Trachte: Blood Flow and Metabolism Flashcards

1
Q

What does the pulmonary artery contain?

A

Mixed venous blood

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2
Q

What’s the PO2 in the pulmonary artery? PCO2?

A

PO2- 40

PCO2- 46

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3
Q

Describe the path of the pulmonary artery?

A

Branches w/ the airways down to the TERMINAL BRONCHIOLES.

Breaks into the PULMONARY CAPILLARIES for gas exchange.

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4
Q

What are pressures in the pulmonary capillaries normally?

A

Usually LOW–little resistance so the heart doesn’t have to work hard to perfuse lungs

25/8 mmHg

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5
Q

What conditions significantly alter pressures in the pulmonary capillaries?

A

CHF
Mitral Valve stenosis

Blood isn’t being pumped adequately so pressure in pulmonary systems begin to rise–> pulmonary edema

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6
Q

What is the mean pressure in the pulmonary capillaries?

A

15 mmHg

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7
Q

What is CO?

A

5 L/min

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8
Q

What is Left atrial pressure?

A

5 mmHg

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9
Q

What’s the pulmonary resistance? How does this compare with systemic resistance?

A

***2 ml/mmHg

systemic is 98/5 which is about 10x higher

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10
Q

What pressures surround the pulmonary capillaries?

A

Alveolar pressure (surrounded by alveoli)

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11
Q

How does pressure around the pulmonary capillaries differ during exhalation and inhalation?

A

exhalation- couple mmHg

Inspiration- subatmospheric

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12
Q

What happens to pulmonary vessels during inspiration?

A

They’re PULLED OPEN

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13
Q

Are there any conditions that radically change the pressure surrounding the vessel?

A
    1. Tension pneumothorax–can shut down blood flow if pressure gets high enough
      1. Positive pressure ventilation–> above atm pressure
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14
Q

Why does pulmonary a. resistance DECREASE w/ an INCREASE in pulmonary a. pressure?

A
  1. RECRUITMENT of additional capillaries in conducting blood flow
  2. DISTENSION of capillaries conducting blood to allow for more blood flow
  3. EXPANSION of lungs reduces resistance
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15
Q

How can alveolar pressure increase resistance?

A

Alveolar pressure can COMPRESS vessels to INCREASE RESISTANCE if it is greater than capillary pressure

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16
Q

How NTs contract vessels to increase resistance?

A

NE
5HT
Histamine

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17
Q

What NTs relax pulmonary vessels to REDUCE resistance?

A

Ach
isoproterenol
prostacyclin–> PGI2 (inhibits platelet agg and causes dilation) prevents MI

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18
Q

What is the fick principle?

A

O2 consumption = CO (CAO2 – CVO2)

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19
Q

What is the equation for pulmonary blood flow?

A

Pulmonary blood flow= VO2/(CAO2 – CVO2)

20
Q

How can you measure concentration of O2 in the arterial blood?

A

Inject a dye

21
Q

Why is there more blood flow to the base of the lung usually than the apex?

A

gravity

22
Q

What are the 3 potential zones of perfusion?

A
  1. Zone 1 : PA > Part > Pvenous
  2. Zone 2: Part > PA > Pvenous
  3. Zone 3: Part > Pvenous > PA
23
Q

What are the characteristics of Zone 1?

A

PA > Part > Pvenous

  1. NO FLOW occurs in this region
  2. This does not occur naturally but can occur in HEMORRHAGE OR POSITIVE BREATHING PRESSURE
  3. NO GAS EXCHANGE
24
Q

What is zone one referred to as? Where is it most likely to occur?

A

alveolar dead space

APEX of the lung

25
Q

What does zone 2 represent?

What determines blood flow in this region?

Does venous pressure influence flow?

A

Part > PA > Pvenous

PRESSURE DIFFERENTIAL between arteries and Alveoli

Venous pressure DOES NOT influence flow

26
Q

Where is zone 2 most likely to occur?

A

APICAL REGION of lung where pressures are the lowest

27
Q

What does zone 3 represent?

A

Part > Pvenous > PA

28
Q

What is flow in zone 3 dependent on? Where does it occur?

A

Arterial/venous pressure difference (normal for the circulatory system)

MIDREGIONS or BASE of lugns

29
Q

What happens during alveolar hpyoxia? What is this mechanism independent of?

A

alveolar hypoxia CONSTRICTS blood vessels perfusing the hypoxic region of the lung

NERVES

30
Q

What is the mechanism for alveolar hypoxia leading to constriction? What does this do to the membrane potential?

A

INHIBITION of voltage gated K channels–>
more K stays inside cell>

DEPOLARIZES cell/DECREASE MEMBRANE POTENTIAL>

INCREASE in Ca leading to vasoconstriction

31
Q

What controls fluid movement out of the pulmonary vasculature?

A

Starling foces

32
Q

What is the formula for fluid escape?

A

Fluid escape = Kf (Pcap – P int) – ∂ (πcap – πint)

33
Q

What are the constant values for fluid escape?

A

Capillary pressure is 15- interstitial pressure can vary

Osmotic pressure is normally 25–> this should keep your lungs dry

34
Q

Why is there a slight leak of fluid out of the lungs? How does this differ from systemic circulations?

A

Lymphatic drainage (20 ml/hr)

MUCH LOWER in systemic circulations b/c of LOWER hydrostatic pressure

35
Q

What are situations when fluid movement is increased?

A

Heart failure–> back up of fluid from heart into lung–> increased fluid in lungs–> SOB

Not enough protein

36
Q

What happens if too much fluid escapes from the lungs?

A

alveolar edema>

SOB

37
Q

What are other functions of the pulmonary circulation?

A
  1. RESERVOIR for blood (we lay down blood drains from legs to lungs)
  2. FILTER blood (thrombi in legs/periphery can’t get to the brain)
38
Q

What does the lung do to ang I?

A

Activates it to Ang II (mediated by ACE)

39
Q

What does the lung do to bradykinin?

A

Inactivates it (mediated by ACE)

40
Q

What affect does the lung have on 5HT levels?

A

Accumulates it and removes it from circulation–> 5HT is a vasoconstrictor

41
Q

What does the lung synthesize?

A

both PGs and leukotrienes

It can also REMOVE leukotrienes from circulation

42
Q

What are PGS and leukotrienes?

A

Bronchoconstrictors

43
Q

What is an important role of PGE in pulmonary/systemic circulation?

A

Keeps DA open in fetal circulation.

44
Q

How do ACE inhibitors cause cough?

A

Prolong bradykinin actions–> COUGH

45
Q

If you wished to treat a patent ductus arteriosus pharmacologically what would you use?

A

Indomethacin (COX inhibitor)