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Pulmonary > Pulmonary Circulation > Flashcards

Pulmonary Circulation Flashcards

1
Q

What happens to pulmonary artery during low O2?

A

vasoconstriction (systemic results to vasodilation)

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2
Q

Why does the pulmonary arteries vasoconstrict in areas with low O2?

A

To shunt blood in areas with more O2

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3
Q

What things influence the rate of diffusion of gases?

A

pressure difference (air-blood)
Area of alveoli for diffusion
Thickness of alveoli tissue

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4
Q

What is the diffusion equation?

A

Vgas = Area/ Thickness * Constant(P1-P2)

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5
Q

Which condition is related to decreased area for gas exchange?

A

Emphysema

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6
Q

Which condition is related to increased thickness?

A

Pulmonary fibrosis

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7
Q

What does diffusion limitation mean?

A

The membrane is the largest obstacle in the alveoli in the gas exchange process (SUCH AS CO carbon monoxide)

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8
Q

What does perfusion limitation mean?

A

The perfusion capacity limits the amount of chemical being exchanged (IE. N2O nitrous dioxide)

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9
Q

Is O2 diffusion or perfusion limited?

A

normal person –> perfusion limited

disease –> diffusion

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10
Q

How to measure diffusion lung function?

A

Diffusing capacity of CO:
Patient inhales small amount of CO –> measures CO exhaled –> compare with predicted

Healthy –> 75-140%
Disease –> <40%

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11
Q

What happens to O2 exchange at rest vs. exercise?

A

At rest:
Blood flow slow –> more opportunity to migrate to blood from alveoli for a given time –> PaO2 reaches the same alveolar PaO2 quicker

At Exercise:
Blood flowing quicker –> less gas exchane happening for a given time –> neeed to travel a greater length in capillary to reach the same PaO2 as alveoli

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12
Q

What increases alveolar vessel resistance?

A

Inspiration –> increased lung volume expands lung and elongates the vessels making them short but narrow

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13
Q

What increases arteriolar resistance?

A

Expiration –> decreases lung volume

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14
Q

When is the pulmonary resistance the lowest?

A

At functional residual capacity (FRC)

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15
Q

What sound can be heard for PTN?

A

Loud P2 –> accentuated second heart sound at left upper sternal border

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16
Q

What is cor pulmonale ?

A

Untreated pulmonary HTN that leads to high RVP, RV hypertrophy (dilation), elevated JVP, lower extremity edema, hepatomegaly

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17
Q

What is the equation to calculate PA prressure?

A

PApressure = CO*PVR + LAP

so increase in CO [left to right shunts], PVR, or LAP [valve disease, CHF] can lead to PTN

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18
Q

What are some secondary causes of PTN?

A 
COPD
chronic pumlonary emboli
pulmonary fibrosis (scleroderma)
Sleep apnea or high altitude
HIV
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19
Q

T or F: 1o PTN is rare

A

T: due to BMPR2 mutation that affects endothelial function

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20
Q

What are the treatments for 1o PTN?

A

A) Bosetan –> antagonist endothelial-1 receptors
B) Sildenafil –> inhibits PDE-5 in smooth muscles of lungs

all PO –> leads to vasodilation

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21
Q

What is normal for PaO2?

A

> 60 mmHg

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22
Q

How to calculate the partial pressure of O2 in the alveoli?

A

PAO2 = PIO2 - (PaCO2/R) = 150 - (PaCO2/0.8)

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23
Q

What is the A-a gradient?

A

difference between alveolar (A) and arterial (a) O2

10-15 mmHg (A-a gradient)

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24
Q

What means if hypoxemic with normal A-a gradient?

A

Alveoli function good but not inhaling a lot of O2

due to hypoventilation or high altitude

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25
Q

In what conditions will hypoxemia and high A-a gradient occur?

A

Alveoli not working, O2 not getting into blood

Fibrosis, Shunt, V/Q mismatch

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26
Q

T or F: CO2 is more sensitive than O2

A

F: O2 is

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27
Q

What happens in a diffusion limiting disease?

A
  • hypoxemia
  • hypercapnea
  • alveolar destruction –> dead space –> further hypercapnia
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28
Q

In a normal lung, what is the V/Q ratio - (aka R)?

A

0.8

29
Q

What does a VQ less than 1 mean?

A

Means Q higher than V (perfusion wasted; going to areas where there isnt enough O2)

30
Q

What is a V/Q of 0 and how does it happen?

A

Means SHUNTING venous blood going to arterial without being oxygenated/ going an area of ventilation –> hypoxemia

31
Q

What are the two types of shunting?

A

Anatomic
- blood bypasses lungs/alveoli completely

Physiologic
- blood goes to non-functional alveoli –> ATELECTASIS

32
Q

T or F: Shunting leads to hypercapnia along with hypoxemia

A

F: hypoxemia induces hyperventilation which keeps CO2 normal

33
Q

What does it mean when V/Q is larger than 1?

A

DEAD SPACE: reduced perfusion relation to ventilation; ventilation is wasted where there isnt enough blood flow

34
Q

What disease may result to a high V/Q?

A

Fribrosis –> damage alveolar vessels –> less perfusion

35
Q

T or F: dead space commonly results to hypercapnia

A

T: less alveoles to take away CO2

36
Q

How can DEAD Space lead to hypoxemia?

A

At a different functioning alveoli: ventilation becomes lower and perfusion become higher (lots of blood is directed to vessels getting ventilation) –> MIMICS SHUNTING (V/Q less than 1) –> blood has less than 99% oxygenated blood

37
Q

What kind of V/Q mismatch does pulmonary edema result to?

A

lower than 1 –> fluid in alveoli reduces ventilation capacity –> leads to hypoxemia

38
Q

How to determine underlying mechanism of inadequate gas exchange (ie. shunt, V/Q mismatch, or dead space)?

A

Look at:

  1. response to 100% O2
  2. Hypercapnia
39
Q

T or F: In cases of shunting, 100% O2 does not improve condition (ie. hypoxemia).

A

T: poor ventilation not resolved at non-functional alveoli

40
Q

T or F: Dead space and V/Q mismatch will correct with 100% O2

A 
T
Dead space (questionable)
41
Q

T or F: 100% O2 does not corrects VQ mismatch in pulmonary edema

A

F: corrects it because, the affected alveoli still have some ventilation gas exchange capacity and so increasing O2 means blood is getting more O2 and hypoxemia is resolved

42
Q

What are causes of elevated PaCO2?

A
  • increased production (fever)
  • decreased ventilation (hypoventilation)
  • increased dead space
43
Q

What is the equation of PaCO2?

A

PaCO2 = CO2 production/ (Tidal Volume - Dead Space)

Alveolar ventilation = Tidal volume - dead space

44
Q

Why doesnt hypercapnia result in shunting/VQ mismatch?

A

Hyperventilation (due to hypoxemia) happens which results to CO2 clearance

45
Q

Which part of the apex has the least blood flow and ventilation?

A

Apex

46
Q

From bottom to top of the lungs, does blood flow or ventilation decrease more quickly?

A

Blood Flow so the VQ greatest at the apex (top) and low at the base

47
Q

T or F: during exercise the VQ ratio approaches 1

A

T

48
Q

Where is the hydrostatic pressure of vessels the greatest in the lungs?

A

At the base (bottom)

49
Q

T or F: alveolar pressure is gravity dependent

A

F: stays the same

50
Q

What is the Bohr effect?

A

When acid (H+) increases in the blood which allows Hb to take the taut form (less O2 affinity) and release O2 to tissues more easily

–> more O2 off-loading per given paO2

51
Q

What does chronic hypoxia induce?

A

Release of erythropotein from the kidneys to increase Hct and Hb, pulmonary HTN, cor pulmonale, higher release of 2,3- BPG

52
Q

Which molecule impacts the cerebral blood flow at the normal range?

A

CO2 (high cause vasodilation)

53
Q

In which disease states CO2 and oxygenation require monitoring?

A

COPD –> may induce hypoventilation (respiratory depression)
ALS –>respiratory muscle failure
Pneumonia –> may hypoventilate

54
Q

Why is ventilation different throughout the lungs?

A

The imbalance in ventilation results from the fact that intrapleural pressure is different in the various regions

  • -> blood more at the base
  • -> lung at the base stretched causing more neg intrapleural pressure at apex
55
Q

T or F: Apical alveoli are more fully expanded than those at the bases

A

T

Bc less pressure to keep it open

56
Q

What is the pressure change between expiratory and inspiratory during normal breathing?

A

decrease of intrapreural pressure by 3 cm H2O

ie. -10 –> -13

57
Q

Where is ventilation and perfusion highest?

A

Base of the lung

58
Q

T or F: pulmonary arterial pressure increases from base to apex

A

F: apex to base it increases

59
Q

From where does the PA enters the lung?

A

At the hilum, branching off from pulmonary trunk

60
Q

T or F: is pulmonary venous pressure dependent on height

A

T

61
Q

Where is VQ highest, and lowest?

A

Ventilation –> TOP (high VQ –> less PaCO2, high PaO2 but very little perfusion)
Perfusion –> BOTTOM (low VQ –> less O2 –> high perfusion and high ventilation)

62
Q

What is an intrapulmonary (physiologic) shunt?

A

venous blood goes through unventilated alveoli, cardiac shunt, shunt channels in lungs

63
Q

Is the pulmonary circulation high flow and low pressure and resistance?

A

Yes

64
Q

When is the arteriole resistance highest?

A

At low lung volumes (RV) the small arterioles are narrow (like the airways) and this increases the arteriolar resistance to blood flow [ie.EXPIRATION]

65
Q

When is the capillary resistance highest?

A

At large lung volumes (TLC) the expanded alveoli stretch the capillaries and cause a high resistance in them [IE. INSPIRATION]

66
Q

What is PVR consist of?

A

capillary resistance AND arteriole resistance

67
Q

Where is PVR lowest?

A

FRC

68
Q

Why does the lung vasocontrict its vessels in areas of hypoxemia?

A

This mechanism is important for shifting blood flow away from lung areas which are not being ventilated.

69
Q

How is high altitude pulmonary edema occur?

A

Hypoxia –> leads to hypoxic arterial vasoconstriction –> one side leads arteriolar vasoconstriction and one side the arteriole receives more blood –> capillary hypertension –> pulmonary edema

Pulmonary (25 decks)

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