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
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
3
Q
To assess myocardial protection it is imperative to
A
assess myocardial function and O2 consumption.
4
Q
Oxygen demand is a concept closely related
A
to the oxygen consumption.
5
Q
Demand =
A
Need
6
Q
Consumption =
A
Actual amount of oxygen consumed per minute.
7
Q
Oxygen consumption will
A
• regenerate ATP used by membrane
transport (Na+/K+-ATPase pump) and by
• Myocyte contraction and relaxation
(myosin ATPase)
8
Q
arrested heart MVO2 (mlO2/MIN/100G)
A
2
9
Q
resting heart rate MVO2 (mlO2/MIN/100G)
A
8
10
Q
heavy exercise MVO2 (mlO2/MIN/100G)
A
70
11
Q
brain (mlO2/MIN/100G)
A
3
12
Q
kidney (mlO2/MIN/100G)
A
5
13
Q
skin (mlO2/MIN/100G)
A
.2
14
Q
resting muscle (mlO2/MIN/100G)
A
1
15
Q
contracting muscle (mlO2/MIN/100G)
A
50
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)
17
Q
If MVO2 Demands are NOT met the heart may be prone to
A
arrhythmias
18
Q
Name 2 points during cardiopulmonary bypass the heart is prone to fibrillate?
A
• Cooling • Postcrossclamp(postischemicepisodes)
19
Q
Why am I worried about fibrillation?
A
• Distension/Overfilling • Muscular/cellular damage • Starlings Curve
20
Q
lowest level MVO2 during bypass
A
When heart is arrested
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)
22
Q
Ischemia is when
A
oxygen delivery ≠ oxygen demand
23
Q
An imbalance of oxygen delivery and demand leads to
A
ANAEROBIC metabolism and the production of lactic acid.
24
Q
Decreased intracellular pH
A
decreases the stability of the cellular and mitochondrial membranes.
25
Decreased intracellular pH also impairs
the Na -> K ATPase leading to calcium influx and calcium overload.
26
ATP generated from AEROBIC metabolism is used preferentially for
myocardial contraction
27
anaerobically produced ATP is used for
cell survival and repair
28
amount of O2 cardiac muscle extracts
>70%
29
ncreased myocardial oxygen demand is met primarily by
an increase in coronary blood flow.
30
Coronary blood flow is dependent on
the transmural gradient:
31
True Coronary Perfusion Pressure. CoPP =
DBP – LVEDP. Not just a pressure drop across, it is perfusion throughout
32
What parameter can we estimate LVEDP from?
PAD
33
A diastolic aortic pressure of 80 and a LVEDP
| pressure of 14 would leave a CPP
of 66 (normal 60-80 mmHg) calculation alert
34
During cardiac arrest, CPP is one of the most important variables in achieving
the return of spontaneous circulation
| which is why CPR compressions are important > respirations
35
min. CPP necessary for survival
15 mmHg
36
Pre-Ischemic Intervention
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
37
Myocardial Preconditioning
Myocardium that has undergone one or more brief periods of ischemia may be better able to tolerate subsequent prolonged ischemia.
38
Myocardial preconditioning can be achieved by
• 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
39
Why give cardioplegia?
• Cardiac quiescence • Bloodless field • Preservation of myocardial function • Induces myocardial hypothermia
40
Four Main Objectives of Hypothermic Cardioplegia are:
• 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
41
History of Myocardial Protection • Pre-1955:
Systemic hypothermia
42
History of Myocardial Protection 1955
Melrose advocated the use of high potassium solutions to induce cardiac quiescence. Caused permanent myocardial injury.
43
History of Myocardial Protection 1956
Lillehei introduced retrograde cardioplegia.
44
History of Myocardial Protection 1973
Gay & Ebert reintroduced hyperkalemic arrest with lower potassium concentrations (<20 mmol), preventing permanent myocardial injury.
45
History of Myocardial Protection 1979
Buckberg & Follette introduced 4:1 blood cardioplegia.
46
Withoutcardioplegicarrest,irreversible ischemic injury to the myocardium would occur within
20 min.
47
When myocardial protection strategies are used, ischemia can be prolonged to
more than 4-5 hours without irreversible damage.
48
Most cardioplegia strategies based on arresting the heart with
high doses of potassium (But that is changing)
49
ction potential can be disrupted
at different phases
50
Mechanism of Depolarizing
| Potassium Arrest
disrupt •3 – K+ efflux
51
Mechanism of Potassium Arrest (What’s Really Going On....)
• 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
Mechanism of Sodium Arrest (What’s Really Going On....)
• • •
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
Mechanism of Depolarizing
| Sodium Arrest
disrupts phase •0 – Na+ influx
54
Myocardial Protection: route of delivery
Antegrade / Retrograde / Ostial / Via conduits / Integrated
55
Myocardial Protection: composition of solution
Crystalloid / Blood / Microplegia
56
Myocardial Protection: temperature
Warm / Tepid / Cold
57
Myocardial Protection: delivery interval
Intermittent / Continuous
58
Myocardial Protection: additives
Electrolyte / Pharmacologic / Metabolic
59
Myocardial Protection: monitoring
emperature / Myocardial pH
60
Myocardial Protection: preparation for reperfusion
This may be underestimated
61
Cardioplegia Catheter Types
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
Single lumen catheters are sized byGauge= to determine diameter size (mm)
gauge
63
Multi-lumen catheters are measured by
french size
64
French size and diameter are
related directly; Larger French=larger diameter
65
Gauge and size are
related inversely; Smaller Gauge= greater diameter
66
French= to determine diameter size (mm)
divide by 3
67
Gauge= to determine diameter size (mm)
1/gauge
68
Antegrade Delivery • Initial dose
= ~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
Subsequent doses antegrade delivery
less in volume and in potassium concentration than the arresting dose.
70
Line pressure depends
on the pressure drop in mmHg (the goal is to maintain root pressure 50-100 mmHg).
71
Flow is generally ___ during antegrade cardioplegia
250-400 mL/min • 150 ml/minute/m2
72
Antegrade Delivery Benefits
* Easy
* Physiological flow pattern
* Quick arrest
* Appropriate distribution to the right and left heart.
* Root is tolerant of higher pressures
73
Antegrade Delivery DISADVANTAGES
• Requires competent aortic valve • Poor distal perfusion in diseased arteries
• Poor subendocardial perfusion (especially in LVH)
RETROGRADE CP
74
Retrograde cardioplegia is given into
The coronary sinus and must be vented out of the heart.
75
A balloon is inflated on the cannula that provides two functions:
• Prevents backflow • Holds cannula in place
76
RETROGRADE FLOW IS
~ 150 - 200 mL/min
77
Flow should be titrated to maintain a coronary sinus pressure of
40 mmHg
78
Retrograde Delivery Benefits
* 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
Retrograde Delivery disadvantages
* 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
Antegrade pros and cons
pros: -Simple -Mimics normal coronary flow
cons: -Requires competent aortic valve -Can interrupt and delay surgery -Advanced CAD
81
retrograde pros and cons
pros: Avoids limitations from AI and advanced CAD -Does not interrupt surgeryAugments de-airing
cons: Catheter placement difficult -Closely monitor pressure
82
integrated pros and cons
pros: Uniform distribution of cardioplegia
cons: Complex -Closely monitor pressures
83
Direct Ostial Delivery
Not as common as antegrade or retrograde.
| Hand-held cannula directly perfuse ostia
84
pressure required for direct ostial delivery
Approximately 250 mmHg required (circuit pressure) • high pressures due to small cannula orifice.
85
flow required for direct ostial delivery
50-150 mL/min flow seen on delivery • Variable with disease and technique • Normal perfusion is 5-8% of cardiac output
86
Doing distal anastamosis first allows
VG cardioplegia to be given
87
Delivery Through Vein Grafts Infusion pressure
50 mmHg
88
Delivery Through Vein Grafts flow rate
50-100 mL/min.
89
Delivery Through Vein Grafts infusion pressure and flow rate allow surgeon to
check the anastomosis and adequacy of flow, and also allows flow to previously underperfused areas.
• Surgeon may use hand-held syringe
90
Delivery Through Grafts Benefit
* 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
delivery through grafts disadvantages
* Requires graft placement • Complexity
| * Distribution only to those areas perfused by graft
92
Integrated Combined Delivery It is common to give
a large arresting dose of antegrade cardioplegia 1-1.5 L, followed by a smaller dose of retrograde cardioplegia 0.5 L.
93
Integrated Combined Delivery more likely
to perfuse all areas of the heart.
94
Integrated Combined Delivery benefits
Benefits of all methods utilized
95
Integrated Combined Delivery disadvantages
Complexity (lots of cricket clamps for a surgeon)
96
So now that we know which direction to give cardioplegia.........How do we know how fast?
• Direct Measurement • Measured directly at the site
• Calculated Measurement • Pressure drop calculation
Flowing blindly might not be a good thing
97
Pressure drop is a decrease in
pressure from one point in a tube to another point
98
frictional forces increase
frictional forces increase (small cannula)
99
The flow is in the direction of
least resistance
100
Pressure drop increases proportionally
shear forces. • High flow velocities and fluid viscosities result in a larger pressure drop. •Low velocity will result in lower pressure drop.
101
We will assume a pressure drop
| across your entire cardioplegia system of
175 mmHg
