Abstract
Objective Totally thoracoscopic cardiac surgery under cardiopulmonary bypass combined with one-lung ventilation has been identified as the trend in cardiac surgery. The aim of this study was to examine the effects of the selective α2 adrenergic receptor agonist dexmedetomidine on the pulmonary function of patients who underwent mitral valve surgery using the totally thoracoscopic technique. Methods Fifty-seven patients who underwent thoracoscopic mitral valve surgery between July 2019 and December 2019 were selected. The patients were randomly divided into the control (Con) group (n = 28) and the dexmedetomidine (DEX) group (n = 29) using the random number table method. Arterial blood gas analyses were performed, and the oxygenation (PaO2/FiO2) and respiratory indexes (P(A-a)O/PaO2) were calculated 5 min after tracheal intubation (T1), 2 h after operation (T2), 6 h after operation (T3), and 24 h after operation (T4). Moreover, the serum cytokines interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and intercellular adhesion molecule-1 (ICAM-1) were detected using the enzyme-linked immunosorbent method at all time points. Chest radiography was performed 24 h after surgery. Peripheral blood samples were collected before and after the operation for a complete hemogram. Additionally, the procalcitonin concentration was measured and recorded when the patients were transported to the intensive care unit (ICU). The postoperative extubation time, length of ICU stay, and pulmonary infection rate were also recorded. Results Inflammatory reaction after surgery was evident. However, the inflammatory cytokines IL-6, TNF-α, and ICAM-1 in the DEX group were lower than those in the Con group after surgery (T2 to T4; P < 0.05). Neutrophil counts and procalcitonin concentration were higher in the Con group than in the DEX group (P < 0.05). In addition, in the DEX group, pulmonary exudation on chest radiography was lower, and pulmonary function, as shown by an increase in oxidation index and decrease in the respiratory index, improved after surgery (P < 0.05). Moreover, the duration of mechanical ventilation in the Con group was 3.4 h longer than that in the DEX group. Conclusion Dexmedetomidine has a protective effect on pulmonary function in patients undergoing mitral valve surgery using a totally video-assisted thoracoscopic technique, which may be related to a reduction in the concentration of inflammatory cytokines in the early perioperative period.
Highlights
Thoracoscopic cardiac surgery has developed rapidly in clinical practice due to its minimally invasive technique and rapid recovery [1]
Thoracoscopic cardiac surgery requires cardiopulmonary bypass (CPB) and the one-lung ventilation (OLV) technique. Both CPB and OLV can result in acute lung injury associated with the systemic inflammatory response syndrome (SIRS) and pulmonary ischemiareperfusion injury, which can lead to pulmonary dysfunction and seriously affect a patient’s prognosis [2,3,4]
Activation of the complement system is considered the initiating factor of postoperative lung injury from CPB [5]. Both the classic and alternative pathways of the complement system are activated during the CPB process, with the intensity of the inflammatory response enhanced through interaction with inflammatory factors such as tumor necrosis factor-α (TNF-α), procalcitonin (PCT), interleukin-1 (IL-1), IL-2, IL-6, and IL-8
Summary
Thoracoscopic cardiac surgery has developed rapidly in clinical practice due to its minimally invasive technique and rapid recovery [1]. Thoracoscopic cardiac surgery requires cardiopulmonary bypass (CPB) and the one-lung ventilation (OLV) technique. Both CPB and OLV can result in acute lung injury associated with the systemic inflammatory response syndrome (SIRS) and pulmonary ischemiareperfusion injury, which can lead to pulmonary dysfunction and seriously affect a patient’s prognosis [2,3,4]. Activation of the complement system is considered the initiating factor of postoperative lung injury from CPB [5] Both the classic and alternative pathways of the complement system are activated during the CPB process, with the intensity of the inflammatory response enhanced through interaction with inflammatory factors such as tumor necrosis factor-α (TNF-α), procalcitonin (PCT), interleukin-1 (IL-1), IL-2, IL-6, and IL-8. The interaction and cascade of cytokines during OLV are the primary mechanisms that cause lung injury [6]
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