Pulmonary Flashcards
Normally, the respiratory quotient is:
- 1.0
- 0.6
- 0.3
- 0.8
0.8
The normal respiratory quotient is 0.8 and probably reflects utilization of a combination of both fats and carbohydrates a fuel sources.
In the upright position, the largest alveoli are found:
- at the lung bases
- in the lingular lobe
- in zone 2
- at the apices
at the apices
In the upright position, the largest alveoli are at the pulmonary apex, whereas the smallest tend to be at the base
Referring to the spirogram below, the vital capacity is best represented by:
A
B
C
D
B
The vital capacity is the maximum volume of gas that can be exhaled following maximal inspiration.
The amount at which airways in the dependent portions of the lung begin to close is referred to as the:
closing volume
closing capacity
functional residual capacity
residual volume
closing capacity
Small airways lack cartilaginous support and depend on radial traction caused by the elastic recoil of surrounding tissue to keep them open. Patency of these airways is highly dependent on lung volume. The volume at which these airways begin to close is called the closing capacity.
The flow-volume loop below that best represents normal lung function is:
A
B
C
D
B
flow-volume loop B demonstrates both normal volumes and flows.
In a patient receiving general anesthesia with controlled ventilation with a tidal volume of 600 mL, the PaCO2 was 42 mmHg and the mixed expired CO2 was 35. From this information, the dead space can be estimated to be:
- 100 mL
- 150 mL
- 200 mL
- cannot be determined from this information
100 mL(?)
Dead space can be estimated using the Bohr equation:
VD/VT = (PACO2 - PECO2)/PACO2
During the administration of general anesthesia, the airway pressures from graph A below were obtained. One hour later, the airway pressures in graph B were noted. Possible explanations for the change include:
- increased compliance
- increased dead space
- kinked endotracheal tube
- increased tidal volume
kinked endotracheal tube
Causes of increased peak inspiratory pressure and unchanged plateau pressure include decreased I:E ratio, increased airway resistance, bronchospasm, kinked endotracheal tube, secretions and foreign body aspiration.
Pulmonary vascular tone is most profoundly affected by:
- alveolar hypoxia
- mixed venous hypoxemia
- a-adrenergic stimulation
- cholinergic stimulation
alveolar hypoxia
Local factors are more important than the autonomic system in influencing pulmonary vascular tone. Both pulmonary arterial and alveolar hypoxia induce vasoconstriction, but alveolar hypoxia is a more powerful stimulus.
While receiving PCA after a lumbar fusion, an 21-year-old male was found to have a PaCO2 of 80 mmHg while breathing room air. From this information, his expected PaO2 would be:
- 55 mmHg
- 85 mmHg
- 100 mmHg
- 150 mmHg
55 mmHg
Large increases in PaCO2 (> 75 mmHg) readily induce hypoxia at room air, but not at high inspired oxygen concentrations.
β-2 stimulation results in:
- bronchodilation and decreased secretions
- bronchodilation and increased secretions
- bronchoconstriction and decreased secretions
- bronchoconstriction and increased secretions
bronchodilation and decreased secretions
Sympathetic activity mediates bronchodilation and decreased secretions via the β-2 receptors. α-1 receptors stimulation also decrease secretions, but may cause bronchospasm.
In patients with decreased lung volume, increasing lung volume with PEEP will:
- decrease dead space
- have little effect on airway resistance
- increase airway resistance
- decrease airway resistance
decrease airway resistance
At low lung volumes, loss of radial traction increases the contribution of small airways to total resistance; airway resistance becomes inversely proportional to lung volume. Increasing lung volume with PEEP can reduce airway resistance.
Hypoxic vasoconstriction has been shown to be inhibited by:
- desflurane
- nitroprusside
- nitrous oxide
- all of the above
all of the above
Inhalation agents, including nitrous oxide can inhibit hypoxic pulmonary vasoconstriction. For volatile agents, the ED50 is about 2 MAC.
Pulmonary capillary oxygen tension corresponds best with:
- alveolar oxygen tension
- PaO2
- mixed venous O2
- FiO2
alveolar oxygen tension
For all practical purposes, pulmonary end-capillary oxygen tension may be considered identical to alveolar oxygen tension; the gradient is normally minute.
The predicted PaO2 in a healthy 90-year-old patient is:
- 72 mmHg
- 83 mmHg
- 94 mmHg
- 100 mmHg
72 mmHg
Arterial oxygen tension can be approximated by the formula:
PaO2 = 102 - (Age/3)
In the adult at rest, oxygen consumption is approximately:
- 150 mL/min
- 250 mL/min
- 500 mL/min
- 1000 mL/min
250 mL/min
In the adult, oxygen consumption is approximately 250 mL/min with carbon dioxide production being 200 mL/min resulting in a respiratory quotient of 0.8.
Surfactant is produced by:
- type I pneumocytes
- type II pneumocytes
- goblet cells
- the basement membrane
type II pneumocytes
Type II pneumocytes are round cells that contain prominent cytoplasmic inclusions. These inclusions contain surfactant, an important substance necessary for normal pulmonary mechanics.
Upper abdominal procedures are associated with a reduction in FRC of approximately:
10 - 15%
20 - 30%
40 - 50%
60 - 70%
60 - 70%
Upper abdominal procedures consistently decrease FRC by 60 - 70%. This effect is maximal on the first postoperative day and usually lasts 7 - 10 days.
Most airway resistance comes from:
- the trachea and vocal cords
- large bronchi
- medium-sized bronchi(before the 7th generation)
- small bronchi)after the 7th generation)
medium-sized bronchi (before the 7th generation)
Normal total airway resistance is about 0.5 - 2 cm H2O/L/s, with the largest contribution coming from medium-sized bronchi (before the 7th generation).
The most sensitive pulmonary function test indicating the presence of increased airway resistance is the:
- FEV1
- FVC
- FEV1/FVC ratio
- FEF25-75%
FEF25-75%
Whereas both FEV1 and FVC are effort dependent, FEF25-75% is effort independent and a more reliable measurement of obstruction. In early obstructive disease the FEF25-75% is often the only abnormality.
Stimulation of vagal afferents and efferents of the bronchi is associated with:
- an increased responsiveness to carbon dioxide
- a decrease in hypoxic drive
- bronchoconstriction
- decreased bronchial secretions
bronchoconstriction
Vagal afferents in the bronchi are sensitive to histamine and multiple noxious stimuli. Vagal activation results in bronchoconstriction, which is mediated by an increase in cGMP.
During general anesthesia in healthy individuals, venous admixture (shunting) usually:
- decreased to 1 - 4%
- increases to 5 - 10%
- increases to over 20%
- remains unchanged from the unanesthetized state
increases to 5 - 10%
General anesthesia commonly increases venous admixture to 5 - 10%, probably as a result of atelectasis and airway collapse in dependent areas of the lung.
The effects of inhalation anesthesia at 1 MAC and greater are to:
- decrease tidal volume and rate
- increase tidal volume and rate
- decrease tidal volume and increase rate
- increase tidal volume and decrease rate
decrease tidal volume and increase rate
At 1.2 MAC, inhalation agents increase ventilatory rate and decrease tidal volume.
Pulmonary function tests that do not depend on patient effort include:
- FVC
- FEV
- FEF25-75%
- FEV1
FEF25-75%
Whereas both FEV1 and FVC are effort dependent FEF25-75% is effort independent and may be a more reliable measurement of obstruction.
Laminar flow in the airways is found:
- in the trachea
- in the mainstem bronchi
- in bronchioles
in bronchioles
β2-adrenergic agonists produce bronchodilation by:
- increasing intracellular cAMP
- increasing intracellular cGMP
- stabilizing mast cells
- blocking histamine and serotonin receptors
increasing intracellular cAMP
Activation of β2-adrenergic receptors on bronchiolar smooth muscle activated adenylate cyclase, which results in the formation of intracellular cAMP.
The lung volume remaining after normal exhalation is the:
- residual volume
- expiratory reserve volume
- functional residual capacity
- closing capacity
function residual capacity
The lung volume at the end of a normal exhalation is called the functional residual capacity (FRC). At this volume, the inward elastic recoil approximates the outward elastic recoil. The FRC is the sum of the expiratory reserve volume and the residual volume and is approximately 2.5 L in volume.
The flow-volume loop below that best represents chronic obstructive pulmonary disease is:
A
B
C
D
A
Loop A demonstrates the elevated lung volumes and diminished expiratory flow associated with COPD.
Capnographic evidence of bronchospasm includes:
- increased slope of phase I
- increased slope of phase II
- increased slope of phase III
- increased slope of phase IV
increased slope of phase III
In the normal capnogram, phase III is nearly flat with a slope approaching zero. With obstruction, the slope of phase III increases.
Patients with long-standing COPD often develop:
- decreased responsiveness to carbon dioxide
- decreased pulmonary artery pressures
- decreased right ventricular pressures
- decreased red cell mass
decreased responsiveness to carbon dioxide
In patients with COPD, chronic hypoxia leads to erythrocytosis, pulmonary hypertension and right ventricular failure (cor pulmonale). Patients gradually develop CO2 retention and loss of sensitivity to arterial CO2 tension.
The dichotomous division of the tracheobronchial tree is estimated to involve:
- 10 divisions
- 17 divisions
- 23 divisions
- 31 divisions
23 divisions
Dichotomous division, starting with the trachea and ending in alveolar sacs, is estimated to involve 23 divisions. Gas exchange can occur only across the flat epithelium, which begins to appear on pulmonary bronchioles (generations 17 - 19).