Respiratory Physiology Flashcards

1
Q

What is the difference between intra-alveolar pressure & intra-pleural pressure?

A

-Intra-alveolar pressure: pressure within the alveoli
-Intra-pleural pressure: pressure exerted outside the lungs within the thoracic cavity (756 mm Hg at rest)

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2
Q

What keeps the lungs stretched apart?

A

-Intrapleural fluid cohesiveness
-Transmural pressure gradient: intra-alveolar pressure is great than intrapleural pressure (expands the lungs)
-Similar gradient exists across the thoracic wall which keep the thoracic cavity compressed

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3
Q

How does air flow into and out of the lungs?

A

Changes in the intra-alveolar pressure brought by respiratory muscle activity

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4
Q

What is Boyle’s Law? How does this relate to inspiration and expiration?

A

-At any constant temperature, the pressure exerted by a gas varies inversely with the volume of gas
-As the volume of gas increases, the pressure exerted by the gas decreases proportionately
-Respiratory muscle do not act directly on the lung of to affect volume; they affect the volume of the thoracic cavity, which in turn affects the volume of the lung by their cohesive interaction

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5
Q

What branch of the ANS controls bronchoconstriction? Bronchodilation?

A

-Parasympathetic=bronchoconstriction
-Sympathetic=bronchodilation

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6
Q

What is alveolar surface tension? What is its function? Why do we need it?

A

-Tension or force exerted by the H2O molecules on the alveolar surface
-Tendency is to oppose the expansion of the alveoli
-Reduces the size of the alveolus
-Results in elastic recoil
-However, too high of a surface tension would
-Collapse the lung
-Low compliance= hard to inflate and stretch
-So you need some surface tension but not too much

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7
Q

How do the pulmonary arterioles respond to decreased levels of oxygen? Is this different from systemic arterioles?

A

-Increase in CO2 induce bronchodilation of airway smooth muscles which increase airflow while decrease in O2 level induce vasoconstriction of the pulmonary arterioles, which decreases blood flow, allowing more O2 transfer between the lungs and capillaries
-Yes; systematic arterioles vasodilate in response to low O2 levels to increase blood flow to the tissues that it supplies

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8
Q

What is pulmonary surfactant? What cells secrete it?

A

Lipid and protein secretion from Alveolar type II cells

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9
Q

What is the difference between obstructive and restrictive lung disease?

A

-Obstructive lung disease: more difficulty emptying the lungs than filling them (Residual Volume goes up)
-Restrictive lung disease: lungs less compliant and can’t expand (Reduced VC- decreased)

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10
Q

What is dead-space volume?

A

Amount of air in the conducting pathways not available for gas exchange

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11
Q

Define partial pressure

A

The individual pressure exerted independently by a particular gas within a mixture of gases

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12
Q

What factors influence gas diffusion?

A

Surface area
Thickness of barrier
Diffusion of coefficient of gas

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13
Q

How is oxygen transported in the blood?

A

-Dissolved: very little amount is directly proportional to the PO2 of blood= PO2 of 100mm Hg=3ml O2 liter of blood
-Bound to hemoglobin: 98.5% of O2 transported; Reduced Hb-no bound oxygen; Oxyhemoglobin (HbO2)=bound to oxygen

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14
Q

What is the law of mass action?

A

A reversible reaction is determined by the concentration of the molecule involved

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15
Q

What does the oxygen Hb dissociation curve tell us?

A

Plateau portion:
-Exists at pulmonary capillaries where O2 is being loaded onto Hb
-At PO2 = 100 mm Hg = % Hb saturation = 97.5%
-Large changes in PO2 do not affect % Hb saturation = blood is carrying more than enough O2 to meet tissue demands
Steep Portion:
-Exists in systemic capillaries = PO2 is between 0 and 60 mm Hg
-O2 dissociates from Hb to flow down its gradient into the tissues
-Allows massive amounts of O2 to be “dropped” off when tissue demands increase

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16
Q

How does hemoglobin promote the movement of oxygen into the blood?

A

-Hb promotes the net transfer of O2 from the alveoli to the blood
-O2 movement into blood is determined by PO2 gradients
-As O2 moves into blood, Hb binds with it, thus decreasing PO2 in the blood
-This facilitates the continuous movement of O2 into the blood
-When alveolar and blood PO2 levels equilibrate, HB is maximally saturated

17
Q

What affects the ability of oxygen to bind to Hb?

A

-Increase in PCO2 decreases the affinity between Hb and O2
-Important at the systemic capillaries
-Increase un acidity decreases the affinity between Hb and O2
-Indication of metabolic activity

18
Q

What is the BOHR effect?

A

Both CO2 and H+ bind reversibly to allosteric sites which alters Hb affinity for O2

19
Q

What is the function of 2,3 DPG?

A

-Decreases the affinity between Hb and O2
-DPG levels increases when arteria HbO2 is below normal
-Allows O2 to be released, but also prevents O2 loading since the RBCs carry DPG throughout the circulatory system

20
Q

How is carbon dioxide transported in the blood?

A

-Physically dissolved (10%)
-Bound to Hb (carbamino hemoglobin 30%)
-As bicarbonate (60%)

21
Q

What is the HALADANE effect?

A

-Removal of O2 from Hb facilitates the “mopping up” of CO2 generated H+

22
Q

What is hypoxia? What are the different types of hypoxia?

A

-Insufficient O2 at the cellular level
-Hypoxic: low arterial PO2 accompanied by inadequate HB saturation
-Respiratory gas exchange defect, below normal alveolar PO2
-High altitude or suffocating environment
-Anemic: reduced O2 carrying capacity of blood
-Decrease in RBC &/or Hb or CO poisoning
-Normal PO2 but blood O2 content is low
-Circulatory: too little oxygenated blood is delivered to tissues
-Heart failure or vessel blockage- arterial PO2 and O2 content are normal
-Histotoxic: O2 delivery is normal but cells can’t use it
-Cyanide poisoning blocks electron transport in cell respiration

23
Q

What is hyperoxia?

A

-Above normal arterial PO2
-Breathing supplemental O2
-Arterial PO2 is increased, but Hb is already saturated
-O2 toxicity=High PO2 can damage some cells

24
Q

What is hypercapnia? What is hypocapnia?

A

-Excess CO2 in the arterial blood
-Caused by hypoventilation
-O2 and CO2 gas exchange is severely hampered
-Lung disease=Co2 accumulation occurs with O2 deficit, but since O2 suffers more=likely to develop hypoxic hypoxia instead
-Below normal arterial PCO2 levels
-Hyperventilation
-Alveolar and arterial PO2 levels increase but again Hb is already fully saturated
-Hyperpnea: increased ventilation to match metabolic needs (exercise)-no change is gas levels

25
Q

What is respiratory acidosis? Respiratory alkalosis?

A

-Respiratory acidosis: Hypercapnia = excess CO2 generated H+
-Respiratory alkalosis: Hypocapnia = less than normal CO2 generated H+