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Taras Mukhin
Taras Mukhin

Cardiopulmonary Bypass Principles And Practice Free Download Pdf


Unfractionated heparin (UFH) is widely used as a reversible anti-coagulant in cardiopulmonary bypass (CPB). However, the pharmacokinetic characteristics of UFH in CPB surgeries remain unknown because of the lack of means to directly determine plasma UFH concentrations. The aim of this study was to establish a pharmacokinetic model to predict plasma UFH concentrations at the end of CPB for optimal neutralization with protamine sulfate.




cardiopulmonary bypass principles and practice free download pdf



We conducted a cross-sectional online survey of 124 cardiothoracic surgeons, cardiovascular anesthesiologists, and perfusionists. Survey questions were designed to assess clinical decision-making patterns of intravenous (IV) fluid utilization in cardiovascular surgery for five types of patients who need volume expansion: (1) patients undergoing cardiopulmonary bypass (CPB) without bleeding, (2) patients undergoing CPB with bleeding, (3) patients undergoing acute normovolemic hemodilution (ANH), (4) patients requiring extracorporeal membrane oxygenation (ECMO) or use of a ventricular assist device (VAD), and (5) patients undergoing either off-pump coronary artery bypass graft (OPCABG) surgery or transcatheter aortic valve replacement (TAVR). First-choice fluid used in fluid boluses for these five patient types was requested. Descriptive statistics were performed using Kruskal-Wallis test and follow-up tests, including t tests, to evaluate differences among respondent groups.


Of the 124 HCPs who completed the survey, 52 (41.9%) were anesthesiologists, 47 (37.9%) were surgeons, and 25 (20.2%) were perfusionists (Table 1). The primary practice setting for most HCPs was a non-university hospital (73.4%) followed by university hospital (26.6%). The average number of bypass surgeries that the HCPs participated in per month was 28.6 for surgeons, 24.7 for anesthesiologists, and 21.4 for perfusionists.


Microcirculatory perfusion disturbances are associated with increased morbidity and mortality in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Technological advancements made it possible to monitor sublingual microcirculatory perfusion over time. The goal of this review is to provide an overview of the course of alterations in sublingual microcirculatory perfusion following CPB. The secondary goal is to identify which parameter of sublingual microcirculatory perfusion is most profoundly affected by CPB.


Microcirculatory perfusion disturbances are commonly reported in patients undergoing cardiac surgery with cardiopulmonary bypass (CPB). Cardiac surgery with CPB is associated with risk of morbidity such as mediastinitis, permanent stroke, acute kidney injury, and acute lung injury [1, 2]. Microcirculatory perfusion disturbances are additionally associated with increased morbidity and mortality in the ICU in patients with cardiogenic shock or sepsis [3, 4]. Interestingly, however, there appears to be an uncoupling of macrocirculatory and microcirculatory hemodynamics [5], meaning that sustainment of systemic hemodynamic parameters during surgery does not guarantee adequate microcirculatory perfusion. Therefore, real-time imaging might be a valuable tool to monitor alterations in microcirculatory perfusion in patients undergoing cardiac surgery with CPB and guide interventions in the perioperative period.


In contrast, no effect of CPB on total vessel density (TVD), small vessel density (SVD), or vessel density (VD) was observed. These observations are in line with recent experimental and theoretical insights [30, 32, 33], suggesting that CPB does not necessarily affect the absolute number of microvessels, but mainly impairs microcirculatory red blood cell flow patterns, as reflected by a reduced number of perfused vessels (PVD). CPB-associated factors such as hemodilution, contact activation, and the induction of a systemic inflammatory response are thought to impair microcirculatory perfusion by affecting both transport and diffusion of oxygen at the microvascular level. Pathophysiological mechanisms include glycocalyx degradation and endothelial, platelet, and leucocyte activation leading to increased endothelial permeability and edema formation, leucocyte extravasation, and microthrombi formation (Fig. 2). These pathophysiological mechanisms involved in cardiopulmonary bypass-associated microvascular alterations and microcirculatory perfusion disturbances were previously discussed in detail [31, 34].


Summary figure. Cardiac surgery with cardiopulmonary bypass impairs microcirculatory perfusion, which is monitored sublingually in patients in the perioperative period. Onset of cardiopulmonary bypass reduces sublingual microcirculatory perfusion reflected by functional capillary density (FCD), proportion of perfused vessels (PPV), and perfused vessel density (PVD) compared to baseline, whereas total vessel density (TVD) remained unaltered. The effect of cardiopulmonary bypass on microvascular flow index (MFI) differed between studies. Pathophysiological mechanisms include systemic inflammation, and activation of complement and coagulation, which causes shedding of the endothelial protective glycocalyx layer leading to endothelial injury. In addition, release of barrier disruptive mediators induce endothelial barrier disruptive signaling, resulting in capillary leakage and edema formation. Activation of the endothelium stimulates the release of nitric oxide (NO), affecting vascular tone and systemic blood pressure. Moreover, induction of endothelial adhesion molecule expression increases leucocyte rolling and extravasation. Also, activation of polymorphonuclear neutrophils causes the release of reactive oxygen species (ROS), contributing to tissue injury. Activation of platelets and coagulation are associated with the formation of microthrombi and microvascular occlusion. Collectively, these mechanisms impair microcirculatory perfusion and contribute to organ injury following cardiac surgery with cardiopulmonary bypass, with clinical and experimental treatment strategies presented in italic in white boxes. IL, interleukin; IFNy, interferon gamma; TNFα, tumor necrosis factor alpha


Tissue hypoperfusion during cardiopulmonary bypass (CPB) affects cardiac surgical outcomes. Lactate, an end product of anaerobic glycolysis from oxygen deficit, is a marker of tissue hypoxia. In this study, we aimed to identify the prognostic value of blood lactate level during CPB in predicting outcomes in adults undergoing cardiac surgeries.


Indications to secure the airway do not differ from recommendations in normothermic patients [8]. Intubation may provoke ventricular fibrillation (VF) in severe hypothermia [132, 133] but the risk is small [8, 134, 135]. There is little published data about anaesthesia in these patients, but the likely effects can be anticipated by extrapolating from studies done on animals, and in patients with induced hypothermia for medical treatment. Most intravenous anaesthetic induction agents cause cardiovascular depression so doses should be small. Ketamine may be safe in pre-existing hypothermia [136], but the sympathomimetic effects could theoretically cause problems for an irritable hypothermic heart [99]. If succinylcholine is used for intubation, the potential for it to increase serum potassium should be considered [137]. Neuromuscular transmission decreases during hypothermia, even in the absence of muscle relaxants [138] and studies performed in animals and humans during hypothermic cardiopulmonary bypass (CPB) have indicated that hypothermia


Unexplained exertional dyspnoea or fatigue can arise from a number of underlying disorders and shows only a weak correlation with resting functional or imaging tests. Noninvasive cardiopulmonary exercise testing (CPET) offers a unique, but still under-utilised and unrecognised, opportunity to study cardiopulmonary and metabolic changes simultaneously. CPET can distinguish between a normal and an abnormal exercise response and usually identifies which of multiple pathophysiological conditions alone or in combination is the leading cause of exercise intolerance. Therefore, it improves diagnostic accuracy and patient health care by directing more targeted diagnostics and facilitating treatment decisions. Consequently, CPET should be one of the early tests used to assess exercise intolerance. However, this test requires specific knowledge and there is still a major information gap for those physicians primarily interested in learning how to systematically analyse and interpret CPET findings. This article describes the underlying principles of exercise physiology and provides a practical guide to performing CPET and interpreting the results in adults.


The objective of this practical introduction is to describe the basic principles of exercise physiology and provide an easy-to-follow approach for those primarily interested in learning how to conduct, analyse and interpret CPET in their clinical practice. For further information, reference is given to the literature [3, 5,6,7, 10, 11, 15,16,17,18,19,20] and the updated reference work [1].


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