A Comparison of Artificial Ventilation and Spontaneous Respiration With Particular Reference to Ventilation-Bloodflow Relationships

Campbell, E. J. M.; Nunn, J.F.; Peckett, B. W.

doi:10.1093/bja/30.4.166

Cited by 98 publications

(20 citation statements)

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“…These are + 2 S.D. of measurements of 90 anaesthetized paralysed subjects accumulated from the data of Nims, Conner & Comroe (1955), Butler & Smith (1957), Howell & Peckett (1957) and Campbell, Nunn & Peckett (1958). These subjects, in addition to being paralysed, were also supine and their average age was greater than our conscious subjects.…”

Section: Increased End-inspiratory Muscle Tensionmentioning

confidence: 68%

The immediate effects of elastic loads on the breathing of man

Campbell¹,

Dinnick²,

Howell³

1961

The Journal of Physiology

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Section: Increased End-inspiratory Muscle Tensionmentioning

confidence: 68%

The immediate effects of elastic loads on the breathing of man

Campbell¹,

Dinnick²,

Howell³

1961

The Journal of Physiology

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“…This may result in decreased oxygenation of blood. [1][2][3] A major cause of this derangement appears to be atelectasis, 4 which cannot be seen on conventional chest x-ray, 5 but was demonstrated by computed tomography (CT) of the chest. [6][7][8] Atelectasis in turn causes pulmonary shunt.…”

mentioning

confidence: 99%

Dynamics of re-expansion of atelectasis during general anaesthesia

Rothen

Neumann

Berglund

et al. 1999

British Journal of Anaesthesia

199

110

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A major cause of impaired gas exchange during general anaesthesia is atelectasis, causing pulmonary shunt. A 'vital capacity' (VC) manoeuvre (i.e. inflation of the lungs up to 40 cm H 2 O, maintained for 15 s) may re-expand atelectasis and improve oxygenation. However, such a manoeuvre may cause adverse cardiovascular effects. Reducing the time of maximal inflation may improve the margin of safety. The aim of this study was to analyse the change over time in the amount of atelectasis during a VC manoeuvre in 12 anaesthetized adults with healthy lungs. I.v. anaesthesia with controlled mechanical ventilation (VT 9 (SD 1) ml kg -1 ) was used. For the VC manoeuvre, the lungs were inflated up to an airway pressure (Paw) of 40 cm H 2 O. This pressure was maintained for 26 s. Atelectasis was assessed by analysis of computed x-ray tomography. The amount of atelectasis, measured at the base of the lungs, was 4.0 (SD 2.7) cm 2 after induction of anaesthesia. The decrease in the amount of atelectasis over time during the VC manoeuvre was described by a negative exponential function with a time constant of 2.6 s. At an inspired oxygen concentration of 40%, Pa O 2 increased from 17.2 (4.0) kPa before to 22.2 (6.0) kPa (Pϭ0.013) after the VC manoeuvre. Thus in anaesthetized adults undergoing mechanical ventilation with healthy lungs, inflation of the lungs to a Paw of 40 cm H 2 O, maintained for 7-8 s only, may re-expand all previously collapsed lung tissue, as detected by lung computed tomography, and improve oxygenation. We conclude that the previously proposed time for a VC manoeuvre may be halved in such subjects. 1999; 82: 551-6 Br J Anaesth

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“…[1][2][3][4][5][6] There is little argument that true veno-arterial shunting consequent upon alveolar collapse is an important contributory factor. Most of the evidence for this is indirect, and the presence of alveolar collapse is inferred from changes in compliance 7 and from the effect on oxygenation of measures designed to overcome the postulated collapse.…”

mentioning

confidence: 99%