test 2 Flashcards

1
Q

the lungs are covered with

A

-pleura

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2
Q

what covers the top of the diaphram

A

-parietal pleura

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3
Q

what is between the parietal pleura and visceral pleura

A

-serous fluid

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4
Q

what happens when our thoracic cage expands

A

-pulls the lungs

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5
Q

Inspiration (normal conditions)

A
  • Diaphragm contracts (pulled down)
  • ­Increases size of thoracic cavity
  • ­Decreases pleural pressure (air comes in) (builds up - pressure) (goes from a place of higher pressure to lower pressure)
  • Lifting up of the thoracic cage
  • Lungs being stretched and pulled
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6
Q

Expiration (normal conditions)

A
  • ­Diaphragm relaxes – domed position
  • ­Lungs recoil
  • ­Increases pleural pressure (force air out)
  • Size of thoracic cavity decreased
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7
Q

PULMONARY PHYSIOLOGY

A

-­Lungs are very elastic
-­Want to collapse
-­Surface tension very high
­-Surfactant Decreases surface tenstion

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8
Q

Bronchial circulation

A

-High pressure, low-flow (small vessels)
-Arterial blood to the tissues of the respiratory system (­1-2% of cardiac output)
-Branches off of thoracic aorta (Oxygenated blood)
-Returns venous blood to left
atrium

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9
Q

Pulmonary circulation

A

-Low pressure, high flow
-Venous blood to pulmonary
capillaries (­Gas exchange)
-Returns arterial blood to left
atrium (­Via Pulmonary veins)

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10
Q

What happens to the lungs when we go on bypass?

A

-­Stop ventilating lungs (­Lungs collapse)
-­Resistance to blood flow increases (­No pulmonary blood flow (Bypassing))
AND (Little bronchial flow (due to resistance))

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11
Q

Atelectasis

A

-Collapse of alveoli (­Can be localized OR ­Can be entire lung)

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12
Q

what happens to the lungs post-CPB

A

­-Some atelectasis remain

  • ­Range in degree of severity
  • can lasts for months after bypass
  • acute respiratory distress syndrome (ARDS)
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13
Q

Degrees of severity of atelectasis

A

­-Micro-atelectasis (Not detectable clinically)
-Complete collapse of entire lobe
­-Intermediate degrees

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14
Q

Factors affecting pulmonary function

A

­-Atelectasis
­-Pleural disruption
­-Impaired lung compliance
-SIRAB (systemic inflammatory response after bypass)

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15
Q

Atelectasis results from (2)

A
  • ­Blockage of small bronchi with mucous

- ­Obstruction of a major bronchus (left side more likely to build up mucous)

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16
Q

What happens during atelectasis?

A
  • air becomes trapped
  • ­Air is absorbed into the pulmonary capillaries and creates negative pressure
  • ­ Alveoli collapse
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17
Q

If alveoli can’t collapse due to fibrosis

A

­-Created negative pressure in alveoli
­-Pulls fluid out of capillary into alveoli
­-Massive collapse of entire lung

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18
Q

Why is atelectasis so common on bypass?

A

-anesthesia give neuromuscular blocker which relaxes the diaphram (moves up) which decreases space in thoracic cavity = pleural pressure increases and less likely to move air

19
Q

Resorption atelectasis

A
  • all air is sucked out

- low ventilation to perfusion ratios (mismatch) resulting in airway obstruction

20
Q

residual atelectasis

A
  • heart lies on lung
  • lung lies on self so the back side of the lung effected
  • retraction helps atelectasis
  • venous cannula
21
Q

what can we do to prevent atelectasis?

A
  • not much
  • must be aware of it!
  • reduce chance of edema (not allowing it to go into the lungs)
  • anesthesia has more control
22
Q

Anesthesia’s role in atelectasis

A

-mechanical ventilation initiates atelectasis

23
Q

Surfactant depletion

A
  • surfactant lowers surface tension
  • anesthesia lowers surfactant function
  • there are huge stores of surfactant
24
Q

atelectasis promotes produciton of pro-inflammatory cytokines which

A

-decrease surfactant synthesis which leads to lung collapse

25
Blind suctioning of the airways can cause damage to
-carina which causes secretions to build up and airway collapse
26
what is the most common lung complication after bypass?
-atelectasis (70% of cases)
27
preoperative contributions to atelectasis
­-Smoking, chronic bronchitis ­-Obesity ­-Cardiogenic Pulmonary Edema
28
intraoperative contributions to atelectasis
­-Passive ventilation | ­-Monotonous ventilator pattern
29
bypass contributions to atelectasis
­-Surfactant inhibition ­-Plasma, lung distension, lung ischemia ­-Increased extravascular lung water (complement activation) ­-Heart rests on left lobe -Open pleural cavity – accumulation of blood and fluid
30
CLINICAL CONSEQUENCES OF ATELECTASIS
-functional residual capacity decreased can decrease by 40-50%
31
pump lung
-acute respiratory failure -­Lungs diffusely congested ­-Intra=alveolar and instersitial edema ­-Hemorrhagic atelectasis ­-Vessel lumen full of neutrophils ­-Diffuse swelling of endothelial cells
32
WHAT MIGHT CAUSE ACUTE LUNG INJURY?
- Embolic load - Complement activation / inflammatory response - Hypoxia of lung tissue - Hemodilution - Elevated pulmonary artery pressure (increase resistance)
33
acute lung failure
-microemboli overload -­Aggregated proteins, ­Platelet fragments, ­Damaged, neutrophils, ­Fibrin, ­Fat globules -Introduction of arterial and cardiotomy filters greatly reduced degenerative lesions in lungs
34
acute lung failure complement activation
- found where blood meets foreign surface | - Provides function for fighting invading organisms
35
opsonization
-coats an invader with antibodies which tags it and stops it from attacking our cells
36
complement and the ECC
- complement exposes neutrophils - become sticky - neutrophils degranulate- break into small pieces and release O2 free radicals which damage endothelial cells (capillary leakage)
37
ACUTE LUNG FAILURE: HYPOXIA
- lung tissue still has metabolic activity - bronchial circulation is still functional - COMPLIMENT IS THE BIGGEST PROBLEM - atelectasis leads to compliment
38
hemodilution to lung injury
- provide potential for lung injury | - does not impair surfactant
39
what is the biggest offender of acute lung failure
COMPLIMENT ACTIVATION
40
acute bronchospasm during CPB
- C5a triggers it | - very rare
41
MANAGEMENT OF BRONCHOSPASM
- Stay on bypass or go back on bypass | - Support patient while anesthesia treats
42
PREVENTION AND TREATMENT OF ACUTE LUNG INJURY
- ECC – attenuate immune response - coat circuit for better biocompatability - Hemofiltration - filter inflammatory mediators - leukocyte depletion - mechanical ventilation (anesthesia) - corticosteroids= decrease immune response to CPB - inhaled Nitric Oxide- causes pulmonary vasodilation and decreases neutrophil adhesion
43
what is the most common complication after bypass
- Acute lung injury | - atelectasis
44
most common cause of acute lung injury
mechanical ventilation