Respiratory Alkalosis Caused by Assist Control Mechanical Ventilation in a Patient with a Bronchopleural Fistula

Author(s):  
Russell F. Pruitt ◽  
William Joseph Messick ◽  
Michael H. Thomason
2019 ◽  
Author(s):  
Sarah Rae Easter ◽  
Nicole A. Smith

Pulmonary edema is characterized by the movement of excess fluid into the alveoli of the lungs.  Although the alterations of cardiovascular and pulmonary physiology in pregnancy may predispose patients to pulmonary edema, it is never normal and constitutes severe maternal morbidity.  The etiologies of pulmonary edema are diverse, ranging from disease processes independent of pregnancy to pathophysiology unique to the gravid state.  The causes of pulmonary edema can be broadly classified as either cardiogenic or noncardiogenic, which constitutes the first important branch point in the diagnosis and management of the disease.  The treatment of pulmonary edema in pregnancy parallels that in the nonpregnant population with an emphasis on maintaining the physiologic alterations of pregnancy through supportive care, including mechanical ventilation if needed.  In all cases of pulmonary edema, the decision to proceed with delivery to improve the maternal status should be considered within the context of the etiology and anticipated disease course, the gestational age, and the goals of care. This review contains  3 figures, 4 tables, and 60 references. Key Words:  Pulmonary edema, respiratory alkalosis, acute respiratory distress syndrome (ARDS), cardiogenic pulmonary edema, transfusion-related acute lung injury (TRALI), transfusion-associated circulatory overload (TACO), mechanical ventilation, extra corporeal membrane oxygenation (ECMO).


1994 ◽  
Vol 77 (5) ◽  
pp. 2079-2085 ◽  
Author(s):  
A. M. Leevers ◽  
P. M. Simon ◽  
J. A. Dempsey

We determined whether normocapnic mechanical ventilation at high tidal volume (VT) and breathing frequency (f) during non-rapid-eye-movement (NREM) sleep would cause apnea. Seven normal sleeping subjects were placed on assist-control mechanical ventilation (i.e., subject initiates inspiration) and VT was gradually increased to 2.1 times eupneic VT (1.17 +/- 0.04 liters). This high VT was maintained for 5 min, the ventilator mode was switched to controlled mechanical ventilation, and f was increased gradually from 9.5 +/- 1.0 (during assist-control mechanical ventilation) to 14.0 +/- 0.7 breaths/min. Normocapnia (end-tidal PCO2 = 44 +/- 1.2 Torr) was maintained throughout the trials. Inspiratory effort was completely inhibited during the period of sustained high VT and f, and apnea occurred immediately after cessation of the passive mechanical ventilation. The duration of the apnea preceding the first inspiratory effort was 20.3 +/- 2.3 s or 7.1 times the eupneic expiratory duration and 5 times the expiratory duration chosen by the subject during assist-control mechanical ventilation. We conclude that inhibition of inspiratory motor output occurs during and after normocapnic mechanical ventilation at high VT and f during NREM sleep. These neuromechanical inhibitory effects may serve to initiate and prolong apnea.


2006 ◽  
Vol 105 (1) ◽  
pp. 14-18 ◽  
Author(s):  
Evans R. Fernández-Pérez ◽  
Mark T. Keegan ◽  
Daniel R. Brown ◽  
Rolf D. Hubmayr ◽  
Ognjen Gajic

Background Respiratory failure is a leading cause of postoperative morbidity and mortality in patients undergoing pneumonectomy. The authors hypothesized that intraoperative mechanical ventilation with large tidal volumes (VTs) would be associated with increased risk of postpneumonectomy respiratory failure. Methods Patients undergoing elective pneumonectomy at the authors' institution from January 1999 to January 2003 were studied. The authors collected data on demographics, relevant comorbidities, neoadjuvant therapy, pulmonary function tests, site and type of operation, duration of surgery, intraoperative ventilator settings, and intraoperative fluid administration. The primary outcome measure was postoperative respiratory failure, defined as the need for continuation of mechanical ventilation for greater than 48 h postoperatively or the need for reinstitution of mechanical ventilation after extubation. Results Of 170 pneumonectomy patients who met inclusion criteria, 30 (18%) developed postoperative respiratory failure. Causes of postoperative respiratory failure were acute lung injury in 50% (n = 15), cardiogenic pulmonary edema in 17% (n = 5), pneumonia in 23% (n = 7), bronchopleural fistula in 7% (n = 2), and pulmonary thromboembolism in 3% (n = 1). Patients who developed respiratory failure were ventilated with larger intraoperative VT than those who did not (median, 8.3 vs. 6.7 ml/kg predicted body weight; P < 0.001). In a multivariate regression analysis, larger intraoperative VT (odds ratio, 1.56 for each ml/kg increase; 95% confidence interval, 1.12-2.23) was associated with development of postoperative respiratory failure. The interaction between larger VT and fluid administration was also statistically significant (odds ratio, 1.36; 95% confidence interval, 1.05-1.97). Conclusion Mechanical ventilation with large intraoperative VT is associated with increased risk of postpneumonectomy respiratory failure.


2012 ◽  
Vol 57 (8) ◽  
pp. 1297-1304 ◽  
Author(s):  
Teresa A Volsko ◽  
Justin Hoffman ◽  
Alecia Conger ◽  
Robert L Chatburn

2010 ◽  
Vol 36 (4) ◽  
pp. 721-722 ◽  
Author(s):  
Valentina Bellato ◽  
G. M. Ferraroli ◽  
D. De Caria ◽  
M. V. Infante ◽  
U. Cariboni ◽  
...  

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