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

Why is this important? TIME IS MUSCLE!

Why is this important?

History 1967 - 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. 1969 - 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

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.

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

Conditions during CPB How does it all work?

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

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!

A heart requiring theatre is essentially a sick heart!

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.

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.

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

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.

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.

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

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): 3058-3060.

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

Can you give the heart a pep Talk BEFORE CPB?

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

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.

Cardioplegia

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

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

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

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

Cardioplegia ROUTE  ANTEGRADE OR RETROGRADE ANTEGRADE  AORTIC ROOT/CORONARY OSTIA AT 60-100 MMHG RETROGRADE  CORONARY SINUS AT 30-50 MMHG

Cardioplegia EXAMPLES

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