Exam 2 - Pulmonary CPB / Initiation-Termination / Charting Flashcards
3 layers of pulmonary linings
- Parietal Pleura
- Serous fluid
- Visceral Pleura
Inspiration
- Lungs expand
- Negative pressure
- Air pulled in
Expiration
- Diaphragm relaxes
- Lungs recoil
- Positive pressure
- Air pushed out
Lung Characteristics
- Very elastic
- High surface tension
- Want to collapse
- Surfactant helps decrease surface tension
- Surface tension forces stronger on smaller alveoli
Bronchial circulation
- high pressure / low flow
- 1-2% of CO
- Arteries branch off thoracic aorta
- Return venous blood to LA
Pulmonary circulation
- Low pressure / high flow
- Deoxy blood to pulmonary caps
- Gas exchange
- Returns O2 blood to LA via pulmonary veins
Lungs on CPB
- 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
Atelectasis
- 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
Lungs post CPB
- 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
Pulmonary problems post CPB
- Atelectasis
- ARDS
- Highly variable for both
- Caused by atelectasis/pleural disruption (lifting)/impaired lung compliance/SIRAB (systemic inflammatory response after bypass)
Atelectasis formation
- 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
How quick can atelectasis form
- 5-10 minutes after anesthesia
- anesthetized patient -> relaxed diaphragm
- increase pleural pressure
Resorption atelectasis
- Airway blocked
- low ventilation:perfusion ratio (Q:V ratio)
- normally equal
Collapsed lungs during CPB due to no flow
- 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
Prevention of atelectasis
- Cannot do much
- decrease compliment activation
- decrease chance of edema
- anesthesia has more control (inflation/deflation)
Surfactant depletion
- anesthesia exposure reduces surfactant
- Lungs on CPB produce cytokines that drop surfactant synthesis
- lungs hurt themselves on CPB
Trauma of Lungs on CPB
- Suction can damage carina
- build up of secretions
- Promotes airway collapse
- careful when suctioning lungs
What happens when cavity is open on CPB
- Blood / fluid can enter
- lung compresses
Supine position on CPB
- decreases FRC (functional residual capacity)
- atelectasis observed in dorsal lung regions post CPB
Most common lung complication of CPB
- Compress lung
- open cavity / supine position / IVC cannulation
Pre-op risks of atelectasis
- smoking
- chronic bronchitis
- obesity
- cardiogenic pulmonary edema
Intraoperative risks of atelectasis
- passive ventilation
- monotonous vent pattern
Bypass risks of atelectasis
- surfactant inhibition
- distension / lung ischemia / compliment activation / open cavity / heart resting on left lobe
Pump lung
- acute respiratory failure
- lungs congested
- interstitial / alveolar edema
- hemorrhagic atelectasis
- high [neutrophil]
Causes of acute lung injury
- embolic load
- compliment activation
- hemodilution
- high pulmonary pressure -> high resistance
Which patients benefit from OPCAB
- COPD
- Pulmonary problems
- Increased airway resistance
Prevention of micro-emboli overload
- More filtration -> more normal the lungs
CPB and pulmonary injury
- CPB -> compliment activation -> pulmonary injury
- hypoxia is not the problem -> still have bronchial circulation
Acute bronchospasm on CPB
- Rare
- If on CPB….stay on
- If off CPB….get on
Prevention / treatment of acute lung injury on CPB
- Heparin coated circuits
- increase biocompatibility
- limit neutrophil activation
- hemofiltration: Z-buff / MUF / hemoconcentrate
- Corticosteroids / prostaglandins / inhaled NO (more for transplants)
Most common complication of lungs post CPB
- acute lung injury (atelectasis)
- common cause is mechanical ventilation
- manipulation of pleura / retraction of lung
- Perfusionists can get rid of pro-inflammatory mediators
