Exam 2 - Pulmonary CPB / Initiation-Termination / Charting Flashcards

1
Q

3 layers of pulmonary linings

A
  • Parietal Pleura
  • Serous fluid
  • Visceral Pleura
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2
Q

Inspiration

A
  • Lungs expand
  • Negative pressure
  • Air pulled in
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3
Q

Expiration

A
  • Diaphragm relaxes
  • Lungs recoil
  • Positive pressure
  • Air pushed out
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4
Q

Lung Characteristics

A
  • Very elastic
  • High surface tension
  • Want to collapse
  • Surfactant helps decrease surface tension
  • Surface tension forces stronger on smaller alveoli
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5
Q

Bronchial circulation

A
  • high pressure / low flow
  • 1-2% of CO
  • Arteries branch off thoracic aorta
  • Return venous blood to LA
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6
Q

Pulmonary circulation

A
  • Low pressure / high flow
  • Deoxy blood to pulmonary caps
  • Gas exchange
  • Returns O2 blood to LA via pulmonary veins
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7
Q

Lungs on CPB

A
  • Stop ventilating and lungs collapse
  • Resistance to flow INCREASES
  • No pulmonary flow (bypassing)
  • Little bronchial flow (due to resistance)
    - vessels are constricted because lungs collapsed
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8
Q

Atelectasis

A
  • Collapse of alveoli
  • localized or entire lung
  • Caused by: blockage of small bronchi w/ mucous
    Obstruction of major bronchus
  • Easier to access R lung due to anatomy / more vertical and in-line
  • Left side more prone to blockage
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9
Q

Lungs post CPB

A
  • Some atelectasis remains to variable degree
  • Micro-atelectasis - not detectable clinically
  • Can collapse entire lobe to degree
  • CPB compromises pulmonary function
    - from days to months
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10
Q

Pulmonary problems post CPB

A
  • Atelectasis
  • ARDS
  • Highly variable for both
  • Caused by atelectasis/pleural disruption (lifting)/impaired lung compliance/SIRAB (systemic inflammatory response after bypass)
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11
Q

Atelectasis formation

A
  • Air trapped in pulmonary caps
  • creates negative pressure and subsequent collapse
  • if can’t collapse (fibrosis)… build negative pressure
    - pulls fluid into alveoli….whole lung collapses
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12
Q

How quick can atelectasis form

A
  • 5-10 minutes after anesthesia
  • anesthetized patient -> relaxed diaphragm
    - increase pleural pressure
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13
Q

Resorption atelectasis

A
  • Airway blocked
  • low ventilation:perfusion ratio (Q:V ratio)
  • normally equal
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14
Q

Collapsed lungs during CPB due to no flow

A
  • Re-expansion after CPB not always 100% successful
  • Residual atelectasis
  • cannula can push on lungs -> collapse
  • back of lung collapses under own weight -> supine patient
  • heart rests on top of lung -> collapse
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15
Q

Prevention of atelectasis

A
  • Cannot do much
  • decrease compliment activation
  • decrease chance of edema
  • anesthesia has more control (inflation/deflation)
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16
Q

Surfactant depletion

A
  • anesthesia exposure reduces surfactant
  • Lungs on CPB produce cytokines that drop surfactant synthesis
    • lungs hurt themselves on CPB
17
Q

Trauma of Lungs on CPB

A
  • Suction can damage carina
  • build up of secretions
  • Promotes airway collapse
  • careful when suctioning lungs
18
Q

What happens when cavity is open on CPB

A
  • Blood / fluid can enter

- lung compresses

19
Q

Supine position on CPB

A
  • decreases FRC (functional residual capacity)

- atelectasis observed in dorsal lung regions post CPB

20
Q

Most common lung complication of CPB

A
  • Compress lung

- open cavity / supine position / IVC cannulation

21
Q

Pre-op risks of atelectasis

A
  • smoking
  • chronic bronchitis
  • obesity
  • cardiogenic pulmonary edema
22
Q

Intraoperative risks of atelectasis

A
  • passive ventilation

- monotonous vent pattern

23
Q

Bypass risks of atelectasis

A
  • surfactant inhibition

- distension / lung ischemia / compliment activation / open cavity / heart resting on left lobe

24
Q

Pump lung

A
  • acute respiratory failure
  • lungs congested
  • interstitial / alveolar edema
  • hemorrhagic atelectasis
  • high [neutrophil]
25
Q

Causes of acute lung injury

A
  • embolic load
  • compliment activation
  • hemodilution
  • high pulmonary pressure -> high resistance
26
Q

Which patients benefit from OPCAB

A
  • COPD
  • Pulmonary problems
  • Increased airway resistance
27
Q

Prevention of micro-emboli overload

A
  • More filtration -> more normal the lungs
28
Q

CPB and pulmonary injury

A
  • CPB -> compliment activation -> pulmonary injury

- hypoxia is not the problem -> still have bronchial circulation

29
Q

Acute bronchospasm on CPB

A
  • Rare
  • If on CPB….stay on
  • If off CPB….get on
30
Q

Prevention / treatment of acute lung injury on CPB

A
  • Heparin coated circuits
  • increase biocompatibility
  • limit neutrophil activation
  • hemofiltration: Z-buff / MUF / hemoconcentrate
  • Corticosteroids / prostaglandins / inhaled NO (more for transplants)
31
Q

Most common complication of lungs post CPB

A
  • acute lung injury (atelectasis)
  • common cause is mechanical ventilation
    • manipulation of pleura / retraction of lung
  • Perfusionists can get rid of pro-inflammatory mediators