Pulmonary Response to Cardiopulmonary Bypass

Question 1

Atelectasis

Answer 1

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

Question 2

most common pulmonary complication (70%)

Answer 2

Atelectasis

Question 3

types of atelactasis

Answer 3

microscopic lobar

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

Question 4

ATELECTASIS

Impaired Oxygenation

Answer 4

decreased functional residual capacity
By 20% after general anesthesia
By 40-50 % after CPB
decreased lung compliance
increased veno-arterial admixture
Alveolar-arterial oxygen gradient P(A-a)O2 increases

Question 5

FACTORS CONTRIBUTING TO ATELECTASIS

 Preoperative

Answer 5

smoking, chronic bronchitis  obesity cardiogenic pulmonary edema

Question 6

FACTORS CONTRIBUTING TO ATELECTASIS Intraoperative

Answer 6

anesthesia: reduced surfactant function passive ventilation monotonous ventilator pattern

Question 7

FACTORS CONTRIBUTING TO ATELECTASIS bypass

Answer 7

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

Question 8

WHAT CAN WE DO TO PREVENT ATELECTASIS?

Answer 8

Not much
Decrease complement activation
Reduce chances of edema
Anesthesia has more control (i.e. how lungs are deflated and re-inflated)
PEEP CPAP OLC (open lung concept)

Question 9

ACUTE LUNG INJURY FROM CPB

Answer 9

 1950’s “Pump Lung”: acute respiratory failure lungs diffusely congested
intra-alveolar and interstitial edema hemorrhagic atelectasis vessel lumina full of neutrophils diffuse swelling of endothelial cells

Question 10

WHAT MIGHT CAUSE ACUTE LUNG INJURY?

Answer 10

Embolic load Membrane damage from immune response

Decreased pulmonary blood flow Hemodilution Elevated pulmonary artery pressure

Question 11

ACUTE LUNG FAILURE: EMBOLI

Answer 11

Emboli can lead to areas of ventilation/perfusion mismatching
aggregated proteins disintegrated platelets damaged neutrophils fibrin
fat globules Introduction of arterial and cardiotomy filters
greatly reduced degenerative lesions in lung Better the filtration – more normal the lungs

Question 12

ACUTE LUNG FAILURE: MEMBRANE DAMAGE

 Complement Activation

Answer 12

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

Question 13

ACUTE LUNG FAILURE: MEMBRANE DAMAGE cont.

Answer 13

Vasoactive compounds from PMNs

 Oxygen free radicals  Ischemia reperfusion injury

Question 14

ACUTE LUNG FAILURE: DECREASED PULMONARY BLOOD FLOW

Answer 14

Lungs isolated from pulmonary circulation during bypass
Lung tissue still has metabolic activity approximately 11 mL/minute at 36 oC approximately 5 to 6 mL/minute at 28 oC
Bronchial circulation is still functional
Complement Localized vasoconstriction

Question 15

ACUTE LUNG FAILURE: HEMODILUTION

Answer 15

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
actually prevents impairment of surfactant

Question 16

ACUTE LUNG FAILURE: ELEVATED PA PRESSURE

Answer 16

Potential cause of pulmonary edema due to Inadequate venting Increased bronchial blood flow
Not direct correlation COMPLEMENT ACTIVATION

Question 17

ACUTE BRONCHOSPASM DURING BYPASS trigger

Answer 17

Rare occurrence
 Trigger
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

Question 18

MANAGEMENT OF BRONCHOSPASM

Answer 18

 Stay on bypass or reinitiate bypass  Rest up to anesthesia
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
potent bronchodilators
halothane sensitizes myocardium to catecholamines – risk of tachyarrhythmias

Question 19

PREVENTION & TREATMENT OF ACUTE LUNG INJURY

Answer 19

 Blood filtration leukocyte depletion removal of endothelin-1
 Coated circuits
 Membrane oxygenators
 Hemodilution avoid homologous blood primes
 Proper LV venting
 Steroids
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

Question 20

PREVENTION & TREATMENT OF ACUTE LUNG INJURY (CONTINUED)

Answer 20

 Prostaglandins may be more protective than corticosteroids
inhibit intravascular pulmonary leukocyte aggregation, activation, and free radical production
need to be careful because of hypotensive effect  Aprotinin
inhibits serine proteases (plasmin & kallikrein) prevents the activation of kininogen and formation of
bradykinin
definitely reduces blood usage by preventing platelet aggregation and inhibiting fibrinolysis
attenuates bradykinin-induced increases in vascular permeability
reduced lung neutrophil accumulation after bypass

Question 21

PREVENTION & TREATMENT OF ACUTE LUNG INJURY (CONTINUED) NO

Answer 21

 Inhaled Nitric Oxide 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
Decreases IL-8 Attenuates neutrophil adhesion and migration Attenuates apoptosis in lungs