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Physiology > Pulmonary Circulation (B2: W7) > Flashcards

Pulmonary Circulation (B2: W7) Flashcards

1
Q

Where do the pulmonary veins lie in relation to other structures of the heart?

A
  • Right pulmonary veins pass behind the R atrium and superior vena cava
  • Left pulmonary veins pass in front of the descending thoracic aorta
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2
Q

How thick are the pulmonary capillaries?

A

0.6 microns - just thick enough to have oxygen pass to blood stream

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3
Q

Where is pulmonary vascular resistance controlled in the lungs?

A

35-45% of pulmonary vascular resistance (PVR) is at the level of the capillaries

  • As opposed to systemic circulation, which is at the level of the arterioles
  • Pulmonary circulation is a low-pressure circuit
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4
Q

What is the transit time across the pulmonary microcirculation?

A
  1. 5-1 second transit time across the microcirculation
    * Alllows enough time to equilibrate O2 and CO2 tensions in alveoli
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5
Q

What factors control pulmonary vascular resistance?

A
  • PPA - PPV / Pulmonary blood flow
    • Pulmonar artery pressure, pulmonary vein pressure, cardiac output
  • This is about 1/10th of the systemic vascular resistance
  • Also depends on left atrial pressures (PLA)
    • As PLA increases, PVR will no longer decrease as a result of increasing PPA
      • Because the vascular bed is nearly fully distended
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6
Q

What happens if alveolar pressure is greater than capillary pressure?

A

Capillaries collapse

  • Capillaries normally near atmospheric pressure (therefore near alveolar pressure) because of surfactant
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7
Q

What factors reduce pulmonary vascular resistance?

A
  • Recruitment: opening of previously used capillaries
  • Distention: increase caliber of already open capillaries
  • Expansion of lung volume: inspiration
    • Causes radial traction and pulls open vessels
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8
Q

What does a Swan-Ganz catheter measure?

A

Pulmonary artery wedge pressure

  • Measures static fluid pressure in pulmonary circuit
  • Reflects left atrial pressure and estimates total body fluid balance
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9
Q

What is considered a normal range of values for pulmonary artery wedge pressure?

A

8-12 mm Hg

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10
Q

How is a Swan-Ganz catheter inserted?

A
  • Enter through internal jugular vein or through subclavian veins
  • SVC → R atrium → R ventricle → pulmonary artery
  • Catheter has a balloon at the end that makes it easier to move through
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11
Q

Describe the distribution of pressures moving through the heart with a Swan-Ganz catheter

A

R atrium - low pressure

R ventricle - high pressure

PCW (distal pulmonary artery) = wedge pressure

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12
Q

What are the three zones that the lung is divided into based on blood flow?

A
  • Zone 1: apex
    • PA>Pa>PV
  • Zone 2: mid-lung
    • Pa>PA>PV
  • Zone 3: base
    • Pa>PV>PA
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13
Q

What is the reason for regional blood flow differences?

A

Hydrostatic pressure

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14
Q

What happens to the distribution of blood flow in the supine position?

A
  • Increased apical blood flow
  • Same basal blood flow
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15
Q

What happens to the distribution of blood flow during mild exercise?

A
  • Increased apical and basal blood flow
  • Decreased regional differences in flow
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16
Q

What happens to the distribution of blood flow in someone who is upside down?

A

Apical blood flow > basal blood flow

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17
Q

Describe the blood flow to zone 1 (apex)

A

The apex is ventilated but not perfused

  • Alveolar pressure exceeds the capillary pressure
  • Dead space ventilation
    • Capillaries are flattened due to increased PA
    • Extra-alveolar capillaries are patent
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18
Q

Describe the blood flow in zone 2 (mid-lung)

A

Blood flow determined by difference between alveolar pressure and arterial pressure

  • PA - Pa
  • “Waterfall effect”
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19
Q

Describe the blood flow to zone 3 (basal)

A

Blood flow determined by usual arteral-venous difference

  • Pa > PV> PA
20
Q

What happens to circulation in the event of hypoxia?

A

Hypoxic vasoconstriction

  • Exact mechanism unknown
  • Certain substances illicit hypoxic vasoconstriction
  • Contraction of arteriolar smooth muscle walls in hypoxic region (PO2 of alveolar gas)
    • Increase in resistance
    • Directs blood to less hypoxic regions
21
Q

At what alveolar pressure does the active control of circulation respond?

A

Responsiveness is greatest at alveolar PO2 < 70 mm Hg

22
Q

What is the effect of nitrous oxide (NO) on active control of circulation?

A

Nitrous oxide is an endothelial-derived releasing factor

  • Formed from L-arginine via guanylate cyclase, forming cGMP
  • Causes smooth muscle relaxation
23
Q

Will inhaling nitrous oxide at 20 ppm decrease pulmonary hypoxic vasoconstriction?

A

No

  • This sounds great in theory, but it’s not great in practice
  • NO doesn’t help adult respiratory distress syndrome (ARDS) at all
24
Q

How does pulmonary circulation respond to high altitude?

A

Generalized vasoconstriction at high altitude

  • Increase in pulmonary arterial pressure (PPA)
25
Q

What goes on with pulmonary circulation at birth?

A
  • Fetus has increased pulmonary vascular resistance
    • Only 15% of CO to lungs
  • At first breath: O2 goes to alveoli
    • Pulmonary vascular resistance decreases
    • Increased pulmonary blood flow
26
Q

What factors inhibit hypoxic vasoconstriction?

A
  • Increased CO
  • Increased pulmonary vascular resistance
  • Hypothermia
  • Acidosis and alkalosis
  • Inhaled anesthetics
  • Calcium channel blockers
  • Positive end-expiratory pressure (PEEP)
    • Holds alveoli open
  • High frequency ventilation
  • Isoproterenol
  • Vasodilators
27
Q

What is used to treat hypoxic vasoconstriction for pulmonary hypertension?

A

Calcium channel blockers

28
Q

What treatment is better to use on neonates for hypoxic vasoconstriction?

A

High frequency ventilation

29
Q

How does Starling’s law apply to water balance in the pulmonary capillaries?

A

Net fluid = K[(Pc - Pi) - ∂(πc - πP)]

K = filtration coefficient

∂ = reflection coefficient

Pc = capillary hydrostatic pressure

Pi = interstitial hydrostatic pressure

πc = colloid osmotic pressure of blood protein

πP = colloid osmotic pressure of intestitial fluid

30
Q

What happens when there is fluid leakage from the pulmonary capillaries?

A
  • Fluid goes to interstitium of alveolar walls via perivascular and peribronchial lymph nodes
  • Interstital edema occurs
    • Transport of excess fluid goes to hilar lymph nodes
31
Q

What causes alveolar edema?

A

Capacity of the lymphatics is exceeded

  • Fluid poors from lymphatics in the interstitium into the alveoli
  • Interferes with gas exchange
    • Problems moving oxygen from the environment into the blood stream
32
Q

What leads to neurogenic pulmonary edema?

A

Increased intracranial pressure

  • Leads to increased pulmonary capillary pressure
  • Can cause trauma to capillaries
    • Increased capillary permeability
    • SPillage of fluid into the alveolar space
33
Q

How does high-altitude pulmonary edema affect pulmonary capillaries?

A

Causes hypoxia-induced vasoconstriction at pre-capillary sites

  • Exact mechanism unknown
34
Q

When does a fetus begin producing its own surfactant?

A

At 36 weeks of gestation

  • Premature babies don’t have surfactant, and alveoli can collapse
  • Infant respiratory distress syndrome
35
Q

What is acute/adult respiratory distress syndrome, and what are its causes?

A
  • Accumulation of proteinaceous fluid in the alveoli due to a number of causes
    • Causes significant ventilation-perfusion (V-Q) mismatch
  • Causes of ARDS
    • Severe trauma
    • Sepsis
    • Pancreatitis
    • Aspiration pneumonia
    • Community-acquired pneumonia
36
Q

How is ARDS treated?

A

Best outcomes are with low tidal volume ventilation strategy (6 CCs)

  • Prevents repetivie trauma from ventilator
    • Volu-traua, baro-trauma
  • Large tidal volume causes more damage (12 CCs)
    • Causes more proteins to accumulate due to inflammation
37
Q

What is the danger of ARDS?

A

60-70% mortality at 30 days

  • Lower in trauma victims
    • Tend to be younger and healthier
  • Higher in alcohol abusers
38
Q

What is transfusion-related acute lung injury (TRALI)?

A
  • Variant of ARDS
    • Usually resolves within 48 hrs - not as long term as ARDS
  • Occurs with massive blood product transfusion, most commonly fresh frozen plasma
    • Blood is replaced with donor blood
    • Different antibodies can cause an inflammatory response
  • Can happen in trauma patients or in people with a GI bleed
  • Mechanism though to be development of anti-granulocyte antibodies which then attack the recipient’s grandulocytes
    • Initiates an inflammatory response in the pulmonary capillaries
39
Q

What are the symptoms of TRALI?

A

Fever, tachycardia, tachypnea

  • Develops within 1-2 hours of transfusion
  • Development of pink, frothy sputum
  • Patients usually extubate within 48 hrs
40
Q

What are the functions of pulmonary circulation aside from gas exchange?

A
  • Reservoir for blood
    • Due to decreased pulmonary vascular resistance
  • Filtration
    • Small thrombi, WBCs
41
Q

How are vasoactive substances activated in the lung?

A

Angiotensin I becomes angiotensin II

  • Via angiotensin converting enzyme (ACE)
  • Found in small pits of capillary endothelial cells
42
Q

What is the effect of bradykinin on pulmonary circulation?

A

Bradykinin causes relaxation of blood vessels

  • By inhibiting ACE
    • Up to 80%
  • Without bradykinin: constriction of blood vessels → hypertension
43
Q

What mechanisms inactivate vasoconstriction in the pulmonary vessels?

A
  • Bradykinin - 80%
  • Serotonin (uptake and storage)
    • Released during anaphylaxis
  • Prostaglandin
  • Norepinephrine - 30%
  • Arachidonic acid
    • To leukotrienes via lipoxygenase
    • To prostaglandins via cyclooxygenase
44
Q

What is the significance of prostaglandin E2 in the fetus?

A

Keeps ductus arteriosus patent

45
Q

What gets broken down in emphysema?

A

Proteins: collagen and elastin of lung framework

  • Broken down by proteases

Physiology (29 decks)

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