Myocardial Preservation 2D.1,2 Flashcards
1
Q
cardiac muscles are ….
A
self contracting, autonomically regulated and must continue to contract in rhythmic fashion
2
Q
structure of cardiac muscles
A
- mononucleated
- arrangement of actin and myosin is like skeletal striated muscle
3
Q
Some of the cardiac muscle cells are ___-___
A
auto-rhythmic
4
Q
____ __ are located b/w cardiac muscle cells
A
intercalated disks
5
Q
intercalated disk contain _____ which provide communicating channels b/w cells
A
gap junctions
6
Q
what do intercalated disk allow?
A
waves of depolarizations to sweep across the cells thus synchronizing muscle contraction
7
Q
Skeletal muscle is ___
A
neurogenic
8
Q
the beat originates in the ___ ____ itself
A
cardiac muscle
9
Q
the heart beat is therefore called _____ (muscle + origin)
A
myogenic
10
Q
cells are rich in ___ ____ at the ____ ____
A
cells are rich in gap junctions at the intercalated discs
11
Q
the heart is said to act as a functional ____ (single cell) even though composed of individual cells
A
syncytium
12
Q
what transmit mechanical force from cell-to-cell
A
desmosomes
13
Q
what is also known as “molecular rivets”
A
desmosomes
14
Q
Sliding of the cardiac myofibrils is regulated by
A
the intracellular concentration of calcium ions released by the sarcoplasmic reticulum
15
Q
when do muscles contract and what is required for this to occur?
A
- muscles contract when sarcomeres shorten
- ATP is required for this to occur
16
Q
Do the sarcomeres shorten during contraction?
A
Yes
the thin and thick filaments that make up sarcomeres slide past one another, causing the sarcomere to shorten while the filaments remain the same length
17
Q
what happens when the sarcomeres contract?
A
- Z lines move closer together
- I band gets smaller
- thin filaments overlap
18
Q
How the sliding filament model works (5 steps)
A
- ATP activates myosin, bringing to higher energy state
- myosin acts binds to an actin filament and changing shape, pulling the actin filament toward the A-band
- ATP binds again, destabilizing the myosin filament and enabling it to bind to another site along the actin filament, increasing the strength of contraction
- all the myosin heads contract simultaneously, shortening all the sarcomeres, causing the muscle to contract
- myosin heads pull the A-band toward the Z-lines
19
Q
the movement of 3 types of ions determines all aspects of cardiac __,___,___
A
cardiac conduction, contraction, and repolarization
20
Q
what is another word for cell to cell conduction
A
depolarization
21
Q
cell to cell conduction through the myocardium is carried by ____ ions
A
Na+ ions
22
Q
Depolarization may be considered an advancing _________ within the heart’s myocytes
A
wave of positive changes (Na+)
23
Q
_____ conduction is due to slow movement of Ca2= ions
A
AV node conduction
24
Q
what produces myocardial contraction
A
the release of free Ca2+ ions into the interiors of the myocytes
25
following depolarization and contraction, _____ is due to the controlled outflow of K+ ions from the myocytes
repolarization
26
sodium ion movement produces cell-to-cell conduction (of depolarization) in the heart except in the..
except the AV node, which depends on the (slow) movement of Ca++ ions
27
calcium ions (ca++) ions cause
myocyte contraction
28
potassium (K+) ions cause
outflow causes repolarization of myocytes
29
Phase 0
depolarization
Na channels open Na in
Na channels close
30
Phase 1
initial repolarization
| K leaves thru K channels
31
Phase 2
Plateau
decrease in K permeability
increase in Ca permeability
Ca influx decreased
K efflux causes AP to flatten out
32
Phase 3
rapid repolarization
| Ca channels close
33
Phase 4
resting membrane potential
-90mV
34
what is myocardial protection
strategies and methods used to attenuate or prevent post-ischemic myocardial dysfunction that occurs during and after heart surgery
35
the main principles of myocardial protection are (2)
- reduction of metabolic activity by hypothermia
- therapeutic arrest of the contractile apparatus and all electrical activity of the myocytes by administering cpg solution
36
what is myocardial injury
inadequate perfusion (blood flow and substrate) to sustain steady-state metabolism at a given level of cardiac work
37
Determinants of Ischemic injury
- duration of ischemia
- amount of collateral blood flow
- O2 demands of the myocardium
- temperature of myocardium
- buffering capacity of myocardium
- edema
38
Ischemia of the human heart can last for
1. for only a few seconds or minutes (angioplasty or angina)
2. for hours (cardiac surgery or infarction
3. for years (chronic ischemic heart disease)
39
why understanding myocardial protection is important
- lead to low output syndrome
- can prolong hospital stay
- prolong cost
- may result in delayed myocardial fibrosis
40
Ischemic/reperfusion injury presents with
low CO
hypotension
reversible or irreversible damage
41
what are some reversible or irreversible damage by inadequate myocardial damage (3)
- EKG abnormalities
- elevated plasma enzymes and proteins such as Toponins I and troponin T , CK-MB (takes 6-9 hrs to show), myoglobin (2-3 hrs from start, 24 hrs back to normal)
- wall motion abnormalities
42
manifestations of reperfusion injury associated with CPB
- reperfusion dysthythmias
- post ischemic systolic and diastolic dysfunction
- myocardial necrosis
- endothelial dysfunction
- wall motion abnormalities
- EKG abnormalities (arrhythmias)
43
what are one of the most important factors in ischemia-reperfusion injury
Ca++
44
Na+ -K+ pump
3 Na out to 2 K into cell
| dependent on ATP availability
45
when ATP is depleted what happens to NA and membrane potential
NA accumulates inside cell
| membrane potential is lowered
46
when ATP is depleted, what happens to Ca++
released from lowered membrane potential
- sarcolemma gated Ca++ channels due to anaerobic metabolism continue
- results in hydrogen ion accumulation (acidosis) and lactic acid production
47
Na+ - H+ pump
acidosis cause further Na+ accumulation
48
3Na+ - 1Ca2+ exchanger
```
function deteriorates due to intracellular Na+ increase
leads to intracellular Ca2+ accumulation
```
49
what is the myocardial ischemic injury list from least to worst damage
- acute ischemic myocardial dysfunction
- myocardial preconditioning
- myocardial stunning
- myocardial hibernation
- myocardial necrosis vs apoptosis
50
acute ischemic myocardial dysfunction
reversible contractile failure
perfusion pressure (decreased due to coronary spasm, thrombus formation)
O2 supply (not adequately met)
immediate recovery
51
Myocardial Preconditioning
reversible
slow energy utilization
reduction in myocardial necrosis
increase protective abilities of myocardium
-recovery is in hrs to days
- a bunch of episodes of baby heart attacks that makes you more tolerant to have one big massive heart attack bc your heart is used to having slower energy utilizations
52
myocardial stunning
- partially reversible
- post-ischemic contractile dysfunction with no morphological injury or necrosis
- may be accompanied by endothelial dysfunction
- occurs from ischemic-reperfusion insult
- mediated by increased intracellular Ca++ accumulation
- recovery in hrs to weeks
- no structural damage
53
myocardial hibernation
partially reversible
related to poor myocardial blood flow (poor wall motion)
chronic
revery is weeks to months
54
myocardial apoptosis
irreversible
"suicide": programmed cell death
intact cell membrane, cell shrinkage, chromatin condensation, phagocytosis w/o inflammation
-myocytes may be salvageable
55
Myocardial Injury
| 3 Surgical Phases
1. antecedent ishcemia
2. protected ischemia
3. reperfusion injury
56
antecedent ischemia
occurs prior to CPB or CPG delivery
| -due to poorly perfused myocardium due to CAD or MI
57
protected ischemia
initiated electively by chemical CPG
-the heart is ischemic (no blood flow) but the metabolic demand of the myocardium are dramatically reduced by systole and hypothermia
58
reperfusion injury happens during...
sustained during intermittent CPG infusions, after X-clamp removal, or after CPB
59
when does the most reperfusion injury occur?
when cross clamp is removed
60
reperfusion injury is caused by
- neutrophil activation
- k+ efflux, membrane depolarization, intracelular H+, Na+, and Ca2+ loading
- release/production of oxygen free radicals (ROS)
- endothelial activation leading to microvascular dysfunction
- activation of the inflammation cascade
61
factors that affect the rate at which ischemic injury evolves
- collateral or non coronary collateral flow
- effects of disease such as: hypertrophy, DM, HTN
- HR, metabolic rate, and tissue temperature
- metabolic response to ischemia (substrate utilization)
- nutirional and hormonal states
- age and gender
62
how does age affect the rate at which ischemic injury evolves
octogenarians have a 3-fold increase risk of death compared with younger adult
63
gender
adult females have up to 1.6 times higher in-hospital mortality rates and higher morbidity than males
64
can deliver blood to the heart via
- bronchial
- mediastinal
- tracheal
- esophageal
- diaphragmatic arteries
- LIMA and RIMA
65
what is normal collateral or non-coronary collateral flow in ml/min
250 ml/min
66
what is an advantage of delivering collateral or non-coronary collateral flow
providing O2 and substrates to ischemic tissues
67
what is a negative of delivering collateral or non-coronary collateral flow
washing out cold CPG soon
68
what are the 4 different types of crystalloid CPG
- intracellular
- extracellulat
- ALM
- Del Nido
69
intracellular CPG
- only used for cold renals
- depolarized arrest
- low or absent concentrations of sodium and calcium (about the same amount that IN the CELL)
- contains potassium and bicarb for buffering
70
extracellular CPG
| aka Buckberg
- depolarized arrest
| - high concentrations of sodium, calcium, and magnesium (same amount found in your extracellular space)
71
ALM CPG
- adenosine, lidocaine, magnesium
- polarized arrest
- arrested membrane potential of -80-85
- benefits: rapidly slows HR, slows AV conduction, CA vasodilation, anti-ischemic, anti-arrhythmic, anti-inflammatory
72
Del Nido CPG
- non glucose based solution given as a single dose that provides up to 180 minutes of cardiac quiescence
- buys you a lot more time
73
what is the cardioplegic technique goals
-reducing energy consumption and oxygen demand so ischemia tolerance of the heart can be prolonged
74
irreversible ischemic damage begins to occur in the human heart after only
20 min
75
irreversible regional injury (necrosis) occurs at
30. min of coronary occlusion
76
with current techniques of myocardial protection, arrest times of more than ____ hrs may be tolerated w/o irreversible damage
4-5 hrs
77
what is the goal of CPG
- perfect surgical repair
- bloodless field
- use of cardio-protective techniques
78
principles of protection for the heart (5)
1. asystole
2. hypothermia
3. buffering
4. avoidance of edema
5. enhancements
79
depolarized arrest
K+
| membrane potential -50 to -60 mV
80
polarized arrest
Na+ channel blockers, adenosine, K+ channel openers
| arrested heart membrane potential of -80 to -85 mV
81
inhibition of Ca++ influx
zero Ca++ in CPG soln
| -inhibiting Ca inhibits the excitation-contraction coupling
82
what is mvO2
myocardial O2 demand (ml O2/min/100g tissue)
83
at temp of 37, what is the mvO2 of a beating full heart
10
84
at 37, what is the mvO2 of a beating empty heart
5.5
85
at temp 37, what is the mvO2 of a fibrillating heart
6.5
86
at temp 37, what is the mvO2 of K+ CPG arrest
1.0
87
a beating heart after x clamp is applied increases
the rate of ATP depletion
88
Asystole does what
conserves myocardial energy reserves
| increase tolerance to ischemia
89
potassium initial dose for arrest
10-30 mEq/L
90
potassium maintenance dose
10 mEq/L every 20-30 min
91
mvO2 demand decreases only __% with hypothermia alone
10%
92
mvO2 demand decreases ___% with hypothermia to 4'C and asystole
97%
93
ways to cool the heart
1. systemic cooling, iced saline lavage, ice slush topically on heart, cooling pads, cold CPG
- PA vent prevents rewarming from bronchial return
94
every 10'C decrease in temp decreases enzyme activity by
50%
95
optimal myocardial temp is
10-15'C
96
acidosis impairs...
enzyme kinetics and metabolism
97
accumulation of hydrogen ions do what to pH
reduce tissue pH
98
what is blood's natural buffer
histidine
99
what is used to buffer
- blood
- tromethamine
- histidine
- bicarbonate
- phosphate
100
what is blood's benefit in buffering
lower incidence of low output syndrome immediately upon reperfusion with blood cardioplegia
101
what is tromethamine (THAM) benefit in buffering
adjust pH prior to admin
102
what is histidine benefit in buffering
promotes anaerobic glycolysis
| improves recovery of high-energy phosphates and contractile function in hypertrophied myocardium
103
what does bicarb do in buffering
adjust pH prior to admin
104
what does phosphate do in buffering
minimize rapid changes in extracellular and intracellular pH values during the bouts of ischemia-reperfusion
105
edema manifest during reperfusion when
water and solutes can escape from leaky capillaries
106
how to avoid edema
- hypersomotic agents such as mannitol, glucose, and albumin
- low reperfision pressures prevent starling forces in trans capillary fluid movement from intravascular to interstium
- hyperosmolar solution may aid myocardial drhydration
- PA vent: prevents ventricle distention and rewarming
107
enhancements
- supply metabolic substrates such as glucose, glutamate and aspartate
- prevent calcium accumulation with CPD and magnesium
- membrane stabilization
- vasodilators
108
adenosine purpose
coronary vasodilator
| enhances cpg delivery
109
magnesium sulfate purpose
calcium channel competitor
| prevents calcium influx
110
lidocaine/procaine
sodium channel blocker
| prevents sodium influx
111
histidine/sodium bicarb/THAM
buffering agent
| counteracts acidosis from ischemia
112
CPG delivery techniques
- hand held syringe
- pressure bag: difficult to determine pressure and volume delivered
- roller pump: precise volume and pressure
- MPS2 myocardial protection system
113
nonrecirculating: single pass CPG system
- used at THI
- 150 micron filter captures any air emboli and particulates as blood exits the outlet chamber
- pressure relief valve protects the heat exchanger from over-pressurization
- low system priming volume
114
recirculating CPG
- closed system
- active cooling/coil ice bath
- minimize dead to decrease amount of warm CPG solution
- not flush w/ CO2 prior to priming
- always crystalloid cog solution
115
continuous CPG system (MPS)
microplegia system
| -post oxygenator blood is the carrier of small concentrated arresting agent and other additives
116
antegrade cpr delivery route
into aortic root
| -protects RIGHT and LEFT side
117
cpg infusion pressure for antegrade cpg on pt with severe CAD
100-150 measured at the root
118
cpg infusion pressure for antegrade cpg on pt w/o CAD
50-90
119
delivery rate of antegrade cpg
250 ml/min
120
if the vent is in the ascending aorta, the vent pump must be
OFF during the delivery of antegrade cpg
121
if the vent is in the LV, the vent should be
ON during antegrade CPG
122
retrograde CPG delivery route
into coronary sinus
| -protects left ventricle mostly
123
max pressure of retrograde CPG
40 mmHg
absolute MAX 50 mmHg
124
reason retrograde doesn't protect right heart
position of balloon can obstruct venous drainage into RA
125
delivery rate for retrograde CPG
150 ml/min
126
if giving retrograde CPG, vent is...
ON during delivery
127
method of venting the heart thru direct LV
- venting thru apex
| - rarely used
128
method of venting the heart thru RSPV
placed in junction of RSPV and left atrium
| -passes into LV thru MV
129
what are the 4 methods of venting the heart
direct LV
RSPV
PA vent
aortic root vent
130
draining the heart drains to reservoir via
roller pump
vacuum source
gravity drainage
131
how to vent the heart during CABG
NO NEED FOR VENTING
| -if heart can't remain decompressed during distal anastomoses a vent should be inserted
132
ostial delivery route for CPG delivery
- rt and left coronary arteries
- important to use during AV operations and subsequent doses of CPG
- avoid high pressures, could damage Ostia
133
cpg flow through left coronary
200 ml/min
134
cpg flow through right coronary
150 ml/min
135
when giving cpg through postal delivery, LV vent must be....
ON during delivery
136
the heart at rest received about __% of CO
5% of CO
137
coronary blood flow is about ___ ml/min
250
138
increases in myocardial oxygen demand must be met by an
increase in coronary blood flow
139
coronary blood flow occurs predominately during
diastole
140
benefits of blood CPG
```
active resuscitation
avoidance of reperfusion damage
limitation of hemodilution
provision of onconicity
buffering
theologic effects
endogenous oxygen free radical scavengers
enhanced oxygen carrying capacity
```
141
warm induction CPG arrest helps
preserve ATP stores
142
reperfusion w/ warm blood CPG helps
myocardial metabolic recovery w/o ATP consumption of contraction
-active resuscitation
143
when is terminal warm induction (hot shot) given
before x clamp removal
144
what is the most commonly used cpg technique
cold blood cpg
145
what is citrate-phosphate-dextrose (CPD) used for
to lower the ionic calcium
146
the buffer is used to maintain
alkaline pH
147
what is the primary advantage of cold blood cpg
- couples the provision of myocardial nourishment with the capacity, through perfusion hypothermia,
- to lower myocardial oxygen demands and the rate and development of ischemic damage
148
what is the rationale for multidose blood cpg
rewarms hearts by replacing any carefully formulated cpg solution with systemic blood at the temp prevailing in the extracorporeal circuit
149
an added benefit of multi dose CPG is that formulation that include buffering and hypocalcemia may
limit reperfusion damage during subsequent doses b/w intermittent ischemic intervals
150
benefits of either warm or cold blood cpg are effective only if
the solutions are delivered to all myocardial regions in sufficient amounts
151
what has helped overcome the limitation of maldistribution of flow of cpg
retrograde CPG
| as good left ventricular protection follows coronary sinus or right atrial perfusion
152
most retrograde perfusion drains via
thebesian veins
153
coronary sinus retroperfusion provides
right ventricular hypothermia
154
venous drainage of the heart is done by what cannulation
retrograde cannulation of coronary sinus
155
why do most surgeons stop the heart with high dose potassium blood cpg and use multi dose lowdose potassium for the reminder of the operation
because hypothermia potentiates electromechanical quiescence
156
cold arrested hearts remain quiescent and both the left and right ventricles recover completely when perfused with
cold retrograde noncardioplegic blood
| 4-10 degree C
157
the advantages of continuous perfusion and nourishment are possible only with non-cog blood because
electromechanical activity returns when warm noncardioplegic blood is delivered either antegrade or retrograde
158
what if continuous perfusion is delivered only via the coronary sinus?
potential right ventricular ischemia
159
What makes it possible to change from "high K+ to low K+ to No K+" during the same procedure and maintain the arrested state
use of cold blood
160
five areas of concern with hyperkalemic cpg
1. unnatural membrane voltages and ionic imbalances
2. coronary vasoconstriction
3. activation the coronary vascular endothelium to become leaky, pro inflammatory and promotes platelet aggregation
4. post operative arrhythmias and conduction disturbances
5. higher incidence of low cardiac output (LOS) from ventricular stunning
161
who is at higher risk for injury to the coronary sinus?
patients with ventricular hypertrophy
162
hypermagnesium can arrest heart by
displacing calcium from receptors in the sarcolemma involved in heart contraction
