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Perf Tech Exam 2 > Topic 11A > Flashcards

Topic 11A Flashcards

1
Q

Coronary blood flow (Qb) is determined by

A

hemodynamic factors such as perfusion pressure (P) and

coronary vascular resistance (R).

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2
Q

The delivery of oxygen (DO2) to the myocardium

(oxygen supply) is determined by two factors:

A

coronary blood flow (CBF)

oxygen content of blood (CaO2)

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3
Q

O2 delivery= [formula]

A

CBF * CaO2

where CBF = ml/min and CaO2= ml O2/ml blood

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4
Q

To assess myocardial protection it is imperative to

assess

A

myocardial function and O2 consumption

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5
Q

Oxygen demand is a concept closely related to

A

oxygen consumption

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6
Q

Oxygen consumption and demand are often used interchangeably although they are not equivalent because:
Demand=
Consumption=

A 
Demand = Need
Consumption= Actual amount of oxygen consumed per minute
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7
Q

Oxygen consumption will: regenerate

A

ATP used by membrane transport (Na+/K+- ATPase pump) and by Myocyte contraction and relaxation
(myosin ATPase)

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8
Q

ml O2/min per 100g (from small chart)
Cardiac state: Arrested Heart
Cardiac state: Resting heart rate “beating working”
Cardiac state: heavy exercise

A

Arrested Heart= 2
Resting heart rate “beating working”= 8
heavy exercise= 70

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9
Q

O2 consumption: ml/min per 100g
Temp: 37C
Beating non-working

A

5.5

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10
Q

O2 consumption: ml/min per 100g
Temp: 32C
Beating non-working

A

5.0

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11
Q

O2 consumption: ml/min per 100g
Temp: 28C
Beating non-working

A

4.0

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12
Q

O2 consumption: ml/min per 100g
Temp: 22C
Beating non-working

A

3.0

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13
Q

O2 consumption: ml/min per 100g
Temp: 37C
Fibrillating

A

6.5

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14
Q

O2 consumption: ml/min per 100g
Temp: 32C
Fibrillating

A

3.9

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15
Q

O2 consumption: ml/min per 100g
Temp: 28C
Fibrillating

A

3.5

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16
Q

O2 consumption: ml/min per 100g
Temp: 22C
Fibrillating

A

2.0

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17
Q

O2 consumption: ml/min per 100g
Temp: 37C
Arrested

A

1.0

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18
Q

O2 consumption: ml/min per 100g
Temp: 32C
Arrested

A

0.9

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19
Q

O2 consumption: ml/min per 100g
Temp: 28C
Arrested

A

0.4

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20
Q

O2 consumption: ml/min per 100g
Temp: 22C
Arrested

A

0.3

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21
Q

ml/min per 100g

organ: brain

A

3

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22
Q

ml/min per 100g

organ: kidney

A

5

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23
Q

ml/min per 100g

organ: skin

A

0.2

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24
Q

ml/min per 100g

organ: resting muscle

A

1

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25
Q

ml/min per 100g

organ: contracting muscle

A

50

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26
Q

There is a unique relationship between MVO2, coronary blood flow (CBF), and the extraction of oxygen from the blood (A-V O2 difference). This relationship is an application of the

A

Fick Principle

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27
Q

Fick Principle= [Formula]

A

MVO2= CBF * (CaO2 − CvO2)

  • CBF= coronary blood flow (ml/min)
  • (CaO2-CvO2) is the arterial-venous oxygen content difference (ml O2/ml blood).
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28
Q

If MVO2 Demands are NOT met the heart may be prone to

A

arrhythmias

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29
Q

Name 2 points during bypass the heart is prone to fibrillate?

A
  1. Cooling

2. Post cross clamp (post ischemic episodes)

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30
Q

how much blood flow through the SVC will you get if the IVC is not yet cannulated when you start going on bypass

A

1/3

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31
Q

consequences of fibrillating

A

Distension/Overfilling
Muscular/cellular damage
Starlings Curve

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32
Q

Cardiac Oxygen Consumption (MVO2) varies ____ during cardiac surgery using bypass

A

widely

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33
Q

MVO2 lowest levels at

A

when heart is arrested

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34
Q

MVO2 highest levels at

A

Shortly after weaning from bypass- Heart is repaying oxygen debt (catch up period-the heart needs time)

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35
Q

ischemia is when

A

oxygen delivery ≠ oxygen demand

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36
Q

An imbalance of oxygen delivery and demand leads to

A

ANAEROBIC metabolism and the production of lactic acid

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37
Q

Decreased intracellular pH decreases the

A

stability of the cellular and mitochondrial membranes

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38
Q

Decreased intracellular pH impairs the

A

Na –> K ATPase leading to calcium influx and calcium overload

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39
Q

ATP generated from AEROBIC metabolism is used

A

preferentially for myocardial contraction

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40
Q

anaerobically produced ATP is used for

A

cell survival and repair

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41
Q

Cardiac muscle extracts much more oxygen than other

organs… %

A

> 70%

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42
Q

Because cardiac muscle extracts more oxygen than other organs, an increased myocardial oxygen demand is met primarily by an…

A

increase in coronary blood flow

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43
Q

Coronary blood flow is dependent on the

A

transmural gradient

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44
Q

True Coronary Perfusion Pressure

CoPP= [Formula]

A

DBP-LVEDP

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45
Q

What parameter can we estimate LVEDP from?

A

Wedging the swan= PA wedge pressure

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46
Q

CPP normal value

A

60-80 mmHg

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47
Q

During cardiac arrest, CPP is one of the most …

A

important variables in achieving the return of spontaneous circulation (which is why CPR compressions are important > respirations)

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48
Q

A pressure gradient of _____ at a minimum may be necessary for survival

A

15 mmHg

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49
Q

On the waveform, at the aortic pressure dicrotic notch, coronary pressure is at its

A

highest

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50
Q

Minimize on going ischemia with

A

nitroglycerin

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51
Q

Wall tension increases MVO2 and increases

52
Q

Myocardial preconditioning=

A

Myocardium that has undergone one or more brief periods of ischemia may be better able to tolerate subsequent prolonged ischemia
-life style choices alter normal values- the body adapts and resets their own “normal” values”

53
Q

Pre-ischemic intervention includes

A

Minimize ongoing ischemia (i.e. NTG)
Prevent ventricular distension
Vent !!!!!!!!!!!!!!

54
Q

Myocardial preconditioning can be achieved by:

A

Ischemia
Drugs
•Bradykinin, nitric oxide, phenylephrine (neosynephrine), endotoxin, adenosine
•Sevoflurane, desflurane, isoflurane

55
Q

Cardiopulmonary bypass itself may override these

other methods and be the ___ preconditioning tool

A

“best”

56
Q

Why give cardioplegia

A

Cardiac quiescence
Bloodless field
Preservation of myocardial function
Induces myocardial hypothermia

57
Q

Four Main Objectives of Hypothermic Cardioplegia

are: (Know these)

A
  1. Immediate/sustained electromechanical arrest
  2. Rapid/sustained homogenous myocardial cooling
  3. Maintenance of therapeutic additives in effective
    concentrations
  4. Periodic washout of metabolic inhibitors
58
Q

History of Myocardial Protection: Pre-1955

A

Systemic hypothermia

59
Q

History of Myocardial Protection: 1955

A

Melrose
-advocated the use of high potassium solutions to induce cardiac quiescence. Caused permanent myocardial
injury.

60
Q

History of Myocardial Protection: 1956

A

Lillehei

-introduced retrograde cardioplegia.

61
Q

History of Myocardial Protection: 1973

A

Gay & Ebert

-reintroduced hyperkalemic arrest with lower potassium concentrations (<20 mmol), preventing permanent myocardial injury

62
Q

History of Myocardial Protection: 1979

A

Buckberg & Follette

-introduced blood 4:1 cardioplegia.

63
Q

Without cardioplegic arrest, irreversible ischemic injury to the myocardium would occur within

A

20 minutes

64
Q

When myocardial protection strategies are

used, ischemic injury can be prolonged to more than

A

4-5 hours without irreversible damage.

65
Q

Most cardioplegia strategies are based on arresting the heart with

A

high doses of potassium (But that is changing)

66
Q

Depolarization= potential becomes more

67
Q

Repolarization= potential becomes more

68
Q

Ion potential step 0:

A

Na+ channels open and more Na+ enters the cell- makes it more positive

69
Q

Ion potential step 1:

A

K+ channels open and K+ begin to leave the cell

70
Q

Ion potential step 2:

A

Na+ becomes more refractory so no more Na+ enters the cell. Ca++ influxes= plateau

71
Q

Ion potential step 3:

A

K+ continues to leave the cell, causes membrane potential to return to resting level- makes it more negative

72
Q

Ion potential step 4:

A

K+ channels close and Na+ channels rest. Extra K+ outside will diffuse away

73
Q

With a blood potassium of 8-10 mEq/L=

A

depolarization of the cell occurs and sodium rushes into the cell

74
Q

When the extracellular potassium is so high the cell

cannot repolarize and the sodium remains…

A

inside the cell.

•sodium gates do not reset: fast-gates remain open; slow gates remain closed

75
Q

As potassium washes out of the extracellular

space…

A

the cells can begin to repolarize

76
Q

Sodium arrest mechanism= Low sodium environment extracellular…

A

Disrupts Na+ gates and influx
•Because the extracellular sodium is low the cell
cannot depolarize.
•sodium gates disrupted

77
Q

Components of Myocardial Protection:

Route of delivery

A 
Antegrade
Retrograde 
Ostial
Via conduits
Integrated
78
Q

Components of Myocardial Protection

Composition of solution

A

Crystalloid
Blood
Microplegia

79
Q

Components of Myocardial Protection

Temperature

A

Warm
Tepid
Cold

80
Q

Components of Myocardial Protection

Delivery interval

A

Intermittent

Continuous

81
Q

Components of Myocardial Protection

Additives

A

Electrolyte
Pharmacologic
Metabolic

82
Q

Components of Myocardial Protection

Monitoring

A

Temperature

Myocardial pH

83
Q

Components of Myocardial Protection

Preparation for reperfusion

A

This may be underestimated…

84
Q

Single lumen catheters are sized by

85
Q

Multi-lumen catheters are measured by

A

french size

86
Q

French size and diameter are related how

A

directly;

Larger French=larger diameter

87
Q

Gauge and size are related how

A

inversely;

Smaller Gauge= greater diameter

88
Q

French= to determine diameter size (mm) divide by

89
Q

Gauge= to determine diameter size (mm)

90
Q

Antegrade Delivery Initial dose adults

A

~10-15 mL/kg

91
Q

Antegrade Delivery Initial dose peds

A

Up to 30mL/kg

92
Q

Antegrade delivery: Keep in mind that if blood

cardioplegia is used, a 1000 mL dose would only be ____ mL of crystalloid at a ratio of 4:1.

93
Q

Antegrade delivery Subsequent doses=

A

less in volume and in potassium concentration than the arresting dose

94
Q

Antegrade delivery: Line pressure depends on the pressure drop in mmHg- the goal is to maintain root pressure of

A

50-100 mmHg

95
Q

Antegrade delivery: Flow is generally

ml/min) and (ml/min/m2

A

250-400 mL/min

150 ml/minute/m2

96
Q

Antegrade Delivery

•Benefits

A 
Easy
Physiological flow pattern
Quick arrest
Appropriate distribution to the right and left heart.
Root is tolerant of higher pressures
97
Q

Antegrade Delivery

• Disadvantages

A

Requires competent aortic valve
Poor distal perfusion in diseased arteries
Poor subendocardial perfusion (especially in LVH)

98
Q

Retrograde cardioplegia is given into the

A

coronary sinus and must be vented out of the heart

99
Q

Retrograde delivery: A balloon is inflated on the cannula that provides two functions

A

Prevents back flow

Holds cannula in place

100
Q

Retrograde Delivery: flow is

A

~ 150-200 mL/min

101
Q

Retrograde Delivery: Flow should be titrated to maintain a coronary sinus pressure

102
Q

Retrograde Delivery: benefits

A

Ideal for aortic valve regurgitation
Good distal perfusion of obstructed arteries
Good subendocardial perfusion
Retrograde flushing of emboli–augments de-airing
Does not impede conduct of case-can run continuously (ie, warm)

103
Q

Retrograde Delivery: disadvantages

A

Catheter placement can be difficult
Impaired right heart protection
Right coronary veins drain into the right atrium
Surgical skill required for placement of cannula
Distracting to perfusionist
Possible coronary sinus rupture

104
Q

Direct Ostial Delivery is Not as common as

A

antegrade or retrograde

105
Q

Direct Ostial Delivery=

A

held cannula directly perfuse ostia

106
Q

Direct Ostial Delivery: how much circuit pressure is required

A

250 mmHg

high pressures due to small cannula orifice

107
Q

Direct Ostial Delivery: flow seen on delivery=

A

50-150 mL/min

Variable with disease and technique

108
Q

Direct Ostial Delivery: Normal perfusion is ___% of cardiac output

109
Q

Vein graft cardioplegia: Doing ____ anastamosis first allows VG cardioplegia to be given

110
Q

Vein graft cardioplegia: Infusion pressure of

111
Q

Vein graft cardioplegia: Flow rate of

A

50-100 mL/min

112
Q

Vein graft cargioplegia: allows the surgeon to check the

A

anastomosis and adequacy of flow, and also allows flow to previously underperfused areas.
• Surgeon may use hand-held syringe

113
Q

Vein graft cargioplegia: Benefits

A
  • Allows antegrade protection of areas of coronary artery disease
  • Obviates limitations from aortic insufficiency and coronary artery disease
  • Allows delivery without need to pressurize aortic root or interrupt surgery
114
Q

Vein graft cargioplegia: Disadvantages

A

Requires graft placement
Complexity
Distribution only to those areas perfused by graft

115
Q

Integrated Combined Delivery: It is common to give a large arresting dose of antegrade cardioplegia ____ L, followed by a smaller dose of retrograde cardioplegia ____ L

A

1-1.5 L

0.5

116
Q

Integrated Combined Delivery: Using this technique, you are more likely to perfuse

A

all areas of the heart

117
Q

Integrated Combined Delivery: benefits

A

Benefits of all methods utilized

118
Q

Integrated Combined Delivery: disadvantages

A

Complexity

lots of cricket clamps for a surgeon

119
Q

Flow Rate and Cardioplegia:Direct Measurement=

A

Measured directly at the site

120
Q

Flow Rate and Cardioplegia:Calculated Measurement=

A

Pressure drop calculation

121
Q

Flow Rate and Cardioplegia: Flowing blindly is

A

NOT a good thing

122
Q

Pressure Drop increases proportionally to

A

to shear forces

123
Q

frictional forces do what to resistance

A 
increase resistance
(small cannula = increased R)
124
Q

The main determinants for pressure drop are

A

velocity and viscosity

125
Q

High flow velocities and fluid viscosities result in a

A

larger pressure drop

126
Q

Low velocity will result in

A

lower pressure drop

Perf Tech Exam 2 (3 decks)

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