1. Damian Gimpel Waikato Cardiothoracic Unit
Myocardial Management during Cardiac Surgery with Cardiopulmonary Bypass
Damian Gimpel
Waikato Cardiothoracic Unit

2. Why is this important?
TIME IS MUSCLE!

3. Why is this important?

4. History
Taber et al  Identified small areas of myocardial necrosis - 30% of the left ventricular myocardium, in a group of patients dying early after cardiac operations.
Najafi et al  acute diffuse subendocardial myocardial infarction was found frequently in patients who died early after valve replacement  myocardial oxygen supply/demand ratios
1970’s – CABG  Hultgren et al  7% occurrence of acute transmural myocardial infarction
1970’s  Development of Cardioplegia, Pharmacological Agents to improve outcomes

5. Conditions during CPB
The amount and distribution of myocardial blood flow are continuously regulated, primarily in response to myocardial oxygen demand.
This flow is determined by coronary perfusion pressure (aortic pressure), tension in the various myocardial layers (related in part to ventricular wall thickness and size), and coronary vascular resistance.

6. During CPB - The heart is deprived of regulatory factors.
Conditions during CPB
During CPB - The heart is deprived of regulatory factors.

7. Conditions during CPB
How does it all work?

8. THEREFORE! Arterial pulse pressure is narrow
mean arterial blood pressure is variable.
The heart is usually more or less empty and smaller
Increased intramyocardial tension and transmural and subendocardial vascular resistance
decreased flow to the subendocardial layer

9. Conditions during CPB flow is determined by
coronary perfusion pressure (aortic pressure)
tension in the various myocardial layers (related in part to ventricular wall thickness and size)
coronary vascular resistance.
THESE ARE ALL EFFECTED!

10. A heart requiring theatre is essentially a sick heart!

11. Vulnerability of the diseased heart
coronary blood supply or the myocardium are not normal  susceptible to ischemic and reperfusion damage.
Hypertrophied ventricles  susceptible to ischemic and reperfusion damage.

12. Vulnerability of the diseased heart
several factors at play.
Increased Transmural gradients of energy substrate utilization are markedly elevated
Xanthine oxidase levels are markedly elevated  Free radicals
Superoxide dismutase levels are markedly decreased  Poor natural defenses
wall characteristics of the hypertrophied ventricle make reperfusion of the subendocardium even more difficult than under normal circumstances.
The heart of the patient with chronic heart failure is chronically depleted in energy charge susceptible to additional acute depletion and damage during ischemia and reperfusion.

13. Damage from Global Myocardial Ischemia
2 concepts:
Myocardial stunning
Myocardial Necrosis

14. Myocardial Cell Stunning
occurs after a state of acutely diminished myocardial blood flow followed by adequate reperfusion.
remains for a time diminished contractility  perfusion/contractility mismatch
characterized by systolic and diastolic dysfunction in the absence of myocardial necrosis
damage caused by ischemia and reperfusion.

15. Myocardial Cell Necrosis
the end stage of a complex process initiated by the onset of global myocardial ischemia, maintained by continuing ischemia, and aggravated by reperfusion.
contractile force declines rapidly, as does myocardial pH.
Oxidative metabolism, electron transport, and ATP production by oxidative phosphorylation (which take place in mitochondria) decline rapidly.
Some ATP is still produced by relatively inefficient anaerobic glycolysis.

16. Myocardial Cell Necrosis
Duration increases  intracellular metabolic deterioration continues
Permeability changes
Loss of intra cardiac proteins, enzymes and molecules

17. Ref: A new shield from the double-edged sword of reperfusion in STEMI , Navin K. Kapur and Richard H. Karas. Eur Heart J (2015) 36 (44):

18. Damage from Reperfusion
Myocardial Cell Damage
Endothelial Cell Damage
Specialized Conduction Cell Damage

19. Can you give the heart a pep Talk BEFORE CPB?

20. Advantageous Conditions during Ischemia
Myocardial glycogen content can be increased by an intravenous infusion of a glucose-insulin-potassium - PHASE II TRIAL

21. Methods of Myocardial Management during Cardiac Surgery
Goals of management is to limit ischaemia by combination of: myocardial hypothermia
electromechanical arrest
Washout
O2 and other substrate enhancement
oncotic manipulation
buffering.

22. Cardioplegia

23. Cardioplegia 2 MECHANISMS
Inhibition of the fast sodium current to prevent conduction of the myocardial action potential
2. Inhibition of calcium activation of myofilaments to prevent myocyte contraction

24. Cardioplegia CRYSTALLOID 2 TYPES:
INTRACELLULAR – LOW / ABSENT CONCENTRATIONS OF SODIUM AND CALCIUM
EXTRACELLULAR – HIGH CONCENTRATIONS OF SODIUM, CALCIUM AND MAGNEISUM

25. Cardioplegia COLD BLOOD CARDIOPLEGIA
- HYPOTHERMIC, HYPOKALAEMIC INDUCED CARDIAC ARREST.

26. COLD BLOOD Cardioplegia
PROVIDES OXYGENATED ENVIRONEMNT
LIMITS HEAMODILUTION
GOOD BUFFERING CAPACITY
PHYSIOLOGICAL PH AND BUFFERING CAPACITY
ENDOGENOUS ANTIOXIDANTS
LESS COMPLEX TO PREPARE

27. Cardioplegia ROUTE  ANTEGRADE OR RETROGRADE
ANTEGRADE  AORTIC ROOT/CORONARY OSTIA AT MMHG
RETROGRADE  CORONARY SINUS AT MMHG

28. Cardioplegia EXAMPLES

29. OTHER METHODS INTERMITTTENT AORTIC CROSS CLAMPING W/ FIBRILLATION
SYSTEMIC HYPOTHERMIA AND ELECTIVE FIBRILLATORY ARREST (SEVERELY CALCIFIED AORTA)
OFF PUMP SURGERY
PHARMACOLOGIC AGENTS  Adenosine, Acadensine, Na-H exchange inhibitors