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Perf Tech > Myocardial Protection and Cardioplegia Part 1 > Flashcards

Myocardial Protection and Cardioplegia Part 1 Flashcards

1
Q

Coronary blood flow (Qb) is determined by

A

hemodynamic factors such as perfusion pressure (P) and coronary vascular resistance (R).
• Q = P/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).
  • O2 Delivery = CBF × CaO2 where CBF = ml/min and CaO2 = ml O2/ml blood
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3
Q

To assess myocardial protection it is imperative to

A

assess myocardial function and O2 consumption.

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4
Q

Oxygen demand is a concept closely related

A

to the oxygen consumption.

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5
Q

Demand =

A

Need

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6
Q

Consumption =

A

Actual amount of oxygen consumed per minute.

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7
Q

Oxygen consumption will

A

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

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8
Q

arrested heart MVO2 (mlO2/MIN/100G)

A

2

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9
Q

resting heart rate MVO2 (mlO2/MIN/100G)

A

8

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10
Q

heavy exercise MVO2 (mlO2/MIN/100G)

A

70

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11
Q

brain (mlO2/MIN/100G)

A

3

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12
Q

kidney (mlO2/MIN/100G)

A

5

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13
Q

skin (mlO2/MIN/100G)

A

.2

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14
Q

resting muscle (mlO2/MIN/100G)

A

1

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15
Q

contracting muscle (mlO2/MIN/100G)

A

50

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16
Q

relationship between MVO2, coronary blood flow (CBF), and the extraction of oxygen from the blood (A-V O2 difference).

A

Fick Principle:

MVO2 = CBF × (CaO2 − CvO2)

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17
Q

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

A

arrhythmias

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18
Q

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

A

• Cooling • Postcrossclamp(postischemicepisodes)

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19
Q

Why am I worried about fibrillation?

A

• Distension/Overfilling • Muscular/cellular damage • Starlings Curve

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20
Q

lowest level MVO2 during bypass

A

When heart is arrested

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21
Q

highest level MVO2 during bypass

A

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

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22
Q

Ischemia is when

A

oxygen delivery ≠ oxygen demand

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23
Q

An imbalance of oxygen delivery and demand leads to

A

ANAEROBIC metabolism and the production of lactic acid.

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24
Q

Decreased intracellular pH

A

decreases the stability of the cellular and mitochondrial membranes.

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25
Q

Decreased intracellular pH also impairs

A

the Na -> K ATPase leading to calcium influx and calcium overload.

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26
Q

ATP generated from AEROBIC metabolism is used preferentially for

A

myocardial contraction

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27
Q

anaerobically produced ATP is used for

A

cell survival and repair

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28
Q

amount of O2 cardiac muscle extracts

A

> 70%

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29
Q

ncreased myocardial oxygen demand is met primarily by

A

an increase in coronary blood flow.

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30
Q

Coronary blood flow is dependent on

A

the transmural gradient:

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31
Q

True Coronary Perfusion Pressure. CoPP =

A

DBP – LVEDP. Not just a pressure drop across, it is perfusion throughout

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32
Q

What parameter can we estimate LVEDP from?

A

PAD

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33
Q

A diastolic aortic pressure of 80 and a LVEDP

pressure of 14 would leave a CPP

A

of 66 (normal 60-80 mmHg) calculation alert

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34
Q

During cardiac arrest, CPP is one of the most important variables in achieving

A

the return of spontaneous circulation

which is why CPR compressions are important > respirations

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35
Q

min. CPP necessary for survival

A

15 mmHg

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36
Q

Pre-Ischemic Intervention

A

Minimize on-going ischemia (i.e. NTG) • Don’t make it worse

Prevent ventricular distension Wall tension increases MVO2 and increases LVEDP Vent !!!!!!!!!!!!!! Don’t make it worse

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37
Q

Myocardial Preconditioning

A

Myocardium that has undergone one or more brief periods of ischemia may be better able to tolerate subsequent prolonged ischemia.

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38
Q

Myocardial preconditioning can be achieved by

A

• Ischemia • Drugs
• Bradykinin, nitric oxide, phenylephrine (neosynephrine), endotoxin, adenosine
• Sevoflurane, desflurane, isoflurane
Cardiopulmonary bypass itself may override these other methods and be the “best” preconditioning tool

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39
Q

Why give cardioplegia?

A

• Cardiac quiescence • Bloodless field • Preservation of myocardial function • Induces myocardial hypothermia

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40
Q

Four Main Objectives of Hypothermic Cardioplegia are:

A

• Immediate/sustained electromechanical arrest
• Rapid/sustained homogenous myocardial cooling
• Maintenance of therapeutic additives in effective concentrations
• Periodic washout of metabolic inhibitors
Hint: This would will make a good m/c question

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41
Q

History of Myocardial Protection • Pre-1955:

A

Systemic hypothermia

42
Q

History of Myocardial Protection 1955

A

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

43
Q

History of Myocardial Protection 1956

A

Lillehei introduced retrograde cardioplegia.

44
Q

History of Myocardial Protection 1973

A

Gay & Ebert reintroduced hyperkalemic arrest with lower potassium concentrations (<20 mmol), preventing permanent myocardial injury.

45
Q

History of Myocardial Protection 1979

A

Buckberg & Follette introduced 4:1 blood cardioplegia.

46
Q

Withoutcardioplegicarrest,irreversible ischemic injury to the myocardium would occur within

A

20 min.

47
Q

When myocardial protection strategies are used, ischemia can be prolonged to

A

more than 4-5 hours without irreversible damage.

48
Q

Most cardioplegia strategies based on arresting the heart with

A

high doses of potassium (But that is changing)

49
Q

ction potential can be disrupted

A

at different phases

50
Q

Mechanism of Depolarizing

Potassium Arrest

A

disrupt •3 – K+ efflux

51
Q

Mechanism of Potassium Arrest (What’s Really Going On….)

A

• With a blood potassium of 8-10 mEq/L, depolarization of the cell occurs and sodium rushes into the cell.
• Because the extracellular potassium is so high the cell cannot repolarize and the sodium remains inside the cell.
• sodium gates do not reset: fast-gates remain open; slow gates remain closed
• As potassium washes out of the extracellular space, the cells can begin to repolarize – you hope.
(post cross clamp)

52
Q

Mechanism of Sodium Arrest (What’s Really Going On….)

A

• • •
Low sodium environment extracellular Disrupts Na+ gates and influx
Because the extracellular sodium is low the cell cannot depolarize.
• sodium gates disrupted • Utilized as “donor” cardioplegia for years

53
Q

Mechanism of Depolarizing

Sodium Arrest

A

disrupts phase •0 – Na+ influx

54
Q

Myocardial Protection: route of delivery

A

Antegrade / Retrograde / Ostial / Via conduits / Integrated

55
Q

Myocardial Protection: composition of solution

A

Crystalloid / Blood / Microplegia

56
Q

Myocardial Protection: temperature

A

Warm / Tepid / Cold

57
Q

Myocardial Protection: delivery interval

A

Intermittent / Continuous

58
Q

Myocardial Protection: additives

A

Electrolyte / Pharmacologic / Metabolic

59
Q

Myocardial Protection: monitoring

A

emperature / Myocardial pH

60
Q

Myocardial Protection: preparation for reperfusion

A

This may be underestimated

61
Q

Cardioplegia Catheter Types

A

H- Medtronic Coronary Ostial Cannula 17 FR
G - Medtronic Coronary Ostial 30055 F – Coronary Ostial 12 G
E – Cobe Aortic Root Cannula 16 G
D – Medtronic Aortic Air Air- Aspirating Needle 16 G
C – DLP Non Aspirating Aortic Root 16 G
B – RMI 9 FR Cardioplegia Retrograde Coronary Sinus
A – 18 mm Baxter 14 FR Retrograde Cardiplegia w/Auto inflating balloon

62
Q

Single lumen catheters are sized byGauge= to determine diameter size (mm)

A

gauge

63
Q

Multi-lumen catheters are measured by

A

french size

64
Q

French size and diameter are

A

related directly; Larger French=larger diameter

65
Q

Gauge and size are

A

related inversely; Smaller Gauge= greater diameter

66
Q

French= to determine diameter size (mm)

A

divide by 3

67
Q

Gauge= to determine diameter size (mm)

A

1/gauge

68
Q

Antegrade Delivery • Initial dose

A

= ~10-15 mL/kg Up to 30 mL/kg in pediatric patients. Keep in mind that if blood cardioplegia is used, a 1000 mL dose would only be 200 mL of crystalloid at a ratio of 4:1.

69
Q

Subsequent doses antegrade delivery

A

less in volume and in potassium concentration than the arresting dose.

70
Q

Line pressure depends

A

on the pressure drop in mmHg (the goal is to maintain root pressure 50-100 mmHg).

71
Q

Flow is generally ___ during antegrade cardioplegia

A

250-400 mL/min • 150 ml/minute/m2

72
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
73
Q

Antegrade Delivery DISADVANTAGES

A

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

74
Q

Retrograde cardioplegia is given into

A

The coronary sinus and must be vented out of the heart.

75
Q

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

A

• Prevents backflow • Holds cannula in place

76
Q

RETROGRADE FLOW IS

A

~ 150 - 200 mL/min

77
Q

Flow should be titrated to maintain a coronary sinus pressure of

A

40 mmHg

78
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)
79
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
80
Q

Antegrade pros and cons

A

pros: -Simple -Mimics normal coronary flow
cons: -Requires competent aortic valve -Can interrupt and delay surgery -Advanced CAD

81
Q

retrograde pros and cons

A

pros: Avoids limitations from AI and advanced CAD -Does not interrupt surgeryAugments de-airing
cons: Catheter placement difficult -Closely monitor pressure

82
Q

integrated pros and cons

A

pros: Uniform distribution of cardioplegia
cons: Complex -Closely monitor pressures

83
Q

Direct Ostial Delivery

A

Not as common as antegrade or retrograde.

Hand-held cannula directly perfuse ostia

84
Q

pressure required for direct ostial delivery

A

Approximately 250 mmHg required (circuit pressure) • high pressures due to small cannula orifice.

85
Q

flow required for direct ostial delivery

A

50-150 mL/min flow seen on delivery • Variable with disease and technique • Normal perfusion is 5-8% of cardiac output

86
Q

Doing distal anastamosis first allows

A

VG cardioplegia to be given

87
Q

Delivery Through Vein Grafts Infusion pressure

A

50 mmHg

88
Q

Delivery Through Vein Grafts flow rate

A

50-100 mL/min.

89
Q

Delivery Through Vein Grafts infusion pressure and flow rate allow surgeon to

A

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

90
Q

Delivery Through Grafts Benefit

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
91
Q

delivery through grafts disadvantages

A
  • Requires graft placement • Complexity

* Distribution only to those areas perfused by graft

92
Q

Integrated Combined Delivery It is common to give

A

a large arresting dose of antegrade cardioplegia 1-1.5 L, followed by a smaller dose of retrograde cardioplegia 0.5 L.

93
Q

Integrated Combined Delivery more likely

A

to perfuse all areas of the heart.

94
Q

Integrated Combined Delivery benefits

A

Benefits of all methods utilized

95
Q

Integrated Combined Delivery disadvantages

A

Complexity (lots of cricket clamps for a surgeon)

96
Q

So now that we know which direction to give cardioplegia………How do we know how fast?

A

• Direct Measurement • Measured directly at the site
• Calculated Measurement • Pressure drop calculation
Flowing blindly might not be a good thing

97
Q

Pressure drop is a decrease in

A

pressure from one point in a tube to another point

98
Q

frictional forces increase

A

frictional forces increase (small cannula)

99
Q

The flow is in the direction of

A

least resistance

100
Q

Pressure drop increases proportionally

A

shear forces. • High flow velocities and fluid viscosities result in a larger pressure drop. •Low velocity will result in lower pressure drop.

101
Q

We will assume a pressure drop

across your entire cardioplegia system of

A

175 mmHg

Perf Tech (14 decks)

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