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Physiology - Renal and Respiratory > Respiratory > Flashcards

Respiratory Flashcards

1
Q

Conducting airways

A

ventilated, but not perfused - nose, mouth, pharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles

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2
Q

Respiratory airways

A

respiratory bronchioles, alveolar ducts, alveolar sacs.

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3
Q

Type 1 pneumocytes

A

95% of respiratory endothelium Form the respiratory membrane

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4
Q

Type 2 pneumocytes

A

5% of respiratory endothelium. Secrete surfectant

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5
Q

Area available for gas exchanges

A

75 square meters

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6
Q

What are some structural determinants of compliance

A

collagen, elastin, and surface tension of small airways and alveoli

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7
Q

What is Hysterisis?

A

It is the dependence of change on past conditions. For the lungs, this means that the compliance curve looks different depending on whether you are inhaling or exhaling.

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8
Q

What happens to compliance in COPD?

A

It increases, because there is less collagen and elastin in the walls.

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9
Q

Main muscle of breathing at rest.

A

Diaphragm

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10
Q

Additional muscles of inspiration at rest

A

external intercostals, interchondrals

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11
Q

Additional muscles of forced inspiration

A

Neck muscles, SCM

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12
Q

What about expiration at rest? How does that work?

A

It is passive.

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13
Q

Forced expiration - what additional muscles are recruited

A

Internal intercostals

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14
Q

Functional Residual Capacity

A

Volume at the end of a quiet expiration

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15
Q

What is the resting equilibrium state of the lungs.

A

The chest wall wants to expand outward, the lungs want to collapse inward. The forces balance.

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16
Q

Transpulmonary pressure?

A

The pressure across the alveolar wall, so it’s basically the difference in pressure between the air inside the lung and the pleural space. Pleural pressure is really low, so that helps keep the alveoli open.

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17
Q

What happens to pleural pressure when the chest expands? Why is that important.

A

It drops real quick. This is important because the low pressure surrounding the lungs makes it expand, which causes the intraalveolar pressure to drop.

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18
Q

Forced Expiratory Volume

A

Inspiratory Maximum - Expiratory maximum (70-80% of vital capacity)

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19
Q

Vital capacity

A

the sum of inspiratory reserve volume, tidal volume, and expiratory reserve volume.

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20
Q

What happens to forced expiratory volume and vital capacity in COPD?

A

Forced Expiratory volume goes down (no shit), and the ratio of forced expiratory volume/vital capacity also goes down.

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21
Q

What happens to forced expiratory volume and vital capacity in restrictive disease?

A

Forced Expiratory volume goes down (again, no shit), and the ratio of forced expiratory volume/vital capacity goes up, because vital capacity is also shrinking.

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22
Q

Where does the blood for the pulmonary circulation come from?

A

It is mixed venous blood from the right ventricle, coming from the IVC, SVC, and carotid sinus.

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23
Q

How do you calculate the partial pressure of oxygen at sea level, and what is it usually, assuming 0% humidity?

A

Fraction O2 * Air pressure
Air is usally 21% oxygen, and Air pressure at sea level is 760 mmHg so:

0.21 * 760mmHg = 160 mmHg

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24
Q

Since humidity is usually higher than 0%, how do you calculate the partial pressure of O2 in humid air?

A

Fraction O2 * (Air pressure-Pressure of Water)

Air is usally 21% oxygen, Air pressure at sea level is 760 mmHg, and partial pressure of water is usually 47mmHg so:

0.21 * (760mmHg - 47mmHg) = 150 mmHg

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25
Q

Anatomic dead space

A

Conducting airways, about 150 mL, cannot be reduced.

26
Q

Physiologic dead space

A

Total volume of lung not participating in gas exchange - variable depending on rate and depth of breathing.

27
Q

How much CO2 is there in the atmosphere? What about in expired air? Why is this important?

A

Atmospheric CO2 is really low - 0.04%, so we can measure expired CO2 to get a good sense of how much respiration is happening.

28
Q

What are the pressures of Oxygen and Carbon Dioxide (PO2 and PCO2) in the pulmonary capillaries before gas exchange? What about in the air?

A

Deoxygenated blood - PO2 - 40, PCO2 - 46

Air - PO2 - 150, PCO2 - 0

29
Q

What are the pressures of Oxygen and Carbon Dioxide (PO2 and PCO2) in the pulmonary capillaries AFTER gas exchange? What about in the air?

A

Deoxygenated blood - PO2 - 100, PCO2 - 40

Air - PO2 - 100, PCO2 - 40

They have to be the same because they reached equilibrium.

30
Q

What are the 3 ways blood can carry O2?

A

Dissolved, modified, or bound to hemoglobin

31
Q

If a gas reaches equilibrium, it is __________ limited

A

Perfusion

32
Q

If a gas does not reach equilibrum, it is _________ limited

A

Diffusion

33
Q

How does CO2 get out of the tissues?

A

It diffuses into the blood. It is hydrated to H2CO3, which loses a Hydrogen to become bicarbonate. It can also bind to deoxyhemoglobin.

34
Q

How does bicarbonate get into RBC’s? And what is “Chloride shift?”

A

Bicarbonate is imported into RBC’s via an exchange with a chloride ion (this is the chloride shift).

35
Q

What do the chloride and bicarbonate levels in venous blood look like compared to arterial blood.

A

They are higher, because more CO2 has been processed into bicarbonate, and more chloride has been “shifted” out of RBC’s to help absorb it.

36
Q

What are some factors that will shift the oxyhemoglobin dissociation curve to the LEFT (making oxygen bind MORE tightly to Hgb)?

A

Decreased temperature, decreased PCO2, Decreased 2,3 BPG, Increased pH.

37
Q

What are some factors that will shift the oxyhemoglobin dissociation curve to the RIGHT (making oxygen bind LESS tightly to Hgb)?

A

Increased temperature, decreased pH, increased PCO2, increased 2,3 BPG.

This is called the Bohr shift - you can think of it like this - as you exercise, you increase your temp and CO2 and lower your pH, so you need to unload O2 more easily, which causes looser binding.

38
Q

The total oxygen content of the blood is the sum of?

A

(Oxygen binding capacity * Hemoglobin % saturation) + Dissolved O2

39
Q

How do alveoli self-regulate their blood flow? what effect does this have?

A

Pneumocytes sense decreased PO2 and the membrane compensates by opening calcium channels, increasing vascular resistance, and decreasing blood flow. This means that the least ventilated alveoli are also the least perfused.

40
Q

What are some chemical signals that dilate small pulmonary blood vessels?

A

NO, prostacyclin

41
Q

What are some chemical signals that constrict small pulmonary blood vessels?

A

Thromboxane,

42
Q

When does the entire lung change its resistance at once? Why is this important?

A

Right after birth, as the lungs are mechanically expanded and aerated, the PO2 goes WAY up, and pulmonary circulation vasodilates, and resistance drops WAY down. This causes increased pulmonary flow, allowing the lungs to be perfused.

43
Q

Tissue that is ventilated, but not perfused is called

A

Dead space

44
Q

Tissue that is perfused, but not ventilated is called

A

A shunt. Examples include ASD, VSD, PDA, and for a R->L shunt, Tetrology.

45
Q

Where in the lungs is ventilation usually the highest? The lowest?

A

The apices, and the bases, respectively.

46
Q

What is the ventilation/perfusion ratio in a normal lung

A

1

47
Q

What is the ventilation/perfusion ratio in dead space

A

Infinite - total ventilation and no perfusion

48
Q

What is the ventilation/perfusion ratio in an underperfused lung?

A

> 1

49
Q

What is the ventilation/perfusion ratio in a poorly ventilated lung?

A

< 1

50
Q

What is the ventilation/perfusion ratio in a shunt?

A

0 - perfused but not ventilated

51
Q

How does the sympathetic system regulate pulmonary airflow?

A

Via Beta 2 receptors and the diaphragm

52
Q

How does that parasympathetic system regulate pulmonary airflow

A

Via the vagus nerve, and Achetylcholine

53
Q

Medullary Inspiration Center

A

Controls respiration during normal, quiet inspiration. Inputs are chemoreceptors and mechanoreceptors, and output is via the phrenic nerve.

54
Q

Peripheral chemoreceptors - location and function.

A

Located in carotid bodies and aortic arch. Send signals to the medullary inspiration center via CN’s IX and X to INCREASE respiration rate. They sense PaO2 primarily, and are generally inactive until it hits around 60mmHg.

55
Q

Central Chemoreceptors - location and function

A

Ventral surace of medulla. Sense CSF pH. Increase respiratory rate when pH drops.

56
Q

Mechanoreceptors - location and function

A

Airway smooth muscle. Decrease respiratory rate by prolonging expiration. There are also some in skeletal muscles and joints that warn your cardiovascular system of oncoming exercise.

57
Q

Medullary expiratory center - location and function

A

Ventral, Medulla, inactive at rest, but active during exercise.

58
Q

Apneustic Center - location and function

A

Pons. Causes prolonged inspiratory gasps with short breaks when the brainstem is damaged (apneustic breathing)

59
Q

Pneumotaxic center - location and function

A

Pons - stops inspiration when the lungs are full.

60
Q

Cortical regulation of respiration - what happens when you voluntarily hypoventilate?

A

As your PCO2 goes up and your PO2 drops, chemoreceptors stimulate an increase in respiratory rate. You won’t be able to override it.

61
Q

Cortical regulation of respiration what happens when you voluntarily hyperventilate?

A

increased oxygenation results in increased CSF pH. This leads to vasoconstriction of the cerebral vasculature and vasodilation everywhere else. This will cause hypoxia and eventual syncope. Once your cortex is out of the picture, your medulla takes over, and normal respiration resumes.

Physiology - Renal and Respiratory (2 decks)

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