MYOCARDIAL

PROTECTION
DR. RHEECHA JOSHI
FCPS RESIDENT
• Myocardial protection refers to strategies and methodologies used
either to attenuate or to prevent post ischemic myocardial
dysfunction that occurs during and after heart surgery

• surgically induced myocardial ischemia is secondary to aortic cross-

clamping

• cessation of coronary blood flow such that oxygen delivery to the

myocardium is insufficient to meet basal myocardial requirements to
preserve cellular membrane stability and viability
• The clinical manifestations of myocardial damage present as

 low cardiac output syndrome due to impaired myocardial contractility,

dysrhythmias,

decreased ventricular compliance or

 segmental myocardial wall motion abnormalities

 Primary mediators of injury :
intracellular Ca2 overload during ischemia and reperfusion
 oxidative stress induced by reactive oxygen species (ROS) generated at the
onset of reperfusion
• decreased cytosolic phosphorylation potential [ATP]-/-([ADP] [Pi]), results
in less free energy from ATP hydrolysis than is necessary to drive the
energy-dependent pumps (sarcoplasmic reticulum Ca2-ATPase, the
sarcolemmal Ca2-ATPase) that maintain intracellular calcium homeostasis
• Restoration of intracellular pH at the onset of reperfusion via Na-H
exchange contributes to intracellular Ca2 overload via reversed Na-Ca2
exchange
Three basic types of injury occur during heart surgery
Myocardial stunning
Apoptosis
MI
Myocardial stunning
• last for only a few hours or persist for several days despite the
restoration of normal blood flow
• Cells are reversibly injured (stunned)
• exhibit no sign of ultrastructural damage
Apoptosis
• is “suicidal” programmed cell death, characterized by retention of an
intact cell membrane, cellshrinkage, chromatin condensation, and
phagocytosis without inflammation
MI
• irreversible injury in the form of infarction, necrosis, and a spectrum
of reperfusion associated pathologies manifested as membrane
destruction, cell swelling, DNA degradation, cytolysis, and the
induction of an inflammatory response collectively called reperfusion
injury
Goals and principles of myocardial
protection
• current cardioprotection strategies are designed to reduce cellular and
subcellular ROS formation and oxidative stress, to enhance the heart’s
endogenous antioxidant defense mechanisms, and to prevent intracellular
Ca2 overload

• principal determinants of myocardial energy utilization are left ventricular

end diastolic wall tension (LVEDP) and electromechanical activity

• majority of cardioprotective strategies now available do allow patients to

undergo conventional and complex heart operations with an operative
mortality rate ranging from less than 2 to 4%
Types of Myocardial Protection
• Cardioplegia
• Off-pump coronary artery bypass surgery (OPCAB)
• Ischemic preconditioning
• on-pump beating-heart surgery
• Intermittent ischemic arrest
NONCARDIOPLEGIC TECHNIQUES
• Intermittent Cross-Clamping with Fibrillation

• Systemic Hypothermia and Elective Fibrillatory Arrest

Intermittent Cross-Clamping with Fibrillation

• intermittent aortic cross clamping with fibrillation and moderate

hypothermic perfusion (30 to 32C)

• Using this approach, CABG can be performed on the unarrested heart

with ascending aorta cannulation and generally a two-stage single
venous cannula
Systemic Hypothermia and Elective
Fibrillatory Arrest
• systemic hypothermia (28C), elective fibrillatory arrest, and
maintenance of systemic perfusion pressure at between 80 and 100
mm Hg

 Limitations
• the surgical field may be obscured by blood during revascularization
• ventricular fibrillation is associated with increased muscular tone, which
can limit the surgeon’s ability to position the heart for optimal exposure
• it is generally not applicable for intracardiac procedures
CARDIOPLEGIC TECHNIQUES
• to arrest the heart rapidly in diastole, create a quiet operating field,
and provide reliable protection against ischemia-reperfusion injury

• Cross-clamping of the aorta without the use of cardioplegia results in

anaerobic metabolism and depletion of myocardial energy stores

• Types: crystalloid cardioplegia and blood cardioplegia

Cold Crystalloid Cardioplegia
Cold Blood Cardioplegia
Warm Blood Cardioplegia
Tepid Blood Cardioplegia

• potassium (20–40 mEq/l), which causes membrane depolarization

• sodium (100–200 mEq/l) minimizes the transcellular sodium gradient
and so reduces intracellular edema
• Chloride ions maintain the electroneutrality of the solution
• a cardioplegic catheter inserted into the aorta proximal to the cross-clamp.The
cold hyperkalemic crystalloid solution then is infused (antegrade) at a volume
that generally does not exceed 1000 mL

• One or more infusions of 300 to 500 mL of the cardioplegic solution may be

administered ( evidence of electrical heart activity resumption or if a prolonged
ischemic time is anticipated)

• can be administered directly into the coronary arteries via cannulation of the
coronary ostia/ can be administered retrograde via a coronary sinus catheter with
or without a self-inflating silicone cuff
Cold Crystalloid Cardioplegia
• provides little substrate and no oxygen to the heart during the period of ischemic
arrest. It functions primarily by arresting the heart at cold temperatures
• two types of crystalloid cardioplegic solutions:
• the intracellular type : by absent or low concentrations of Na and Ca
• the extracellular type: higher concentrations of sodium, calcium, and magnesium

• Both types avoid concentrations of potassium 40 mmol/L (10 - 40

mmol/L) ,contain bicarbonate for buffering, and are osmotically balanced

• the perioperative MI rate is < 4%, and the operative mortality rate is < 2%
Cold Blood Cardioplegia
• combining autologous blood obtained from the extracorporeal circuit
while the patient is on CPB with a crystalloid solution consisting of citrate-
phosphate-dextrose (CPD), tris-hydroxymethyl- aminomethane (tham) or
bicarbonate (buffers), and potassium chloride approximately 30 mmol/L

• the temperature of the solution usually is lowered between 12 and 4C

• The ratio of blood to crystalloid varies among centers, with the most
common ratios being 8:1, 4:1, and 2:1
• The oxygen demand of the heart is reduced by nearly 90% by simply
arresting the heart at normothermia

• maintenance of arrest during the cross-clamp period is accomplished

by readministering the solution every 15–20 minutes to deliver
potassium and wash out metabolic byproducts

• A low potassium solution (12–15 mEq/L) is used to maintain the

arrest while avoiding an excess potassium load; the high-potassium
solution should be used if the heart resumes any activity.
• rationales for using blood as a vehicle for hypothermic potassium-induced cardiac
arrest include
1. It can provide an oxygenated environment.
2. It can provide a method for intermittent reoxygenation of the heart during arrest.
3. It can limit hemodilution when large volumes of cardioplegia are used.
4. It has an excellent buffering capacity.
5. It has excellent osmotic properties.
6. The electrolyte composition and pH are physiologic.
7. It contains a number of endogenous antioxidants and free-radical scavengers.
8. It can be less complex than other solutions to prepare.
Warm Blood Cardioplegia
• Since enzymatic and cellular reparative processes function better at normothermia,
warm cardioplegia gives excellent results

• the sodium potassium ATPase is kept intact, helping to limit the amount of cellular
swelling and third space edema within the myocardium. Also it prevents damage to
the coagulation enzymes, thus reducing bleeding once cardiopulmonary bypass is
terminated

• must be given continuously or with only brief interruptions to protect the heart

• When given continuously, it can obscure the operative field and cause hemodilution
• To minimize hemodilution from excessive cardioplegia administration, the
“miniplegia” system that simply adds potassium to the blood is useful

• how long the warm heart can tolerate an ischemic event, which may occur
when the infusion is interrupted, flow rates are reduced owing to an
obscured surgical field, or a maldistribution of the cardioplegic solution
occurs

• the use of warm cardioplegia is associated with increased incidence of

neurologic deficits (the incidence of permanent neurologic deficits was
threefold greater in the warm blood group (3.1 versus 1.0%)
• can be used as an adjunct to cold cardioplegia
Warm induction
• involves administering 500 mL of warm cardioplegia immediately after aortic cross-
clamping
• brief period of time during which oxygen can be used to repair cell damage and
replace energy stores
Terminal warm blood cardioplegia (“hot shot”) only blood/non cardioplegic
• a terminal infusion of warm blood cardioplegia before removing the cross-clamp
accelerates myocardial metabolic recovery
• The heart tends to remain asystolic for several minutes after removal of the aortic
cross-clamp, during which time the heart is able to “repair” cellular processes or
replenish energy stores while the oxygen demand is low
Tepid Blood Cardioplegia
• a number of studies are performed to determine the optimal temperature of
cardioplegia solution

• Tepid blood cardioplegia : 32 C to 20 C

• the tepid antegrade cardioplegia was the most effective in reducing anaerobic
lactate acid release during the arrest period

• Whether tepid cardioplegia confers better protection over other current

methodologies remains to be determined
SECP substrate enhanced cardioplegia
Methods of Delivery
ACP /antegrade cardioplegia delivery
• Antegrade infusion pressure : 60 and 80 mmHg

• care must be taken to eliminate air from the aortic root when the cardioplegia is
readministered

• The efficacy of ACP delivery is compromised by

• severe coronary artery stenosis and is often dependent on collateral flow/ High pressure
during infusion
• sufficient root distention may not be achieved in patients with more than mild aortic
insufficiency. antegrade cardioplegia will be infused partially into the left ventricle and will
not be distributed into the myocardium very effectively.
• Light manual pressure applied to the right ventricle will help close the left ventricular
outflow tract
Retrograde cardioplegia (RCP) delivery
• is easy to administer, either intermittently or continuously, and does not interrupt
the flow of an operation
• Careful monitoring of coronary sinus pressure during the administration of
retrograde cardioplegia is essential
• if it is too high (>50 mm Hg), coronary sinus rupture can occur
• if it is too low (< 20 mm Hg), there is usually a problem with catheter malposition
/the balloon is not inflated or not occluding the coronary sinus
• If low retrograde infusion pressure : the presence of a left superior vena cava.
the vessel is occluded with a tourniquet only if an intact innominate vein is
present. If the innominate vein is absent, only antegrade cardioplegia is used
• Retrograde cardioplegia has the theoretical advantage of ensuring a
more homogeneous distribution of the cardioplegic solution to
regions of the heart that are poorly collateralized

• can result in a poor distribution of the solution to the right ventricle

• variable venous anatomy of the hear, coronary sinus anomalies

Cardioplegia temperature
• Crystalloid cardioplegia solutions : 4 ° C
• Cold blood solutions : 10–16 ° C
• Warm blood solutions : 37 ° C

Adequacy of cardioplegia distribution is confirmed by monitoring

myocardial temperature/ placed in the septum first
• Temperature is generally kept below 15 ° C
• pH probe
THANK YOU!
References
• Manual of perioperative care in adult cardiac surgery- Robert M Bojar
• Cardiac surgery in the Adult- Lawerence H Cohn
• Surgery of the chest- Sabiston and Spencer
• Cardiothoracic Surgery Fritz J. Baumgartner