End-respiratory pressure ventilation and sulfobromophthalein sodium excretion in dogs

1977 ◽  
Vol 43 (4) ◽  
pp. 714-720 ◽  
Author(s):  
E. E. Johnson ◽  
J. Hedley-Whyte ◽  
S. V. Hall

Sulfobromophthalein sodium (BSP) 25 mg/kg body wt was given as a single iv injection to 32 fasted dogs. Serum samples at 3, 5, 10, 20, 30, 45, 60, 80, and 120 min postinjection were analyzed for total concentration of BSP and from 30 to 120 min for percent conjugated BSP. Four groups were compared: spontaneous ventilation; intermittent positive-pressure ventilation (IPPV) and continuous positive-pressure ventilation (CPPV) (2 groups). During CPPV, one group of dogs was given a continuous infusion of cholecystokinin octapeptide (CCK-8, 1 ng/kg per min). Central venous pressure averaged 11.3 +/- 0.7 (SE) cmH2O in dogs with CPPV + CCK-8 and 11.8 +/- 0.8 (SE) cmH2O in dogs with CPPV alone. At 3, 5, and 10 min postinjection serum BSP levels were similar in all groups. From 30 to 120 min postinjection serum levels of both free and conjugated BSP were higher in dogs ventilated with CPPV alone than in any other group (P less than 0.01). Dogs given CCK-8 during CPPV had serum BSP levels that were statistically similar to dogs breathing spontaneously or ventilated with IPPV. We conclude that CPPV impairs BSP excretion. This effect is counteracted by CCK-8.

1975 ◽  
Vol 39 (6) ◽  
pp. 937-942 ◽  
Author(s):  
E. E. Johnson ◽  
J. Hedley-Whyte

Resistance to flow through the choledochoduodenal junction was measured during constant perfusion (0.8 ml saline/min). In eight dogs, intermittent positive-pressure ventilation (IPPV) and continuous positive-pressure ventilation (CPPV) were compared. Pressure in the common bile duct was always higher during JPPV than IPPV. With the first application of CPPV the rate of intravenous fluid was adjusted to maintain constant Hct. Mean hepatic venous pressure (Phv) increased from 6.6 to 11.5 cmH2O (P less than 0.001). Mean pressure in the common bile duct increased (P less than 0.001) from 11.6 to 14.1 cmH2O. The average increase in resistance was 21%. Changes reversed with return to IPPV. During the second application of CPPV, intravenous fluid was increased to maintain constant arterial pressure. Phv increased to 12.8 cmH2O and pressure in the common bile duct increased to 15.0 cmH2O (30% increase). In four additional dogs, choledochoduodenal resistance during continuous CPPV was reduced by intravenous vasopressin, intravenous norepinephrine and intraducta phenylephrine. CPPV increases resistance to flow through the choledochoduodenal junction, probably by vascular engorgement.


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.


1989 ◽  
Vol 66 (5) ◽  
pp. 2223-2230 ◽  
Author(s):  
M. Skaburskis ◽  
R. P. Michel ◽  
A. Gatensby ◽  
A. Zidulka

We have previously shown (Am. Rev. Respir. Dis. 136: 886–891, 1987) improved cardiac output in dogs with pulmonary edema ventilated with external continuous negative chest pressure ventilation (CNPV) using negative end-expiratory pressure (NEEP), compared with continuous positive-pressure ventilation (CPPV) using equivalent positive end-expiratory pressure (PEEP). The present study examined the effect on lung water of CNPV compared with CPPV to determine whether the increased venous return created by NEEP worsened pulmonary edema in dogs with acute lung injury. Oleic acid (0.06 ml/kg) was administered to 27 anesthetized dogs. Supine animals were then divided into three groups and ventilated for 6 h. The first group (n = 10) was treated with intermittent positive-pressure ventilation (IPPV) alone; the second (n = 9) received CNPV with 10 cmH2O NEEP; the third (n = 8) received CPPV with 10 cmH2O PEEP. CNPV and CPPV produced similar improvements in oxygenation over IPPV. However, cardiac output was significantly depressed by CPPV, but not by CNPV, when compared with IPPV. Although there were no differences in extravascular lung water (Qwl/dQl) between CNPV and CPPV, both significantly increased Qwl/dQl compared with IPPV (7.81 +/- 0.21 and 7.87 +/- 0.31 vs. 6.71 +/- 0.25, respectively, P less than 0.01 in both instances). CNPV and CPPV, but not IPPV, enhanced lung water accumulation in the perihilar areas where interstitial pressures may be most negative at higher lung volumes.


2004 ◽  
Vol 101 (4) ◽  
pp. 1015-1017 ◽  
Author(s):  
Henning Pontoppidan ◽  
Srinivasa N. Raja

Continuous positive-pressure ventilation in acute respiratory failure. By Kumar A, Falke KJ, Geffin B, Aldredge CF, Laver MB, Lowentein E, Pontoppidan H. N Engl J Med 1970; 283:1430-6. Reprinted with permission. Continuous positive-pressure ventilation was used in eight patients with severe acute respiratory failure. Cardiac output and lung function were studied during continuous positive-pressure ventilation (mean end-expiratory pressure, 13 cm H2O) and a 30-min interval of intermittent positive-pressure ventilation. Although the mean cardiac index increased from 3.6 to 4.5 l/min per square meter of body surface area, the mean intrapulmonary shunt increased by 9% with changeover to intermittent positive-pressure ventilation. Satisfactory oxygenation was maintained in all patients during continuous positive-pressure ventilation with 50% inspired oxygen or less. With intermittent positive-pressure ventilation, arterial oxygen tension promptly fell by 161 mm of mercury, 79% occurring within 1 min. Prevention of air-space collapse during expiration and an increase in functional residual capacity probably explain improved oxygenation with continuous positive-pressure ventilation. In four patients, subcutaneous emphysema or pneumothorax developed. Weighed against the effects of prolonged hypoxemia, these complications were not severe enough to warrant cessation of continuous positive-pressure ventilation.


2017 ◽  
Vol 62 (4) ◽  
pp. 334
Author(s):  
K. PAVLIDOU (Κ. ΠΑΥΛΙΔΟΥ) ◽  
I. SAVVAS (Ι. ΣΑΒΒΑΣ) ◽  
T. ANAGNOSTOU (Τ. ΑΝΑΓΝΩΣΤΟΥ)

Mechanical ventilation is the process of supporting respiration by manual or mechanical means. When normal breathing is inefficient or has stopped, mechanical ventilation is life-saving and should be applied at once. The ventilator increases the patient's ventilation by inflating the lungs with oxygen or a mixture of air and oxygen. Ventilators play an important role in the anaesthetic management of patients, as well as in the treatment of patients in the ICU. However, there are differences between the anaesthetic ventilators and the ventilators in ICU. The main indication for mechanical ventilation is difficulty in ventilation and/or oxygenation of the patient because of any respiratory or other disease. The aims of mechanical ventilation are to supply adequate oxygen to patients with a limited vital capacity, to treat ventilatory failure, to reduce dyspnoea and to facilitate rest of fatigued breathing muscles. Depression of the central nervous system function is a pre-requirement for mechanical ventilation. Some times, opioids or muscle relaxants can be used in order to depress patient's breathing. Mechanical ventilation can be applied using many different modes: assisted ventilation, controlled ventilation, continuous positive pressure ventilation, intermittent positive pressure ventilation and jet ventilation. Furthermore, there are different types of automatic ventilators built to provide positive pressure ventilation in anaesthetized or heavily sedated or comatose patients: manual ventilators (Ambu-bag), volumecontrolled ventilators with pressure cycling, volume-controlled ventilators with time cycling and pressure-controlled ventilators. In veterinary practice, the ventilator should be portable, compact and easy to operate. The controls on most anaesthetic ventilators include settings for tidal volume, inspiratory time, inspiratory pressure, respiratory rate and inspiration: expiration (I:E) ratio. The initial settings should be between 10-20 ml/kg for tidal volume, 12-30 cmH2 0 for the inspiratory pressure and 8-15 breaths/min for the respiratory rate. Mechanical ventilation is a very important part of treatment in the ICU, but many problems may arise during application of mechanical ventilation in critically ill patients. All connections should be checked in advance and periodically for mechanical problems like leaks. Moreover, complications like lung injury, pneumonia, pneumothorax, myopathy and respiratory failure can occur during the course of mechanical ventilation causing difficulty in weaning.


Author(s):  
Bayane Sabsabi ◽  
Ava Harrison ◽  
Laura Banfield ◽  
Amit Mukerji

Objective The study aimed to systematically review and analyze the impact of nasal intermittent positive pressure ventilation (NIPPV) versus continuous positive airway pressure (CPAP) on apnea of prematurity (AOP) in preterm neonates. Study Design In this systematic review and meta-analysis, experimental studies enrolling preterm infants comparing NIPPV (synchronized, nonsynchronized, and bi-level) and CPAP (all types) were searched in multiple databases and screened for the assessment of AOP. Primary outcome was AOP frequency per hour (as defined by authors of included studies). Results Out of 4,980 articles identified, 18 studies were included with eight studies contributing to the primary outcome. All studies had a high risk of bias, with significant heterogeneity in definition and measurement of AOP. There was no difference in AOPs per hour between NIPPV versus CPAP (weighted mean difference = −0.19; 95% confidence interval [CI]: −0.76 to 0.37; eight studies, 456 patients). However, in a post hoc analysis evaluating the presence of any AOP (over varying time periods), the pooled odds ratio (OR) was lower with NIPPV (OR: 0.46; 95% CI: 0.32–0.67; 10 studies, 872 patients). Conclusion NIPPV was not associated with decrease in AOP frequency, although demonstrated lower odds of developing any AOP. However, definite recommendations cannot be made based on the quality of the published evidence. Key Points


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