Vincent R. Conti

Prospective Study of Blunt Aortic Injury: Multicenter Trial of the American Association for the Surgery of Trauma

BACKGROUND Blunt aortic injury is a major cause of death from blunt trauma. Evolution of diagnostic techniques and methods of operative repair have altered the management and posed new questions in recent years. METHODS This study was a prospectively conducted multi-center trial involving 50 trauma centers in North America under the direction of the Multi-institutional Trial Committee of the American Association for the Surgery of Trauma. RESULTS There were 274 blunt aortic injury cases studied over 2.5 years, of which 81% were caused by automobile crashes. Chest computed tomography and transesophageal echocardiography were applied in 88 and 30 cases, respectively, and were 75 and 80% diagnostic, respectively. Two hundred seven stable patients underwent planned thoracotomy and repair. Clamp and sew technique was used in 73 (35%) and bypass techniques in 134 (65%). Overall mortality was 31%, with 63% of deaths being attributable to aortic rupture; mortality was not affected by method of repair. Paraplegia occurred postoperatively in 8.7%. Logistic regression analysis demonstrated clamp and sew (p = 0.002) and aortic cross clamp time of > or = 30 minutes (p = 0.01) to be associated with development of postoperative paraplegia. CONCLUSIONS Rupture after hospital admission remains a major problem. Although newer diagnostic techniques are being applied, at this time aortography remains the diagnostic standard. Aortic cross clamp time beyond 30 minutes was associated with paraplegia; bypass techniques, which provide distal aortic perfusion, produced significantly lower paraplegia rates than the clamp and sew approach.

Mitral regurgitation following acute myocardial infarction

Mitral valve regurgitation (MR) is a frequent Doppler echocardiographic finding in patients after acute myocardial infarction (AMI) and an independent predictor of long-term cardiovascular mortality. Reported risk factors include advanced age, prior myocardial infarction, infarct extension, and recurrent ischemia. During the early phase of AMI, transient ischemic MR is common and rarely causes hemodynamic compromise. However, when several chordae tendineae or a papillary muscle ruptures, acute left atrial and ventricular volume overload ensues, leading to abrupt hemodynamic deterioration with cardiogenic shock. Auscultation may be unrevealing due to decreased turbulence. Hence, the importance of a high index of suspicion for acute MR in any patient with acute pulmonary edema in the setting of AMI, especially if left ventricular systolic function is well preserved. Later, ventricular remodeling may lead to MR through annular dilatation or papillary muscle migration with malcoaptation of the leaflets. The widespread availability, ease of use and non-invasive nature of Doppler echocardiography have made it the standard diagnostic tool for detecting MR. Mechanical reperfusion of the infarct-related artery seems to be superior to fibrinolysis in decreasing its incidence acutely and in the long run. Nevertheless, when acute severe MR occurs, unless rapidly diagnosed and treated, this dreaded complication is associated with high morbidity and mortality. Prompt surgical intervention after hemodynamic stabilization is essential to ensure a good short-term and long-term prognosis. This review discusses the incidence, long-term prognosis, associated risk factors, complex pathophysiology, time of occurrence, clinical manifestations, diagnosis, and management of patients with MR after AMI.

Adverse effects of postoperative infusion of shed mediastinal blood

BACKGROUND Postoperative infusion of shed mediastinal blood has been used in an effort to decrease blood usage after cardiac operations. Recent experience has suggested that this practice may actually lead to a delayed increase in bleeding. METHODS In a prospective, randomized study, 40 patients undergoing coronary artery bypass grafting with shed mediastinal blood collected in a cardiotomy reservoir were divided into two equal groups and studied during their first 4 hours in the intensive care unit. Shed mediastinal blood was directly infused in group I (n = 20), whereas in group II (n = 20), it was not. In group II, if a sufficient volume of red cells was present to allow processing (n = 5), washed red cells were infused. Variables studied before and after infusion were the amount of blood lost and infused, homologous blood transfused, complete blood count and differential, serum fibrinogen, fibrin split products, D-dimers, clotting factors, prothrombin time, activated partial thromboplastin time, thromboelastograms, plasma-free hemoglobin, complement factors C3 and C4, creatine kinase and its MB isoenzyme, and body temperature. RESULTS After infusion of shed mediastinal blood, elevated levels of fibrin split products and D-dimers were found in significantly more patients in group I. The thromboelastogram index was normal in 76% of patients in group II but in only 12.5% in group I. Group I also had an increase in band neutrophils, a greater number of febrile patients, higher serum levels of creatine kinase, its MB isoenzyme, and plasma-free hemoglobin, and greater blood loss during hours 3, 4, and 5 in the intensive care unit. The volume of red cells in shed mediastinal blood (hematocrit, 9% to 10%) was small, resulting in clinically insignificant autotransfusion when infused directly, and insufficient for cell processing in most patients. CONCLUSIONS These data support those in previous studies that direct infusion of shed mediastinal blood does not save substantial amounts of autologous red cells and can cause a delayed coagulopathy and other adverse effects that may be harmful to patients postoperatively.

Myocardial Ischemia: Correlation of Mitochondrial Adenine Nucleotide and Respiratory Function

State 3 respiration of rat heart mitochondria decreased approximately 60% after 20 min normothermic in vitro ischemia. After 20 min ischemia, the levels of intramitochondrial adenine nucleotides (ATP + ADP + AMP) decreased to approximately 20% of control values, with a rapid loss between 10 and 20 min. Also, the exchangeable adenine pool of the mitochondria decreased 60% after 20 min ischemia. State 4 respiration was not affected by the ischemic insult. The adenine nucleotide translocase activities of mitochondria from control and ischemic hearts were too high to measure accurately. Therefore, the effects of ischemia on adenine nucleotide translocase activity could not be established. However, 1 microM carboxyatractyloside did not impair state 3 respiration of control mitochondria, but did inhibit the adenine translocase activity by at least 80%. Moreover, titration of state 3 respiration with carboxyatractyloside produced sigmoidal curves for mitochondria from control and ischemic tissue. State 3 respiration correlated well with the total mitochondrial adenine nucleotides and the exchangeable adenine pool (r = 0.63 and 0.78, respectively). Data collected from isolated perfused rat hearts also showed a good correlation between state 3 respiration and the exchangeable adenine nucleotides (r = 0.92). In this study, mitochondria were isolated from hearts that were either perfused, made ischemic for 30 min by aortic cross-clamp, or reperfused for 10 min after the aortic cross-clamp. The slopes and y-intercepts of the regression lines were similar for the in vitro ischemic and the perfusion studies. There was no significant difference between the effects of ischemia on the state 3 and uncoupled respiratory rates.(ABSTRACT TRUNCATED AT 250 WORDS)

Air embolism during cardiopulmonary bypass

Sudden and unexpected death during an operation is a calamity which never fails to strike terror to the heart of the boldest surgeon. Although death is a frequent and familiar visitor wherever human beings exist, nevertheless its sudden and unforeseen advent conveys with it more than the usual halo of sadness, and when such a scene transpires in the operating room it leaves impressions which neither time nor space can erase ... Believing that it is good practice to prepare for war in time of peace, I intend on this occasion to call your attention to one of the most dreaded and, I may add, one of the most uncontrollable causes of sudden death I

Hemodynamic action of calcitonin gene-related peptide in the isolated rat heart

The effects of calcitonin gene-related peptide (CGRP) on heart rate, coronary flow, pressure development, and time to ischemic contracture were studied in the isolated, perfused rat heart. A bolus of CGRP (2640 pmols) caused significant increases in heart rate and coronary flow; these effects were sustained for at least five minutes after injection. The increase in coronary flow was independent of heart rate, since CGRP caused an increase in coronary flow in non-beating (potassium-arrested) hearts. The dose-response of CGRP was studied using five doses (65, 218, 658, 1320 and 2640 pmols) given as bolus injections. Although the increase in heart rate was apparently dose-dependent, significant increases above baseline were observed only with the two highest doses. In contrast, coronary flow increased significantly above baseline with the injection of all but the lowest dose of CGRP. Ten minutes after injection of CGRP, all hearts were made ischemic. The time to onset of ischemic contracture was approximately 11 minutes for those hearts that received 65 pmols of CGRP; however, for those hearts receiving all other doses of CGRP, the time to onset of contracture was approximately 8 minutes. We conclude that CGRP significantly decreases the resistance of the coronary vascular bed, and that it may be an important regulator of regional blood flow in the heart.

Comparison of two topical collagen-based hemostatic sponges during cardiothoracic procedures.

The need for topical hemostasis during cardiothoracic procedures continues to fuel the development of additional hemostatic products with a focus on minimizing cost and increasing efficacy. The efficacy of a recently approved collagen-based topical hemostatic agent (Hemostagene, Coletica, S.A., Lyon, France) was tested in a prospective randomized trial of 60 consecutive patients undergoing cardiothoracic surgical procedures. Comparisons to a control collagen sponge (Helistat, Integra Life Sciences, Inc., Plainsboro, NJ) were made and hemostasis was considered successful if bleeding was controlled in 10 min or less. We employed a unique hemorrhage grading scale to more closely assess the relative effectiveness of these different topical agents. Overall, Hemostagene and Helistat achieved a successful hemostasis rate of 75% and 77%, respectively, with no statistically significant difference. The Hemostagene sponge was deemed easier to handle when compared to control. During the study, neither of the products was associated with complications attributable to the topical sponge. In conclusion, Hemostagene had improved handling characteristics yet was equal to Helistat at topical hemostasis, adding an alternative to the topical hemostatic market.

Life-threatening intrathoracic complications during treatment with extracorporeal membrane oxygenation.

Extracorporeal membrane oxygenation (ECMO) has been successful (greater than 80% survival) in 35 centers in greater than 900 newborns with severe respiratory failure having an estimated mortality of greater than 80% on conventional management. During the last 3 years we have treated 79 newborns with 74 survivors (94%). Their diagnoses included meconium aspiration, persistent fetal circulation, respiratory distress syndrome, congenital diaphragmatic hernia, and sepsis. Seven patients (9%) had life-threatening intrathoracic complications requiring emergent intervention while on ECMO: tension hemothorax (3), tension pneumothorax (2), and pericardial tamponade (2). Pericardial tamponade and tension hemothorax and pneumothorax show a similar pathophysiology of increasing intrapericardial pressure and decreasing venous return. Perfusion is initially maintained by the nonpulsatile flow of the ECMO circuit before further decrease in venous return results in decreasing ECMO flow and progressive hemodynamic deterioration. Each of the seven patients demonstrated a clinical triad that includes increasing PaO2 and decreasing peripheral perfusion (as evidenced by decreasing pulse pressure and decreasing SvO2) followed by decreasing ECMO flow with progressive deterioration. The diagnoses were confirmed by transillumination, chest x-ray, or cardiac echocardiogram. Initial emergent placement of a percutaneous drainage catheter was temporizing in all seven cases. However, four patients required emergent thoracotomy for definitive treatment while still on ECMO. All seven patients were weaned from ECMO and are short-term survivors (6 months to 3.5 years). As use of ECMO for newborn severe respiratory failure increases, responsible physicians must be familiar with life-threatening intrathoracic complications and appropriate treatment strategies.

Postischemic recovery of mitochondrial adenine nucleotides in the heart.

BackgroundAdenine nucleotides (AdNs) are lost from the mitochondrial fraction of the heart cell during ischemia. It is unknown whether this pool of AdNs can be replenished after reperfusion. The purpose of this study was to evaluate the postischemic recovery of the mitochondrial AdN pool. Methods and ResultsThe left anterior descending coronary artery (LAD) of the canine heart was occluded for 30 minutes followed by either no reflow, 30-minute reflow, 1-day reflow, or 7-day reflow. Systolic shortening in the TAD-supplied region was absent during occlusion but recovered to approximately 30% of preocclusion values during early reperfusion. Mitochondrial and tissue AdNs (ATP, ADP, and AMP) were determined in the LAD-supplied and left circumflex-supplied (control) regions of the heart. The AdN content (expressed as percent of control values) of mitochondria from the LAD region was 55±101% (p<0.002), 64±7% (p<0.001), 81±6% (p<0.03), and 94±8% for the no-reflow, 30-minutereflow, 1-day-reflow, and 7-day-reflow groups, respectively. The AdN content (expressed as percent of control values) of tissue samples from the LAD region was 52±9% (p<0.002), 48±12% (p<0.02), 68±5% (p<0.002), and 70±9% for the no-reflow, 30-minute-reflow, 1-day-reflow, and 7-day-reflow groups, respectively. There was a good correlation between mitochondrial and tissue AdN (r=0.95). Using initial exchange rates, adenine nucleotide translocase activities of mitochondria from the LAD and control regions were not significantly different. State 3 respiration of LAD mitochondria was depressed (approximately 25%, p<0.05) only in the no-reflow group. Acceptor control ratios of the LAD mitochondria were not significantly different from control values in any group. Conclsions. After 30 minutes of regional ischemia, postischemic restoration of the mitochondrial AdN pool occurs between 1 and 7 days; this restoration is preceded by recovery of respiratory and adenine nucleotide translocase functions. Although the abnormally low levels ofAdN persist in the mitochondrial compartment during the early reperfusion period, postischemic contractile dysfunction cannot be explained by depressed mitochondrial respiratory activity.

Intermittent ischemia produces a cumulative depletion of mitochondrial adenine nucleotides in the isolated perfused rat heart.

The purpose of the present study was to determine if repetitive myocardial ischemia would result in the cumulative loss of mitochondrial adenine nucleotides. Isolated perfused rat hearts were subjected to continuous or intermittent ischemia. A single 5-minute period of continuous ischemia did not result in a significant decrease in the mitochondrial adenine nucleotide pool; a single 10-minute period of ischemia resulted in a decrease of approximately 17%. Next, the adenine nucleotide content of mitochondria from preischemic and 30-minute continuous ischemic hearts was compared with two groups of hearts undergoing intermittent ischemia (both groups receiving a total of 30 minutes of ischemia). One group received three 10-minute episodes of ischemia interrupted by 5-minute periods of reperfusion (3 x 10-minute intermittent ischemia); the other intermittent ischemic group received six 5-minute episodes of ischemia interrupted by 5-minute periods of perfusion (6 x 5-minute intermittent ischemia). The mitochondrial adenine nucleotide content (expressed as nanomoles per nanomole cytochrome a) for the preischemic and 30-minute continuous ischemic hearts was 14.7 +/- 0.6 and 8.0 +/- 0.4, respectively. The mitochondrial adenine nucleotide content of the 3 x 10-minute intermittent ischemia group (8.5 +/- 0.5) was not significantly different from the 30-minute continuous ischemic group. The mitochondrial adenine nucleotide content of the 6 x 5-minute intermittent ischemia group (11.0 +/- 0.6) was significantly larger than that of the 30-minute continuous and the 3 x 10-minute intermittent ischemia groups (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)