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A1 > Pulmonary Circulation > Flashcards

Pulmonary Circulation Flashcards

1
Q

PAPs

A

25/10 mean 15

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2
Q

Where do pulmonary vessels branch of into?

A

Alveolar vessels- closely related to acini, can become compressed with high PEEP
Extra alveolar- Larger and thicker, do not compress with high PEEP,

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3
Q

Vascular resistance / lung volume graph

A

“J” shape, high resistance at low volumes, low resistance at medium volumes, high resistance at high volumes

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4
Q

How is blood flow directed to the lungs?

A

With increased CO, lungs RECRUIT mainly
Recuit- opens more vessels as any muscle does during work out
Also distend to a smaller amount

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5
Q

Functional Capillary volume

A

70ml (1ml/kg) at rest
200ml maximal volume during exercise

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6
Q

How fast does gas exchange occur?

A

.25 seconds, but stays in network for .75 seconds

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7
Q

How much blood is in the lungs

A

500 ml- 50% of weight of lungs
More than any other organ

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8
Q

Capacitance resevoir of lungs

A

can alter from 50% to 200% of resting volume
Prevents change in blood return to RV from affected LV filling pressures of 2-3 cardiac cycles

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9
Q

Chief mechanism of fall in PVR during exercise

A

Recruitment

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10
Q

Distension

A

Internal vessel pressure rises and opens capillary beds
Elevated LA pressure extends capillary beds (mitral regurg, LV failure)
Leads to lung congestions and ultimately HF
Seen at high vascular pressures

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11
Q

Pleural pressure on expiration

A

Pleural pressure less negative than -5mm H2O
Higher pressures decrease venous return
Less RV ejection pressure

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12
Q
A
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13
Q

What increases PVR?

A

Higher and lower lung volumes

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14
Q

How do extra alveolar and alveoli react during breathing?

A

Extra alveolar dilate on inspiration
Alveolar compress during inspirating

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15
Q

How does mechanical ventilation effect alveolar pressure?

A

Increases alveolar pressure- can decrease CO or increase VQ mistmatch
- Increase amount of ZONE 2
- Increase in resistance to ZONE 2

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16
Q

Where does bronchial blood circulation return to?

A

RA via azygos vein
Conducting airways to terminal bronchioles, & pleura, interlobar spaces, pulmonary arteries and veins
1-2% of cardiac output
The rest of the bronchial blood exits lung by small anastomeses with pulmonary veins to contribute to normal venous mixture (R to L shunt)

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17
Q

How much fluid do the lymphatic system remove?

A

20 ml/hr
Hydrostatic forces (slightly negative) are responsible

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18
Q

VO2 at rest

A

Oxygen consumption/ minute
300 ml/min
CO= O2 Consumption (VO2)/ AV O2 differences

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19
Q

Fick principle

A

One method of determining CO, blood flow thru lungs

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20
Q

Indicator dilution principles

A

Dye injected into venous circulation
Diluted concentration measured on arterial side
Thermodilution technique also commonly used to measure CO

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21
Q

Blood flow at different levels

A

Top lung- low
Middle lung- higher
Bottom lung- Peaks but drops at very bottom

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22
Q

Pressure gradient from gravity on systemic BP

A

0.74mm Hg/cm
In supine position- arterial pressure is higher in feet than in head

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23
Q

What are the two zero reference points for hydrostatic pressure

A

RA
Middle lung

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24
Q

Zone 1 formula

A

PA> Pa> Pv
High pressure in alveoli
No blood flow- capillaries are collapsed by alveolar pressure

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25
Q

Zone 2 formula

A

Pa> PA> Pv
Moderate bloow flow
Waterfall effect

26
Q

Zone 3 formula

A

Pa> Pv> PA
Most blood flow
Hydrostatic pressure causes distention and recruitment, which decrease resistance

27
Q

What does pressure in the alveoli depend on?

A

Hydrostatic pressure
Gravity
Transmural compressive pressure
Lung volume

28
Q

What does blood flow (PVR) depend on?

A

Pressures in the pulmonary vessels relative to alveolar pressure

29
Q

Zone 4

A

Abnormal condition of reduced blood flow
High PVR
Causes- LV failure, MV stenosis
Pulmonary edema

30
Q

What expands zone 1?

A

Decreased PAP- shock, hypovolemia
Increased PA- high PEEP
Occlusion of blood vessels- PE

31
Q

What reduces Zone 1?

A

Increased PAP- infusion or bolus
Reduced hydrostatic effect- standing to supine, change in pt position

32
Q

Regulation of pulmonary blood flow is ___

A

Active- altering vascular smooth muscle tone in pulmonary arterioles

33
Q

What is active regulation of pulmonary vessels mediated by?

A

Local metabolic influences

34
Q

What does an increase in sympathetic outflow cause in pulmonary vasculature

A

Stiffening of PV walls- vasoconstriction

35
Q

PVR vasoconstrictors

A

Reduced PaO2
Increased PCO2
Histamines
Levo
Thromboxane A2

36
Q

PVR Vasodilators

A

Increased PaO2
NO
Prostaglandin I2

37
Q

Thromboxane A2

A

Potent vasoconstrictor
Product of cell membrane arachidonic acid metabolism
Constricts pulmonary arterial and venous smooth muscle

38
Q

When is Thromboxane A2 produced?

A

Acute lung injury by macrophages, leukocytes, endothelial cells
Effect localized because of short half time of seconds

39
Q

Prostacyclin (Prostaglandin I2)

A

Potent vasodilator
Inhibitor of platelet activation

40
Q

How is prostaglandin I2 made?

A

By endothelial cells as a product of arachidonic acid metabolism

41
Q

NO

A

Potent endogenous dilator
Localized effect
Toxic at high concentrations- binds to HGB 200000x more than oxygen

42
Q

How is NO formed?

A

From L arginine which causes smooth muscle relaxation through synthesis of cyclic GMP
NO activates guanylyl cyclase and increases cGMP

43
Q

How do NTG and sodium nitroprusside work?

A

Same as NO
From L arginine which causes smooth muscle relaxation through synthesis of cyclic GMP
NO activates guanylyl cyclase and increases cGMP

44
Q

PAO2 effect on blood flow

A

Low PAO2 causes vasoconstriction
High PAO2 causes vasodilation

45
Q

PH causes ______ in the body

A

Increase in hypoxia
High PVR
Hypoventilation
Low inspired PO2
High PCO2
Pain
Histamine release
RV hypertrophy/ cor pulmonale
Tricuspid regurgitation

46
Q

PH

A

Serious condition
Transplant only effective treatment

47
Q

What causes non uniform and regional ventilation?

A

Airway resistance Compliance
Hydrostatic effects

48
Q

The distribution of ventilation in the lung is _____

A

Nonuniform caused by gravity/ hydrostatic pressure
Bottom receives more ventilation due to increased compliance

49
Q

Decreased compliance ___ lung volumes

A

reduces

50
Q

A-a PO2 levels

A

Alveolar arterial differences
Normal- 10-15mmHg

51
Q

What causes high Aa gradients?

A

Intrinsic pulmonary disease- shunting

52
Q

Most common cause of inefficient O2/CO2 exhange

A

Mismatch V/Q ratio

53
Q

Shunt

A

Perfused but not ventilated (think alveoli shrinks up)
Small shunts are normal

54
Q

True anatomical (R-L) shunts

A

Bronchopulmonary venous anastomoses
Intracardiac thesbian veins
Mediastinal veins
Pleural veins

55
Q

Venous admixture of blood

A

“Wasted ventilation”
R-L shunt

56
Q

L-R shunt

A

Does not affect systemic arterial oxygen tension
Oxygen in R heart increased

57
Q

R-L shunt

A

Pulmonary venous admixture
A portion of CO does not participate in gas exchange

58
Q

HPV

A

Hypoxic pulmonary constriction
Blood diverts to better ventilated areas

59
Q

HPV causes/ enhancements

A

Hypoxia
Hypercapnia & acidosis

60
Q

Pleural pressure during inspiration
Volumes in RV and LV

A

More negative than -5mm H2)
Lower pressure allows for more venous return to right heart
Higher RV pressure
LV ejects less blood

61
Q

How are alveolar dimensions controlled?

A

Not by autonomic or hormone control
Alveolar capillaries contribute to 40% resistance
Alveolar arterioles contribute to 50% of resistance (compared to 75% of SVR)

A1 (122 decks)

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