scholarly journals Pulmonary edema in a pediatric patient undergoing ureteroscopy: a case report

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Irfan Tuna Dusgun ◽  
Cengiz Sahutoglu ◽  
Taner Balcioglu

Abstract Background This report demonstrates a case of pediatric pulmonary edema, detected due to the overuse of irrigation fluids during ureteroscopy. Case presentation A 7-year-old girl was hospitalized due to the large number of opaque stones in the right kidney. After extubation, the patient’s oxygen saturation dropped down to 85%, and respiratory distress was observed. It was determined that the surgical team used 5 Lt 0.9% NaCl solution as irrigation fluid. Positive pressure ventilation with mask continued, and intravenous bolus injection of furosemide was administered to the patient with a preliminary diagnosis of pulmonary edema. Conclusions In prolonged operations, patients should be checked for the presence of pulmonary edema with lung auscultation, and noninvasive mechanical ventilation and diuretic treatment should be instituted if necessary.

1989 ◽  
Vol 67 (2) ◽  
pp. 817-823 ◽  
Author(s):  
J. I. Sznajder ◽  
C. J. Becker ◽  
G. P. Crawford ◽  
L. D. Wood

Constant-flow ventilation (CFV) maintains alveolar ventilation without tidal excursion in dogs with normal lungs, but this ventilatory mode requires high CFV and bronchoscopic guidance for effective subcarinal placement of two inflow catheters. We designed a circuit that combines CFV with continuous positive-pressure ventilation (CPPV; CFV-CPPV), which negates the need for bronchoscopic positioning of CFV cannula, and tested this system in seven dogs having oleic acid-induced pulmonary edema. Addition of positive end-expiratory pressure (PEEP, 10 cmH2O) reduced venous admixture from 44 +/- 17 to 10.4 +/- 5.4% and kept arterial CO2 tension (PaCO2) normal. With the innovative CFV-CPPV circuit at the same PEEP and respiratory rate (RR), we were able to reduce tidal volume (VT) from 437 +/- 28 to 184 +/- 18 ml (P less than 0.001) and elastic end-inspiratory pressures (PEI) from 25.6 +/- 4.6 to 17.7 +/- 2.8 cmH2O (P less than 0.001) without adverse effects on cardiac output or pulmonary exchange of O2 or CO2; indeed, PaCO2 remained at 35 +/- 4 Torr even though CFV was delivered above the carina and at lower (1.6 l.kg-1.min-1) flows than usually required to maintain eucapnia during CFV alone. At the same PEEP and RR, reduction of VT in the CPPV mode without CFV resulted in CO2 retention (PaCO2 59 +/- 8 Torr). We conclude that CFV-CPPV allows CFV to effectively mix alveolar and dead spaces by a small bulk flow bypassing the zone of increased resistance to gas mixing, thereby allowing reduction of the CFV rate, VT, and PEI for adequate gas exchange.


Author(s):  
Antoine Vieillard-Baron

Knowledge of heart–lung interactions is key to manage haemodynamics in mechanically ventilated patients (see also Chapter 5). It allows intensivists to understand the meaning of blood and pulse pressure respiratory variations (PPV). Unlike spontaneous breathing, positive pressure ventilation increases blood pressure and pulse pressure during inspiration following by a decrease during expiration. This is called reverse pulsus paradoxus and includes a ‘d-down’ and a ‘d-up’ effect. No variation means no effect of mechanical ventilation on the heart and especially on the right heart. In case of significant PPV, tidal volume usually reduces right ventricular stroke volume by way of reducing preload where systemic venous return is decreased (fluid expansion is useful to restore haemodynamics, when impaired) or increasing afterload (obstruction of pulmonary capillaries due to alveolar inflation and, in this case, fluid expansion is useless or even sometimes deleterious). Clinical examination as well as evaluation of respiratory variations of superior vena cava by echo, helps to distinguish between these two situations. By studying the beat-by-beat changes in echo parameters induced by positive pressure ventilation heartbeat by heartbeat, echocardiography is perfectly suited to study heart–lung interactions and then to propose an appropriate optimization in case of haemodynamic impairment.


1976 ◽  
Vol 40 (4) ◽  
pp. 568-574 ◽  
Author(s):  
P. C. Hopewell ◽  
J. F. Murray

We compared the effects of continuous positive-pressure ventilation (CPPV), using 10 cmH2O positive end-expiratory pressure (PEEP), with intermittent positive-pressure ventilation (IPPV), on pulmonary extravascular water volume (PEWV) and lung function in dogs with pulmonary edema caused by elevated left atrial pressure and decreased colloid osmotic pressure. The PEWV was measured by gravimetric and double-isotope indicator dilution methods. Animals with high (22–33 mmHg), moderately elevated (12–20 mmHg), and normal (3–11 mmHg) left atrial pressures (Pla) were studied. The PEWV by both methods was significantly increased in the high and moderate Pla groups, the former greater than the latter (P less than 0.05). There was no difference in the PEWV between animals receiving CPPV and those receiving IPPV in both the high and moderately elevated Pla groups. However, in animals with high Pla, the Pao2 was significantly better maintained and the inflation pressure required to deliver a tidal volume of 12 ml/kg was significantly less with the use of CPPV than with IPPV. We conclude that in pulmonary edema associated with high Pla, PEEP does not reduce PEWV but does improve pulmonary function.


1981 ◽  
Vol 240 (6) ◽  
pp. H821-H826 ◽  
Author(s):  
J. E. Fewell ◽  
D. R. Abendschein ◽  
C. J. Carlson ◽  
E. Rapaport ◽  
J. F. Murray

To determine whether alterations in the mechanical properties (i.e., stiffening) of the right and left ventricles contribute to the decrease in right and left ventricular end-diastolic volumes during continuous positive-pressure ventilation (CPPV), we studied six dogs anesthetized with chloralose urethane and ventilated with a volume ventilator. We varied ventricular volumes by withdrawing or infusing blood. Pressure-volume curves, constructed by plotting transmural ventricular end-diastolic pressures against ventricular end-diastolic volumes, did not change during CPPV (12 cmH2O positive end-expiratory pressure) compared to intermittent positive-pressure ventilation (IPPV, 0 cmH2O end-expiratory pressure). We conclude that decreased ventricular end-diastolic volumes during CPPV result primarily from a decrease in venous return. Alterations in the mechanical properties of the ventricles do not play a significant role in this response.


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