Myocardial Preservation 2D.1,2 Flashcards
cardiac muscles are ….
self contracting, autonomically regulated and must continue to contract in rhythmic fashion
structure of cardiac muscles
- mononucleated
- arrangement of actin and myosin is like skeletal striated muscle
Some of the cardiac muscle cells are ___-___
auto-rhythmic
____ __ are located b/w cardiac muscle cells
intercalated disks
intercalated disk contain _____ which provide communicating channels b/w cells
gap junctions
what do intercalated disk allow?
waves of depolarizations to sweep across the cells thus synchronizing muscle contraction
Skeletal muscle is ___
neurogenic
the beat originates in the ___ ____ itself
cardiac muscle
the heart beat is therefore called _____ (muscle + origin)
myogenic
cells are rich in ___ ____ at the ____ ____
cells are rich in gap junctions at the intercalated discs
the heart is said to act as a functional ____ (single cell) even though composed of individual cells
syncytium
what transmit mechanical force from cell-to-cell
desmosomes
what is also known as “molecular rivets”
desmosomes
Sliding of the cardiac myofibrils is regulated by
the intracellular concentration of calcium ions released by the sarcoplasmic reticulum
when do muscles contract and what is required for this to occur?
- muscles contract when sarcomeres shorten
- ATP is required for this to occur
Do the sarcomeres shorten during contraction?
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
what happens when the sarcomeres contract?
- Z lines move closer together
- I band gets smaller
- thin filaments overlap
How the sliding filament model works (5 steps)
- 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
the movement of 3 types of ions determines all aspects of cardiac __,___,___
cardiac conduction, contraction, and repolarization
what is another word for cell to cell conduction
depolarization
cell to cell conduction through the myocardium is carried by ____ ions
Na+ ions
Depolarization may be considered an advancing _________ within the heart’s myocytes
wave of positive changes (Na+)
_____ conduction is due to slow movement of Ca2= ions
AV node conduction
what produces myocardial contraction
the release of free Ca2+ ions into the interiors of the myocytes
following depolarization and contraction, _____ is due to the controlled outflow of K+ ions from the myocytes
repolarization
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
calcium ions (ca++) ions cause
myocyte contraction
potassium (K+) ions cause
outflow causes repolarization of myocytes
Phase 0
depolarization
Na channels open Na in
Na channels close
Phase 1
initial repolarization
K leaves thru K channels
Phase 2
Plateau
decrease in K permeability
increase in Ca permeability
Ca influx decreased
K efflux causes AP to flatten out
Phase 3
rapid repolarization
Ca channels close
Phase 4
resting membrane potential
-90mV
what is myocardial protection
strategies and methods used to attenuate or prevent post-ischemic myocardial dysfunction that occurs during and after heart surgery
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
what is myocardial injury
inadequate perfusion (blood flow and substrate) to sustain steady-state metabolism at a given level of cardiac work
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
Ischemia of the human heart can last for
- for only a few seconds or minutes (angioplasty or angina)
- for hours (cardiac surgery or infarction
- for years (chronic ischemic heart disease)
why understanding myocardial protection is important
- lead to low output syndrome
- can prolong hospital stay
- prolong cost
- may result in delayed myocardial fibrosis
Ischemic/reperfusion injury presents with
low CO
hypotension
reversible or irreversible damage
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
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)
what are one of the most important factors in ischemia-reperfusion injury
Ca++
Na+ -K+ pump
3 Na out to 2 K into cell
dependent on ATP availability
when ATP is depleted what happens to NA and membrane potential
NA accumulates inside cell
membrane potential is lowered
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
Na+ - H+ pump
acidosis cause further Na+ accumulation
3Na+ - 1Ca2+ exchanger
function deteriorates due to intracellular Na+ increase leads to intracellular Ca2+ accumulation
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
acute ischemic myocardial dysfunction
reversible contractile failure
perfusion pressure (decreased due to coronary spasm, thrombus formation)
O2 supply (not adequately met)
immediate recovery
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
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
myocardial hibernation
partially reversible
related to poor myocardial blood flow (poor wall motion)
chronic
revery is weeks to months
myocardial apoptosis
irreversible
“suicide”: programmed cell death
intact cell membrane, cell shrinkage, chromatin condensation, phagocytosis w/o inflammation
-myocytes may be salvageable
Myocardial Injury
3 Surgical Phases
- antecedent ishcemia
- protected ischemia
- reperfusion injury
antecedent ischemia
occurs prior to CPB or CPG delivery
-due to poorly perfused myocardium due to CAD or MI
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
reperfusion injury happens during…
sustained during intermittent CPG infusions, after X-clamp removal, or after CPB
when does the most reperfusion injury occur?
when cross clamp is removed
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
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
how does age affect the rate at which ischemic injury evolves
octogenarians have a 3-fold increase risk of death compared with younger adult
gender
adult females have up to 1.6 times higher in-hospital mortality rates and higher morbidity than males
can deliver blood to the heart via
- bronchial
- mediastinal
- tracheal
- esophageal
- diaphragmatic arteries
- LIMA and RIMA
what is normal collateral or non-coronary collateral flow in ml/min
250 ml/min
what is an advantage of delivering collateral or non-coronary collateral flow
providing O2 and substrates to ischemic tissues
what is a negative of delivering collateral or non-coronary collateral flow
washing out cold CPG soon
what are the 4 different types of crystalloid CPG
- intracellular
- extracellulat
- ALM
- Del Nido
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
extracellular CPG
aka Buckberg
- depolarized arrest
- high concentrations of sodium, calcium, and magnesium (same amount found in your extracellular space)
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
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
what is the cardioplegic technique goals
-reducing energy consumption and oxygen demand so ischemia tolerance of the heart can be prolonged
irreversible ischemic damage begins to occur in the human heart after only
20 min
irreversible regional injury (necrosis) occurs at
- min of coronary occlusion
with current techniques of myocardial protection, arrest times of more than ____ hrs may be tolerated w/o irreversible damage
4-5 hrs
what is the goal of CPG
- perfect surgical repair
- bloodless field
- use of cardio-protective techniques
principles of protection for the heart (5)
- asystole
- hypothermia
- buffering
- avoidance of edema
- enhancements
depolarized arrest
K+
membrane potential -50 to -60 mV
polarized arrest
Na+ channel blockers, adenosine, K+ channel openers
arrested heart membrane potential of -80 to -85 mV
inhibition of Ca++ influx
zero Ca++ in CPG soln
-inhibiting Ca inhibits the excitation-contraction coupling
what is mvO2
myocardial O2 demand (ml O2/min/100g tissue)
at temp of 37, what is the mvO2 of a beating full heart
10
at 37, what is the mvO2 of a beating empty heart
5.5
at temp 37, what is the mvO2 of a fibrillating heart
6.5
at temp 37, what is the mvO2 of K+ CPG arrest
1.0
a beating heart after x clamp is applied increases
the rate of ATP depletion
Asystole does what
conserves myocardial energy reserves
increase tolerance to ischemia
potassium initial dose for arrest
10-30 mEq/L
potassium maintenance dose
10 mEq/L every 20-30 min
mvO2 demand decreases only __% with hypothermia alone
10%
mvO2 demand decreases ___% with hypothermia to 4’C and asystole
97%
ways to cool the heart
- systemic cooling, iced saline lavage, ice slush topically on heart, cooling pads, cold CPG
- PA vent prevents rewarming from bronchial return
every 10’C decrease in temp decreases enzyme activity by
50%
optimal myocardial temp is
10-15’C
acidosis impairs…
enzyme kinetics and metabolism
accumulation of hydrogen ions do what to pH
reduce tissue pH
what is blood’s natural buffer
histidine
what is used to buffer
- blood
- tromethamine
- histidine
- bicarbonate
- phosphate
what is blood’s benefit in buffering
lower incidence of low output syndrome immediately upon reperfusion with blood cardioplegia
what is tromethamine (THAM) benefit in buffering
adjust pH prior to admin
what is histidine benefit in buffering
promotes anaerobic glycolysis
improves recovery of high-energy phosphates and contractile function in hypertrophied myocardium
what does bicarb do in buffering
adjust pH prior to admin
what does phosphate do in buffering
minimize rapid changes in extracellular and intracellular pH values during the bouts of ischemia-reperfusion
edema manifest during reperfusion when
water and solutes can escape from leaky capillaries
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
enhancements
- supply metabolic substrates such as glucose, glutamate and aspartate
- prevent calcium accumulation with CPD and magnesium
- membrane stabilization
- vasodilators
adenosine purpose
coronary vasodilator
enhances cpg delivery
magnesium sulfate purpose
calcium channel competitor
prevents calcium influx
lidocaine/procaine
sodium channel blocker
prevents sodium influx
histidine/sodium bicarb/THAM
buffering agent
counteracts acidosis from ischemia
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
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
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
continuous CPG system (MPS)
microplegia system
-post oxygenator blood is the carrier of small concentrated arresting agent and other additives
antegrade cpr delivery route
into aortic root
-protects RIGHT and LEFT side
cpg infusion pressure for antegrade cpg on pt with severe CAD
100-150 measured at the root
cpg infusion pressure for antegrade cpg on pt w/o CAD
50-90
delivery rate of antegrade cpg
250 ml/min
if the vent is in the ascending aorta, the vent pump must be
OFF during the delivery of antegrade cpg
if the vent is in the LV, the vent should be
ON during antegrade CPG
retrograde CPG delivery route
into coronary sinus
-protects left ventricle mostly
max pressure of retrograde CPG
40 mmHg
absolute MAX 50 mmHg
reason retrograde doesn’t protect right heart
position of balloon can obstruct venous drainage into RA
delivery rate for retrograde CPG
150 ml/min
if giving retrograde CPG, vent is…
ON during delivery
method of venting the heart thru direct LV
- venting thru apex
- rarely used
method of venting the heart thru RSPV
placed in junction of RSPV and left atrium
-passes into LV thru MV
what are the 4 methods of venting the heart
direct LV
RSPV
PA vent
aortic root vent
draining the heart drains to reservoir via
roller pump
vacuum source
gravity drainage
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
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
cpg flow through left coronary
200 ml/min
cpg flow through right coronary
150 ml/min
when giving cpg through postal delivery, LV vent must be….
ON during delivery
the heart at rest received about __% of CO
5% of CO
coronary blood flow is about ___ ml/min
250
increases in myocardial oxygen demand must be met by an
increase in coronary blood flow
coronary blood flow occurs predominately during
diastole
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
warm induction CPG arrest helps
preserve ATP stores
reperfusion w/ warm blood CPG helps
myocardial metabolic recovery w/o ATP consumption of contraction
-active resuscitation
when is terminal warm induction (hot shot) given
before x clamp removal
what is the most commonly used cpg technique
cold blood cpg
what is citrate-phosphate-dextrose (CPD) used for
to lower the ionic calcium
the buffer is used to maintain
alkaline pH
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
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
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
benefits of either warm or cold blood cpg are effective only if
the solutions are delivered to all myocardial regions in sufficient amounts
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
most retrograde perfusion drains via
thebesian veins
coronary sinus retroperfusion provides
right ventricular hypothermia
venous drainage of the heart is done by what cannulation
retrograde cannulation of coronary sinus
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
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
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
what if continuous perfusion is delivered only via the coronary sinus?
potential right ventricular ischemia
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
five areas of concern with hyperkalemic cpg
- unnatural membrane voltages and ionic imbalances
- coronary vasoconstriction
- activation the coronary vascular endothelium to become leaky, pro inflammatory and promotes platelet aggregation
- post operative arrhythmias and conduction disturbances
- higher incidence of low cardiac output (LOS) from ventricular stunning
who is at higher risk for injury to the coronary sinus?
patients with ventricular hypertrophy
hypermagnesium can arrest heart by
displacing calcium from receptors in the sarcolemma involved in heart contraction
