
Introduction
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While the number of publications each year in cardiac anesthesia is enormous there are a select group of interesting articles highlighting controversies in current practice or new techniques, medications, procedures which may change practice down the road. The purpose of this article is to review some of these articles. While by no means a systematic review, this article highlights some of the more interesting papers from the cardiac anesthesia and surgical literature from 2007. The articles focus on areas such as: methods to reduce both cerebral dysfunction and renal dysfunction, myocardial protection inhaled volatile anesthetic agents, and methods to reduce atrial fibrillation.
Mathematical modeling, based on fundamental principles from engineering may help clinical trial design, aiding in answering problems that remain in cardiac surgery, such as management of carotid artery stenosis in patients undergoing cardiopulmonary bypass (CPB), hematocrit during CPB, adequacy of oxygen delivery during CPB, adequacy of blood pressure management during CPB, filtration during bypass for renal failure, bypass circuit pacification, carbon dioxide wound insufflation and neurological events, and pulsatile to nonpulsatile flow during CPB. In addition, mathematical modeling may help explain deficiencies of previous work that have failed to clarify what to do.
From the first description of the “systemic inflammatory response” in the early 1990s, it has been recognized that this is a multifaceted response of the body to the combined insult of cardiothoracic surgery with bypass, involving causation by “activation of complement, coagulation, fibrinolytic, and kallikrein cascades, activation of neutrophils with degranulation and protease enzyme release, oxygen radical production, and the synthesis of various cytokines from mononuclear cells.” Yet the intervening 15 years have seen a narrowing of research into individual systems and interventions naively targeted at single pathways without achieving clinically meaningful benefits. The time has come to redefine the systemic inflammatory response so that research can be more productively focused on objectively measuring and interdicting this multisystem disorder. A key concept of this new understanding is that translation into a hard adverse event occurs when the systemic imbalance is combined with a localized trigger. Triggers might be inadvertently provided by transient episodes of ischemia/malperfusion to vulnerable organs or handling trauma to major vessels. Future research should be directed at suppressing systemic activation with
The early postoperative care of a heart transplant recipient remains challenging, even in experienced centers with a long tradition of excellence. Approximately 10% to 20% of heart transplant recipients experience potentially life-threatening right ventricular dysfunction intraoperatively and early postoperatively due to an elevated pulmonary vascular resistance. In addition, heart transplant recipients experience a high risk of perioperative hemorrhage, as well as opportunistic infection and rejection. The authors describe a case of severe right ventricular dysfunction in a 46-year-old male several hours after heart transplantation for a dilated cardiomyopathy. This patient was salvaged by judicious multimodality therapy including the use of adrenergic agents, phosphodiesterase inhibitors, inhaled nitric oxide, and extracorporeal membrane oxygenation. The risk factors for the development of early graft failure after heart transplantation are reviewed, along with the principles of appropriate management of this complication.
Because anesthesia affects the integrity of the autonomic nervous system, anesthesiologists use vital signs to maintain respiratory and circulatory homeostasis. However, patients with genetic predispositions or with autonomic dysfunctions are at risk of severe complications from anesthesia. For these patients, the monitoring of vital signs may not give sufficient warning to avoid complications. The development of methods to measure autonomic tone could be of interest to anesthesiologists because they could warn of changes in autonomic tone before vital signs are affected. New noninvasive methods are being developed to obtain measurements of parasympathetic and sympathetic output allowing for the monitoring of perioperative autonomic tone. These measurements are based on analysis of heart rate and blood pressure variability. In this report, the principals of the analysis of heart rate and blood pressure variability will be explained and the usefulness of these methods to anesthesiologists will be discussed.
Blunt traumatic thoracic aortic injury (BTTAI) is a lethal injury associated with a prehospital mortality of 80% to 90%. Patients arriving in the emergency room and considered appropriate to undergo emergency open surgical repair still have a mortality rate of 15% to 30% because of severe associated injuries. Conventional open surgical repair requires a left thoracotomy, single lung ventilation, aortic-cross clamping and unclamping, with or without the adjunct use of partial or full cardiopulmonary bypass and systemic heparinization. All this leads to significant physiological stress and surgical trauma resulting in perioperative complications such as major blood loss, coagulopathy, myocardial infarction, stroke, respiratory failure, renal failure, bowel infarction, and paraplegia. Despite advances in anesthesia, critical care medicine, and surgical techniques, a recent meta-analysis showed no definite improvement in operative mortality over the past decade, following open surgical repair in patients with BTTAI. Endovascular repair of BTTAI does not require a thoracotomy, single lung ventilation, aorticcross clamping and unclamping, or systemic heparinization. As a result, endovascular repair of BTTAI has emerged as an effective, minimally invasive treatment alternative, especially in patients with severe concomitant injuries, which may be prohibitive to open surgical repair. Recent published studies have shown that endovascular repair of BTTAI is associated with lower morbidity, mortality, stroke, and paraplegia/paraparesis rates, when compared with open surgical repair of BTTAI.
Despite major improvements in perfusion techniques over the past 50 years, it is still not possible to formulate a clear definition of what is meant by optimal perfusion. In part this is due to the lack of sufficient evidence-based data and in part because of the complex pathophysiology that takes place during cardiac surgery with cardiopulmonary bypass. To find an answer we need to understand the exact mechanism of the inflammatory reaction triggered by the cardiopulmonary bypass. However, it is clear that further improvement of the cardiopulmonary bypass components alone will be sufficient. Only a combined strategy can further improve cardiopulmonary bypass—related morbidity and mortality. Such a combined strategy will embrace perfusion techniques as well as a pharmacological approach. It will also require a continuous monitoring of the microcirculation. The latter will not only allow to rapidly sense changes in the quality of perfusion but, even more important, also make it possible to intervene at the moment of deterioration. Recent research shows that such an approach has positive an impact on cardiopulmonary bypass—related morbidity postoperatively.
Blood has been described as the most precious and personal substance in the world. Current directions in cardiac surgery are moving away from transfusing donor “Allogeneic” blood products, and towards improving methods of saving and preserving the patient's own “autologous” blood. Nothing else comes close to the natural healing abilities and homeostasis that one's own whole blood offers. No substitute, whether it is human or artificial, will ever work as well with fluid shifts, hemostasis and homeostasis. News reports today commonly feature severe blood shortages and research documenting recognized transfusion risks such as how older stored blood can put heart surgery patients at increased risk and others that point to the morbidity and mortality associated with its use. Therefore the medical community is moving towards more effective blood utilization by minimizing the exposure to donated blood. Current techniques are saving as much as possible of the patient's own blood that might otherwise be mismanaged or lost during surgery. Techniques, such as Ultrafiltration, that quickly concentrate and reinfuse whole blood back to the patient are the best choice. Admission to discharge hemovigilance requires a concerted multidisciplinary team effort with multimodal tools available in the coagulation armamentarium to effectively avoid this form of organ transplant. Improving outcomes and reducing morbidity and mortality in cardiac surgery takes place at the microcirculatory capillary level and with control of Hemostasis. Cardiac teams need to effectively communicate and minimize blood loss and hemodilution and reverse it, for state of the art blood management in Cardiac surgery.
Hemostasis management of the cardiac surgical patient has changed following the withdrawal of aprotinin for use in cardiac surgical patients. The challenge to minimize blood loss and reduce exposure of cardiac surgical patients to blood products continues to grow with patients presenting being older and sicker and more complex procedures being performed. The cardiac surgery team has many options available for it to consider; although current recommendations strongly support the use of cell salvage as one process to assist in this challenge, other options need to be equally critically evaluated.
Despite nearly 2 decades of published reports and clinical trials demonstrating the relative safety and efficacy of aprotinin in adult cardiac surgical patients at increased risk of bleeding—culminating in an official endorsement of the usage of aprotinin in such patients from both cardiac surgery and anesthesiology subspecialty committees—several more recent studies have raised profound concerns regarding the safety of aprotinin in these same patients. These studies and the implications thereof have ultimately resulted in the withdrawal of aprotinin from clinical usage internationally. This article will briefly review these developments with the hope of understanding how this abrupt turnabout took place and will attempt to understand how such events can be avoided in the future.