Topic 3: Pulmonary Response to CPB Flashcards
Atelectasis
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
most common pulmonary complication?
(70%)
ATELECTASIS
With Atelectasis – variable degree remains when lungs are re-expanded and ventilated
microscopic
lobar
hard to differentiate mechanical changes caused by bypass versus other parts of the surgery
Impaired Oxygenation
decreased functional residual capacity
— After general anesthesia?
By 20% after general anesthesia
Impaired Oxygenation
decreased functional residual capacity
— After CPB?
By 40-50 % after CPB
Impaired Oxygenation (4)
decreased functional residual capacity
decreased lung compliance
increased veno-arterial admixture
Alveolar-arterial oxygen gradient
P(A-a)O2 increasesFactors contributing to Atelectasis? Pre operative (3)
smoking, chronic bronchitis
obesity
cardiogenic pulmonary edema
Factors contributing to Atelectasis?
Intraoperative (3)
anesthesia: reduced surfactant function
passive ventilation
monotonous ventilator pattern
Factors contributing to Atelectasis?
Bypass (5)
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
what can we do to prevent ATELECTASIS?
Not Much
What can we do to prevent Atelectasis – Anesthesia controls what?
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)
Continuous positive airway pressure (CPAP) is?
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.
Positive end-expiratory pressure (PEEP) is
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.
Open Lung Ventilation - OLC
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.
– “Pump Lung”: acute respiratory failure characteristics? (5)
lungs diffusely congested intra-alveolar and interstitial edema hemorrhagic atelectasis vessel lumina full of neutrophils diffuse swelling of endothelial cells
What might cause Acute Lung Injury ? (5)
Embolic load Membrane damage from immune response Decreased pulmonary blood flow Hemodilution Elevated pulmonary artery pressure
Emboli can lead to areas of ventilation/perfusion mismatching which can lead to what? (5)
aggregated proteins disintegrated platelets damaged neutrophils fibrin fat globules
Better the filtration=
more normal the lungs
Introduction of arterial and cardiotomy filters greatly reduced what?
degenerative lesions in lung
Acute Lung Failure - MEMBRANE DAMAGE
Complement Activation
Vasoactive compounds from PMNs
Oxygen free radicals
Ischemia reperfusion injury
Acute Lung Failure – Complement Activation
— 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)
ALF - Decreased Pulmonary Blood FLow
Lungs isolated from pulmonary circulation
during bypass
Lung tissue still has metabolic activity
Bronchial circulation is still functional
Complement
Lung tissue still has metabolic activity
– @36C
approximately 11 mL/minute at 36C
Lung tissue still has metabolic activity
– @ 28C
approximately 5 to 6 mL/minute at 28C
ALF — Complement does what to pulmonary BF?
Localized vasoconstriction
ALF - Hemodilution
–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
Hemodilation and surfactant ?
actually prevents impairment of surfactant
Elevated PA pressure —-
Potential cause of pulmonary edema due to what 2 things?
Inadequate venting
Increased bronchial blood flow
ALF - Elevated PA pressure ?
No direct correlation between ALF and elevated PA pressure
COMPLEMENT ACTIVATION
Potential cause of pulmonary edema
Triggers for acute bronchospasm during bypass ? (8)
-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
Management of Bronchospasm ?
Stay on bypass or reinitiate bypass
Rest up to anesthesia
Anesthesia management of bronchospasm? (4)
-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
During bronchospasm volatile anesthetic agents can be given through pump - and what do they do?
-potent bronchodilators
-halothane sensitizes myocardium to catecholamines
–risk of tachyarrhythmias
Prevent/Treatment of Acute Lung Injury – by Blood filtration (2)?
leukocyte depletion
removal of endothelin-1
Prevent/Treatment of Acute Lung Injury – by Steroids characteristics? (3)
—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)
may be more protective than corticosteroids
Prostaglandins
Prostaglandins inhibit what? have what effect?
inhibit intravascular pulmonary leukocyte aggregation, activation, and free radical production
need to be careful because of hypotensive effect
Aprotinin inhibits/reduces what? (4)
- 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
Aprotinin attenuates what?
attenuates bradykinin-induced increases in vascular permeability
Inhaled Nitric Oxide characteristics/actions (4)
-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
Inhaled Nitric Oxide anti-inflammatory properties?
Decreases IL-8
Attenuates neutrophil adhesion and migration
Attenuates apoptosis in lungs
Inhaled Nitric Oxide – endogenous production is reduced post CPB, what does this reduction potentiate?
Potentiates pulmonary hypertension
Which drug inhibits serine proteases (plasmin & kallikrein) and prevents the activation of kininogen and formation of bradykinin?
Aprotinin
What inhibit intravascular pulmonary leukocyte aggregation, activation, and free radical production?
Prostaglandins
Steroids do not affect activation and release of what?
C3a activation or leukocyte elastase release
