Pathophysiology of cardiopulmonary bypass
Cardiopulmonary Bypass: Advances in Extracorporeal Life Support, Elsevier, ss.135-154, 2022
- Yayın Türü: Kitapta Bölüm / Araştırma Kitabı
- Basım Tarihi: 2022
- Doi Numarası: 10.1016/b978-0-443-18918-0.00009-7
- Yayınevi: Elsevier
- Sayfa Sayıları: ss.135-154
- Anahtar Kelimeler: Blood–air interface, cardiopulmonary bypass, coagulation system, complement system, contact system, cytokines, extracorporeal circulation, inflammation, ischemia-reperfusion injury, pathophysiology, systemic inflammatory response syndrome
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Numerous cardiac surgical procedures are currently conducted around the world using cardiopulmonary bypass (CPB). The contribution of the techniques and equipment of CPB to morbidity and mortality following cardiothoracic surgery remains unclear despite extensive clinical and experimental research has been done over many years. The pathophysiology of the CPB-related systemic inflammatory response is multifactorial and has two main courses: “early phase or contact activation” and “late phase or ischemia-reperfusion injury.” The early phase occurs as a result of the use of CPB and contact of blood with nonphysiological surfaces, with an acute-phase reaction of protease cascades, leukocyte, and platelet activation by introducing systemic inflammatory responses involving cellular and humoral interactions. The late phase results from endotoxemia and coagulation disorders due to ischemic-reperfusion injury via cardioplegic arrest by cross-clamping the aorta and heparin/protamine reactions. The generation of inflammatory responses manifests mainly as subclinical organ dysfunctions, but the reactions can be profoundly amplified to produce a multiorgan dysfunction that can manifest as capillary leak syndrome, coagulopathy, respiratory failure, myocardial dysfunction, renal insufficiency, and neurocognitive decline. The pathophysiological aspects of CPB are driven by plasma proteins and cellular systems that have essential effects on cardinal organ systems. Minimizing these cascades and curbing the extent of the inflammatory responses produce the body a multifactorial defense-circuit.