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Anesthesia based on Nebuchanedzzer II > Basic - Cardiology/Heme > Flashcards

Basic - Cardiology/Heme Flashcards

1
Q

How do diuretics (ie. furosemide) affect the frank starling curve (Cardiac output vs EDV)?

A

reduces cardiac filling pressures along the same ventricular function curve

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2
Q

What does the frank-starling curve represent?

A

how the contractile force of the myocardium (stroke volume or cardiac output) is dependent on the sarcomere length (diastolic filling volume or preload) immediately before contraction

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3
Q

Summary of cardiovascular system changes with aging: (4)

A
  1. Decreased ventricular compliance
  2. Decreased beta-receptor responsiveness
  3. Increased SNS activity
  4. Increased stiffness of large arteries
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4
Q

In pts with reduced diastolic function, LVEDP is (increased/decreased), and preload is more dependent on _____

A

Increased (elevated)

Atrial kick

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5
Q

Complete heart block (aka third degree heart block) is associated with ischemia involving the ______artery and typically involves the ________

A

RCA
PDA supplying the Inferior wall of the LV

*ischemia of LAD will damage the distal conducting system (bundles branches, purkinje system)

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6
Q

in 85% of patients, the ____ branches off the Right Coronary artery and supplies the _____

A

posterior descending artery (PDA)

posterior 1/3 of the interventricular septum and posteromedial papillary muscle

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7
Q

The supply of the SA node does not depend on coronary dominance (like the PDA is), the SA node is supplied by the RCA in __% of patients, and LCA in __%

A

RCA 60%

LCA 40%

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8
Q

The L main artery gives rise to ____.

Does it supply the AV node?

A

L circumflex
LAD

No

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9
Q

What does the LAD supply?

A
  1. Anterior wall of the heart
  2. Interventricular septum
  3. Bundle branches
  4. Purkinje system

*blockage of the LAD will not cause complete heart block

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10
Q

What does the L circumflex artery supply?

A

The posterior and lateral walls of the LV

- in 15% it also supplies the PDA (L dominant)

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11
Q

Treatment for hemophilia A?

A

Factor VIII
Desmopressin

*FFP not recommended bc it poses infxn risk and lg volumes are needed

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12
Q

Factor VIII levels have to decrease < __% to alter hemostasis.

A

30%.
- During surgery, pts with hemophilia A are advised to have factor VIII activity lvl of 30-40% for mild hemorrhages and 50% for severe hemorrhages

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13
Q

what blood products contain factor VIII?

A

FFP and cryoprecipitate

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14
Q

Treatment for hemophilia B?

A

Recombinant factor IX

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15
Q

Treatment for hemophilia C?

A

supportive

- Deficiency is from Factor XI, but there is a high risk of thrombotic events

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16
Q

Nitroglycerin MOA

A

direct acting venodilator via activation of cGMP production

- added benefit of coronary vasodilation

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17
Q

How do carvedilol and nicardipine affect preload?

A

minimal effect on preload

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18
Q

Carvedilol MOA

A

nonselective BB
- acts on SNS to slow heart

alpha blocking

  • modest vasodilation
  • minimal effect on preload
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19
Q

Nicardipine MOA

A

CCB

  • ARTERIOLOAR vasodilation -> decreases afterload and SVR
  • minimal effect on preload
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20
Q

Sodium nitroprusside MOA

A

direct acting vasodilator via conversion to nitric oxide in vascular smooth muscle -> increase cGMP levels

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21
Q

How does hyperventilation increase the risk of citrate toxicity?

A

It decreases ionized calcium ions (think perioral tingliness when people hyperventilate)
- Citrate toxicty is actually d/t HYPOcalcemia (citrate binding with calcium)

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22
Q

Signs of citrate toxicity?

A

Same as hypocalcemia

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23
Q

Citrate toxicity is highest when which blood product is given?

A

FFP

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24
Q

What does FFP contain?

A
  1. All clotting factors,
  2. fibrinogen
  3. plasma proteins (albumin),
  4. electrolytes,
  5. physiologic anticoagulants (C, S, antithrombin)
  6. added anticoagulants (citrate)
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25
Q

What is the primary mech behind delayed hemolytic transfusion reaction (DHTR)?

A

Donor red cell antigens

  • Typically the recipient was already exposed to antigens through prior transfusion or pregnancy
  • Recipient antibody and complement attack on donor cells
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26
Q

What is the primary mech behind acute hemolytic transfusion reactions?

A

ABO incompatibility

  • (recipient antibody and complement attack on donor cells)
  • Fatal
  • Most often d/t clerical error
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27
Q

Signs of acute hemolytic transfusion reactions when pts are awake vs under GA?

A

Awake
- Fever, chills, CP, N/V

GA
- Hemoglobinuria, bleeding diathesis, hypotension

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28
Q

What is the primary mech behind febrile transfusion reactions?

A

Donor cytokines and antibodies reacting to recipient leukocyte antigens

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29
Q

What is the primary mech behind Graft vs host disease (GVHD)?

A

lymphocytes in donor blood reacting against recipient tissues

  • recipient is unable to reject the donor lymphocyte bc of immunodeficiency or immunosuppression
  • irradiated blood can decrease risk
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30
Q

Leading cause of death related to blood transfusions

A

1) transfusion related acute lung injury (TRALI) 55%
- noncardiogenic pulmonary edema

2) Hemolytic transfusion reaction (22%)
- Non-ABO > ABO

3) Infection

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31
Q

Diagnostic criteria for TRALI (4)

A
  1. Sudden onset hypoxemia (< 6 hours from last blood product)
  2. B/l “fluffy” infiltrates on CXR
  3. No appreciable change in cardiac filling pressures or increased L atrial pressures
  4. All other etiologies for ALI r.o
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32
Q

What is NOT a good treatment for TRALI

A
  1. diuretics
    - this is a noncardigenic pulmonary edema: will worsen hypotension
  2. Corticosteroids
    - avoid just like in ARDS

*Lung protective ventilation strategies are safe. Most pts require ventilatory support, IV fluids, and vasopressors.

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33
Q

What is the primary mech behind TRALI?

A

anti-granulocyte antibodies from donor -> attack activated recipient leukocytes sequestered in lungs -> pulmonary inflammatory response

*P:F ratio typically 200-300mmHg

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34
Q

Hyperkalemia EKG findings

A
  1. Widening of QRS complex

2. Peak T waves

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35
Q

The R wave should be small in lead V1. Throughout the precordial leads (V1-V6), the R wave becomes larger — to the point that the R wave is larger than the S wave in lead V4.
Name Disorders associated with large R wave in lead V1

A
  1. right bundle branch block
  2. Wolff-Parkinson-White syndrome
  3. Posterior wall MI
  4. R atrial enlargement/RVH
  5. Duchenne muscular dystrophy
    - isolated posterior wall hypertrophy
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36
Q

What does cryoprecipitate contain?

A
  1. vWF
  2. Fibrinogen
  3. Fibronectin
  4. Factor VIII
  5. Factor XIII
  6. Factor C

*does NOT contain VII

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37
Q

According to ACC/AHA guidelines for pts undergoing PCI for ischemic heart disease, what is the rule for perioperative dual antiplatelet therapy?

A

BMS:

  • DAPT for 1 month after stent placement
  • only ASA in periop period

DES:

  • DAPT for 6 months
  • think des for 6
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38
Q

Normal pulmonary artery pressure? What is it elevated in?

A

6-12mmHg

CHF

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39
Q

When should perioperative beta blockers be started on patients preoperatively (but not the day of surgery)?

A

If they have 3/more risk factors for CAD

  • h.o ischemic Heart disease
  • CHF
  • stroke
  • DM
  • CKD
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40
Q

Most sensitive lead for detecting MI?

A

V5, when used alone

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41
Q

Why is lead II generally looked at on continuous ECG monitoring?

A

It gives the largest P wave

- good for rhythm change

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42
Q

What is the most sensitive combination for detecting ischemia on continuous ECG monitoring?

A

II + V4 (82%)
II + V5 (80%)

II + V4 + V5 = 90%

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43
Q

Ischemia criteria on ECG

A

ST segment depression (>1 mm)

  1. Slope of the segment must be horizontal or downsloping
  2. Commonly indicates endocardial ischemia

ST segment elevation (>0.1 mV in > 2 contiguous leads)

  1. Indicates transmural ischemia or reciprocal change in a lead oriented opposite to the primary vector with subendocardial ischemia
  2. Typically seen in cardiac surgery during wean from CPBG d/t disruption of coronary blood flow
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44
Q

Pts with prolonged K value (slope of angle) on TEG, would probably benefit from:

A

Cryoprecipitate
- remember it contains fibrinogen

  1. vWF
  2. Fibrinogen
  3. Fibronectin
  4. Factor VIII
  5. Factor XIII
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45
Q

Cryoprecipitate contains ____ mg/unit of fibrinogen. 10 units of cryo contains ____ mg of fibrinogen.

A

200mg/u

10u cryo = 2000mg

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46
Q

What is the benefit if receiving leukoreduced blood transfusions (eliminate donor leukocyte in blood)?

A

avoids transfusion-related immunomodulation (TRIM)
- proinflammatory and immunosuppressive effects in allogenic blood

Decreases risk of febrile transfusion reaction

*neg effects are almost all speculative

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47
Q

The only established clinical effect of transfusion-related immunomodulation (TRIM)

A

Enhanced survival of renal allografts

- found before potent immunosuppressive regimens were done

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48
Q

Most common complication following autologous blood transfusion?

A

Infection d/t improperly stored blood

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49
Q

Why can autologous blood be beneficial?

A

does not contain non-self antigens to trigger allogenic hemolytic/nonhemolytic reactions

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50
Q

Storage of pRBCsis associated with what changes in:

  • 2,3 DPG
  • pH
  • CO2
  • K
A

during storage, erythocytes remain metabolically active (anaerobic)

Decrease in:

  • 2,3 DPG
  • pH

Increase in:

  • CO2
  • K (moves out of pRBC to maintain electroneutrality w. H+ generated during anaerobic metabolism)
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51
Q

Normal Central venous pressure (CVP)

A

4-6

  • BP in the vena cava, near the RA
  • if CVP is high = overhydration
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52
Q

Formula for oxygen delivery (DO2)

A

CO * CaO2 * 10

CaO2 = arterial oxygen content

*notice that peripheral vasoconstriction does not increase DO2 bc it does not increase CO or CaO2

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53
Q

Formula for CaO2 (arterial oxygen content)

A
  1. 34 * hgb * SaO2 + (0.003 * PaO2)

* notice that PaO2 contributes relatively less to overall arterial oxygen content than CO, hgb, or SaO2

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54
Q

What does it mean when a blood is “screened”?

A
  1. Screen for unexpected antibody status mixing of pt red cells w/ commercial reagents that contain most clinically important RBC antigens implicated in hemolytic transfusion reactions
  2. Determine pt ABO status:
    - Mixing pt red cells with commercial type O RBCs for anti-A, anti-B, anti-AB, anti-D antibodies
  • if negative = pt can be safely transfused with ABO and Rh compatible blood
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55
Q

What does it mean when blood is “crossmatched”?

A

pts plasma and donor RBCs are mixed to determine compatibility and ensure no serious transfusion reaction

56
Q

Why is giving type O blood in a pt who has a positive antibody screen significant??

A

bc type O blood has both anti-A and anti-B ANTIBODIES

*it has no antigens

57
Q

Type AB blood has what antigens and antibodies?

A

A and B antigens
No antibodies
- can receive AB, A, B, and O blood

*universal recipient

58
Q

What type blood is the universal recipient and donor?

A

Universal recipient: AB blood

Universal donor: O blood

59
Q

Pts with IgA deficiency who receive blood transfusions are at increased risk of ____

A

allergic reaction to antigens in donor blood

- can be severe anaphylaxis or mild urticaria

60
Q

Thrombotic thrombocytopenic purpura (TTP) is a disorder of _____. And can benefit from which blood product?

A

platelet destruction

FFP

  1. All clotting factors,
  2. fibrinogen
  3. plasma proteins (albumin),
  4. electrolytes,
  5. physiologic anticoagulants (C, S, antithrombin)
  6. added anticoagulants (citrate)
61
Q

Which blood product is at substantially higher risk of contamination and transfusion associated sepsis?

A

Platelets

62
Q

Simple febrile reactions to blood products are usually d/t ____

A

antibodies that the host has formed against HLAs present on donor leukocytes
- febrile period is mild, short lived, tx with acetaminophen

63
Q

Which mechanism of epinephrine makes it a med of choice in Vfib?

A

ALPHA receptor mediated vasoconstriction
- increases coronary and cerebral perfusion pressure

*note that the beta response can increase myocardial work

64
Q

How does metformin cause lactic acidosis, which can be associated with a 50% mortality rate?

A

Metformin reduces the activity of pyruvate dehydrogenase and the transport of mitochondrial reducing agents
->
Increase anaerobic metabolism as pyruvate accumulates
-> gets converted to lactate

65
Q

Should metformin be continued in the periop period?

A

yes

66
Q

Lab test to monitor enoxaparin response

A

factor Xa activity

67
Q

LMWH is cleared by the ____.

A

kidney

68
Q

Unfractionated Heparin MOA

- Monitored by tracking ___

A

binds and enhances antithrombin III

  • inactivates thrombin (factor II), Xa, other factors in intrinsic pathway
  • monitor PTT
69
Q

Enoxaparin MOA

- Monitored by tracking ___

A

binds and enhances effects of AT3 through conformational change
- factor Xa

70
Q

Treatment of AT3 deficiency

A

Administer AT3 or FFP

71
Q

How does positive lusitropy affect LVEDP?

A

reduces it

72
Q

How does phenylephrine affect preload and afterload?

A

increases both

-alpha 1 receptor agonist

73
Q

How does phenylephrine affect stroke volume?

A

Depends

  • if pts are on steep portion of frank starling curve (volume dependent), they will have increase in SV d/t increase in preload
  • if pts are on flat portion of curve (volume independent), they will not have any increase in stroke volume from increase in preload, and the increase in afterload reduces further cardiac output
74
Q

Which blood products are stored frozen and are only thawed on demand?

A

FFP and cryoppt

- low risk of infxn

75
Q 
What the the normal values for:
Cardiac output
Cardiac index
Stroke volume
Stroke volume index
A

Cardiac output: 4-8 L/min
Cardiac index: 2.5 - 4.0
Stroke volume: 60-100mL/beat
Stroke volume index: 33-47

76
Q

The _____ reflex helps maintain arterial blood pressure through a negative feedback loop

A

baroreceptor reflex

77
Q

Which BB is metabolized by RBC esterases?

A

Esmolol

78
Q

Cardioselective BB mneumonic

A

BEAM

  • Bisoprolol
  • Esmolol
  • Atenolol
  • Metoprolol
79
Q

Carvedilol, Propanolol and labetalol targets which receptors since they are nonselective?

A

Carvedilol

  • B1
  • B2
  • A1

Propanolol

  • B1
  • B2

Labetalol

  • B1
  • B2
  • A1
80
Q

Which BB has minimal effects on pts with reactive airway disease? Where are they metabolized?

A

atenolol

  • kidneys
  • (ATNolol - ATN also affects kidneys)

metoprolol
- liver

81
Q

Nicardipine MOA

A

ARTERIOLAR vasodilator

- decreases BP primarily by afterload reduction (minimal effect on preload)

82
Q

Fenoldopam MOA

A

short acting dopamine receptor agonist

  • profound peripheral vasodilation via cAMP stimulation
  • reduces preload and afterload
  • stimulates diuresis and natriuresis (useful in stimulating kidney perfusion while simultaneously treating HTN)
83
Q

Nitroglycerin MOA

A

direct acting VENOUS vasodilator by activating cGMP

- added benefit of coronary vasodilation

84
Q

Sodium Nitroprusside MOA

A

direct acting ARTERIOLAR AND VENOUS vasodilator by increaing cGMP

85
Q

Nesiritide MOA

A

recombinant form of brain natriuretic peptide (BNP)

  • vasodilation
  • diuresis
  • natriuresis

*BNP is counter-regulatory to angiotensin II, norepi, and endothelin

86
Q

Nesiritide only current indication for treatment

A

acutely decompensated CHF

87
Q

What is defined as an “old” vs acute vs recent MI?

A

Old: occurred > 30 d ago

Acute: 7-30 d ago

Recent < 7 days ago

88
Q

What constitute active cardiac conditions?

A
  1. Unstable coronary syndrome
    - acute/recent MIs
    - unstable angina
  2. Decompensated HF
  3. Significant arrhythmias
    - high grade AV block (II/III)
    - uncontrolled supraventricular tachy (ie:afib) > 100bpm
    - symptomatic bradycardia
  4. Severe valvular disease
89
Q

Severe aortic stenosis:

  • peak vel
  • mean PG
  • AVA (cm2)
  • Indexed AVA
  • Vel ratio (DI)
A
  • peak vel: >4
  • mean PG: >40
  • AVA (cm2): <1
  • Indexed AVA: <0.6
  • Vel ratio (DI): < 0.25
90
Q

When do you use infective endocarditis abx prophylaxis in pts undergoing dental procedure?

A

Dental procedure must involve mucosal or gingival procedures

Pt has high risk cardiac condition:

  1. Prosthetic heart valve
  2. Previous endocarditis
  3. Congenital heart disease
    - only if its unrepaired, recently repaired, or repaired with residual defects
  4. Cardiac transplant recipient w/ valvular disease
91
Q

When do you use infective endocarditis abx prophylaxis in pts undergoing Respiratory tract procedures?

A

Respiratory procedures must be invasive and involve incision and biopsy of resp mucosa (ie: T+A, NOT bronchoscopy)

Pt has high risk cardiac condition:

  1. Prosthetic heart valve
  2. Previous endocarditis
  3. Congenital heart disease
    - only if its unrepaired, recently repaired, or repaired with residual defects
  4. Cardiac transplant recipient w/ valvular disease
92
Q

Milrinone MOA

  • how does it affect inotropy and vasculature?
  • How does it affect the frank starling curve?
A

PDE 3 inhibitor

  • improved inotropy
  • vasodilation
  • Leftward (Decreased EDV)
  • Upward (increased CO)
93
Q

Nicardipine and hydralazine

- How does it affect the frank starling curve?

A

They are vasodilators

- improved ventricular function (CO), while reducing cardiac filling pressures

94
Q

Factors that improve defibrillation

A
  1. Electrode gel
  2. Biphasic defibrillation
    - Low energy (200J)
  3. Larger electrodes
95
Q

Defibrillation vs cardioversion?

A

Defib: unsynchronized shock
- depolarizes entire myocardium

Cardioversion

  • Synchronized with QRS complex to deliver shock on R wave.
  • Avoids R on T phenomenon
96
Q

If a pts major adverse cardiac event (MACE) is >1%, what do you do next?

A

Check functional capacity

- if < 4 METS, obtain further study

97
Q

On the wiggers diagram, CVP tracing includes 3 waves (a, c, v) and 2 descents (x, y), what do they represent?

A

3 waves (a, c, v)

  • a: RA contraction
  • c: RV contraction
  • v: Filling of RA

2 descents (x, y)

  • x: emptying RV
  • y: passive emptying of RA
98
Q

On CVP tracing:

Cannon a wave is seen with _____.

Large cv-wave is seen with ____.

Large a-wave_____.

A

Cannon a wave is seen with AV dissociation.

Large cv-wave is seen with TR.

Large a-wave tricuspid stenosis.

________

  • a: RA contraction
  • c: RV contraction
  • v: Filling of RA
  • x: emptying RV
  • y: passive emptying of RA
99
Q

Ventricular hypertrophy (increases/decreases) wall tension

A

decreases
- increase in pressure or radius of the ventricle increases wall tension, so it compensates that increasing wall thickness, to decrease wall tension

*decreases wall tension, but becomes less compliant

100
Q

____ is the most imporatnt parameter regulating the myocardial oxygen supply demand relationship?

A

Heart rate

101
Q

Vasopressin acts on V1 receptors, which stimulates what?

A

water retention, peripheral vasoconstriction

  • -> increases SVR and afterload
  • -> improve MAP and cerebral and coronary perfusion
102
Q

Can vasopressin cause pulmonary vasoconstriction?

A

no, there are no V1 receptors in lungs

*epi and alpha-1 agonists can though

103
Q

The right ventricle is perfused during (diastole/systole)

A

both
- but receives greatest perfusion during peak/late systole, early diastole

*diff from LV that is perfused only during diastole

104
Q

_______ potentiates the effects and toxicity of digoxin.

A

Hypokalemia

- monitor K in pts receiving loop diuretics

105
Q

digoxin MOA

A

Inhibits Na-K ATPase
- increases intracellular Na [ ] –> inc intracellular Ca [ ]

Positive inotrope

106
Q

First line vasopressor in pts with a TBI, inc urine output, and hypotension

A

Vasopressin

- vasoconstrictor and ANTI-diuretic

107
Q

Why does ABO incompatible blood cause increase in bilirubin levels?

A

Incompatible transfused erythrocytes are rapidly destroyed -> hemolysis -> free hgb is metabolized to bilirubin (both indirect and direct bilirubin) will be elevated.

108
Q

During acute hemolytic transfusion reactions, what happens to PT/INR and PTT? Fibrinogen?

A

Both increase

*fibrinogen decreases

109
Q

Why is FFP generally transfused with pRBCs during MTPs?

A

in order to prevent development of dilutional coagulopathy

110
Q

What is myasthenia gravis d/t?

A

antibodies destroying post-synaptic ACh receptors

111
Q

Factors that decrease the release of ACh?

A
  1. Antibiotics (clindamycin, polymixin)
  2. Magnesium (antagonizes Ca2+)
  3. Hypocalcemia
  4. Anticonvulsants
  5. DIuretics (furosemide)
  6. Eaton-Lambert syndrome: inhibits P-type calcium channels
  7. Botulinum toxin: inhibits SNARE poteins
112
Q

Can Calcium channel blockers interfere with ACh release?

A

no
- it blocks L-type channels, not P-type calcium channels

*Lambert eaton inhibits P-type CC

113
Q

Both botulinum and tetanus toxin inhibits _____. Whats the difference?

A

SNARE proteins

Botulinum: affects peripheral nerves

Tetanus: affects CNS

114
Q

How much FFP do you need for warfarin reversal?

A

10-15mL/kg

115
Q

Warfarin MOA

A

inhibits vit K dependent coag factor synthesis in the liver (II, VII, IX, X)

1972

116
Q

What is warfarin induced skin necrosis d/t?

A

after warfarin initiation, there is an initial shift towards clotting
- protein C: half life of 6 hours

117
Q

What is P50?

A

Hgb molecule is 50% saturated with oxygen

- normally 27mmHg

118
Q

An increase and decrease in P50 affects hgb affinity for O2 how?

A

Increase P50:

  • decreases hgb affinity for O2, release O2 to tissues
  • Right shift

Decrease P50:

  • increases hgb affinity for O2
  • Left shift
119
Q

What is hetastarch (HES) made of?

A

6% hydroxyethyl starch
electrolytes
glucose
lactate

120
Q

How does hetastarch (HES) cause platelet dysfunction?

A

reduces availability of glycoprotein IIb-IIIa on platelets

121
Q

St. John’s wort is used to treat depression and

PMS. What are some negative side effects?

A

CYP3A4 inducer ->increased metabolism (decreased efficiacy) of digoxin, warfarin, cyclosporine, anticonvulsants

122
Q

What herbal supplements are linked to platelet dysfunction?

A
  1. Ginger
  2. GInko
  3. Garlic
  4. Vit E
123
Q

(FFP/PCC) is preferred to rapidly reverse warfarin?

A

PCC > FFP

  • PCC contains Vit K dep coag factors (II, VII, IX, and X)
  • more [ ], lower INR, rapid onset
124
Q

what are the physiological effects of acute normovolemic hemodilution (giving pt fluid, then take their blood and save for later)?

A
  1. decrease blood viscosity
  2. decrease peripheral vascular resistance
  3. increased cardiac output
  4. inc regional blood flow
125
Q

Timeframe for anaphylactic transfusion reaction vs TRALI (both manifest after blood products and can have increased pulmonary pressures)?

A

anaphylactic transfusion reaction: w/in 1 hr

TRALI: w/in 6 hours

126
Q

How does the content of dissolved gases (O2 and CO2) change with temperature?

A

It doesn’t, the partial pressure changes

- Ie: PO2 and PCO2 can change with temp, but O2 and CO2 content has not

127
Q

As pt temperature drops, what happens to pH, PaO2m PCO2?

A

pH will be higher
pCO2 will be lower
paO2 will be lower

128
Q

Maximum allowable blood loss equation

A

MABL = [EBV * kg * (starting Hct - target Hct)] / starting Hct

129
Q 
Estimated blood volume (mL/kg) for:
Premature infant: 
Full term newborn: 
Infant (3 mo-1yr): 
Child (1-12 yr): 
Adult Female: 
Male:
A 
Premature infant: 100  
Full term newborn: 85
Infant (3 mo-1yr): 75
Child (1-12 yr): 70
Adult Female: 60
Male: 70
130
Q

What is the only factor in FFP that is easily degraded (unstable) above 4C?

A

Factor VIII
- Factor V is next

*this is why FFP needs to be frozen for storage

131
Q

______ is the carrier molecule for factor VIII, which is ultimately activated by ___

A

vWF

IIa

132
Q

Why doesn’t FFP have a high risk for GvH or CMV transmission?

A

It doesn’t carry a sig quantity of viable leukocytes

133
Q

Laboratory evidence of Acute hemolytic transfusion rxn?

A

Hemolysis +

+ direct antiglobulin test

134
Q

What does a positive direct antiglobulin (Coombs) test confirm?

A

the presence of antibodies to the RBC components

- does not prove or disprove acute hemolytic rxn

135
Q

Diff betwn direct and indirect coombs test?

A

Direct:
- antibodies present against on RBC surface

Indirect:

  • free antibodies in blood against RBC
  • used in testing samples prior to blood transfusion and prenatal testing of pregnant women
136
Q

What is coronary steal phenomenon?

A

When meds that cause coronary vasodilation causes redirection of blood flow away from stenotic lesions (that are already maximally dilated), thus worsening ischemia

137
Q

What are surrogates for LVEDP?

A

PCWP
PAOP
LAP

Anesthesia based on Nebuchanedzzer II (38 decks)

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