of Patterns of Subendocardial Reperfusion and Left Ventricular Performance after Ischemia

Ninety-three dogs were studied with normothermic or hypothermic ischemia for 60 or 90 minutes, with or without potassium cardioplegia. Radioactive-labeled microspheres (9 ± 1) were injected into the aortic perfusion cannula just prior to aortic cross-clamping and at 2, 6, and 10 minutes after the clamp was released. Left ventricular (LV) function was analyzed with a right heart bypass model before and 45 minutes after the ischemia period. Changes in LV function were defined as the arithmetic difference in the center of mass between preischemia and postischemia computer-drawn Sarnoff curves.Regardless of technique of myocardial protection, increased subendocardial flow 2 minutes after ischemia correlated strongly with preservation of LV function (p < 0.01). Well-preserved hearts showed a rapid return to normal levels of coronary blood flow (p < 0.01). In contrast, a delay in the peaking of subendocardial flow to 10 minutes was associated with poor function (p < 0.01). There was a high correlation between ultrastructural morphology and LV function. While well-preserved hearts show early preferential subendocardial perfusion, the poorly protected myocardium is unable to restore adequate subendocardial flow early in the reperfusion period.     

Prevention of Ischemic Spinal Cord Injury Following Aortic Cross-Clamping: Use of Corticosteroids

Prior to proximal aortic cross-clamping, baseline measurements of spinal cord blood flow and function were done. Blood flow was evaluated with radioactive microspheres and function determined by assessment of somatosensory evoked potential (SEP). Group 1 (N = 6) animals had aortic cross-clamping for 5 minutes after ischemic spinal cord dysfunction (SEP loss) was documented. Group 2 (N = 9) underwent aortic cross-clamping for 10 minutes after loss of SEP. Group 3 (N = 6) also underwent 10 minutes of cross-clamping after initial SEP loss, but were treated intravenously with methylprednisolone (30 mg per kilogram of body weight) 10 minutes prior to cross-clamping and again 4 hours postoperatively. After release of the cross-clamp, the animals were allowed to recover and serial evaluations of spinal cord blood flow and neurological status were carried out for seven days. Group 1 animals recovered uneventfully without evidence of neurological injury. Group 2 animals sustained a 67% incidence of permanent spastic paraplegia (p = 0.02 versus Group 1). In contrast, methylprednisolone-treated animals sustained no clinically detectable neurological injury (p = 0.02 versus Group 2). Measurements of spinal cord blood flow at the time of SEP loss revealed similar degrees of spinal cord ischemia in all groups. No significant differences were observed in the duration of aortic cross-clamping prior to SEP loss among the three groups. The data indicate that short periods of cross-clamping (5 minutes) following SEP loss are well tolerated, whereas longer periods (10 minutes) are associated with a high incidence of paraplegia. This injury can be prevented if an adequate dose of methylprednisolone is given before and after cross-clamping. Beneficial effects of steroid administration do not appear to be related to changes in spinal cord blood flow, but may be related to protective effects on cellular and subcellular components. Clinical investigations employing this regimen of corticosteroid protection during surgical procedures on the thoracoabdominal aorta appear to be indicated.     

Effect of noncoronary blood flow upon myocardial mitochondrial function during hypothermic anoxic arrest

Mongrel dogs (23) were subjected to the experimental study characterizing the effect of noncoronary blood flow upon myocardial mitochondrial respiration. Anoxic arrest for 60 minutes was obtained by cross-clamping of the aorta under hypothermic cardiopulmonary bypass, and heart was reperfused for 10 minutes, then heart was excised to obtain the endocardium, epicardium of the left ventricle and ventricular septum for study of mitochondrial function and myocardial blood flow. Myocardial blood flow was measured with carbonized plastic tracer⁴⁶Sc during cross-clamping of the aorta. Noncoronary blood flow showed equal distribution in the left ventricle and septum with flow of 0.16±0.23 ml/min/100g (endocardium). Mitochondrial respiratory function following 60 minutes of hypothermic anoxic arrest at 20°C recovered to normal level, and also no correlation was demonstrated between noncoronary blood flow during cross-clamping of the aorta and mitochondrial respiratory function. It was concluded that noncoronary blood flow was negligible with respect to the oxygen demand at 20°C of myocardial temperature, and that noncoronary blood flow during cross-clamping of the aorta was not correlated to mitochondrial protection from ischemia.     

Ultrastructural integrity of human ventricular myocardium following cardioplegic arrest.

The appearance of the ventricular myocardium in 6 patients electing coronary bypass operation was evaluated by electron microscope before and after aortic cross-clamping. Bypassing protocol included the induction of hypothermic cardioplegia by intermittent aortic root perfusion, with potassium chloride added to cold blood serving as the cardioplegic agent. Cross-clamp intervals ranged from 66 to 125 minutes. Ultrastructural alterations following bypass manipulations, and distinct from those observed before cross-clamping, were limited to the presence of extensive myocardiocytic pooling of glycogen. Scrutiny of the intramyocardial capillary bed following perfusion with the cardioplegic solution revealed no abnormalities attributable to, or intensified by, the bypass maneuver. These findings indicate that hypothermic potassium cardioplegia, as specified, is not injurious to human myocardial ultrastructure.     

Analysis of diastolic function in patients undergoing aortic aneurysm repair and impact on hemodynamic response to aortic cross-clamping

OBJECTIVES: The purpose of this study was to analyze left ventricular diastolic function in patients undergoing aortic aneurysm repair and to investigate the effects of laparotomy and aortic cross-clamping on diastolic function. DESIGN: Prospective clinical study. SETTING: University hospital. PARTICIPANTS: Forty-five consecutive patients undergoing open aortic aneurysm repair. INTERVENTIONS: Left ventricular diastolic function and hemodynamic variables were evaluated using transesophageal Doppler echocardiography and a pulmonary artery catheter at baseline, after laparotomy, and at 1 and 10 minutes after cross-clamping. Diastolic function was determined by Doppler derivatives of mitral inflow (E/A ratio, deceleration time of early inflow) and pulmonary venous flow (S/D ratio). MEASUREMENTS AND MAIN RESULTS: Twenty of 39 patients revealed signs of diastolic dysfunction at baseline. Of these 20 patients, 14 displayed delayed relaxation and 6 displayed a pseudonormal filling pattern. Patients with pseudonormal filling exhibited a lower stroke volume (p = 0.02) and cardiac index (p < 0.01) in comparison to patients with normal diastolic function. Laparotomy was associated with an improvement of diastolic function in 9 of 20 patients with preexisting diastolic dysfunction. Only 3 patients suffered impairment of diastolic function after cross-clamping. The hemodynamic response to cross-clamping did not differ between patients with normal and abnormal diastolic function. CONCLUSIONS: About 50% of patients undergoing aortic aneurysm repair exhibit signs of diastolic dysfunction. The majority of these patients showed delayed relaxation. Patients with pseudonormal filling displayed a significantly lower cardiac index. Laparotomy resulted in an improvement in diastolic function in about half of patients with preexisting diastolic dysfunction. The effects of cross-clamping on diastolic function are minimal.     

Myocardial blood flow and oxygen consumption in the empty-beating, fibrillating, and potassium-arrested hypertrophied canine heart

Myocardial oxygen consumption and blood flow distribution were examined in severely hypertrophied canine hearts in the empty-beating, fibrillating, and pharmacologically arrested states. Hypertrophy was produced using a subcoronary valvular aortic stenosis model that mimics the clinical situation of aortic valvular stenosis. Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer, which had been validated by the Van Slyke-Neill method. Transmural blood flow was measured in each state using microspheres, and perfusion pressure was maintained at 80 mm Hg. Oxygen consumption in the empty-beating hypertrophied heart was found to be the same as that previously reported for normal hearts. Blood flow was evenly distributed in the empty-beating heart, with an endocardial/epicardial ratio of 0.99 +/- 0.15 (SEM) milliliters per minute per gram of left ventricular weight. Oxygen consumption failed to increase significantly with fibrillation; however, blood flow distribution favored the subepicardium, suggesting that oxygen consumption determinations in the fibrillating hypertrophied heart may not accurately reflect metabolic demand. Basal oxygen consumption of the hypertrophied heart as determined by the potassium-arrested, blood-perfused model was the same as that previously described for normal hearts. Blood flow during potassium arrest favored the subendocardium (endocardial/epicardial ratio = 1.14 +/- 0.27 ml/min/gm LV weight).     

Functional recovery of hearts after cardioplegia and storage in University of Wisconsin and in St. Thomas' Hospital solutions

There are conflicting reports of the beneficial effects of University of Wisconsin (UW) cardioplegic solution used in heart preservation techniques. Therefore we investigated the efficacy of myocardial protection in adult rat hearts subjected to single-dose infusion (3 minutes) of nonoxygenated cardioplegic solutions (UW or St. Thomas' Hospital solution No. 2 [STH]) and stored at 4 degrees C by immersion in the same solution or in saline solution. Isolated working-heart preparations (n = 8 per group) were used to assess the prearrest (20 minutes' normothermic perfusion) and postischemic left ventricular functions. Four groups of hearts underwent 5, 8, 10, and 20 hours of cold ischemia (4 degrees C) in UW solution. Hearts stored for 8 to 20 hours showed no postischemic recovery of cardiac pump function (aortic flow, 0%), had decreased levels of myocardial high-energy phosphates, and were highly edematous (50% to 70% increased). After 5 hours of storage there was also poor recovery of aortic flow, coronary flow, and aortic pressure (55.0% +/- 19.4%, 67.1% +/- 5.1%, and 58.1% +/- 11.7%, respectively) but good recovery of adenosine triphosphate, creatine phosphate, and guanosine triphosphate (18.54 +/- 1.42, 29.99 +/- 2.05, and 1.64 +/- 0.14 mumol/gm dry weight, respectively). In contrast, hearts arrested and stored in STH solution for 5 hours rapidly established normal left ventricular functions (aortic flow, 111.5% +/- 2.5%; cardiac output, 99.1% +/- 1.2%; coronary flow, 85.0% +/- 3.4%; heart rate, 95.8% +/- 2.7%; and aortic pressure, 94.6%). A group of hearts arrested with STH solution but stored in saline solution recovered more slowly, had only partial return of function (aortic flow, 73.6% +/- 14.8%; p less than 0.01 vs STH/STH group), and had significantly greater tissue water content (8.020 +/- 0.080 vs 6.870 +/- 0.126 ml/gm dry wt; p less than 0.01). These results demonstrate the superior preservation of explanted hearts at 4 degrees C obtained by STH cardioplegic solution compared with UW solution under conditions used for transplantation.     

Regional changes in myocardial acid production during ischemic arrest: a comparison of sanguineous and asanguineous cardioplegia

Regional differences in myocardial acid production have not been characterized during administration of either asanguineous or sanguineous cardioplegia. To investigate this, miniature glass pH electrodes were placed in the right ventricular (RV) myocardium, the left ventricular subendocardial (LV endo) region, and the subepicardial (LV epi) region in a canine model. Multiple doses of either blood cardioplegia (Group 1; N = 11) or crystalloid cardioplegia (Group 2; N = 11) were administered during 4 hours of aortic cross-clamping. The accumulation of hydrogen ions during the cross-clamp period was greater in Group 2 than Group 1 in the LV endo region (629 +/- 79 nm/L versus 66 +/- 31 nm/L; p less than 0.001), the LV epi region (623 +/- 66 nm/L versus 72 +/- 32 nm/L; p less than 0.001), and the RV myocardium (814 +/- 296 nm/L versus 150 +/- 54 nm/L; p less than 0.05). Within each group, the time course of myocardial pH and the accumulation of hydrogen ions did not differ among the LV endo region, LV epi region, and the RV myocardium (p = not significant). These data indicate that transmural and interventricular differences in myocardial pH and hydrogen ion accumulation are not produced in the vented, arrested canine heart. In addition, when compared with asanguineous cardioplegia, blood cardioplegia globally and transmurally reduces acid accumulation during ischemic arrest.     

Ventricular Fibrillation: Its Effect on Myocardial Flow,Distribution, and Performance

Subendocardial ischemia develops in hearts that are fibrillated during cardiopulmonary bypass when: (1) the normal ventricle is fibrillated with a sustained electrical stimulus, (2) the hypertrophied ventricle is allowed to fibrillate spontaneously, (3) the fibrillating heart becomes distended, or (4) the perfusion pressure is reduced to approximately 50 mm Hg. Myocardial hypothermia reduces cardiac oxygen requirements during fibrillation but does not prevent ischemia when perfusion pressure falls to levels frequently attained during clinical open-heart operations. The ischemia occurs because flow cannot rise sufficiently to meet the metabolic demands of ventricular fibrillation. The forces interacting to impede adequate flow to the subendocardium during ventricular fibrillation are: (1) the compressive forces exerted on subendocardial muscle by the strength of fibrillation, (2) the compressive forces resulting from raised intracavitary pressure due to occlusion or malfunction of the ventricular vent, and (3) the evolution of myocardial edema as ischemia is prolonged.We have abandoned the use of ventricular fibrillation in clinical open-heart operations and now allow the heart to beat continually with adequate perfusion pressure. We have not needed to use inotropic drugs postoperatively after aortic or mitral valve replacement since adopting this technique.     

Coronary artery bypass grafting in patients with poor left ventricular function using retrograde continuous cold blood cardioplegia]

Patients with poor left ventricular function or those requiring urgent surgery may have more extensive ischemic myocardial injury if myocardial preservation is incomplete. We have performed coronary artery bypass grafting (CABG) aimed at complete revascularization in such cases using RC-CBCP, which is considered more effective on myocardial preservation during aortic cross-clamping in particular to protect ischemic area distal to severe coronary artery stenosis or obstruction. In the present study, in 25 patients with poor left ventricular function (left ventricular ejection fraction; LVEF less than or equal to 0.3) including 10 patients who required urgent surgery, the operative results were evaluated. All the distal and proximal anastomoses of grafts (average 2.5 grafts) were completed during one aortic cross-clamping using RC-CBCP, therefore graft flow was obtained immediately after release of the aortic clamping. Though this method required 142 minutes of a mean aortic cross-clamping time, myocardial protection was considered to be preferable judging from postoperative isoenzymatic evaluation and improved ventricular function. Fifteen patients with elective CABG were all alive and restored to NYHA class I to II. Among 10 patients requiring urgent CABG, 4 patients with acute myocardial infarction died but others were restored to NYHA class I to II. We conclude that it is important to aim at complete coronary revascularization in patients with poor left ventricular function and RC-CBCP achieves more effective myocardial protection during CABG in the patients.     

Does adenosine pharmacologically precondition human myocardium during coronary bypass surgery?

AIM: Adenosine (Ado) triggers ischemic preconditioning. We investigated whether Ado provides additional myocardial protection in patients during intermittent aortic cross-clamping (IAC) bypass surgery. METHODS: The placebo group was made of 15 male of 66+/-8 years while the Ado group was made of 19 male of 65+/-10 years. The patients of the Ado group had a 3-vessel heart disease and were treated with elective surgery. With the aortic cross-clamping, Ado or vehicle were infused over 10 min at systemic pressure together with sufficient blood via the aortic root. Blood samples before anaesthesia and onset of ECC, 1 hour after end of surgery, and on day 1 and 2 post-surgery to assess CK-MB and troponin I were performed. Hemodynamic measures (heart rate, left ventricular pressure, max/min pressure rise, central venous pressure) before installation and 15 min after completion of the coronary artery bypass. Different ECGs for electrophysiological analyses were performed. RESULTS: Hemodynamic and laboratory measures revealed no significant advantages of either protocol. Mortality rate was zero in both groups. CONCLUSIONS: The comparable outcome is likely due to cardioprotection provided by both IAC bypass surgery and hypothermia, which might obscure beneficial effects of pharmacological preconditioning in patients with good left ventricular function (ejection fraction >50%). As the benefit might have been marginal, it may well become apparent in a larger study on patients with more severe left ventricular dysfunction.     

Cardiac and renal responses to cross-clamping of the descending thoracic aorta

The present study was performed to document the relative efficacy of commonly applied techniques used adjunctively during 1 hour of descending thoracic aortic cross-clamping. Renal and cardiac responses were determined by standard laboratory methods. There were four experimental groups: (1) heparin-bonded shunt; (2) partial femoral-femoral bypass; (3) sodium nitroprusside; (4) control. Each of the experimental groups showed abnormal hemodynamic responses during cross-clamping. Elevations in left ventricular end-diastolic pressure (LVEDP) and systolic blood pressure were common events during clamping, and cardiac output often decreased. Nevertheless, left ventricular performance curves after cross-clamping showed similar increases in left ventricular stroke work (LVSW) with increasing preload. In addition, left ventricular biopsy specimens showed preservation of myocardial high-energy phosphate stores and essentially normal ultrastructural integrity. Radioactive microspheres generally showed increased myocardial blood flow during and after cross-clamping, but no evidence of preferential subendocardial ischemia. Examination of renal function showed a marked decrease in urine output, glomerular filtration rate, and renal plasma flow during cross-clamping. Following the release of the cross-clamp, renal function returned to 50% to 85% of baseline status. Since we could find no major advantage of any of the techniques employed under the present experimental conditions, we suggest that all of the techniques should be part of the surgical armamentarium and the particular preoperative and/or intraoperative findings in a specific case should determine which technique is most appropriate for a given patient.     

Identification and control of noncoronary collateral blood flow

To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 microns in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions:vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries. Without effective LV venting, LV intracavitary pressure rose to 7.0 +/- 0.1 mm Hg (mean +/- standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 +/- 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 +/- 3.5 ml/min and myocardial blood flow fell to 0.3 +/- 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent. These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic-pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.     

Monitoring of somatosensory evoked potentials during surgical procedures on the thoracoabdominal aorta. I. Relationship of aortic cross-clamp duration, changes in somatosensory evoked potentials, and incidence of neurologic dysfunction

To determine if intraoperative monitoring of somatosensory evoked potentials detects spinal cord ischemia, we subjected 21 dogs to aortic cross-clamping distal to the left subclavian artery. Group I animals (short-term studies, n = 6) demonstrated decay and loss of somatosensory evoked potentials at 8.5 +/- 1.1 minutes after aortic cross-clamping. During loss of somatosensory evoked potentials, significant decreases in spinal cord blood flow occurred in cord segments below T6. Significant reactive hyperemia occurred without normalization of somatosensory evoked potentials after reperfusion. Fifteen Group II animals (long-term studies) were studied to determine the relationship between duration of spinal cord ischemia (evoked potential loss) and subsequent incidence of paraplegia. Extension of aortic cross-clamping for 5 minutes after loss of somatosensory evoked potentials in six dogs resulted in no paraplegia (mean cross-clamp time 12.7 +/- 0.6 minutes). Prolongation of aortic cross-clamping for 10 minutes after evoked potential loss in nine dogs (mean cross-clamp time 17.6 +/- 0.6 minutes) resulted in a 67% (6/9) incidence of paraplegia 7 days postoperatively (p = 0.02 versus 10 minutes of aortic cross-clamping). These findings demonstrate that simple aortic cross-clamping uniformly results in spinal cord ischemia and that such ischemia is detectable by monitoring of somatosensory evoked potentials. Duration of ischemia, as measured by the time of evoked potential loss during the cross-clamp interval, is related to the incidence of postoperative neurologic injury.