Chapter 306e - Disturbances of Respiratory Function Flashcards

1
Q

How thin is the membrane between alveolar gas and the alveolar capillary?

A

“blood flowing through alveolar wall capillaries is separated from alveolar gas by an extremely thin membrane of flattened endothelial and epithelial cells, across which respiratory gases diffuse and equilibrate.”

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2
Q

What is the area estimated for the alveolar superface area? How do you explain the discrepance between this area and the volume of the thoracic cavity?

A

“To provide an enormous alveolar alveolar surface area (typically 70m2) for blood-gas diffusion within the modest volume of a thoracic cavity (typically 7L), nature has distributed both blood flow and ventilation among millions of tiny alveoli through multigenerational branching of both pulmonary arteries and bronchial airways.”

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3
Q

The respiratory muscles should be considered part of the chest wall aswell as the neuromuscular system.
True or False?

A

True.
“the mass of respiratory muscles is part of the chest wall, while the force these muscles generate is part of the neuromuscular system”

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4
Q

Define elastic recoil pressure of the lung.

A

“Due both to surface tension at the air-liquid interface between alveolar wall lining fluid and alveolar gas and to elastic recoil of the lung tissue itself, the lung requires a positive transmural pressure difference between alveolar gas and its pleural surface to stay inflated; this difference is called the elastic recoil pressure of the lung, and it increases with lung volume.”

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5
Q

Explain the mechanism of air trapping in healthy and pathological lungs.

A

“At zero inflation pressure, even normal lungs retain some air in the alveoli because the small peripheral airwaysw are tethered open by radially outward pull from inflated lung parenchyma attached to adventitia; as the lung deflates during exhalation, those small airways are pulled open progressively less, and eventually they close, trapping some gas in the alveoli. This effect can be exaggerated with age and especially with obstructive airway diseases, resulting in gas trapping at quite large lung volumes.”

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6
Q

When is it that the respiratory sistem is at a resting point?

A

“a passive resting point of the respiratory system is attained when alveolar gas pressure equals body surfase pressure (i.e., when the transrespiratory system pressure is zero). At this volume (called the functional residual capacity [FRC]) the otward recoil of the chest wall is balanced exactly by the inward recoil of the lung. As these recoils are transmited through the pleural fluid, the lung is pulled both outward and inward simultaneously at FRC, and thus its pressure falls below atmospheric pressure (typically, -5cmH2O).”

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7
Q

Explain the dynamics of the passive respiratory system (lungs plus chest wall).

A

“because the lung and chest wall function in mechanical series, the pressure required to displace the passive respiratory system (lungs plus chest wall) at any volume is simply the sum of the elastic recoil pressure of the lungs and the transmural pressure across the chest wall. When plotted against respiratory system volume, this relationship assumes a sigmoid shape, exhibiting stiffness at high lung volumes (imparted by the lung), stiffness at low lung volumes (imparted by the chest wall or sometimes by airway closure), and compliance in the middle range of lung volumes.”

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8
Q

The limitation to the flow of a fluid is given by the frictional resistance. However, during rapid exhalation, the resistance cannot be explained alone by this factor. What then can explain this phenomenon?

A

“This phenomenon is called dynamic airflow limitation, and it occurs because the bronchial airways through which air is exhaled are collapsible rather than rigid.”

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9
Q

The velocity of airflow is much greater in the central airways than in the peripheral airways.
True or False?

A

True.

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10
Q

How do you explain limitation of airflow?

A

“If an individual tries to exhale more forcefully, the local velocity increases further and reduces airway size further, resulting in no net increase in flow. Under these circumstances, flow has reached its maximum possible value, or its flow limit.”

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11
Q

Name conditions in which the expiratory flow are (i) increased and (ii) decreased.

A

(i) pulmonary fibrosis
(ii) ephysema and “diseases that narrow the airway lumen at any transmural pressure (…) or that cause excessive airway collapsibility.”

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12
Q

How do you explain that limitation to inspiratory flow rarely occurs in diffuse pulmonary diseases?

A

“The Bernoulli effect also applies during inspiration, but the more negative pleural pressures during inspiration lower the pressure outside of airways, thereby increasing transmural pressure and promoting airway expansion. Thus inspiratory airflow limitation seldom occurs due to diffuse pulmonary airway disease. Conversely, extrathoracic airway narrowing (e.g., due to a tracheal adenoma or post-tracheostomy stricture) can lead to inspiratory airflow limitation.”

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13
Q

What is the most efficient way to increase ventilation with the least increase in work breathing?

A

“a modest increase of ventilation is most efficiently achieved by increasing tidal volume but not respiratory rate, which is the normal ventilatory response to lower-level exercice. At high levels of exercise, deep breathing persists, but respiratory rate also increases. The pattern chosen by the respiratory controller minimizes the work of breathing.”

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14
Q

Explain the pathophysiology of increased work of breathing in obstructive pulmonary diseases.

A

“The work of breathing also increases when disease reduces the compliance of the respiratory system or increases the resistante to airflow (…) the latter occurs in obstructive airway diseaes (…). Furthermore, severe airflow obstruction can functionally reduce the compliance of the respiratory system by leading to dynamic hyperinflation.”

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15
Q

Do patients with obstructive diseaes, such as asthma and chronic bronchitis, sense difficulty in inhaling? And if so, why so?

A

“At these high lung volumes, the respiratory system is much less compliant than at normal breathing volumes, and thus the elastic work of each tidal breath is also increased. The dynamic pulmonary hyperinflation that accompanies severe airflow obstruction causes patients to sense difficulty in inhaling - even though the root cause of this pathophysiologic abnormality is expiratory airflow obstruction.”

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16
Q

What is the “respiratory rate”?

A

Ratio between oxygen uptake and average rate of metabolic CO2 production (R = VCO2/VO2).

17
Q

How efficient is diffusion of oxygen?

A

“Diffusion through the alveolar membrane is so efficient in the human lung that in most circumstances a red blood cell’s hemoglobin becomes fully oxygen saturated by the time the cell has traveled just one-third the lenght of the alveolar capillary.”

18
Q

How do you explain that hypoxemia is refractory to supplemental inspired oxygen?

A

“(1) raising the inspired FiO2 has no effect on alveolar gas tensions in nonventilated alveoli and (2) while raising inspired FiO2 does increase PaCO2 in ventilated alveolie, , the oxygen content of blood exiting ventilated units increases only slightly, as hemoglobin will already have been nearly fully saturated and the solubility of oxygen in plasma is quite small.”

19
Q

How do you explain increased frictional resistante in an acute episode of asthma?

A

“During an episode of acute asthma, luminal narrowing due to smooth muscle constriction as well as inflammation and thickening within the small- and medium-sized bronchi raise frictional resistance and reduce airflow.”

20
Q

Name the hallmark of pulmonary hyperinflation related to lung volumes.

A

Elevated Total Lung Capacity.

21
Q

How do you explain that arterial hypoxemia is not seen at rest until emphysema becomes very severe?

A

“However, because porly ventilated emphysematous acini are also poorly perfused (due to loss of their capillaries), arterial hypoxemia usually is not seen at rest until emphysema becomes very severe.”

22
Q

How is it possible to measure absolute lung volumes?

A

Inert gas dilution and body pletysmogrraphy.

23
Q

What is the main drawback of measuring lung volumes with inert gas dilution?

A

“A drawback of this method is that regions of the lung that ventilate poorly (e.g., due to airflow obstruction) may not receive much inspired inert gas and so do not contribute to its dilution. Therefore, inert gas dilution (especially in the single-breath method) often underestimates true lung volumes.”

24
Q

How much lower is the total lung capacity (TLC) comparing different races?

A

“In addition, races influences lung volumes; on average, TLC values are ~12% lower in African Americans and 6% lower in Asian Americans than in Caucasian Americans.”

25
Q

FEV1/FVC normalized means that there is no obstruction to airflow.
True or False?

A

False.
Although FEV1/FVC usually means that there is no obstruction to airflow, since it is a fraction, it can be “artifactually normal” with reduced FEV1 “compensated” with reduced FVC. “To circumvent this problem, it is useful to compare FEV1 as a fraction of its predicted value with TLC as a fraction of its predicted value. In health, the results are usually similar. In contrast, even an FEV1 valute that is 95% of its predicted value may actually be relatively low if TLC is 110% of its respective prediced value. In this case, airflow obstruction may be present, despite the “normal” value for FEV1.”

26
Q

What is the normal pressure detected for maximal effort on inhalation or exhalation?

A

+/-60cmH2O

27
Q

Name the conditions that are associated with an elevated DL50.

A

“DL50 decreases in diseases that thicken or destroy alveolar membranes (e.g., pulmonary fibrosis, emphysema), curtail the pulmonary vasculature (e.g., pulmonary hypertension), or reduce alveolar capillary hemoglobin (e.g., anemia). Single-breath diffusing capacity may be elevated in acute congestive heart failure, astha, polycythemia, and pulmonary hemorrhage.”