Topic 3: Pulmonary Response to CPB Flashcards

1
Q

Atelectasis

A

A complete or partial collapse of a lung or

a lobe of the lung-develops when the alveoli become deflated and don’t inflate properly

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2
Q

most common pulmonary complication?

A

(70%)

ATELECTASIS

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3
Q

With Atelectasis – variable degree remains when lungs are re-expanded and ventilated

A

microscopic
lobar

hard to differentiate mechanical changes caused by bypass versus other parts of the surgery

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4
Q

Impaired Oxygenation
decreased functional residual capacity
— After general anesthesia?

A

By 20% after general anesthesia

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5
Q

Impaired Oxygenation
decreased functional residual capacity
— After CPB?

A

By 40-50 % after CPB

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6
Q

Impaired Oxygenation (4)

A
decreased functional residual capacity
decreased lung compliance
increased veno-arterial admixture
Alveolar-arterial oxygen gradient
      P(A-a)O2 increases
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7
Q
Factors contributing to Atelectasis?
Pre operative (3)
A

smoking, chronic bronchitis
obesity
cardiogenic pulmonary edema

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8
Q

Factors contributing to Atelectasis?

Intraoperative (3)

A

anesthesia: reduced surfactant function
passive ventilation
monotonous ventilator pattern

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9
Q

Factors contributing to Atelectasis?

Bypass (5)

A

surfactant inhibition
plasma, lung distention, lung ischemia
increased extravascular lung water (complement activation)
heart rests on immobile left lower lobe
open pleural cavity–accumulation of blood and fluid

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10
Q

what can we do to prevent ATELECTASIS?

A

Not Much

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11
Q

What can we do to prevent Atelectasis – Anesthesia controls what?

A

Anesthesia has more control (i.e. how lungs
are deflated and re-inflated)
PEEP (post-end expiratory pressure)
CPAP (Continuous positive airway pressure)
OLC (open lung concept)

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12
Q

Continuous positive airway pressure (CPAP) is?

A

the use of continuous positive pressure to maintain a continuous level of positive airway pressure in a spontaneously breathing patient. It is functionally the same as PEEP as both are used to stent alveoli open and recruit alveoli of the lungs for more surface area for ventilation.

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13
Q

Positive end-expiratory pressure (PEEP) is

A

the pressure in the lungs (alveolar pressure) above atmospheric pressure (the pressure outside of the body) that exists at the end of expiration.
The two types: are extrinsic PEEP (PEEP applied by a ventilator) and intrinsic PEEP (PEEP caused by a non-complete exhalation). Pressure that is applied or increased during an inspiration is termed pressure support.

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14
Q

Open Lung Ventilation - OLC

A

a strategy that is utilized by several modes of mechanical ventilation to combine low tidal volume and applied PEEP to maximize recruitment of alveoli. The low tidal volume aims to minimize alveolar overdistention and the PEEP minimizes cyclic atelectasis. Working in tandem the effects from both decrease the risk of ventilator-associated lung injury.

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15
Q

– “Pump Lung”: acute respiratory failure characteristics? (5)

A
lungs diffusely congested
intra-alveolar and interstitial edema
hemorrhagic atelectasis
vessel lumina full of neutrophils
diffuse swelling of endothelial cells
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16
Q

What might cause Acute Lung Injury ? (5)

A
Embolic load
Membrane damage from immune response
Decreased pulmonary blood flow
Hemodilution
Elevated pulmonary artery pressure
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17
Q

Emboli can lead to areas of ventilation/perfusion mismatching which can lead to what? (5)

A
aggregated proteins
disintegrated platelets
damaged neutrophils
fibrin
fat globules
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18
Q

Better the filtration=

A

more normal the lungs

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19
Q

Introduction of arterial and cardiotomy filters greatly reduced what?

A

degenerative lesions in lung

20
Q

Acute Lung Failure - MEMBRANE DAMAGE

A

Complement Activation
Vasoactive compounds from PMNs
Oxygen free radicals
Ischemia reperfusion injury

21
Q

Acute Lung Failure – Complement Activation

A

— Found wherever blood meets foreign surface
hemodialysis
leukophoresis
— Provides several functions for fighting invading organisms
leukocyte activation
cytolysis
(opsonization makes bacterial cells vulnerable to phagocytosis by attaching various items)

22
Q

ALF - Decreased Pulmonary Blood FLow

A

Lungs isolated from pulmonary circulation
during bypass
Lung tissue still has metabolic activity
Bronchial circulation is still functional
Complement

23
Q

Lung tissue still has metabolic activity

– @36C

A

approximately 11 mL/minute at 36C

24
Q

Lung tissue still has metabolic activity

– @ 28C

A

approximately 5 to 6 mL/minute at 28C

25
Q

ALF — Complement does what to pulmonary BF?

A

Localized vasoconstriction

26
Q

ALF - Hemodilution

A

–Concern with decrease in colloid osmotic
pressure and movement of fluid into the
intracellular space
–Studies seem to indicate the accumulation of
pulmonary extravascular water is not affected
by the type of priming solution
–Hemodilution does not appear to harm the lungs

27
Q

Hemodilation and surfactant ?

A

actually prevents impairment of surfactant

28
Q

Elevated PA pressure —-

Potential cause of pulmonary edema due to what 2 things?

A

Inadequate venting

Increased bronchial blood flow

29
Q

ALF - Elevated PA pressure ?

A

No direct correlation between ALF and elevated PA pressure
COMPLEMENT ACTIVATION
Potential cause of pulmonary edema

30
Q

Triggers for acute bronchospasm during bypass ? (8)

A

-activation C5a (fulminant bronchospasm)
-cold urticaria syndrome (release histamine when exposed to cold)
-preexisting bronchospastic disease
instrumentation
-secretions
-cold anesthetic gas in patients with -hyperactive airways
-allergic reactions to antibiotics or protamine
-drugs that induce histamine release

31
Q

Management of Bronchospasm ?

A

Stay on bypass or reinitiate bypass

Rest up to anesthesia

32
Q

Anesthesia management of bronchospasm? (4)

A

-administration of beta selective agonists directly into endotracheal tube
(albuterol, metaproterenol)
-small IV boluses of epinephrine followed by continuous low-dose infusion
-IV lidocaine given to decrease airway hyperactivity
-volatile anesthetic agents can be given through pump

33
Q

During bronchospasm volatile anesthetic agents can be given through pump - and what do they do?

A

-potent bronchodilators
-halothane sensitizes myocardium to catecholamines
–risk of tachyarrhythmias

34
Q

Prevent/Treatment of Acute Lung Injury – by Blood filtration (2)?

A

leukocyte depletion

removal of endothelin-1

35
Q

Prevent/Treatment of Acute Lung Injury – by Steroids characteristics? (3)

A

—does not affect C3a activation or leukocyte
elastase release
—may inhibit increase in leukotriene B4 and tissue plasminogen activator
—may actually cause other problems
(increased blood loss, low cardiac output syndrome)

36
Q

may be more protective than corticosteroids

A

Prostaglandins

37
Q

Prostaglandins inhibit what? have what effect?

A

inhibit intravascular pulmonary leukocyte aggregation, activation, and free radical production
need to be careful because of hypotensive effect

38
Q

Aprotinin inhibits/reduces what? (4)

A
  • inhibits serine proteases (plasmin & kallikrein)
  • prevents the activation of kininogen and formation of bradykinin
  • reduced lung neutrophil accumulation after bypass
  • definitely reduces blood usage by preventing platelet aggregation and inhibiting fibrinolysis
39
Q

Aprotinin attenuates what?

A

attenuates bradykinin-induced increases in vascular permeability

40
Q

Inhaled Nitric Oxide characteristics/actions (4)

A

-Endogenous production reduced post CPB
(Potentiates pulmonary hypertension)
-Provides potent vasodilation in the pulmonary vasculature
-Used to treat elevated pulmonary vascular resistance
-Some anti-inflammatory properties

41
Q

Inhaled Nitric Oxide anti-inflammatory properties?

A

Decreases IL-8
Attenuates neutrophil adhesion and migration
Attenuates apoptosis in lungs

42
Q

Inhaled Nitric Oxide – endogenous production is reduced post CPB, what does this reduction potentiate?

A

Potentiates pulmonary hypertension

43
Q

Which drug inhibits serine proteases (plasmin & kallikrein) and prevents the activation of kininogen and formation of bradykinin?

A

Aprotinin

44
Q

What inhibit intravascular pulmonary leukocyte aggregation, activation, and free radical production?

A

Prostaglandins

45
Q

Steroids do not affect activation and release of what?

A

C3a activation or leukocyte elastase release