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Orange Book Flashcards

1
Q
  1. For hollow fiber oxygenators, where is blood and gas in relation to the fiber?
  2. Describe what happens when you increase or decrease sweep and how CO2 is removed.
A
  1. Blood on outside of fiber
    Gas on inside of fiber
  2. Increased sweep= less CO2 on outside of fiber= a higher conc. Gradient from blood to gas= less CO2 in blood

Decreased sweep= more CO2 on the outside of fiber= a lower conc. Gradient from blood to gas= more CO2 in blood

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2
Q 
What are the micron sizes for each filter:
Gas line filters= 
Pre-bypass filters=
Crystalliod cardioplegia filters = 
Arterial line filters = 
Leukodepletion filters = 
Blood cardioplegia filters = 
Blood transfusion filters =
A 
Gas line = 0.2 microns
Pre-bypass filters 0.2 microns
Crystalliod cardioplegia filters = 0.2 microns
Arterial line filters = 40 microns
Leukodepletion filters = 40 microns
Blood cardioplegia filters = 40 microns
Blood transfusion filters = 40 microns
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3
Q

How do screen filters work?

A

removes particles by mechanical retention and impaction. They have a specific pore size and remove air by velocity separation and venting.

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4
Q

How do depth filters work?

A

creates a tortuous path between fibers and retains particles mechanically. There is not a specific pore size. Air is removed by entrapment during transit of blood through the pathway between fibers.

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5
Q

What are the top 5 most common places to place a vent

A
  1. Aortic root
  2. Left ventricle
  3. Right superior pulmonary vein
  4. Left ventricular apex = (most dangerous)
  5. Left atrium or pulmonary artery
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6
Q

What are the 5 reasons for venting the heart during CPB

A
  1. Prevent distension of the heart
  2. Reduce myocardial re-warming
  3. To evacuate air from cardiac chambers during the de-airing phase
  4. To improve surgical exposure
  5. To create a dry surgical field
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7
Q

Why should suction pressure and duration should be keep to a minimum

A

it is possible for air to get to the arterial side by being introduced into the venous reservoir and possibly not getting captured, then into the oxygenator, and still avoiding capture. And then finally into the arterial line

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8
Q
  1. What does the heart do when it is with out blood?

2. What does the heart do when blood is reintroduced to the heart?

A
  1. When heart is without blood, it continues to use ATP to fuel metabolic reactions anaerobically- Resulting in depletion of energy reserves and build up of products of anaerobic metabolism ex: lactic acid
  2. Myocardial contractility is diminished when blood is reintroduced to the heart due to a build up of products of anaerobic metabolism but contractility will get better when ATP reserves are restored
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9
Q

How do you reduce metabolic state of heart during CPB?

A
  1. Cardioplegia arresting the heart

2. Using cold cardioplegia and by cooling the body

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10
Q

Cardioplegia produces ________ cardiac arrest

A

Cardioplegia produces DIASTOLIC cardiac arrest

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11
Q

What are 3 cardioplegia delivery sites for antegrade delivery?

A
  1. Aortic root
  2. Coronary ostia
  3. Saphenous vein graft
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12
Q

What is the cardioplegia delivery site for retrograde delivery?

A
  1. Coronary sinus
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13
Q
  1. How do hemoconcentrators work?
  2. What is the typical fluid removal rate?
  3. What size molecules are removed?
  4. What can they be used to treat?
A
  1. Have semi-permeable membranes (hollow fibers) that permit passage of water and electrolytes out of blood.
  2. Fluid removal is 30-50mL/min
  3. Typically molecules smaller than 20,000 Daltons are removed
  4. Can be used to manage hyperkalemia and acidosis. Also used to concentrate blood to increase HCT
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14
Q

Name the 3 types of in-line monitoring systems used during CPB

A
  1. Electrochemical electrodes
  2. Cuvettes - placed in circuit
  3. Light absorbance or reflectance of infrared light signals - placed on circuit tubing
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15
Q

What 3 things do miniature circuits reduce?

A
  1. Reduce foreign surface exposure
  2. Reduced priming volume
  3. Reduced blood-air contact
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16
Q

What 3 things do miniature circuits NOT include

A
  1. Reservoir
  2. Heat exchanger
  3. Cardiotomy suction
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17
Q

Why is it nearly impossible to not use blood containing primes for infants and neonates?

A

priming volume is far greater than their blood volume

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18
Q

What does hemodilution do?

A

decreases viscosity which increases microcirculation

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19
Q

What is DO2 influenced by

A
  1. pump flow rate
  2. Arterial oxygen content ( this being primarily determined by hematocrit)
    (*and hgb and SaO2 and PaO2)
    Formula: (1.39xHgbxSaO2 + (.003xPaO2)) x Flow [lpm]
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20
Q

What is VO2 influenced by

A
  1. Temperature
  2. Level of anesthesia
    (*and CO and the Art/Ven oxy content difference)
    Formula: Flow [lpm] x 10 x (aO2 content- vO2 content)
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21
Q

Define Autologous priming

A
  1. Clear Prime Replacement

2. Retrograde Autologous Prime/Venous Autologous Prime

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22
Q

What are the 3 types of priming solutions used

A
  1. Crystalliod
  2. Colloid
  3. Blood
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23
Q

What negative results does 5% Dextrose have as a priming solution

A
  1. metabolism of glucose leads to hypotonic solutions

2. Hyperglycemia worsens neurological outcome

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24
Q

What does a hypotonic solution cause

A

fluid moves from extracellular space to intracellular space and cell burst

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25
Q

What does a hypertonic solution cause

A

fluid moves intracellular space to extracellular space and cell shrivels (crenation)

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26
Q

What does an isotonic solution cause

A

tonicity is the same on both sides of the semi-permeable membrane= no fluid shifts

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27
Q

What organs most vulnerable to fluid shifts

A
  1. brain

2. Lungs

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28
Q

What does Intracellular fluid gain cause

A

cerebral or pulmonary edema and impairs organ function

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29
Q

What 2 things are metabolized to bicarbonate in the liver

A

lactate and acetate

-thus solutions containing these components will produce a near ideal physiological solution

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30
Q

What does Hyperchloremia cause? Why?

A

acidosis

* Chloride/Bicarb shift: Extracellular Cl- pushes bicarb intracellular causing acidosis

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31
Q

Why are colloid prime solution are beneficial

A

They combat the effects of hemodilution by helping to maintain colloid oncotic pressure. This increases the concentration of albumin and other circulating plasma proteins.

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32
Q

In theory, colloid solutions a can have what negative affect

A

During CPB a systemic inflammatory response is experienced causing widening of the tight junctions between endothelial cells allowing colloids to escape into the interstitial spaces promoting edema.

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33
Q

What are 3 negative effects of colloid primes

A
  1. Interfere with coagulation
  2. Starches can stay in body for years
  3. Albumin poses infection hazards
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34
Q

Mannitol as a colloidal fluid has what 2 benefits

A
  1. potent osmotic diuretic (rather than raising the oncotic pressure of the prime)
  2. Scavenger of free radicals
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35
Q

Where are most of the proteins required for the coagulation cascade are produced

A

They are produced by the liver as inscribe precursors which are modified into clotting factors.

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36
Q

What are the 2 coagulation pathways and how are they activated?

A
  1. Intrinsic pathway= is activated by contact with collagen from damaged blood vessels or any negatively charged surface
  2. Extrinsic pathway= is activated by contact with tissue factor from the surface of extravascular cells
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37
Q

Both coagulation pathways end in what?

A

Both routes end in a final common pathway - the proteolytic activation of thrombin and the cleaving of fibrinogen to form a fibrin clot

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38
Q

Which coagulation pathway is dominant

A

The intrinsic pathway is the dominant route with the extrinsic pathway acting synergistically

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39
Q

What are the 4 benefits of heparin

A
  1. fast onset of action
  2. Measurable
  3. Reversible
  4. Titratable
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40
Q

Describe Heparins molecular weight and structure

A

Molecular weights
Native Heparin = 3-40 kDA
Unfractionted heparin = 12-15 kDA

Is a member of the glycoaminoglycan family of carbohydrates (also including heparan sulfate in this group and consist of a variably sulfated repeating disaccharide unit that is negatively charged at physiological pH.

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41
Q

What naturally releases Heparin in the body (2)

A
  1. Mast cells

2. Basophils

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42
Q

Heparin is commercially derived from what (2)

A
  1. Bovine Lung

2. Porcine intestinal mucosa

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43
Q

Describe Heparin’s mechanism of action

A

Heparin contains a specific pentasaccharide sulfation sequence which binds to AT- III causing a conformational change which results in increased AT-III activity. Heparin binding to AT-III increases AT-III’s activity up to 1000-fold

The activated AT- III then inactivates thrombin along with other proteases (12, 11, 9, 10, 2)

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44
Q

Heparin is most active against what? (2)

A

thrombin and Xa

*Heparin also increases the activity of heparin cofactor II which inhibits thrombin

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45
Q

What is Heparin’s half-life at doses of 300-400 Units/kg

A

2.5 hours

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46
Q

What 4 things prolong the ACT: (these can affect the ACT, even when not enough heparin is given)

A
  1. Hypothermia
  2. Hemodilution
  3. Platelet function abnormalities
  4. Low fibrinogen
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47
Q

Define heparin resistance

A

The failure to raise the ACT to expected levels despite an adequate dose and plasma conc. of heparin. Administering 600-800 units/kg may be necessary to obtain an ACT level sufficient for CPB

Congenital or acquired AT-III deficiency are associated with heparin resistance.

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48
Q

Why is hemodilution not a cause of ATIII deficiency

A

Hemodilution decreases AT-III levels however, hemodilution does not cause heparin resistance, because it causes dilution of procoagulant factors.

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49
Q

What is the most common reason why ATIII deficiency occurs

A

Prior treatment with heparin causes depletion or dysfunction of AT-III and is the likely reason the patient will present heparin resistance

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50
Q

What can be given to treat ATIII deficiency before CPB

A

Give ATIII or FFP

*Recombinant forms of AT-III are used to treat congenital deficiency

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51
Q

HIT develops in what % of patients receiving heparin

A

5%

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52
Q

Describe the 2 forms of HIT

A
  1. Mild- involves a transient decrease in platelet count
    A) these patients can receive heparin for cardiac surgery
  2. Severe- an immune-mediated decrease in the platelet count
    A) occurs later in heparin therapy (5-14 days after administration)
    B) Antibodies are formed against platelet factor 4 (PF4) and heparin, these antibodies bind to and activate platelets and causes the platelet count to drop extremely low
    C) When there is endothelial injury, this propagation of platelet activation makes it more likely to form platelet clots (white clots) and thrombosis
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53
Q

What are the 3 laboratory diagnosis of HIT? Which is the gold standard?

A
  1. Functional assay - detects platelet activation that is dependent on heparin in the presence of sera and UFH
  2. Antibody-based assay (serotonin release assay) - is the gold standard when a patient’s serum is exposed to heparin. The test uses the patient’s serum and platelets.
  3. Heparin-induced platelet activation (HIPAA)
  4. Platelet-rich plasma aggregation assay (PRP)
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54
Q

What do you do for a patient with a history of HIT but is negative for antibodies?

A

can receive unfractionated heparin

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55
Q

What so you do for a patient with acute HIT

A

delay surgery until HIT antibodies are negative or use alternative anticoagulant such as bivalrudin or hirudin. A combination of unfractionated heparin and anti platelet agents such as epoprostenol or tirofiban are also recommended.

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56
Q 
LOW-MOLECULAR WEIGHT HEPARIN (LMWH):
1- How is it administered?
2- Whats the half life?
3- What patients should not receive it?
4- What are 3 problems with it
A
  1. Intravenously administered
  2. Half-life at least 5 hours (twice as much as UFH)
  3. Not recommended for HIT patients
  4. A) Problem is that it only reverses factor IIa inhibition and leaves the predominant factor Xa inhibition intact.
    B) Problem is it complicates heparin monitoring because APTT and presumably ACT are much less sensitive to Xa inhibition and will not accurately measure the full anticoagulant effect.
    C) Factor Xa monitoring requires, more complex testing
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57
Q

How do DIRECT THROMBIN INHIBITORS (DTIs) work? Name 3?

A

directly inhibit the procoagulant and prothrombotic actions of thrombin and do not require a cofactor. There advantage is that they do not react with nor produce heparin-dependent antibodies

  • LEPIRUDIN
  • ARGATROBAN
  • BIVALIRUDIN
58
Q 
LEPIRUDIN
1- Half life?
2- Monitoring?
3- How is it reversed/eliminated?
4- How is it metabolized?
5- Benefit?
A
  1. Half-life 80 minutes
  2. Monitored by aPTT or ACT
  3. No antidote, however can be eliminated by hemofiltration
  4. metabolized by the kidneys requiring dose adjustments in patients with renal insufficiency
  5. A benefit is that it lacks cross-reactivity with heparin antibodies so it Can be used in HIT patients
59
Q 
ARGATROBAN
1- Half life?
2- Monitoring?
3- How is it reversed/eliminated?
4- How is it metabolized?
5- Benefit?
A
  1. half-life is 45-55 minutes
  2. Monitored by aPTT or ACT
  3. No antidote
  4. metabolized in the liver requiring dose adjustments in patients with moderate liver disease
  5. Lacks cross-reactivity with heparin antibodies so it Can be used in HIT patients (Widely used in HIT patients requiring percutaneous coronary intervention)
60
Q 
BIVALIRUDIN
1- Half life?
2- Monitoring?
3- Dose
4- How is it metabolized?
5- Benefit?
A
  1. Half-life 25 minutes
  2. Monitored by aPTT, ACT, or ecarin clotting time
  3. Dose is 1mg/kg bolus followed by a 2.5mg/kg/hr infusion
  4. Metabolized by proteolytic enzymes present in the blood and by the kidneys. Therefore, minor dose adjustments are necessary for patients with renal insufficiency.
  5. Widely used in percutaneous coronary intervention, even in patients without HIT
61
Q

How does protamine work? What is the normal dose?

A

Protamine is a naturally occurring polypeptide with multiple cationic sites, a “polycation” that binds and inactivates heparin.

Recommended dose range of protamine for heparin reversal is 1-1.3mg protamine/100U of heparin

62
Q

Why must Protamine be administered slowly

A

to prevent hypotension

63
Q

Describe the 3 types of protamine reactions

A
  1. Type I reaction - results from rapid administration resulting in decreases in both systemic and pulmonary arterial pressures, decreased preload, and will experience hypotension
  2. Type II reaction - is immunological and is categorized as: IIA = anaphylaxis, IIB = anaphylactoid, IIC = non-cardiogenic pulmonary edema
  3. TYPE III reactions - are caused by heparin/protamine ionic complexes that can adhere in the pulmonary circulation and cause pulmonary vasoconstriction. This results in catastrophic pulmonary hypertension and resultant right heart failure.
64
Q

What are 4 alternatives to protamine

A

PLATELET FACTOR 4
METHYLENE BLUE
HEPARINASE
HEXADIMETHRINE (no longer used in USA bc of renal toxicity)

65
Q

How does the Hemochron ACT machine work

A
  1. is an automated variation of Lee-White clotting time
  2. Uses activator (celite or kaolin) to activate clotting, then measures the clotting time in a test tube or cartridge
  3. Normal baseline levels = 80-140 sec
    Adequate for CPB = 400-480sec
    OPCAB = >300sec (partial heparination)
  4. ACT is altered by hemodilution and hypothermia, as a result ACT levels do not correlate with heparin concentration nor with anti-factor Xa activity
66
Q

How does the Hepcon ACT machine work

A
  1. Uses protamine titration assays to determine blood heparin level.
  2. Can also provide a dose-response curve for an individual patient and how much heparin to administer in order to reach a target ACT prior to CPB
67
Q

High Dose Thrombin Time (HiTT) test - measures the conversion of fibrinogen to fibrin by thrombin. Unlike an ACT- HiTT is not affected by (3)

A

A) hemodilution
B) hypothermia
C) aprotinin

68
Q

How does THROMBOELASTOGRAPHY (TEG) work?

What do the R, K, alpha angle, and MA represent?

A

Measures the viscoelastic properties of blood as it is induced to clot under a low shear environment resembling sluggish venous flow
R= clotting time from start of test to the initial fibrin formation
K=speed to reach a specific level of clot strength
Alpha=acceleration (kinetics) of fibrin build up and cross-linking (clot strengthening)
MA=highest point representing the ultimate strength of the clot

69
Q

What are 4 causes of bleeding after CPB

A

A) platelet dysfunction
B) Hemodilution
C) Protein Activation/Consumption
D) Fibrinolysis

70
Q

Thrombocytopenia following CPB is due to (3)

A
  1. Hemodilution
  2. Platelet consumption
  3. Platelet Sequestration
71
Q

What is the is the main hemostasis defect during CPB. This is caused by: (6)

A 
Platelet dysfunction 
1. Contact with extracorporeal surfaces
2. Hypothermia
3. Down-Regulation receptors
4. Exposure to heparin
5, Exposure to protamine
6. Patients on antithrombotic medications preoperatively
72
Q

Contact of blood with CPB circuit results in SIRS, which has many components of activation, which are: (6)

A
  1. Kallikrein-Bradykinin system
  2. complement system
  3. Intrinsic pathway
  4. extrinsic pathway
  5. Common pathway
  6. Fibrinolysis
73
Q

What other condition can SIRS cause

A

may cause disseminated intravascular coagulation (DIC) by aggravating consumption factors

74
Q

HEPARIN REBOUND May be observed after adequate reversal of heparinization. May be explained by: (2)

A
  1. Redistribution of protamine to the peripheral compartments
  2. Peripherally bound heparin to the central compartment
75
Q

Hypothermia causes impaired hemostasis due to (5)

A
  1. Sequestration of platelets
  2. Transient platelet dysfunction
  3. Activation of a specific heparin-like inhibitor of Xa
  4. Slowing of enzymatic reactions involved in the coagulation cascade
  5. Accentuation of fibrinolysis
76
Q

How do antifibrinolytic work? Name 2 and the doses

A

produces a structural change preventing the conversion of plasminogen to plasmin

  1. £- aminocaparoic acid (EACA) 100-150mg/kg bolus
  2. Tranexamic acid (TA)10-50mg/kg bolus
77
Q

How does APROTININ work

A

A serine protease inhibitor

-inhibitis the formation of factor XIIa. As a result, both the intrinsic pathway and fibrinolysis are inhibited.

78
Q

How does DESMOPRESSIN work? what does it treat

A

releases Von Willebrand factors (VWF) from normal endothelial cells and is used in treatment of hemophilia.
3) Factor VIII coagulant activity increases 2 to 20 fold in addition to an increase in factor XII levels

79
Q

With a bleeding patient, the Platelets should be maintained above?

A

100K

80
Q

Depletion of clotting factors should be treated with?

A

FFP

81
Q

Depletion of fibrinogen should be treated with?

A

Cryo

82
Q

what is Recombinant factor VIIa

A

vitamin K-dependent glycoprotein that promotes hemostasis by activating the extrinsic pathway.

83
Q

With arterial cannulation, Pressure gradients greater than 100mmHg can cause?

A

excessive hemolysis

84
Q

If the aorta is too calcified to cannulate- what is the alternative spot?
If the fem artery is too calicied to cannulate- what is the alternative spot?

A

Fem Artery

Subclavian or Innominate

85
Q

How do you cannulate a porcelain aorta

A

minimization of aortic handling such as OPCAB or DHCA may be appropriate

86
Q

when is peripheral cannulation most commonly used (4)

A
  1. Redo-sternotomy
  2. Aorta not suitable for cannulation due to calcification
  3. Aortic aneurysm
  4. Minimally invasive surgery
87
Q

name 4 benefits of axillary canulation

A
  1. If patient has an Ascending Aortic Dissection - to avoid the risk of inadvertent retrograde perfusion into the false lumen of the dissection which can occur with femoral cannulation
  2. :ess likely than the femoral artery to have atherosclerotic disease or dissection
  3. Has good collateral flow, with less risk of limb ischemia
  4. Provides antegrade flow with reduced risk of cerebral embolization
88
Q

The degree of venous drainage is determined by: (3)

A
  1. The patient’s central venous pressure,
  2. The difference in height between the patients thorax and the top of the blood level in the venous reservoir
  3. The resistance exerted by the circuit (cannulae, lines, connectors)
89
Q

CVP is influenced by: (2)

A
  1. Intravascular volume

2. Venous compliance

90
Q

What can excessive drainage cause

A

can cause the veins to collapse around the cannulae, with intermittent reduction in drainage, with the potential for generation of gaseous emboli in the circuit; a phenomenon called cavitation.

91
Q

what fraction of blood is drained by the SVC and IVC

A

SVC 1/3

IVC 2/3

92
Q

Why are Snares are placed around vessels with Bicaval cannulae? (3)

A
  1. Patient’s entire venous return flows into the CPB circuit
  2. Air doesn’t get into venous line when RA is opened
  3. Blood doesn’t leak past cannulae and enter into the RA
    * This is referred to as caval occlusion or total CPB and is the technique of choice if right heart is to be opened.
93
Q

What are some averse effects of cardiotomy suction

A

Blood from the field is highly activated with regards to:

  1. Coagulation factors
  2. Fibrinolytic mediators
  3. Leukocytes
  4. Platelets

It is a major source of:

  1. Hemolysis - major contributor amount of air co-aspirated
  2. Microparticles
  3. Fat
  4. Cellular aggregates
  5. Inflammatory mediators (tumor necrosis factor alpha, IL-6, C3a, endotoxins)
  6. Platelet injury
  7. Platelet loss
94
Q

Oxygen capacity formula

A

1.34x Hb + 0.003 x PO2

95
Q

Oxygen content formula

A 
CaO2= 1.34 x Hb (SaO2) + .003 x PaO2
CvO2= 1.34 x Hb (SvO2) + .003 x PvO2
96
Q

Oxygen transfer formula

A

(SaO2-SvO2 x 1.34 x Hb x Q(L/min))/100

97
Q

INDICES OF ADEQUATE TOTAL PERFUSION ARE (3)

A
  1. PH
  2. Lactate
  3. SvO2 (hemoglobin oxygen saturation in venous blood)
    - a low SvO2 during CPB indicates an imbalance between DO2 and VO2
98
Q

Inadequate perfusion can be due to: (5)

A
  1. Insufficient pump flow
  2. Insufficient HCT
  3. Hemoglobin oxygen saturation
  4. Inadequate anesthesia
  5. Increased temperature
99
Q

Research supports: adults at normothermia to have a minimum flow index of ?

A

1.8 L/min/m2

100
Q

An acceptable MAP is that which provides adequate tissue perfusion

  • Adequate tissue perfusion is influenced by: (2)
  • MAP is determined by: (2)
A

Adequate tissue perfusion is influenced by:

  1. Pump Flow
  2. Core body temperature

MAP is determined by:

  1. Flow rate
  2. Arteriolar resistance
101
Q

In general, higher pressures should be maintained in the presence of known: (5)

A
  1. Cerebrovascular disease
  2. Carotid stenosis
  3. Renal dysfunction
  4. Coronary disease
  5. Left ventricular hypertrophy
102
Q

ON Commencement of CPB, there is a drop in systemic vascular pressure due to : (2)

However as CPB continues, there is a progressive increase in SVR pressure due to: (5)

A
  1. decrease viscosity
  2. Systemic inflammatory response syndrome (SIRS)
  3. equilibration of fluid between vascular and tissue compartments causing
  4. Hemoconcentration from diuresis
  5. Urination
  6. Increase in blood viscosity seen with hypothermia
  7. Progressive increase in circulating levels of catecholeamines and renin as part of the stress response of CPB
103
Q

Pulmonary artery and Left Atrial Pressure should be close to _____ while on CPB

  • Useful during CPB to monitor left ventricular distension particularly in cases where increased back flow to the left heart is expected, such as (3)
    1. Cyanotic heart disease
    2. Large bronchial flow in chronic lung disease
    3. Aortic regurgitation
A

Zero

  1. Cyanotic heart disease
  2. Large bronchial flow in chronic lung disease
  3. Aortic regurgitation
104
Q

Central Venous Pressure on bypass is expected to be close to zero and no more than in single digits. An increase in CVP indicates impaired venous drainage to the reservoir. Increased CVP due to: (3)

A
  1. Cannula size to small
  2. Obstruction of venous line or cannula tip
  3. Insufficient height difference between patient and reservoir
105
Q

What is the consequence of an increase in CVP during bypass? If the CVP is persistently high and uncorrected, what should be done?

A

Reduced effective perfusion of critical organs which results in edema. The liver is particularly sensitive to reduced flow as nearly 3/4 of hepatic blood flow occurs at near venous pressure
If persistently high CVP is uncorrected, patient’s head and eyes should be observed for signs of engorgement and consideration given to altering the venous cannula to improve drainage

106
Q

Following removal of the aortic cross clamp and resumption of myocardial activity, persistent ST segment changes may be related to ischemia from (2)

A
  1. Inadequate re-vascularization
  2. Coronary ostial obstruction
    * incorrectly seated aortic valve
    * air/particulate embolization
107
Q

What is the principle reason for hypothermic CPB

A

to protect the heart and other organs by reducing metabolic rate and therefore, oxygen requirements

108
Q

In the myocardium, hypothermia does what: (3)

A
  1. Sustains intracellular reserves of high-energy phosphates
  2. Preserves higher intracellular pH
  3. Preserves electrochemical neutrality
109
Q

Is Systemic hypothermia uniform

A

Systemic hypothermia is NOT uniform due to different blood flow to different vascular beds
*High blood flows and slower cooling ensures less variation in systemic hypothermia

110
Q

What is the goal of rewarming

A

to achieve uniform normothermia - vasodilators can be used to promote more uniform rewarming by distributing greater blood flow and therefore heat from the core to peripheries

111
Q

Avoid rapid changes in temperature or excessive blood temperatures - which can result in: (4)

A
  • microbubble formation due to reduced solubility of gases in blood as temperature increases
  • denaturing of plasma proteins
  • hemolysis
  • cerebral injury
112
Q

What 3 things should you do upon rewarming

A
  1. Increase flows to warm patient faster and to provide more oxygen to patient by blood passing through oxygenator more times a minute
  2. Increase FiO2 to provide more O2 as consumption and metabolism increases
  3. Increase sweep to remove increased levels of CO2 produced from patients metabolism increasing from rewarming. At this period you may see a rapid drop in SVO2
113
Q

What is the max temp gradient? what temps are observed? what are the target temps?

A

A gradient of 10 Celsius between water temp in heater cooler and arterial blood should not be exceeded

Patient should be rewarmed using arterial blood temperature and patient core temperature as guides to the rate and extent of rewarming. The target arterial blood temperature is between 37.5 and 38 degrees Celsius

114
Q

FOR EVERY 1 degree drop in temperature, what is the associated drop in oxygen demand ?

A

FOR EVERY 1 degree drop in temperature, there is an associated 7% drop in oxygen demand

For example, a 7 degree reduction in temperatures, results in a 50% drop in oxygen demand

115
Q 
HYPOTHERMIA TEMPERATURE 
Normothermic:
Mild:
Moderate:
Deep:
Profound:
A 
Normothermic: 36-37
Mild: 32-35
Moderate: 28-31
Deep: 18-27
Profound:
116
Q

Hypothermia is used as a technique in order for flows to be safely reduced. Too high a flow at a reduced temperature may: (4)

A
  1. Cause blood damage
  2. Impede the surgery by flooding the field
  3. Cause an excessive rise in venous pressure
  4. Cause warming of the heart when cardioplegia has been used
117
Q

Indications for diuretic use during CPB include: (3)

A
  1. Hyperkalemia - treated with furosemide
  2. Hemoglobinuria - treated with mannitol which generates alkaline urine
  3. Hemodilution
118
Q

Metabolic acidosis during CPB is almost always the result of ?

A

hypoperfusion leading to oxygen delivery inadequate to meet metabolic demands for aerobic respiration

119
Q

VO2 is reduced by approximately ___ for every ___ degree Celsius reduction in the core temperature below normothermia

A

VO2 is reduced by approximately 50% for every 7 degree Celsius reduction in the core temperature below normothermia
30 degrees = 50%
23 degrees = 25%
16 degrees = 12.5%
decrease of metabolic demand of the same organ at 37 degrees Celsius

120
Q

describe how hypothermia effects left and right shifts for the OXYHEMOGLOBIN DISSOCIATION CURVE

A

Left shift = at colder temp, hemoglobin has a greater affinity for binding O2 and is also released less readily

Right shift = at warmer temp, hemoglobin has a weaker affinity for binding O2 and is also released more readily

121
Q

DHCA dramatically lowers the body’s metabolic demand while protecting organs, particularly the brain during a period in which perfusion is suspended

This technique utilizes profound hypothermia, with or without the use of aortic cross clamping and delivery of cardioplegia, to facilitate surgery to the: (4)

A
  1. Left ventricular outflow tract
  2. Aortic valve
  3. Ascending aorta
  4. Great Vessels
122
Q

describe Alpha Stat management

A
  1. Arterial gas samples are NOT corrected for sample temp and the resulting acidosis remains untreated during cooling
  2. Benefits: maintains function of intracellular enzyme systems and preserves cerebral autoregulation
123
Q

describe pH Stat management

A
  1. Arterial gas samples are temp corrected and CO2 is added to the gas inflow of the CPB circuit so that the PCO2 and hence the pH is corrected to the same levels as during normothermia. Meaning this approach increases the total carbon dioxide content of the blood as the temp falls in order to maintain fixed temperature-corrected pH values.
  2. benefits: results in cerebral vasodilation (hence higher levels of O2 to the brain and enhanced distribution of blood flow)
124
Q

At what temperature does the differences in Alpha Stat and pH Stat become profound

A

25C

125
Q

what is the most common electrolyte disturbance during CPB

A

K+

126
Q

name 6 ways to lower K+ levels

A 
A) insulin and dextrose
B) bicarbonate
C) Calcium
D) Hyperventilating
E) Z-buff "zero balance hemofiltration"
F) Lasix 20-40mg
127
Q

how does temperature effect K+ levels

A

Colder temp = potassium stays intracellularly

Warmer temp = potassium exit the cells

128
Q

name 3 ways to lower Ca++ levels

A

A) Hemodilution
B) Chelation by preservatives in bank blood
C) Hemofiltration

129
Q

name 2 ways to lower magnesium sulfate levels

A

A) hemofiltration

B) high volume diuresis (particularly loop diuretics)

130
Q

Hyperglycemia is associated with poor patient outcomes. Specifically perioperative hyperglycemia has been associated with higher incidences of: (3)

A

A) Mediastinitis
B) Wound Infections
C) Neurocognitive deficits

131
Q

Define sieving coefficient

A

measure of hemofilter efficiency and is directly elated to solute molecular size
- Solutes with weights of 20,000 Daltons are unable to pass through the hemofilter pores. (Hgb, RBC, plasma proteins, clotting factors)

132
Q

whats the difference btwn hemofiltration and dialysis

A

The hemofilter workes by transmembrane pressure (TMP) or hydrostatic pressure differential and not by osmotic pressures. Hemodialysis works by osmotic pressures which creates separation of solutes and fluids

133
Q

Name 3 ways to increase hemofiltration

A
  1. Increase flow
  2. Suction
  3. clamping outflow of hemofilter forcing more fluid out of the effluent line
134
Q

what is a normal transmembrane pressure for a hemofilter

A

100-500 mmHg

135
Q

What happens if the heart continues to beat during aortic cross clamping

A

intracellular depletion of high-energy phosphates ensues and results in impaired recovery of function.

136
Q

Damaged myocardium causes the release of these chemical markers: (2)

A
  1. Troponin

2. Creatine phosphokinase

137
Q

The clinical manifestations of myocardial damage may present as low cardiac output syndrome due to: (4)

A
  1. Impaired myocardial contractility
  2. Dysrhythmias
  3. Decreased ventricular compliance
  4. Segmental myocardial wall motion abnormalities
138
Q

How much K+ is needed to arrest the heart

A

The essential requirement for attainment of rapid diastolic cardiac arrest is 20-40mEq/L of Potassium, which causes membrane depolarization.

139
Q

Why is Magnesium Sulfate added to CPG solutions

A

helps stabilize myocardial membrane by inhibiting myosin phosphorylase, which protects ATP reserves for post-ischemic activity

140
Q

what the disadvantage of Hypothermic crystalloid cardioplegia

A

Inhibits the Na/K ATP pump which results in Myocardial Edema and consequent activation of platelets, leukocytes, and complement.

141
Q

when giving retro cpg and you are getting low flows and high pressures, what does that indicate

A

catheter is advanced too far and should be withdrawn slightly

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