This document discusses various strategies for myocardial protection during cardiac surgery. It describes how ischemia and reperfusion injury can damage the myocardium. The goals of myocardial protection are to reduce oxygen demand, maintain adequate perfusion, and minimize injury during reperfusion. Techniques discussed include cardioplegic arrest, hypothermia, venting, intermittent clamping, and pharmacological additives to cardioplegia solutions. The optimal method balances protection against procedural complexity and aims to prevent intraoperative damage and ensure postoperative cardiac function.

1. MYOCARDIAL PROTECTION
GOAL
TO PROTECT THE
MYOCARDIUM FROM
INTRAOPERATIVE DAMAGES
MYOCARDIAL PROTECTION
GOAL
TO PROTECT THE
MYOCARDIUM FROM
INTRAOPERATIVE DAMAGES

2. PATHOPHYSIOLOGY OF SURGICAL
ISCHEMIA
 Myocardial injury in surgical setting occurs
1. Pre cpb
2. During cpb
3. After cpb(post ishemic reperfusion)

3. Determinants of ishemic injury
 Accumilation of tissue
metabolites(lactate,co2 and hydrogen ions)
 Duration of ishemia
 Baseline health of tissue
 Distinction b/w Global and regional ishemia

4. Mechanisms of myocardial ischemic
injury
 Depletion of high energy phosphates
 Intracellular acidosis.
 Alteration in intracellular calcium.
 Direct myocellular injury from ischemia.
 Oxygen derived free radicals generation
upon reperfusion.
 Myocardial edema from ischemia and
reperfusion.

5. Cessation of Myocardial Blood
Flow
mitochondria
cellular pO2 < 5mmHg within
seconds
oxidative phosphorilation
stops
cytosol
anaerobic glycolysis
glycogen
glucose-6-phosphate
pyruvate
lactate
cellular acidosis
depletion of ATP

6. Depletion of ATP < 50% of Normal
Level-
irreversible lethal cell injury
 glycolysis is blocked
 increasing cellular acidity
 protein denaturation
 structural, enzymatic, nuclear changes

7. Severity and duration of ischemia
 The potential for myocardial injury related to
duration of warm ischemia
To reduce the severity of postischemic injury
1. Rapid arrest
2. Venting LV to decrease O2 requirements
3. Imposing cardiac hypothermia
• Safe period 15 to 45 mts. Up to 4hrs with
hypothermic intermittant cardioplegia

8. WHAT DETERMINES MYOCARDIAL
OXYGEN DEMAND
 Stroke volume
 Aortic pressure or wall stress on LV
 Heart rate
 Basal metabolic rate

9. How to reduce myocardial oxygen
demand ?
 CPB and diastolic arrest substantially
reduces cardiac load by 50%
 Hypothermia
 Ventricular decompression with venting
 Regional ischemia results in
1. subendocardial infarction
2. contractile dysfunction

10. REPERFUSION INJURY
 Defined as pathology that developes as a
consequence of events occuring after
restoration of blood flow

11. Factors contributing reperfusion injury
 Calcium influx into cells
 Generation of oxygen free radicals(sources
mitocondria, vascular endothelium)
 Neutrophil activation
 Complement activation

12. Manifestations of Reperfusion injury
Produces numerous abnormalities as listed
 Reperfusion dysarhythmias
 Postischemic systolic and diastolic dysfunction
 Myocardial necrosis
 Endothelial dysfunction
 Apoptosis(cell death)
 Myocardial edema
 Microvascular injury(no reflow)

13. How to minimize reperfusion injury ?
 Decrease extracellular calcium
 Addition of antioxidants like superoxide
dismutase,glutathione
 Controlled reperfusion
 mannitol

14. Myocardium, Coronary Flow
 coronary blood flow: 250 ml/min
 entirely during diastole
~ aortic diastolic pressure minus LVDP
~ duration of diastole
 pressure < 150 mmHg
 oxygenated by superb membrane
oxygenator-”the lungs”

15. Myocardial Protection
encompass all the strategies employed during
cardiac surgery
 preoperative phase
 operative phase
– global myocardial ischaemic time
– reperfusion
 postoperative phase

16. Myocardial oxygen cosumption
Reduction Oxygen Demand
Normothermic Arrest (37ο
C) 1mL/100g/min 90%
Hypothermic Arrest (22ο
C) 0.30 mL/100g/min
Hypothermic Arrest (10ο
C) 0.14 mL/100g/min ~ 97%

17. Myocardial oxygen consumption
contd.,
 Normal working myocardium consumes
8ml/100gm of oxygen/minute.
 Empty beating heart consumes
5.6ml/100gm/minute.
 Potassium arrested heart consumes
1.1ml/100gm/mt
 Myocardial cooling reduces the consumption
to .3ml/100gm/mt of myocardium

18. HYPOTHERMIA
 lowers metabolic rate
 decrease myocardial energy requirements
 promoting electromechanical quiescence
 every 10 0C in temperature, VO2 halved

19. Normothermic Ischaemia
(canine heart)
 20 minutes- completely reversible
 40 minutes- half the cells are necrotic
 1 hour- lethal for all cells

20. Cardioplegic Strategies
 sufficient reduction of oxygen demands
 delivery to all cardiac regions

21. Types of Cardioplegia
crystalloid
blood

22. Types of Cardioplegia
 crystalloid
Pros
 Inexpensive
 Simplicity
 Availability
Cons
 Hemodilution
 No buffering
 No oxygen carrying
capacity
Blood
Pros
 Oxygen carrying ability
 Buffering capacity
 Osmolarity,electrolyte
 Free radical scavenging
ability
Cons
 Cost
 complexity

23. Cardioplegic Temperature
cold (9 0
C)
tepid (29 0
C)
warm (37 0
C)

24. Cardioplegic Route
antegrade (aorta)
retrograde (coronary sinus)

25. Antegrade Cardioplegia
Advantages
 Produces prompt arrest.
 Simple
 Mimics normal coronary
flow
pitfalls
 poor distribution in coronary
patients unless delivered
through the vein grafts
 poor distribution in patients
with aortic regurgitation
 risk of ostial injury from direct
perfusion (during AVR)
 interruption of procedure
during mitral surgery

26. Retrograde Cardioplegia
 perfusion pressure < 40 mmHg
prevent perivascular haemorrhage and
oedema!
 flow rate = 200mL/min

27. Retrograde Cardioplegia
advantages
 distribution of CP to
regions supplied by
occluded or stenosed
vessels
 improved subendocardial
CP delivery
 flushing of air and/or
atheromatous debris
 Does not impede surgery
pitfalls
 shunting of CP into
ventricular cavities via
Thebesian channels
 perfusion defects especially
right ventricle and posterior
septal regions
 Catheter placement can be
difficult
 complex

28. Blood Cardioplegia
1980’s
 improved oxygen carrying capacity and delivery until
electromechanical quiescence developed
 enhanced myocardial oxygen consumption
 preserved high-energy phosphate stores
 buffering changes in pH
 use of free radical scavengers (superoxide dismutase,
catalase, and glutathione)
 provide appropriate osmotic environment for myocardial
cells and lessen the myocardial oedema

29. “The heart takes up oxygen over time
rather than by dose,
so that blood cardioplegic solutions must
be delivered over a time interval, rather
than by volume”

30. Cold Blood Cardioplegia
advantages
 lowers myocardial oxygen
demands
pitfalls
 hypothermic inhibition of
mitochondrial enzymes
 shifting oxyhaemoglobin
dissociation curve to left
 activating platelets,
leukocytes, complement
 impaired membrane
stabilization

31. Microplegia
 A cardioplegia technique that mixes blood
from CPB circuit with small quantities of
concentrated additives.(Pottssium)
 Relies on precision pumps to deliver
accurate quantities of additives.
 Minimizes crystalloid quantity of cardioplegia
solution.

32. Warm Induction
“resuscitation of the heart”
 severe left ventricular dysfunction
 cardiogenic shock
preischaemic depletion of energy stores
warm induction showed improved aerobic
metabolism and LV function in dogs

33. Warm Reperfusion (hot-shot)
 early myocardial metabolic recovery while
maintaining electro-mechanical arrest
 repletion of energy stores
 maintenance of unnecessary contractile activity

34. Continuous Warm Cardioplegia
 avoidance of direct myocellular injury
inflicted by any cold solution or
environment
 increased rate of perioperative stroke and
neurological events

35. Cardioplegia delivery schedule
Intermittent
Pros
 Improved exposure
 Lower cardioplegia
volume
Cons
Increased inter-dose
myocardial acidosis
Continuous
Pros
 Normal perfusion
 Increased postop LV
function
 Decreased ionotropic
requirement
Cons
 Wet field,Complex

36. Myocardial monitoring technique
Temperature
Pros
 Ease of use
Cons
 Location dependent
 Temp not equivalent to
protection
Ph
Pros
 Potential to alter
surgical conduct and
improve protection.
Cons
 Specialized equipment
 Efficacy unclear

37. Cardioplegia Additives
Drug Advantage Dis adv
Nicorandil Less plegia/Kcl Cost
requirement
reduced periop
coronary spasm
preconditioning
reduced need of
catacolamines post op

38. Cardioplegia additives contd
 L-argine
Advantages
1. Decreased myocardial enzyme release
2. Reduced postop cytokine levels
3. Reduced pulmonary artery wedge pressure
Disadvantages
1. Cost
2. complexity

39. Cardioplegia additives contd
 Insulin
Advantages
1. Increased survival and improved LV
function in some studies
Disadvantages
1. Complexity
2. Efficacy unclear

40. Substrate Enhancement of
Cardioplegia
 Krebs-cycle intermediates
– glutamate
– aspartate
 Insulin-improves LV function
 Nitric oxide (NO) / L-arginine decreases myocardial
enzyme release,reduces cytokine levels and reduces
pulmonary artery wedge pressure

41. “during all phases ventricular distension
must be avoided to prevent the rise of
ventricular oxygen demands produced by
increased wall tension”

42. Myocardial protection without
cardioplegia
 Ventricular fibrillation
 Ventricullar fibrillation with intermittent cross
clamping.
 Off-pump surgery.

43. Ventricular Fibrillation with
Intermittent Aortic Cross-clamping
 induces global ischaemia with fibrillation,
followed by anoxic arrest and electrical silence
on the ECG

44. Ventricular Fibrillation with
Intermittent Aortic Cross-clamping
Advantages
 cumulative cross-clamp times are less than with
cardioplegia
 the myocardium is intermittently perfused with oxygenated
blood
 increasing areas of myocardium are reperfused during the
course of the procedure
Disadvantages
 Repeated aortic clamping
 Anastomotic time limited

45. Therapies Under Investigation
Physiological
superoxide dismutase
catalase
nitric oxide
Pharmacological
mannitol
allopurinol
antioxidants
Physical
ischaemic preconditioning
hypothermia
hypoxic reperfusion

46. THANK YOU