Mean Functional Residual Capacity Research Articles

Lung Volume and Blood Oxygenation after Intermittent Positive Pressure Breathing

Functional residual capacity (FRC) was measured in 12 postoperative patients and in one preoperative patient before and after they received intermittent positive pressure breathing (IPPB) with room air for ten minutes at a peak delivered pressure of 15 cm H2O. Ten patients had a normal or low pretreatment FRC. After cessation of IPPB, the mean FRC decreased further. Arterial oxygen tensions, measured in 11 of the 13 patients, decreased in all 11 from a pretreatment mean of 67.8 +/- 4.3 mm Hg to an immediate posttreatment mean of 57.7 +/- 4.2 mm Hg. In five patients repeated arterial blood gases were measured. At 30 minutes, their arterial oxygen tensions had returned to the pre-IPPB values. This study demonstrates that the routine use of IPPB in postoperative patients accentuates preexisting hypoxia and, therefore, must be used with caution.

Lung volume and blood oxygenation after intermittent positive pressure breathing.

Functional residual capacity (FRC) was measured in 12 postoperative patients and in one preoperative patient before and after they received intermittent positive pressure breathing (IPPB) with room air for ten minutes at a peak delivered pressure of 15 cm H2O. Ten patients had a normal or low pretreatment FRC. After cessation of IPPB, the mean FRC decreased further. Arterial oxygen tensions, measured in 11 of the 13 patients, decreased in all 11 from a pretreatment mean of 67.8 +/- 4.3 mm Hg to an immediate posttreatment mean of 57.7 +/- 4.2 mm Hg. In five patients repeated arterial blood gases were measured. At 30 minutes, their arterial oxygen tensions had returned to the pre-IPPB values. This study demonstrates that the routine use of IPPB in postoperative patients accentuates preexisting hypoxia and, therefore, must be used with caution.

Ventilation-perfusion imbalance after head trauma.

To investigate the role of ventilation-perfusion (VA/Q) imbalance in the hypoxemia observed after head injury, 5 male subjects (17 to 26 years of age) with isolated head trauma and subsequent hypoxemia were studied. Disturbances of ventilation and perfusion were assessed using the steady-state elimination of six inert gases of different solubilities. Paired studies were conducted during mechanical ventilation with a volume-cycled ventilator and during spontaneous ventilation. Distributions recovered from studies of spontaneous ventilation show a mode of ventilation and perfusion near a VA/Q of 1.0. In addition, 41% of the cardiac output was distributed to a second population of lung units with low VA/Q (less than 0.1) and shunt. During mechanical ventilation, perfusion to these regions of low VA/Q decreased to 21% of the cardiac output, whereas shunt fraction was unchanged. This was associated with a marked broadening of the VA/Q mode near 1.0, relative to the studies during spontaneous ventilation. Mean functional residual capacity during mechanical ventilation was not different from that during spontaneous ventilation. These results suggest that head injury can lead to hypoxemia through a failure of VA/Q regulatory mechanisms.

Respiratory mechanics in conscious sheep: response to methacholine.

Most currently used animal models of allergic airway diseases differ from human asthma in that induced bronchospasm in the former is not accompanied by pulmonary hyperinflation. In the present investigation, we chose unsedated, restrained sheep to determine the effect of cholinergic bronchial provocation on respiratory mechanics, functional residual capacity (FRC), and arterial blood gases. Seven animals had been actively sensitized by intramuscular injections of Ascaris suum extract, and four untreated animals served as controls. After inhalation of nebulized 1% methacholine solution, mean pulmonary resistance increased significantly in the sensitized sheep from a base line of 2.4 +/- 0.7 (SD) cmH2O/(l/s) to a peak value after 5 min of 7.9 +/- 4.0 cmH2O/(l/s). This was accompanied by a significant increase of mean FRC from 0.99 +/- 0.14 liters to 1.31 +/- 0.24 liters. The observed changes were transient, and after 60 min, pulmonary resistance and FRC had returned to base-line values. No significant changes occurred in static lung compliance, PaO2, PaCO2, and pH. In the control animals, methacholine provocation did not produce changes in pulmonary function. These results indicate that, in sensitized conscious sheep, induced bronchospasm is associated with pulmonary hyperinflation.

Respiratory mechanics in normal hamsters.

Lung volumes and quasi-static deflation volume-pressure relationships were measured in male golden hamsters anesthetized with pentobarbital. Volume was measured with a pressure plethysmograph, and pleural pressure was estimated by the use of a water-filled esophageal catheter. Mean body weight +/- SE was 122.3 +/-3.0 g, mean lung weight was 0.74 +/- 0.2 g or about 0.6% of body weight. Mean lung volume at 25 cmH2O transpulmonary pressure (TLC25) was 7.2 +/- 0.14 ml, 9.78 +/- 0.17 ml/g lung weight or 5.92 +/- 0.06 ml/100 g body weight. Mean functional residual capacity was 2.4 +/- 0.06 ml or 33.3% of TLC25. Mean vital capacity was 5.2 +/- 0.13 ml. Mean quasi-static compliance of lung was 0.63 +/- 0.03 ml/cmH2O. Chord compliance of chest wall between lung volumes of 1 and 4 ml above RV was 3.39 +/- 0.53 ml/cmH2O. At FRC, the chest wall recoiled inward, so that pleural pressure was positive (1.4 +/- 0.13 cmH2O) and the lung was resisting further collapse. The slope of the lung's deflation volume-pressure curve changed at FRC, ERV was small (0.36 +/- 0.03 ml), and RV was determined by complete airway closure. Thus the mechanisms determining FRC are unusual and include an influence of airway closure.

Lung mechanics in hypervolemic pulmonary edema.

Extravascular thermal volume of the lung (ETVL) is a double indicator dilution technique of use in measuring pulmonary edema. ETVL and lung mechanics measurements were followed to find a less invasive monitor of pulmonary edema than the double indicator dilution technique. Pulmonary edema was induced by overloading the dogs' circulation with dextran. Phases of overload were defined on the basis of a previous electron microscopic study (Noble et al., Can. Anesthetists Soc. J. 21:275, 1974) of lung biopsies relating anatomic changes to physiologic measurements of ETVL and central blood volume (CBV). Congestion occurred when CBV was elevated and ETVL was not, interstitial edema when ETVL was elevated but smaller than 60% above control and alveolar edema when ETVL greater than 85% above control. Once the dogs were in alveolar edema, they were mechanically ventilated with 4, 8, 12, and 16 cmH2O end-tidal pressure (CPPV). Mean functional residual capacity (FRC) for all 15 dogs did not change up to the time CPPV was applied. Pulmonary resistance did not rise until alveolar edema was present. Once in pulmonary edema, lung compliance always fell as lung water increased. In individual dogs, the compliance fall was directly proportional to the rising lung water. However, the variations in slope and beginning point among dogs made it difficult to predict the amount of lung water from dynamic compliance values. PaO2 fell markedly in alveolar edema as a result of a widened A-a gradient. CPPV did not decrease lung water but did increase FRC and PaO2.

Pulmonary Gas Trapping in Premature Infants

Extract: Measurements of thoracic gas volume and functional residual capacity were performed serially from birth on 26 premature infants to determine the presence and time course of gas trapping. Nitrogen washouts were carried out on 16 of these infants and urinary-alveolar nitrogen gradients (uADN2) were measured in 7. The infants were divided into two groups, those above and those below 1750 g birth weight. Trapped gas was documented in both groups, but in the smaller infants the condition persisted for a longer time. The mean thoracic gas volume (TGV) in infants over 1750 g birth weight was 2.0 ± 0.7 ml/cm at birth, with a mean functional residual capacity (FRC) of 1.3 ± 0.4 ml/cm; by day 9, the TGV and FRC were 1.5 ± 0.3 and 1.2 ± 0.2 ml/cm, respectively. Infants under 1750 g birth weight had a mean TGV of 1.7 ± 0.2 ml/cm at birth with an FRC of 0.9 ± 0.2 ml/cm; by week 2 of life, mean TGV and FRC were 0.9 ± 0.2 and 0.8 ± 0.2 ml/cm, respectively. When gas trapping was present, nitrogen washouts and uADN2 indicated that the lung was a single well ventilated space with no evidence of an abnormal distribution of ventilation. This indicated that ventilation of the trapped areas was so small that it could not be measured. The possibility that gas trapping is related to the presence of lung fluid and very compliant airways is considered. Speculation: Low birth weight infants have been shown to have high airway resistance, compliant airways, and low lung volume. This combination of findings has been associated with airway closure in adults. The possibility arises that a volume of gas is “trapped” with each expiration until airways are sufficiently stiff and remain patent with every breath.

Evaluation of the forced oscillation technique for the determination of resistance to breathing.

Total respiratory resistance (R(T)) was measured by the application of a sine wave of airflow to the mouth at the resonant frequency of the respiratory system. The mean respiratory resistance of 42 normal subjects, measured at a mean functional residual capacity of 3.3 liters, was 2.3, SD +/- 0.5, cm H(2)O/liter per sec, and the resonant frequency was between 5 and 8 cycle/sec. The airway resistance measured in these same subjects with the body plethysmograph at a mean panting thoracic gas volume of 3.5 liters was 1.3, SD +/- 0.3, cm H(2)O/liter per sec. Total respiratory resistance was found to vary inversely with lung volume (V) measured plethysmographically; prediction formulae for normal subjects based on this relationship are: R(T) (mean) = 7.1/V, R(T) (range) = 4.0/V to 11.6/V where V is in liters and R(T) is in cm H(2)O/liter per sec. When these criteria were applied to subjects with thoracic disease the following results were obtained: 17 subjects with obstructive lung disease all had elevated total respiratory resistance; 9 subjects with diffuse lung disease without airway obstruction all had normal respiratory resistance; all but 1 of 5 obese subjects and all but 2 of a heterogeneous group of 9 subjects without airway obstruction had normal respiratory resistance. Failure to take lung volume into account resulted in a considerable decrease in the ability to discriminate between obstructive and nonobstructive lung disease on the basis of the forced oscillation test. The resonant frequency of the respiratory system of patients with obesity or nonobstructive lung disease was similar to that obtained in the normal group; accurate evaluation of resonant frequency in subjects with obstructive lung disease was frequently not possible. The combined resistances of lung, thoracic wall and abdominal tissues were found to account for less than 43% of the total respiratory resistance in normal subjects and were only slightly increased by the presence of obesity, restrictive diseases of the thoracic wall, and hyperinflation of the thorax. The forced oscillation method is potentially of value in the study of resistance to breathing of patients who cannot undergo body plethysmography, such as acutely ill, anesthetized, or unconscious subjects. Accurate evaluation of R(T) requires an independent measure of lung volume as well as careful attention during measurements to the airflow rate, phase of respiration, and the adequacy of cheek compression and laryngeal relaxation.