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BCC > CPB (Heart/Lung/Heme) > Flashcards

CPB (Heart/Lung/Heme) Flashcards

1
Q

How does ischemia while on CPB cause myocardial damage?

A

Ischemia leads to depletion of high energy phosphate bonds leading to lactate, acidosis, cellular edema, impaired Ca handling, and loss of membrane integrity –> myocardial contractile dysfunction

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2
Q

How does the CPB circuit cause myocardial damage?

A

Systemic inflammatory response from the plastics (cytokines, complement system, O2 free radicals)

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3
Q

What are the causes of myocardial injury from CPB?

A

Ischemia + CPB circuit itself + reperfusion injury + surgical trauma

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4
Q

How do we decrease myocardial O2 consumption on bypass?

A

Decompression fo the heart which decreases wall tension (40%) + hypothermia (11%) + asystole via cardioplegia (34%); can also perform ischemic preconditioning

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5
Q

How does cardioplegia protect the heart on CPB?

A

Hypothermic solution (less O2 demand) + arrest of the heart + pharmacologic agents to reduce ischemia and reperfusion injury is added

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6
Q

Is cardioplegia or a beating but empty and fibrillation heart more protected?

A

K+ arrested hearts have a 4-fold reduction in O2 consumption compared to a fibrillated, empty heart

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7
Q

What is added to cardioplegia solutions to prevent Ca+ accumulation?

A

Citrate (CPD), Ca channel blockers, magnesium, and low Na+ (decreases Na/Ca exchange antiport)

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8
Q

What is added to cardioplegia solutions to avoid edema?

A

Hyperosmolarity additives (i.e. glucose, K+, mannitol, albumin)

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9
Q

What can be added to cardioplegia solutions to avoid O2 radicals?

A

Allopurinol, nitric oxide, SOD/CAT (superoxide dismutase plus catalase)

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10
Q

What pressure should you not exceed while giving retrograde cardioplegia?

A

40mmHg (risk of coronary sinus rupture if you are over this)

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11
Q

What are the limitations of retrograde cardioplegia?

A

RV is not protected well (thebesian veins drain directly into the RV and not via the coronary sinus) + cannual may be distal to the great cardiac vein + if there is a persistent left SVC

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12
Q

What are risk factors for myocardial dysfunction after CPB?

A

Preop LV dysfunction + acute ischemia + advanced age + cross-clamp time + CPB time + perioperative bleeding + enlarged cardiac chambers

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13
Q

What is the mortality rate if one has prolonged mechanical ventilation (>72 hours) after cardiac surgery?

A

21-43% mortality rate; prolonged ventilation occurs in 7.5-10% of patients

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14
Q

How does the CPB circuit cause lung injury?

A

SIRS: CPB causes neutrophil activation and mobilization of other pro-inflammatory mediators that adhere to the pulmonary endothelium which can release proteolytic enzymes and O2 free radicals causing lung injury

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15
Q

How does ischemia and reperfusion cause lung injury?

A

Decreased pulmonary blood flow during CPB (no blood through PA) causes ischemic injury + reperfusion injury

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16
Q

What are risk factors for post-operative respiratory failure after cardiac surgery per Filsoufi et al?

A

Preop renal failure + female + EF < 30% + double valve procedures + active endocarditis + >70yo + heart failure + reoperations + emergent procedures + previous MI + prolonged CPB time (>180 min)

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17
Q

What are risk factors for ARDS in isolated valve surgeries per Chen et al?

A

Age + cirrhosis + massive transfusion + tricuspid valve replacement

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18
Q

What are the most common clinical manifestations of lung injury after CPB?

A

Atelectasis (from LLL compression during surgical exposure + apnea) and pleural effusions (left is more common, postop bleeding into left thoracic space + pulmonary edema + surgical trauma imparing lymphatic drainage)

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19
Q

Does using CPAP or ventilating the lungs during CPB improve clinical outcomes?

A

No although CPAP did improve the A-a gradient vs apnea

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20
Q

How do RBCs contribute to clotting?

A

They expose procoagulants on their surface which contributes to thrombin generation

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21
Q

How does hemodilution from CPB affect coagulation?

A

Dilution of coagulation factors + reduces RBC’s role in coagulation (clot stability)

22
Q

How does hypothermia affect the oxyhemoglobin dissociation curve?

A

It shifts it to the left, impairing O2 offloading at the tissue

23
Q

Why do we see hemolysis on CPB?

A

Mechanical sheer stress and turbulence within the CPB circuit + contact with non-endothelial surfaces and air + pressure gradients for venous drainage (vacuum) + cardiotomy suction use

24
Q

What are other risks of having hemolysis on CPB?

A

Damage to RBCs can cause release of free Hgb and heme which is a potent scavenger of nitric oxide (vasodilator) -> causes vasoconstriction and reduces microcirculatory function (worsening tissue hypoxia); Free heme can combine with endogenous hydrogen peroxide to form free radicals as well

25
Q

What % of blood volume is made up of white blood cells?

A

1% (99% is made up by RBCs)

26
Q

What happens with white blood cells when on CPB?

A

Activation of WBCs due to contact with non-endothelial surfaces (mediated by Kallikrein and complement system C5a); C5a causes neutrophil chemotaxis, degranulation and superoxide generation -> ultimately leads to tissue edema

27
Q

How do monocytes released from WBCs during CPB cause damage?

A

Releases proinflammatory cytokoines and they express tissue factor which promotes thrombin generation and activates coagulation; they can also conjugate with platelets and cause thrombocytopenia

28
Q

What is released by leukocytes that degrade and destabilize clots?

A

Elastase and Cathepsin G

29
Q

What is a white thrombus?

A

Platelet plug built up at the site of an endothelial defect, usually starting with a GP1a receptor binding to vWF and subsequent activation of GPIIb/IIIa receptors

30
Q

What does fibrin do in platelets for clot formation?

A

Additional platelet activator that recruits more platelets; makes the white thrombus turn into a red thrombus

31
Q

Why does thrombocytopenia occur with CPB?

A

Hemodilution + platelet adhesion to circuit surfaces + mechanical disruption, sheer strees + sequestration in pulmonary and splenic tissue + consumptive coagulopathy

32
Q

Why does thrombocytopathies occur with CPB?

A

Excessive platelet activation during CPB leads to a blunted response to stimulation (via ADP, collagen, thrombin) + Heparin effects (interferes with platelet-vWF interactions) + protamine (activates platelets as well leading to sequestration) + complement activation leading to more platelet activation

33
Q

How does heparin affect platelets?

A

Causes serotonin release + increased ADP-induced/collagen-induced/epi-induced aggregation + decreased thrombin-induced aggregation + opposes prostacyclin-induced aggregation + increased PF4 release + increase in bleeding time + decreased platelet count + P-selectin expression + suppresses alpha granule release (at higher doses)

34
Q

What is one possible explanation for platelet activation causing dysfunction?

A

Being on CPB causes platelets to be activated -> produces a population of granule-depleted platelets that cannot contribute to a platelet plug

35
Q

What can you do to reduce platelet dysfunction after CPB?

A

Reduce platelet damage and activation (i.e. reducing platelet sheer or coated circuits) + prevent exposure to CPB (i.e. ANH)

36
Q

How do endothelial cells cause a coagulopathy on CPB?

A

They upregulate anticoagulant and fibrinolytic pathways, causing thrombin generation and simultaneous fibrinolysis during CPB which sets up for a consumptive coagulopathy

37
Q

What makes up the contact system in coagulation?

A

Factor XI + Factor XII + kallikrein + high-molecular weight kininogen

38
Q

How does the complement system affect coagulation?

A

The complement system normally amplifies the inflammatory response, C5a (neutrophil activation) and membrane attack complex amplify inflammation, cell lysis, and platelet degranulation causing platelet dysfunction

39
Q

What factors make up the intrinsic pathway?

A

Factor XIIa causes Factor XI to become Factor XIa which causes Factor IX to become Factor IXa

40
Q

What factors make up the extrinsic pathway?

A

Tissue factor exposed by endothelial cells complexes with Factor VIIa

41
Q

What factors make up the common pathway?

A

Factor Xa + Factor Va are activated by both the intrinsic and extrinsic systems; these take prothrombin to thrombin which prevents fibrinogen breakdown into fibrin

42
Q

What is the predominant method of coagulation that gets activated during CPB?

A

The intrinsic pathway by the contact system via Factor XII leading to thrombin generation

43
Q

What is heparin rebound?

A

Inadequate heparin reversal with protamine caused by protein binding or endothelial sequestration that preserves heparin from neutralization

44
Q

What are our endogenous anticoagulants?

A

Antithrombin (neutrolizes thrombin) + Tissue factor pathway inhibitor (binds and inactivates Factor Xa and TF-Factor VIIa complex) + Activated protein C

45
Q

How does activated protein C work?

A

Slows down the procoagulant process by inactivating Factor VIIa and Factor Va and also neutralizes plasminogen activator inhibitor-1; it is aided by Protein S

46
Q

What is the purpose of the fibrinolytic system?

A

Prevent clot formation in non-injured vessels and maintain blood fluidity

47
Q

What does plasmin do?

A

Formed from plasminogen, it breaks down fibrin into soluble fibrin degradation products and inactivates Factor Va and Factor VIIIa

48
Q

What does t-PA do?

A

Tissue plasminogen activator = mediates intravascular plasminogen activation, causing dissolution of fibrin in circulation

49
Q

What happens to the fibrinolytic pathway during CPB?

A

Profibinolytic activity is increased caused by endothelial cell activation and t-PA release leading to 100-fold increase in plasmin generation (which breaks down fibrin)

50
Q

How does TXA work?

A

Protease inhibitor that binds to plasminogen which prevents it from becoming plasmin -> this reduces fibrinolysis

BCC (29 decks)

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