Intro to Pulm Physiology Flashcards

1
Q
A

Gas flow rate

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2
Q

E

A

expired gas

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3
Q

I

A

inspired gas

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4
Q

A

A

alveolar gas

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5
Q

a

A

arterial blood

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6
Q

v

A

venous blood

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7
Q
A

mixed venous blood = pulmonary arterial blood, bc it’s a mixture of all the venous blood from all over the body

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8
Q

What is the difference between ventilation, gas exchange, and gas transport?

A

Ventilation = Atmosphere <–> Alveolar space

Gas exchange = Alveolar space <–> Blood

Gas transport = Blood <–> Tissues

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9
Q

Hypercapnia

A

Too much CO2 in the blood

Leads to increased cerebral blood flow/intracranial pressure, acedemia

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10
Q

Hypoxemia

A

Not enough O2 in the blood

Leads to tissue hypoxia, inhibition of cellular aerobic respiration, death

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11
Q

What is the relationship between partial pressure of a gas and the fraction of the gas? Equation?

A

Partial pressure and fraction of gas are directly proportional

Pgas = Fgas x Ptotal

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12
Q

What is atmospheric pressure at sea level?

A

760 mmHg

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13
Q

What makes inspired gas different than atmospheric gas?

A

Your body warms it up and adds water vapor to saturate it

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14
Q

How much partial pressure of water vapor is added to air that you breathe in?

A

47 mmHg

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15
Q

Negative pressure ventilation

A

Subatmospheric pressures in the chest generate air flow

“spontaneous” breathing = tidal breathing

Iron lung

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16
Q

Positive pressure ventilation

A

Suparatmospheric pressure outside the chest generate air flow

Machine/ventialator does this

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17
Q

What is normal RR?

A

10-16 breaths per minute

18
Q

Tidal volume = VT

A

Volume of gas inspired in a normal breath

About 0.5 L

19
Q

Minute ventilation

A

Volume of gas expired or inspired in a minute

About 6-7 L/min

20
Q

Tachypnea

A

Increased RR

21
Q

Hypopnea

A

Small tidal volume

Synonymous to shallow breathing

22
Q

Dead space

A

Ventilated but does not participate in gas exchange

23
Q

Anatomic dead space

A

Normal, part of your anatomy

Includes trachea, bronchi, bronchioles

About 1 ml/lb ideal body weight

24
Q

Physiologic Dead Space

A

Anatomic dead space + diseased areas not participating in gas exchange

25
Q

Which parts do participate in gas exchange?

A

Alveolar space = respiratory bronchioles, alveolar ducts, alveolar sacs

26
Q

What is the relationship between minute ventilation, dead space ventilation, and alveolar ventilation?

A

Where V(dot)E = minute ventilation

V(dot)D = dead space ventilation

V(dot)A = Alveolar ventilation

27
Q

What are the 4 main ways that alveolar ventilation are regulated?

A

peripheral chemoreceptors (CO2, O2, H+), central chemoreceptors (H+), lung stretch receptors, muscle and joint receptors

Includes: inspiratory inhibition reflex/Hering-Breuer reflex, Irritant receptors, J receptors (respond to pulm edema)

28
Q

What is the strongest influence of control over breathing?

A

Central chemoreceptors: sense H+ in brain arterial blood

If pH goes down, tells your body to breathe faster

29
Q

What is the relationship between CO2 and H+ in the blood?

A

CO2 <–> H2CO3 <–> H+ + HCO3-

If CO2 levels rise, then H+ levels increase and pH goes down, which is a signal to the brain to increase ventilation

30
Q

What can the peripheral chemoreceptors sense?

A

Located in carotid and aortic bodies

Elevated H+ (low pH)

Increase in arterial PCO2

Decrease in arterial PaO2

31
Q

What is the best way to measure alveolar ventilation?

A

Measure alveolar CO2!

Unlike O2, it’s pretty constant: there is no inspired CO2

Transferred VCO2 messes with the value of VCO2 a little bit BUT the rate of transfer of CO2 from pulm circ/tissue to alveolus is constant when you are at rest

32
Q

What is the equation for partial pressure of CO2 in the alveolus?

A

PACO2 = 863 x V(dot)CO2/V(dot)A

The amount of CO2 in your alveoli is:

  • directly proportional to the amount of CO2 moving from capillary blood to alveolus (this is your “input” of CO2)
  • inversely proportional to your alveolar ventilation (this is your “drainage:” if you increase alveolar ventilation, you’ll take more CO2 out of the lung & ppCO2 will go down)
33
Q

What is a simplified version of the equation for PCO2?

Why can we rewrite the equation in this way?

A

PACO2 = K’/V(dot)A

Because V(dot)CO2 is constant at rest

34
Q

What is the easiest way to calculate alveolar flow?

A

V(dot)A = K’/PaCO2

We can measure arterial PCO2!!! Alveolar PCO2 = arterial PCO2 because the CO2 has equilibrated between the alveolus and pulmonary capillary PCO2, which becomes pulmonary venous & becomes left atrial & aortic & all the arteries

35
Q

What is the normal range for PaCO2 (arterial)?

A

37-42 mmHg

36
Q

What does low PaCO2 indicate?

A

Less than 37 mmHg

Hypocapnia/hypocarbia

Due to alveolar hyperventilation

37
Q

What does high alveolar PaCO2 indicate?

A

Hypercapnia/hypercarbia: elevated alveolar PCO2

Due to alvolar hypoventilation

38
Q

What causes alveolar hyperventilation?

A

Hypoxemia

Acidemia

Stimulation of lung receptors

Drugs: aspirin, progestins

Pain

Anxiety

Fever

Pregnancy

Exercise

Note: hypercapnia causes increased respiratory drive but it’s impossible to have both hypercapnia and alveolar hyperventilation at the same time

39
Q

What are signs of increased work of breathing?

A

Accessory muscle use

Tachypnea

Nasa flaring

Paradoxical breathing: when belly moves in while chest moves out secondary to diaphragmatic weakness which is due to muscle fatigue

40
Q

What can cause alvolar hypoventilation?

A

Decreased respiratory drive/effort (drugs, sleep, breath holding)

Neuromuscular incompetence i.e ALS patient with weak muscles

Muscle fatigue due to increased load i.e. AIDS patient has increased dead space due to pneumonia

Loss of respiratory system integrity (crushed chest, complete airway obstruction)

41
Q

What are sources of dead space that’s not normal?

A

Adding external dead space: scuba, ventilator tubing, breathe through a straw

New dead space created from alveolar space: due to a pulmonary embolism that blocks blood flow to a section of alveoli

42
Q

Why does increased dead space due to pulmonary embolism lead to alveolar hypoventilation?

A

Normal homeostasis leads to increased PaCO2 which leads to increased minute ventilation and increased alveolar ventilation which ultimately brings down the PaCO2 to normal levels

But when you have dead space due to pulmonary embolism, you get increased PaCO2 which leads to increased minute ventilation & increased ventillation of the dead space –> eventually you get increased work of breathing & your muscles get fatigued –> alveolar hypoventilation