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Perf tech II > test 5 > Flashcards

test 5 Flashcards

1
Q

myocardial protection pre-1955

A

Systemic hypothermia

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2
Q

1955 myocardial protection

A

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

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3
Q

1956 myocardial protection

A

-Lillehei introduced retrograde cardioplegia

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4
Q

1973 myocardial protection

A

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

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5
Q

1979 myocardial protection

A

-Buckberg & Follette introduced blood cardioplegia

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6
Q

europe myocardial protection

A

š-Bretschneider HTK (histadine, tryptophan, alpha ketoglutarate)
š -Low Calcium, low sodium, procaine with histadine buffers
š -Non-depolarizing arrest
š NOW – Custodial HTK
-St. Thomas Solution (London)
š -Intracellular ionic concentration
š -Normocalcemia, hyperkalemia (16mmol/L)
š -NOW – Plegiol in US

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7
Q

Coronary Blood flow is determined by hemodynamic factors

A

-š Perfusion pressure
š- Coronary Vascular Resistance
š -Q = P/R

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8
Q

Delivery of Oxygen (DO2) to myocardium (oxygen supply) is determined by two factors:

A
  • Coronary blood flow (ml/min)
    š- Oxygen content of the blood (ml O2 /mL blood)
    š -O2 Delivery = CBF x CaO2
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9
Q

Consumption and Demand often used interchangeably

A

-š Not equal
š -Demand = Need
š -Consumption = Actual amount of oxygen consumed per minute

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10
Q

how is oxygen used

A

-š Regenerate ATP
š *Na/K-ATPase pump
-š Myocyte contraction and relaxation

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11
Q

Oxygen consumption (mL O2/min per 100g):
arrested heart\
resting heart rate
heavy exercise

A

2
8
70

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12
Q

using hypothermia and fibrillation

A

-reduces workload of the heart

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13
Q

Lowest level of Cardiac Oxygen Consumption

A

-When heart is arrested

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14
Q

Highest level of Cardiac Oxygen Consumption

A
  • Shortly after weaning from bypass

š *Heart is repaying oxygen debt

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15
Q

Ischemia results when oxygen delivery does not meet

A

-Oxygen demand
-šSupply/Demand
š *Normally – Supply is greater than demand – Ratio >1
š *With Ischemia – Supply is less than demand – Ratio <1
-ANAEROBIC metabolism
š -Production of lactic acid

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16
Q

result of the lactic acid buildup

A

š- Decreased intracellular pH
š -decreases the stability of the cellular membranes
š -Decreases the stability of the mitochondrial membranes.
š -Impairs Na-K ATPase
*šLeads to calcium influx
*šCalcium overload

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17
Q

ATP generated from aerobic metabolism is used preferentially for 1_________, whereas anaerobically produced ATP is used for 2___________

A
  1. myocardial contraction (work)

2. Cell survival and repair (work to survive)

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18
Q

increase in heart demand for oxygen, what needs to be done

A
  • increase in coronary blood flow

- can’t extract more

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19
Q

Coronary blood flow is dependent on the and normal flow pressure

A
  • transmural gradient
  • Coronary Perfusion Pressure = DBP - LVEDP
  • normal 60-80 mmHg
  • Pressure gradient of at least 15mmHg may be necessary for survival
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20
Q

coronary blood flow during isovolumetric contraction and ejection compared to diastole

A
  • flow is lower than during diastole
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21
Q

Myocardial Protection: Pre-Ischemic Intervention

A 
-š Minimize on-going ischemia
š *Pharmacology (ie. Nitroglycerin)
-š Prevent ventricular distension
š *Vent!!!
-š Myocardial preconditioning
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22
Q

Myocardial Protection: Preconditioning

A
  • Myocardium that has undergone one or more brief periods of ischemia may be better able to tolerate subsequent prolonged ischemia.
  • getting the heart used to ischemia
  • for beating heart it might help
  • also used when myocardial protection not optimal
23
Q

Myocardial preconditioning can be achieved by

A
  • ischemia
  • drugs
  • Cardiopulmonary bypass itself may override these other methods and be the “best” preconditioning tool
24
Q

Why give Cardioplegia?

A
  • Cardiac quiescence
    š- Bloodless field
    š- Preservation of myocardial function
    š- Induces myocardial hypothermia
25
Q

Goals of Hypothermic Cardioplegia

A
  • š Immediate / sustained electromechanical arrest
  • š Rapid / sustained homogenous myocardial cooling
  • š Maintenance of therapeutic additives in effective concentrations
  • š Periodic washout of metabolic inhibitors
26
Q

Without cardioplegic arrest

A
  • šIrreversible ischemic injury šwithin 20 minutes
27
Q

With myocardial protection strategies

A
  • Can prolong ischemia to more than 4-5 hours without irreversible damage
28
Q

Normal Cardiac Action Potential

A 
PHASES:
•0 – Na+ influx
•1 – Transient K+ efflux
•2 – Ca++ influx
•3 – K+ efflux
•4 – Na/K ATPase
29
Q

Mechanism of Potassium Arrest

A
  • šWith a blood potassium of 8-10 mEq/L, depolarization of the cell occurs and sodium rushes into the cell.
  • šBecause 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
    š- After AoXC, potassium washes out of the extracellular space (Repolarization)
  • stops phase 3
30
Q

Mechanism of Custodial-HTK (“Low Sodium”)

A
  • stops phase 0

- nonpolarizing phase

31
Q

Mechanism of Del Nido (“Low Calcium”)

A
  • stops phase 2
  • stop contraction phase
  • still depolarized but arresting in this phase
32
Q

Components of Myocardial Protection

A
  • š Route of delivery
  • antegrade / retrograde / both / directly into opstia / conduits
  • š Composition of solution
  • Crystalloid / Blood / Microplegia
  • š Temperature
  • Delivery interval
  • Intermittent / Continuous
  • š Additives
  • š Monitoring
  • š Preparation for reperfusion (hotshot)
33
Q

Antegrade pros

A
  • Simple

* Mimics normal coronary flow

34
Q

Antegrade cons

A
  • Requires competent Aortic Valve
  • Can interrupt surgery
  • Advanced CAD
35
Q

Retrograde pros

A
  • Avoids limitations from AI and CAD
  • Doesn’t interrupt surgery
  • Augments de-airing
36
Q

Retrograde cons

A

• Catheter placement difficult
• Closely monitor
pressure

37
Q

Integrated (both) pros

A

• Uniform distribution of cardioplegia

38
Q

Integrated (both) cons

A
  • Complex

* Closely monitor pressures

39
Q

Antegrade Delivery

A
  • šInitial dose = ~10-15 mL/kg
  • šUp to 30 mL/kg in pediatric patients.
  • 4:1 CPG = 4 parts blood = 800mL AND š1 part CPG = 200mL
  • šSubsequent doses are
  • šLess Volume
  • šLower potassium concentration
40
Q

Antegrade Delivery pressures and flow

A
  • šLine pressure:
    *š125-150 mmHg
    š *Goal : Maintain a ROOT pressure of 50- 100mmHg
  • šFlow is generally 250-400 mL/min
    *š150 ml/minute/m2
41
Q

Antegrade Delivery Benefits

A 
-š Easy
š- Physiological flow pattern
š- Quick arrest
š- Appropriate distribution to the right and left heart.
š- Root is tolerant of higher pressures
42
Q

Antegrade Delivery disadvantages

A

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

43
Q

Retrograde Delivery

A
  • šDelivered into Coronary Sinus
    *šMust be vented
    š- A balloon is inflated on the cannula that provides two functions:
    *šPrevents backflow
    *šHolds cannula in place
    *šFlow is ~200 mL/min
    *šFlow should be titrated to maintain a coronary sinus pressure of 30-40 mmHg.
44
Q

Retrograde Delivery benefits

A

-š Ideal for aortic valve regurgitation
-š Good distal perfusion of obstructed arteries
-š Retrograde flushing of emboli – augments de-airing
-š Does not impede conduct of case - can run continuously
š *Warm continuous

45
Q

Retrograde Delivery disadvantages

A

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

46
Q

Direct Ostial Delivery

A

-š Not as common as traditional antegrade or retrograde.
š *Position dependent
-š Hand-held cannula used to directly perfuse ostia
š *AVR
š *Aneurysm / Dissection
-š 250-300 mmHg required (circuit pressure)
š *High pressures due to small cannula orifice.
-š 150-250 mL/min
š *Normal perfusion is 5-8% of cardiac output

47
Q

Delivery Through Grafts

A
  • šAfter the initial dose for CABG, may infuse cardioplegia directly into the vein grafts.
    š *Infusion pressure of 50 mmHg
    š *Flow rate of 50-100 mL/min.
  • Surgeon may use hand-held syringe
48
Q

Delivery Through Grafts Allows surgeon to check

A
  • šAnastamosis
  • šAdequacy of flow
  • šFlow to previously under-perfused areas
49
Q

Delivery Through Grafts benefits

A
  • Allows antegrade protection of areas of coronary artery disease
  • š Obviates limitations from aortic insufficiency and coronary artery disease
  • š Allows delivery without need to pressurize aortic root or interrupt surgery
50
Q

Delivery Through Grafts disadvantage

A

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

51
Q

Integrated Delivery

A
  • šIt is common to give a large arresting dose of antegrade cardioplegia, followed by a smaller dose of retrograde cardioplegia.
  • šMore likely to perfuse all areas of the heart.
52
Q

Integrated Delivery benefits

A
  • šBenefits of all methods utilized
53
Q

Integrated Delivery disadvantages

A
  • šComplexity

Perf tech II (16 decks)

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