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Conduct of Pulmonary Bypass > Myocardial Preservation 2D.1,2 > Flashcards

Myocardial Preservation 2D.1,2 Flashcards

1
Q

cardiac muscles are ….

A

self contracting, autonomically regulated and must continue to contract in rhythmic fashion

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2
Q

structure of cardiac muscles

A
  • mononucleated

- arrangement of actin and myosin is like skeletal striated muscle

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3
Q

Some of the cardiac muscle cells are ___-___

A

auto-rhythmic

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4
Q

____ __ are located b/w cardiac muscle cells

A

intercalated disks

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5
Q

intercalated disk contain _____ which provide communicating channels b/w cells

A

gap junctions

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6
Q

what do intercalated disk allow?

A

waves of depolarizations to sweep across the cells thus synchronizing muscle contraction

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7
Q

Skeletal muscle is ___

A

neurogenic

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8
Q

the beat originates in the ___ ____ itself

A

cardiac muscle

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9
Q

the heart beat is therefore called _____ (muscle + origin)

A

myogenic

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10
Q

cells are rich in ___ ____ at the ____ ____

A

cells are rich in gap junctions at the intercalated discs

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11
Q

the heart is said to act as a functional ____ (single cell) even though composed of individual cells

A

syncytium

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12
Q

what transmit mechanical force from cell-to-cell

A

desmosomes

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13
Q

what is also known as “molecular rivets”

A

desmosomes

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14
Q

Sliding of the cardiac myofibrils is regulated by

A

the intracellular concentration of calcium ions released by the sarcoplasmic reticulum

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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

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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

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17
Q

what happens when the sarcomeres contract?

A
  • Z lines move closer together
  • I band gets smaller
  • thin filaments overlap
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18
Q

How the sliding filament model works (5 steps)

A
  1. ATP activates myosin, bringing to higher energy state
  2. myosin acts binds to an actin filament and changing shape, pulling the actin filament toward the A-band
  3. ATP binds again, destabilizing the myosin filament and enabling it to bind to another site along the actin filament, increasing the strength of contraction
  4. all the myosin heads contract simultaneously, shortening all the sarcomeres, causing the muscle to contract
  5. myosin heads pull the A-band toward the Z-lines
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19
Q

the movement of 3 types of ions determines all aspects of cardiac __,___,___

A

cardiac conduction, contraction, and repolarization

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20
Q

what is another word for cell to cell conduction

A

depolarization

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21
Q

cell to cell conduction through the myocardium is carried by ____ ions

A

Na+ ions

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22
Q

Depolarization may be considered an advancing _________ within the heart’s myocytes

A

wave of positive changes (Na+)

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23
Q

_____ conduction is due to slow movement of Ca2= ions

A

AV node conduction

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24
Q

what produces myocardial contraction

A

the release of free Ca2+ ions into the interiors of the myocytes

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25
Q

following depolarization and contraction, _____ is due to the controlled outflow of K+ ions from the myocytes

A

repolarization

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26
Q

sodium ion movement produces cell-to-cell conduction (of depolarization) in the heart except in the..

A

except the AV node, which depends on the (slow) movement of Ca++ ions

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27
Q

calcium ions (ca++) ions cause

A

myocyte contraction

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28
Q

potassium (K+) ions cause

A

outflow causes repolarization of myocytes

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29
Q

Phase 0

A

depolarization
Na channels open Na in
Na channels close

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30
Q

Phase 1

A

initial repolarization

K leaves thru K channels

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31
Q

Phase 2

A

Plateau

decrease in K permeability
increase in Ca permeability
Ca influx decreased
K efflux causes AP to flatten out

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32
Q

Phase 3

A

rapid repolarization

Ca channels close

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33
Q

Phase 4

A

resting membrane potential

-90mV

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34
Q

what is myocardial protection

A

strategies and methods used to attenuate or prevent post-ischemic myocardial dysfunction that occurs during and after heart surgery

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35
Q

the main principles of myocardial protection are (2)

A
  • reduction of metabolic activity by hypothermia
  • therapeutic arrest of the contractile apparatus and all electrical activity of the myocytes by administering cpg solution
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36
Q

what is myocardial injury

A

inadequate perfusion (blood flow and substrate) to sustain steady-state metabolism at a given level of cardiac work

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37
Q

Determinants of Ischemic injury

A
  • duration of ischemia
  • amount of collateral blood flow
  • O2 demands of the myocardium
  • temperature of myocardium
  • buffering capacity of myocardium
  • edema
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38
Q

Ischemia of the human heart can last for

A
  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)
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39
Q

why understanding myocardial protection is important

A
  • lead to low output syndrome
  • can prolong hospital stay
  • prolong cost
  • may result in delayed myocardial fibrosis
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40
Q

Ischemic/reperfusion injury presents with

A

low CO
hypotension
reversible or irreversible damage

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41
Q

what are some reversible or irreversible damage by inadequate myocardial damage (3)

A
  • 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
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42
Q

manifestations of reperfusion injury associated with CPB

A
  • reperfusion dysthythmias
  • post ischemic systolic and diastolic dysfunction
  • myocardial necrosis
  • endothelial dysfunction
  • wall motion abnormalities
  • EKG abnormalities (arrhythmias)
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43
Q

what are one of the most important factors in ischemia-reperfusion injury

A

Ca++

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44
Q

Na+ -K+ pump

A

3 Na out to 2 K into cell

dependent on ATP availability

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45
Q

when ATP is depleted what happens to NA and membrane potential

A

NA accumulates inside cell

membrane potential is lowered

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46
Q

when ATP is depleted, what happens to Ca++

A

released from lowered membrane potential

  • sarcolemma gated Ca++ channels due to anaerobic metabolism continue
  • results in hydrogen ion accumulation (acidosis) and lactic acid production
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47
Q

Na+ - H+ pump

A

acidosis cause further Na+ accumulation

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48
Q

3Na+ - 1Ca2+ exchanger

A 
function deteriorates due to intracellular Na+ increase 
leads to intracellular Ca2+ accumulation
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49
Q

what is the myocardial ischemic injury list from least to worst damage

A
  • acute ischemic myocardial dysfunction
  • myocardial preconditioning
  • myocardial stunning
  • myocardial hibernation
  • myocardial necrosis vs apoptosis
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50
Q

acute ischemic myocardial dysfunction

A

reversible contractile failure
perfusion pressure (decreased due to coronary spasm, thrombus formation)
O2 supply (not adequately met)
immediate recovery

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51
Q

Myocardial Preconditioning

A

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

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52
Q

myocardial stunning

A
  • 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
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53
Q

myocardial hibernation

A

partially reversible
related to poor myocardial blood flow (poor wall motion)
chronic
revery is weeks to months

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54
Q

myocardial apoptosis

A

irreversible
“suicide”: programmed cell death
intact cell membrane, cell shrinkage, chromatin condensation, phagocytosis w/o inflammation
-myocytes may be salvageable

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55
Q

Myocardial Injury

3 Surgical Phases

A
  1. antecedent ishcemia
  2. protected ischemia
  3. reperfusion injury
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56
Q

antecedent ischemia

A

occurs prior to CPB or CPG delivery

-due to poorly perfused myocardium due to CAD or MI

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57
Q

protected ischemia

A

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

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58
Q

reperfusion injury happens during…

A

sustained during intermittent CPG infusions, after X-clamp removal, or after CPB

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59
Q

when does the most reperfusion injury occur?

A

when cross clamp is removed

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60
Q

reperfusion injury is caused by

A
  • 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
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61
Q

factors that affect the rate at which ischemic injury evolves

A
  • 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
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62
Q

how does age affect the rate at which ischemic injury evolves

A

octogenarians have a 3-fold increase risk of death compared with younger adult

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63
Q

gender

A

adult females have up to 1.6 times higher in-hospital mortality rates and higher morbidity than males

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64
Q

can deliver blood to the heart via

A
  • bronchial
  • mediastinal
  • tracheal
  • esophageal
  • diaphragmatic arteries
  • LIMA and RIMA
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65
Q

what is normal collateral or non-coronary collateral flow in ml/min

A

250 ml/min

66
Q

what is an advantage of delivering collateral or non-coronary collateral flow

A

providing O2 and substrates to ischemic tissues

67
Q

what is a negative of delivering collateral or non-coronary collateral flow

A

washing out cold CPG soon

68
Q

what are the 4 different types of crystalloid CPG

A
  • intracellular
  • extracellulat
  • ALM
  • Del Nido
69
Q

intracellular CPG

A
  • 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
Q

extracellular CPG

aka Buckberg

A
  • depolarized arrest

- high concentrations of sodium, calcium, and magnesium (same amount found in your extracellular space)

71
Q

ALM CPG

A
  • 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
Q

Del Nido CPG

A
  • 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
Q

what is the cardioplegic technique goals

A

-reducing energy consumption and oxygen demand so ischemia tolerance of the heart can be prolonged

74
Q

irreversible ischemic damage begins to occur in the human heart after only

A

20 min

75
Q

irreversible regional injury (necrosis) occurs at

A
  1. min of coronary occlusion
76
Q

with current techniques of myocardial protection, arrest times of more than ____ hrs may be tolerated w/o irreversible damage

A

4-5 hrs

77
Q

what is the goal of CPG

A
  • perfect surgical repair
  • bloodless field
  • use of cardio-protective techniques
78
Q

principles of protection for the heart (5)

A
  1. asystole
  2. hypothermia
  3. buffering
  4. avoidance of edema
  5. enhancements
79
Q

depolarized arrest

A

K+

membrane potential -50 to -60 mV

80
Q

polarized arrest

A

Na+ channel blockers, adenosine, K+ channel openers

arrested heart membrane potential of -80 to -85 mV

81
Q

inhibition of Ca++ influx

A

zero Ca++ in CPG soln

-inhibiting Ca inhibits the excitation-contraction coupling

82
Q

what is mvO2

A

myocardial O2 demand (ml O2/min/100g tissue)

83
Q

at temp of 37, what is the mvO2 of a beating full heart

A

10

84
Q

at 37, what is the mvO2 of a beating empty heart

A

5.5

85
Q

at temp 37, what is the mvO2 of a fibrillating heart

A

6.5

86
Q

at temp 37, what is the mvO2 of K+ CPG arrest

A

1.0

87
Q

a beating heart after x clamp is applied increases

A

the rate of ATP depletion

88
Q

Asystole does what

A

conserves myocardial energy reserves

increase tolerance to ischemia

89
Q

potassium initial dose for arrest

A

10-30 mEq/L

90
Q

potassium maintenance dose

A

10 mEq/L every 20-30 min

91
Q

mvO2 demand decreases only __% with hypothermia alone

A

10%

92
Q

mvO2 demand decreases ___% with hypothermia to 4’C and asystole

A

97%

93
Q

ways to cool the heart

A
  1. systemic cooling, iced saline lavage, ice slush topically on heart, cooling pads, cold CPG
    - PA vent prevents rewarming from bronchial return
94
Q

every 10’C decrease in temp decreases enzyme activity by

A

50%

95
Q

optimal myocardial temp is

A

10-15’C

96
Q

acidosis impairs…

A

enzyme kinetics and metabolism

97
Q

accumulation of hydrogen ions do what to pH

A

reduce tissue pH

98
Q

what is blood’s natural buffer

A

histidine

99
Q

what is used to buffer

A
  • blood
  • tromethamine
  • histidine
  • bicarbonate
  • phosphate
100
Q

what is blood’s benefit in buffering

A

lower incidence of low output syndrome immediately upon reperfusion with blood cardioplegia

101
Q

what is tromethamine (THAM) benefit in buffering

A

adjust pH prior to admin

102
Q

what is histidine benefit in buffering

A

promotes anaerobic glycolysis

improves recovery of high-energy phosphates and contractile function in hypertrophied myocardium

103
Q

what does bicarb do in buffering

A

adjust pH prior to admin

104
Q

what does phosphate do in buffering

A

minimize rapid changes in extracellular and intracellular pH values during the bouts of ischemia-reperfusion

105
Q

edema manifest during reperfusion when

A

water and solutes can escape from leaky capillaries

106
Q

how to avoid edema

A
  • 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
Q

enhancements

A
  • supply metabolic substrates such as glucose, glutamate and aspartate
  • prevent calcium accumulation with CPD and magnesium
  • membrane stabilization
  • vasodilators
108
Q

adenosine purpose

A

coronary vasodilator

enhances cpg delivery

109
Q

magnesium sulfate purpose

A

calcium channel competitor

prevents calcium influx

110
Q

lidocaine/procaine

A

sodium channel blocker

prevents sodium influx

111
Q

histidine/sodium bicarb/THAM

A

buffering agent

counteracts acidosis from ischemia

112
Q

CPG delivery techniques

A
  • hand held syringe
  • pressure bag: difficult to determine pressure and volume delivered
  • roller pump: precise volume and pressure
  • MPS2 myocardial protection system
113
Q

nonrecirculating: single pass CPG system

A
  • 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
Q

recirculating CPG

A
  • 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
Q

continuous CPG system (MPS)

A

microplegia system

-post oxygenator blood is the carrier of small concentrated arresting agent and other additives

116
Q

antegrade cpr delivery route

A

into aortic root

-protects RIGHT and LEFT side

117
Q

cpg infusion pressure for antegrade cpg on pt with severe CAD

A

100-150 measured at the root

118
Q

cpg infusion pressure for antegrade cpg on pt w/o CAD

A

50-90

119
Q

delivery rate of antegrade cpg

A

250 ml/min

120
Q

if the vent is in the ascending aorta, the vent pump must be

A

OFF during the delivery of antegrade cpg

121
Q

if the vent is in the LV, the vent should be

A

ON during antegrade CPG

122
Q

retrograde CPG delivery route

A

into coronary sinus

-protects left ventricle mostly

123
Q

max pressure of retrograde CPG

A

40 mmHg

absolute MAX 50 mmHg

124
Q

reason retrograde doesn’t protect right heart

A

position of balloon can obstruct venous drainage into RA

125
Q

delivery rate for retrograde CPG

A

150 ml/min

126
Q

if giving retrograde CPG, vent is…

A

ON during delivery

127
Q

method of venting the heart thru direct LV

A
  • venting thru apex

- rarely used

128
Q

method of venting the heart thru RSPV

A

placed in junction of RSPV and left atrium

-passes into LV thru MV

129
Q

what are the 4 methods of venting the heart

A

direct LV
RSPV
PA vent
aortic root vent

130
Q

draining the heart drains to reservoir via

A

roller pump
vacuum source
gravity drainage

131
Q

how to vent the heart during CABG

A

NO NEED FOR VENTING

-if heart can’t remain decompressed during distal anastomoses a vent should be inserted

132
Q

ostial delivery route for CPG delivery

A
  • rt and left coronary arteries
  • important to use during AV operations and subsequent doses of CPG
  • avoid high pressures, could damage Ostia
133
Q

cpg flow through left coronary

A

200 ml/min

134
Q

cpg flow through right coronary

A

150 ml/min

135
Q

when giving cpg through postal delivery, LV vent must be….

A

ON during delivery

136
Q

the heart at rest received about __% of CO

A

5% of CO

137
Q

coronary blood flow is about ___ ml/min

A

250

138
Q

increases in myocardial oxygen demand must be met by an

A

increase in coronary blood flow

139
Q

coronary blood flow occurs predominately during

A

diastole

140
Q

benefits of blood CPG

A 
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
Q

warm induction CPG arrest helps

A

preserve ATP stores

142
Q

reperfusion w/ warm blood CPG helps

A

myocardial metabolic recovery w/o ATP consumption of contraction
-active resuscitation

143
Q

when is terminal warm induction (hot shot) given

A

before x clamp removal

144
Q

what is the most commonly used cpg technique

A

cold blood cpg

145
Q

what is citrate-phosphate-dextrose (CPD) used for

A

to lower the ionic calcium

146
Q

the buffer is used to maintain

A

alkaline pH

147
Q

what is the primary advantage of cold blood cpg

A
  • 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
Q

what is the rationale for multidose blood cpg

A

rewarms hearts by replacing any carefully formulated cpg solution with systemic blood at the temp prevailing in the extracorporeal circuit

149
Q

an added benefit of multi dose CPG is that formulation that include buffering and hypocalcemia may

A

limit reperfusion damage during subsequent doses b/w intermittent ischemic intervals

150
Q

benefits of either warm or cold blood cpg are effective only if

A

the solutions are delivered to all myocardial regions in sufficient amounts

151
Q

what has helped overcome the limitation of maldistribution of flow of cpg

A

retrograde CPG

as good left ventricular protection follows coronary sinus or right atrial perfusion

152
Q

most retrograde perfusion drains via

A

thebesian veins

153
Q

coronary sinus retroperfusion provides

A

right ventricular hypothermia

154
Q

venous drainage of the heart is done by what cannulation

A

retrograde cannulation of coronary sinus

155
Q

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

A

because hypothermia potentiates electromechanical quiescence

156
Q

cold arrested hearts remain quiescent and both the left and right ventricles recover completely when perfused with

A

cold retrograde noncardioplegic blood

4-10 degree C

157
Q

the advantages of continuous perfusion and nourishment are possible only with non-cog blood because

A

electromechanical activity returns when warm noncardioplegic blood is delivered either antegrade or retrograde

158
Q

what if continuous perfusion is delivered only via the coronary sinus?

A

potential right ventricular ischemia

159
Q

What makes it possible to change from “high K+ to low K+ to No K+” during the same procedure and maintain the arrested state

A

use of cold blood

160
Q

five areas of concern with hyperkalemic cpg

A
  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
Q

who is at higher risk for injury to the coronary sinus?

A

patients with ventricular hypertrophy

162
Q

hypermagnesium can arrest heart by

A

displacing calcium from receptors in the sarcolemma involved in heart contraction

Conduct of Pulmonary Bypass (2 decks)

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