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Perf tech II > test 2 > Flashcards

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
Q

Blind suctioning of the airways can cause damage to

A

-carina which causes secretions to build up and airway collapse

26
Q

what is the most common lung complication after bypass?

A

-atelectasis (70% of cases)

27
Q

preoperative contributions to atelectasis

A

­-Smoking, chronic bronchitis
­-Obesity
­-Cardiogenic Pulmonary Edema

28
Q

intraoperative contributions to atelectasis

A

­-Passive ventilation

­-Monotonous ventilator pattern

29
Q

bypass contributions to atelectasis

A

­-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
Q

CLINICAL CONSEQUENCES OF ATELECTASIS

A

-functional residual capacity decreased can decrease by 40-50%

31
Q

pump lung

A

-acute respiratory failure
-­Lungs diffusely congested
­-Intra=alveolar and instersitial edema
­-Hemorrhagic atelectasis
­-Vessel lumen full of neutrophils
­-Diffuse swelling of endothelial cells

32
Q

WHAT MIGHT CAUSE ACUTE LUNG INJURY?

A
  • Embolic load
  • Complement activation / inflammatory response
  • Hypoxia of lung tissue
  • Hemodilution
  • Elevated pulmonary artery pressure (increase resistance)
33
Q

acute lung failure

A

-microemboli overload
-­Aggregated proteins, ­Platelet fragments, ­Damaged, neutrophils, ­Fibrin, ­Fat globules
-Introduction of arterial and cardiotomy filters greatly
reduced degenerative lesions in lungs

34
Q

acute lung failure complement activation

A
  • found where blood meets foreign surface

- Provides function for fighting invading organisms

35
Q

opsonization

A

-coats an invader with antibodies which tags it and stops it from attacking our cells

36
Q

complement and the ECC

A
  • complement exposes neutrophils - become sticky
  • neutrophils degranulate- break into small pieces and release O2 free radicals which damage endothelial cells (capillary leakage)
37
Q

ACUTE LUNG FAILURE: HYPOXIA

A
  • lung tissue still has metabolic activity
  • bronchial circulation is still functional
  • COMPLIMENT IS THE BIGGEST PROBLEM
  • atelectasis leads to compliment
38
Q

hemodilution to lung injury

A
  • provide potential for lung injury

- does not impair surfactant

39
Q

what is the biggest offender of acute lung failure

A

COMPLIMENT ACTIVATION

40
Q

acute bronchospasm during CPB

A
  • C5a triggers it

- very rare

41
Q

MANAGEMENT OF BRONCHOSPASM

A
  • Stay on bypass or go back on bypass

- Support patient while anesthesia treats

42
Q

PREVENTION AND TREATMENT OF ACUTE LUNG INJURY

A
  • 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
Q

what is the most common complication after bypass

A
  • Acute lung injury

- atelectasis

44
Q

most common cause of acute lung injury

A

mechanical ventilation

Perf tech II (16 decks)

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