Why and how to protect the heart intraoperatively.

1. Dr Dhanesh Kumar

2. DEFINITION
Strategies and methodologies used either
to attenuate or to prevent post-ischemic
myocardial dysfunction that occurs during
and after heart surgery.

3. 1.Protect against ischemic injury
during surgery on a motionless,
bloodless heart.
2.Allow effective post-ischemic
myocardial resuscitation
Goals of Myocardial
protection

4. WHY NEED FOR
PROTECTION
CONDITIONS OF CPB
- Transmural & subendocardial resistance increased
- VF increases intramyocardial tension more
- Circulating vasoactive agents
- Circulating blood: itself highly abnormal
VULNERABILITY OF DISEASED HEART
Hypertrophied heart
- Xanthine oxidase more, Superoxide dismutase less
- Wall characterstics

5. Chronic heart failure
- Energy stores decreased
- Hemodynamical unstability
SURGICAL REQUIREMENTS
-Bloodless field
-quiescent heart

6. Spectrum of myocardial
ischemic injury
Acute ischemic dysfunction
Preconditioning
Stunning
Hibernation
Necrosis vs. Apoptosis

7. Acute ischemic
dysfunction
Reversible contractile failure
Perfusion pressure
O2 supply
Inmediate recovery

8. Preconditioning
Reversible
Slowed energy utilization
Reduction in myocardial necrosis
Increase protective abilities of
myocardium
Presented as a normal proper
protective reaction of the ischemic
myocardium
Recovery in Hrs

9. Stunning
Partially Reversible
May be accompained by endothelial
dysfunction (NO) causing reduced
coronary blood flow
Result of ischemia-reperfusion insult
Mediated by increased intracellular
Ca accumulation
Recovery in Hrs, Wks

10. Hibernation
Partially Reversible
Related to poor myocardial
blood flow
Chronic
Recovery Wks, Months

11. Necrosis
Irreversible
Hyper contracture - “contracture
band necrosis”, “stone heart”
Osmotic/ionic dysregulation,
membrane injury
Cell swelling&disruption
Lysis

12. Apoptosis
Irreversible
Death signal
Cell shrinkage
Cytoplasmic and nuclear condensation
Phagocytosis

13. Reperfusion Injury
1. STUNNED MYOCARDIUM
2. REPERFUSION ARRHYTHMIAS: VT/VF
3. STONE HEART
IT IS A CRITICAL POINT OF NO RETURN
-DISRUPTION OF MYOFIBRILS
-EVIDENT CONTRACTION BAND
4. ENDOTHELIAL CELL DAMAGE
5. CONDUCTION TISSUE DAMAGE

14. Cellular effects of
ischemia
Altered membrane potential
Altered ion distribution(increase
intracellularCa++/Na++)
Cellular swelling
Cytoskeletal Disorganisation
Increased hypoxantine
Decreased ATP
Decreased phosphocreatine
Decreased Glutatione
Cellular Acidosis

15. Straqtegies for
myocardial protection
Increase the O2 supply
Decrease oxygen demand
Metabolic intervention
Prevention of increased demand
Substrate availability

16. Myocardial O2
consumption at 37°C
Beating (full, perfused)
10ml/100gm/min
Beating (empty, perfused)
55ml/100gm/min
Fibrillating(empty, perfused)
65ml/100gm/min
K+ Cardioplegia(empty, cross-clamped)
10ml/100gm/min

17. Myocardial O2 consumption
ml/100gm/min
Temperature °C
Beating (empty)
Fibrillating (empty)
K+ cardioplegia
37 32 28 22
55 50 40 29
65 38 30 20
10 08 06 03

18. CARDIOPLEGIA
solutions
1.St. Thomas' Solution
2.Bretschneider Solution
3.University of Wisconsin
Solution
4.Custodiol HTK
5.Celsior
6.Buckberg
7.Delnido

19. Cardioplegic
Composition
Blood vs Crystalloid
Buffers
Calcium
Potassium
Free radical scavengers
Others

20. St.Thomas solution
KCL=59.65mg
Mgcl2=162.65mg
Procaine hydrochloride =13.64mg

21. Principles of
cardioplegic protection
Arrest
Myocardial protection
Reversibility
Low toxicity

22. Cardioplegia - Options
No cardioplegia
Cardioplegia
Type ( blood vs crystalloid, cont. vs intermittent )
Route ( antegrade vs retrograde )
Temperature ( warm vs cold )
Additives
Special consideration ( Acute infarction, Neonate)

23. Mechanism of Cardioplegic
Protection
Mechanical arrest ( K – induced, 80%
reduction in O2 consumption)
Hypothermia (10-15% further reduction in
O2 consumption)
Aerobic metabolism – oxygenated
cardioplegia
Maintain hypothermic arrest with
readministration every 20-25 min
Retrograde delivery LV, RV protection

24. Other consideration
Protect from rewarming,
Systemic hypothermia,
Aortic/ventricular vents,
Total bypass (caval
occlusion)
Acute Ischemia
-Warm induction
-Substrate enhancement
Controlled reperfusion
Warm,hypocalcemic,alkali-
ne cardioplegia
-Retrograde or low flow-
pressure antegrade
perfusion
-Energy replacement while
arrested
-Uniform warming

25. Blood vs Crystalloid
O2 carrying capacity ( Hematocrit 15 – 20 %)
Buffers –histidine
Free radical scavengers in RBCs
Improved rheologic / oncotic properties
Metabolic substrate

26. Buffers
THAM
Histidine
NaHCO3
Slightly alkaline reperfusion

27. Calcium, Potassium
Small amounts of calcium ( 0.1 – 0.5 mM/L )
Ca chelated in blood with citrate
10 –100 mM/L of potassium ( first dose
highest )
> 30 mM/L – endothelial dysfunction

28. Free radical scavengers.
Others
Allopurinol
Propofol
Deferoxamine
Metabolic substrates ( adenosine, nucleotid
transport inhibitors...)
K- channel openers ( Nicorandil )

29. The ways of
pharmacological therapy
 Addition of metabolites or cofactors
 Activation of enzymes or complexes
 Control of synthesis of mitochondrial
factors, or genesis of mitochondria, and
protection of mitochondria
 Improving Ph balance in the ischemic
heart
 Drugs -CCB’S , Lidoflazine.

30. Strategy for controlling
Paco2 and pH
ALPHA STAT-Use pH measured at
37deg. C and uncorrected for temp. of
blood .Ph maintained at 7.4
pH STAT- Same values of pH and
Paco2 ,corrected to the temp. of the
patient’s blood ,during hypothermia as
at normothermia.This represents a state
of respiratory acidosis and hypercarbia.

32. THANK
YOU