Is difficult to perform.
Can be used to assess the efficacy of bronchodilators.
Is unaffected by dynamic compression of the airways.
Is reduced in patients with fibrosis but not COPD.
Increases with age.
Turbulence in the trachea.
Action of the diaphragm.
Contraction of the intercostal muscles.
Power of the abdominal muscles.
Compression of the airways.
Decreased expiratory flow rate when related to lung volume.
Abnormally high flow rate early in expiration.
Detecting fixed upper airway obstruction.
Measuring the response to bronchodilator drugs.
Differentiating between chronic bronchitis and emphysema.
Detecting resistance in small peripheral airways.
Detecting fatigue of the diaphragm.
It is usually normal in mild COPD.
The slope of phase 3 is increased in chronic bronchitis.
In phase 3, well-ventilated units empty last.
In normal subjects the last expired gas comes from the base of the lung.
The expiratory flow rate should be as fast as possible.
Increased lung compliance.
Increase in the number of small airways.
Increased radial traction on the airways.
Increased elastic recoil of the lung.
Hypertrophy of the diaphragm
A. Decreases with age.
B. Is highly reproducible.
C. Is affected by the small, peripheral airways.
D. Is most informative in patients with severe lung disease.
E. Is normal in mild COPD.
Blood temperature is reduced.
PCO2 is reduced.
Blood pH is raised.
Concentration of 2,3-DPG in the red cell is raised.
Hydrogen ion concentration is reduced.
Arterial oxygen saturation.
Plasma bicarbonate concentration.
Mixed respiratory and metabolic acidosis.
Uncompensated respiratory acidosis.
Fully compensated respiratory acidosis.
Uncompensated metabolic acidosis.
Fully compensated metabolic acidosis.
Residence at high altitude.
The condition is rare.
Most patients are lean.
Treatment by continuous positive airway pressure (CPAP) is often effective.
Treatment by CPAP tends to cause systemic hypertension.
Snoring is uncommon.
Increase arterial PO2 during moderate exercise.
Increase the uptake of halothane given during anesthesia.
Decrease arterial PCO2 during resting breathing.
Increase resting oxygen uptake when the subject breathes air.
Increase maximal oxygen uptake at extreme altitude.
Respiratory alkalosis with metabolic compensation.
Acute respiratory acidosis.
Metabolic acidosis with respiratory compensation.
Metabolic alkalosis with respiratory compensation.
A laboratory error.
A primary respiratory alkalosis with metabolic compensation.
A normal alveolar–arterial PO2 difference.
An arterial O2 saturation of less than 70%.
The sample was mistakenly drawn from a vein.
A partially compensated metabolic acidosis.
Can be measured with a single spirometer.
Is often larger when measured by helium dilution than with a body plethysmograph.
Is reduced during an attack of asthma.
Is determined by a balance between the elastic recoil of the lung and chest wall.
Falls with increasing age.
Is raised by increasing lung volume.
Is reduced by inhaling β2 agonists.
Is increased by destruction of alveolar walls.
Is unaffected by secretions in the airways.
Is increased by atrophy of bronchial smooth muscle.
Abnormally high levels of lactate in the blood.
Abnormally low ventilation.
Abnormally high cardiac output.
Increased lung compliance.
Reduced diffusing capacity of the lung.
Capillary blood volume.
PCO2 of mixed venous blood.
Damage to pulmonary capillaries by increased alveolar pressure.
Chronic stimulation of bronchial mucous glands by cigarette smoking.
Destruction of lung elastin by excessive action of neutrophil elastase.
Excessive amounts of exercise.
Hyperventilation at high altitude.
Causes severe bronchitis with emphysema.
Results in emphysema at a relatively early age.
Is caused by infections in early childhood.
Is common in heterozygotes for the Z gene.
Tends to be most marked in the upper regions of the lung.
More cough productive of sputum.
Smaller lung volumes.
Decreased lung elastic recoil.
Greater tendency to develop cor pulmonale.
None of the above.