Effect of patient positioning on pneumothorax rate following fine needle lung aspiration.
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Biomedical subjects
Publications and source records attributed to A Zidulka.
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The clearance of mucus in the trachea during high frequency chest wall compression (HFCWC) was studied in nine anesthetized dogs. High frequency chest wall compression was applied by oscillating the pressure in a thoracic cuff such that it produced oscillatory tidal volumes of 25 to 100 cc at frequencies of 3 to 17 Hz. The tracheal mucus clearance rate (TMCR) was determined by direct observation of the rate of displacement of a charcoal particle spot by means of a fiberoptic bronchoscope. Baseline TMCR during spontaneous breathing averaged 8.2 +/- 5.6 mm/min in the 9 dogs. The TMCR during 2 min of HFCWC was increased at 5, 8, 11, 13, 15, and 17 Hz but not at 3 Hz. The enhancement of clearance was most pronounced in the range of 11 to 15 Hz, reaching a peak value of 340% of control at 13 Hz. These studies suggest that HFCWC might be of considerable potential benefit as a mode of chest physiotherapy.
Mean inspiratory flow, occlusion pressure and end-tidal PCO2 were measured in six healthy, sitting subjects, during breathing air and rebreathing carbon dioxide, before and after pentazocine 0.5 mg kg-1 i.v. and again after naloxone 20 micrograms kg-1. Pentazocine reduced the occlusion pressure and inspiratory flow responses at a given PCO2 during carbon dioxide rebreathing and these effects were antagonized by naloxone. The relationship of inspiratory flow and end-tidal carbon dioxide during rebreathing was used to measure the PCO2 value at which mean inspiratory flow was 1 litres-1. Occlusion pressure at this PCO2 was reduced in all the subjects by pentazocine, suggesting that the generation of inspiratory flow required less muscle activity. This effect was antagonized by naloxone.
We attempted to see what the effect of position was on the rate of pneumothorax formation. In 6 anesthetized spontaneously breathing dogs in the left decubitus position, a chest tube was inserted into the right hemithorax. A right-sided pneumothorax was induced by percutaneous transthoracic insertion of a 20-gauge needle into the lung. Once a constant rate of pneumothorax formation occurred, the dogs were alternated between 3 min of no evacuation by the chest tube with the puncture site up (left decubitus) or down (right decubitus). The pneumothorax that accumulated was always evacuated immediately thereafter with the chest tube in the highest position (left decubitus). In every case, the rate of pneumothorax formation decreased with the puncture site down rather than with it up. Furthermore, this maneuver caused the site of leak to completely seal 11 of 21 times in which the puncture site was placed dependent. There was, however, no significant change in the rate of pneumothorax formation with the puncture site kept in the nondependent position. These results are consistent with the hypothesis that placing the site of pleural gas leak in the most dependent position causes a reduction in alveolar size as well as the alveolar to pleural pressure gradient in the region surrounding the leak. Both of these factors would tend to slow the rate of pneumothorax formation and allow sealing of the puncture site.
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In anesthetized and paralyzed pigs in the left decubitus position we obstructed, at functional residual capacity (FRC), either the right middle and lower lobes, or a small posterior basal lung unit, and then passively inflated the unobstructed remaining lung. Measurements were made of alveolar pressure in the obstructed and unobstructed lung regions as well as of esophageal pressure. The tendency of the obstructed lung region to inflate as the remainder of the lung was inflated was assessed by an index (A), which was the end-inspiratory pressure difference between unobstructed and obstructed alveolar pressures, normalized by the change in elastic recoil of unobstructed lung. With the chest wall intact, inflation of unobstructed lung resulted in a tendency to inflate the obstructed regions. This tendency was abolished with the chest wall removed. In a second group of pigs with the basilar lung unit obstructed, the height of the unit was changed by turning a pig from right to left decubitus positions. In each position A was assessed with both spontaneous and positive pressure ventilation. The magnitude of A was found to vary directly with the magnitude of caudal diaphragmatic motion and was greatest with the lung unit dependent and with spontaneous ventilation. These results suggest that lung-chest wall interaction was a more important factor tending to preserve homogenous inflation than lung tissue interdependence.
The right lower lobes (RLL) of intact horizontal dogs were obstructed at FRC during spontaneous breathing and artificial ventilation (IPPB). At end inspiration, pressure within the RLL became less than tracheal pressure, and pressure in the lower esophagus declined to a greater extent than in the upper esophagus. Tidal pressure swings in the obstructed RLL were larger than in the esophagus during spontaneous breathing but smaller during IPPB implying that the elastic recoil of the RLL decreased during inspiration at the mediastinal side. All these changes were intensified during RLL atelectasis and counteracted by strapping of the lower chest wall. These results indicate that: (a) around a lobe moving out of phase with the rest of the lung, a force is created tending to minimize the lobar volume differences; (b) the obstructed lobe is deformed during inflation of the rest of the lung; (c) esophageal (and hence pleural) pressure gradient is modified by this localized intrapulmonary pathology apparently due to shape interactions between chest wall and lung.
Continuous negative external chest pressure was used to increase the functional residual capacity in 6 dogs, and the effects were compared with the effects of increasing functional residual capacity using positive end-expiratory pressure. Cardiac index and mixed venous O2 stauration each decreased from control values during positive end-expiratory pressure, but did not decrease with continuous negative external chest pressure. Continuous negative external chest pressure may provide an alternative to positive end-expiratory pressure for increasing the functional residual capacity of patients in whom the latter causes unacceptable decreases in venous return and cardiac output.
The effects of acute lobar obstruction on pleural surface pressure in supine dogs were examined. The right lower lobes (RLL) were obstructed at FRC in some dogs while in others the left lung and RLL were both obstructed at FRC. At the end of the subsequent inspiration, costal surface pressure was less over the obstructed lobe than over the unobstructed right upper lobe. Alveolar pressure within the obstructed RLL decreased relative to tracheal pressure at end inspiration resulting in an inflating pressure being applied to the obstructed lobe. In most dogs elastic recoil increased at the lateral costal margin of the obstructed RLL implying the application of a deforming pressure to the obstructed lobes. The tendency to inflate and deform the obstructed RLL was greater during spontaneous breathing than during artificial ventilation.
The effect of acute obstruction of the right lower lobes (RLL) on the relative perfusion of different lung regions was studied using Xenon-133 in anesthetized artificially ventilated supine dogs. When the RLL were obstructed at functional residual capacity (FRC) and the rest of the lung was inflated to a transpulmonary pressure of 10 or 20 cm H2O (1 cm H2O = 94.1 N/m2), relative perfusion increased within 10 s to the obstructed lobes by 59 and 92%, respectively. The increase was less marked but still present (17 and 42%, respectively) when obstruction was maintained for 15 min, at a time when arterial hypoxemia had occurred. Hence, there was increased perfusion to an obstructed hypoxic region. The perfusion distribution correlated with the difference in alveolar pressure between the obstructed lobes and the unobstructed lobes such that relative perfusion was always increased to the low alveolar pressure region.
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High frequency chest wall compression (HFCWC) was studied as a method of assisting ventilation in six spontaneously breathing anesthetized dogs. Under a constant level of anesthesia, the dogs became hypercapneic after airflow obstruction was created by metal beads inserted in the airways. HFCWC was achieved by a piston pump rapidly oscillating the pressure in a modified double blood pressure cuff wrapped around the lower thorax. Thirty minute periods of spontaneous ventilation were alternated with thirty minute periods of spontaneous breathing plus HFCWC at 3, 5 or 8 Hz. The superimposition of HFCWC to spontaneous ventilation resulted in little change in the PaO2. The PaCO2, however, was reduced in every case from a mean of 6.55 +/- 0.59 to 4.72 +/- 0.32 kPa at 3 Hz (p less than 0.05), 6.92 +/- 0.57 to 3.9 +/- 0.45 kPa at 5 Hz (p less than 0.01) and 7.10 +/- 0.65 to 4.56 +/- 0.59 kPa at 8 Hz (p less than 0.05). This occurred despite a decrease in spontaneous minute ventilation. We conclude that HFCWC can assist in elimination of CO2 in obstructed spontaneous breathing dogs with hypercapnea.
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