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Myocardial protection

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Information about Myocardial protection
Education

Published on October 30, 2008

Author: ramachandran

Source: authorstream.com

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Myocardial Protection in Children : Myocardial Protection in Children Seoul National University Children's Hospital Pediatric Cardiac Surgery Jeong Ryul Lee, MD Introduction : Introduction In regard of the myocardial protection and cardioplegia, the basic theories and the clinical practices do not show much differences between those on the adult and the child. However, in a certain situation, myocardium of child with congenital heart anomalies has been undergoing hemodymamic and metabolic derrangements from birth, which may require more finely defined perioperative stratigies not to aggravate the damages or even to improve it. Here, I would like to describe the brief theoretical, historical and practical backgrounds of various myocardial protection schemes in child to share the ideas of making a fantastic cardioplegia cocktail, with you. Ⅰ. MYOCARDIAL PROTECTION GENERAL : Ⅰ. MYOCARDIAL PROTECTION GENERAL 1. Temperature: (1) Hypothermia is the first tried method for myocardial protection. Hufnagel used iced slush in 1961. (2) Primary effects of hypothermia 1) Heart rate falls. 2) Vascular resistance increases. 3) Blood pressure falls 4) Oxygen consumption falls. 5) Blood properties change - Increased viscosity, Hb-O2 affinity, gas solubility 6) Changes in patterns of substrate metabolism 7) Reduced rate of physical biochemical reaction 8) Decreased membrane fluidity 9) Water becomes viscous, less ionized, and undergoes conformational change Slide 4: (3) Secondary effects of hypothermia 1) Impaired perfusion 2) Metabolic acidosis 3) Tissue hypoperfusion and hypoxia 4) Shift in acid base balance 5) Altered metabolism 6) Depressed metabolism 7) Reduction of energy O2 demand 8) Decreased energy production 9) Decreased function of membrane bound enzymes 10) Failure of ionic homeostasis 11) Cell swelling 12) Improved membrane protection 13) Depressed metabolism 14) Alkaline shift in neutrality 15) Ice formation Slide 5: (4) Common pitfalls of cooling technique 1) Insufficient cold cardioplegic solution delivered to the myocardium 2) Cardioplegic solution not cold enough 3) Excessive entry of warm blood into the cold heart 4) Excessive heart gain from the environment 5) Airembolism during reinfusion of cardioplegic solution 6) Ineffective topical cooling because the irrigating fluid is not cold enough, the flow rate too low or distribution over the heart uneven 7) Myocardial temperature not monitored 8) Cold injury due to ice-slush 9) Arterial pressure too low during reperfusion 2. Blood or Crystalloid / Artificial blood (Fluosol-DA) : 2. Blood or Crystalloid / Artificial blood (Fluosol-DA) (1) Crystalloid 1) European solutions 1964 : Bretschneider 1,2,3 : ICF, low Na, no Ca, Prociane University of Goetingem, Physiology / Dr. Bretschneider HJ 1978 : Bretschneider 4,7 : no procaine, Mg, Histidine-Trytophan buffer : 1975 : St. Thomas No.1 : ECF, high K, high Ca, Mg, procaine Rayne institute / Dr. Hearse DJ 1986 : St. Thomas No.2 (Plegisol) :Reduce Na/K/Ca, Add HCO3, remove procaine 1992 : the most recent St. Thomas report J Thorac Cardiovasc Surg 1992;104:344-56 superior protection with hypocalcemic solution (0.1mmol) Slide 8: 2) North-American solutions 1968 : Stanford : high potassium, low sodium, bicarbinate 1978 :UAB, high K, low Na, normocalcemic, HCO3, mannitol, albumin 1987 : MGH, Dr. Boggs : cold acalcemic oxygenated Slide 9: 1991 : UW, organ preservant Slide 10: (2) Blood cardioplegia 1) 1955 : Melrose high potassium (35mEq/L) normothermic arrest not myocardial preservant, but just motionless heart producer 2) 1984 : University of Toronto / Dr. SE Fremes blood cardioplegia (2:1) Slide 11: 3) 1987 : MGH / Dr. WM Daggett cold oxygenated diluted blood cardioplegia (1:4) 4) 1989 : UCLA / Dr. GD Buckberg Blood cardioplegia(4:1), warm induction, modified reperfusion 4-1) Cardioplegic solution Slide 12: 4-2) Cardioplegic composition 5) 1992 : SNUCH / Dr. Lee JR cold diluted oxygenated blood cardiaoplegia (1:4) hypocalcemic, cold induction, cold maintenance Slide 13: 6) 1992 : University of Toronto / Dr. Lichtenstein Continuous warm blood cardioplegia / Intermittent warm blood cardioplega blood:crystalloid = 4:1 Slide 14: Pitfalls) - poor operative field - focal global ischemic damage due to uneven cooling - very short allowable ischemic period (15 min) 3. Various additives : ions, substrates, osmolarity, buffer, onconicity, membrane stabilizer : 3. Various additives : ions, substrates, osmolarity, buffer, onconicity, membrane stabilizer (1) ions 1) K 1-1) Ideal level :15-35 mEq/L 1-2) Electrophysiologic role - Changing resting membrane potential [K]ECF= 6mEq/L ---> RMP=-68mV - Major ion for repolarization - Pacemaker potential= pacemaker depol= diastolic depol : Hyperpolarization (due to delayed K repolarization current) induses Ca conductance. - Exchange with Na by NA-K pump Slide 16: 1-3) Expected effects of K arrest - Decreased O2 consumption - Rapid cessation of electrical activity - Prevention of ischemic contracture - Decreased tissue impedance - Conservation of high energy phosphate stores - Synergistic myocardial protection with hypothermia 1-4) High K vs Low K Slide 17: 2) Na 2-1) Ideal level : 120-150 mEq/L 2-2) Electrophysiologic role - Major ion for phase 1 depolarization Depolarization induces rapid Na influx by m-gate opening followed by h-gate closure. - Exchange with K by Na-K pump - Exchange with Ca by Na-Ca exchange mechanism 2-3) High Na vs Low Na Slide 18: 3) Ca 3-1) Ideal Ca level : not definite yet 3-2) Roles : - Maintenance of membrane integrity Glycocalyx bound calcium is 10% of total bound calcium. - Major ion for SA, AV node phase 1 depolarization - Major ion for phase 2 depolarization of cardiac muscle slow inward current causes prolonged refractory period. - Pacemaker potential - K channel activator at the end of plateu-phase - SL bound-Ca induced SR-Ca release (Rianodide) - Induce actin-myosin cross bridge - Neutralization of membrane negativity - Exchange with Na by Na-Ca exchange mechanism - pumped out of the cell by Ca-pump - Resorbed into SR by Ca-pump Slide 19: 3-3) Various Ca-concentrations 3-4) Pathology related with calcium Slide 20: 4) Mg 4-1) Ideal level of Mg : 15 mEq/L Mg is the second most intracellular cation. 4-2) Electrophysiologic role - Compete with Ca at membrane binding site - Inhibit Ca-induced Ca-release from SR - Block Na-channel 4-3) Kirsch : 200 mmol/L Mg for cardiac arrest (2) Metabolic enhancement 1) Glk solution 2) Glutamate/Aspartate : secondary cardioplegia - energy source : transamination & malate aspartate shuttle - buffering capacity - anaerobic ATP production in mitochondria 3) FDP Slide 21: (3) Buffer and PH 1) Ideal PH at various temperature 37'C(7.4), 28'C(7.7), 20'C(7.8), 17'C(8.0) 2) alpha-stat / PH-stat strategies 3) Buffering capacity Hb (60) > histidine (40) > >> THAM > Tris, HCO3(1) glutamate, phosphate cf) THAM : decrease ECF NA and increase Ca influx (4) Osmolarity 1) Ideal : slightly hyperosmolar (300-340 mOsm) 2) Extreme hyperosmolarity causes cellular dehydration(370 mOsm<) (5) Onconicity (6) Antiinflammatory agents : - leukocyte-depletion - steroid - monoclonal antibodies II. MYOCARDIAL PROTECTION IN CHILDREN : II. MYOCARDIAL PROTECTION IN CHILDREN 1. Goal 2. Characteristics of immature myocardium : 2. Characteristics of immature myocardium Immature : - more immature structural element -poor ability to increase cardiac output with increased preload - poor ability to tolerate increase afterload - importance of glycolysis during ischemia - dependence on ectracelluar calcium (1) Structural differences 1) smaller myocardial size 2) Heart comprises a greater mass proportion of body mass at birth 3) increased type Ⅰ/Ⅲ collagen ratio 4) myofiber more randomly oriented 5) mitochondria fewer and less developed Slide 24: (2) Functional differences 1) Weaker -for any given point on a length-tension curve, immature myocardium generates less force - myocardial compliance reduced - less capacity to increase stroke volume with increased preload 2) Compensatory -increased contractility secondary to elevated adrenergic state -greater sensitivity of stroke volume to increased afterload Slide 25: (3) Metabolic differences 1) dependent more on carbohydrate 2) greater glycogen store 3) superior anaerobic glycolytic ATP production 4) more ATP precursor after ischemia 5) less developed sarcoplasmic reticulum, T-tubule system Slide 26: (4) Preoperative stresses ( abnormal physiologic state ) 1) acute hypoxia and acidosis 2) chronic hypoxia Slide 27: 3) pressure and volume overload Slide 28: 4) increased non-coronary blood flow 3. Five phases of myocardial protection : 3. Five phases of myocardial protection - Pre-arrest period - Induction of arrest - Maintenance of arrest - Reperfusion period - Post-reperfusion syndrome Slide 30: (1) Pre-arrest period Myocardium entering cardioplegic arrest in a state of depleted high energy phosphate and/or glycogen is more vulnerable to reperfusion injury. * Judicious pre-arrest mamagement - infusion of metabolic substrrates and free radical scavengers - improvement of hypoxia - decreasing pressure and volume overloads - improvement of metabolic and functional status of the heart Slide 31: (2) Inductional of arrest 1) Goal of inductional cardioplegia Rapid complete electromechanical arrest 2) Reqirements - uniform distribution - infusion pressure monitoring - rapid arrest with potassium-based cardioplegia - heart decompression (CPB +/- venting) 3) Cold induction - Rapid high potassium-based cardioplegia - This method is more than enough to the non-energy depleted child myocardium. Slide 32: 4) Warm induction cardioplegia 4-1) Thoery - Metabolic abnormalities may be reversed by initial dose of warm sububstrate- inhanced blood cardioplegia - warm induction allows myocardium to undergo reparative anaerobic metabolism when oxygen and substrate supply exceed demand. 4-2) Methods - Initial cardioplegic dose of high potassium, warm, substrate enhanced blood cardioplegia delivered to the depressed heart on full cardioplulmocary bypass. - Once resuscitation is complete, cardioplegia is switched to low-potassium, cold cardioplegia Slide 33: 4-3) Advantages of warm induction - High ATP level, high oxygen utilization - Better ventricular function 4-4) Special remark: - Particularly valuable in instances where the pediatric heart is suspected of being energy depleted ( eg. hypoxia ) - Not necessary in selective pediatric procedures in non energy depleted heart Slide 34: (3) Maintenance cardioplegia 1) Goal prevent ischemia during arrest period by decreasing oxygen demand 2) Important tools - hypothermia - electromechanical arrest - mechanical decompression - control of non-coronary collateral flow - intermittent delivery of cardioplegia Slide 35: (4) Reperfusion 1) Stratigies to reduce reperfusion injury 1-1) Controlled reperfusion Reperfusion with warm modified blood cardioplegia prior to release of cross clamp 1-2) Variables : pressure and osmolarity, ionic calcium level substrate enhancement, neutrophil content, free radical scavengers 2) Reperfusion solution - buffered, hypocalcemic, hyperosmolar, substrate enhancement superoxide dismutase and catalase, mechanical leukocyte depletion Slide 36: (5) Post-reperfusion period 1) Excessive functional demands hinder the ability of the myocyte to repair damage sustained during arrest and reperfusion. 2) Need low threshold for insertion ventricular assist device 4. Distribution of cardioplegia : 4. Distribution of cardioplegia (1) Retrograde cardioplegia 1) Indications - Particularly useful in case of aortic insufficiency and where the aortic root is opened - Combination of antegrade and retrograde cardioplegia may maximize distribution. Slide 38: 2) Studies on retrograde cardioplegia 2-1) Porcine and canine model - Vast majority of flow to anterior ventricular septum and left ventricle. - Pronounced lack of capillary flow to right ventricle 2-2) Human - Capillary flow/gm myocardium to the RV is approximately a quarter of the amount that is to the left ventricle during blind transatrial retrograde coronary cannulation - Direct cannulation with occlusion by purse-string of the coronary sinus ostium increases RV reperfusion from 1/2 to near identical capillary flow as compared to the LV. - Approximately 1/3-2/3 of retrograde cardioplegia is shunted through the besian veins into the ventricular cavities : decreased capillary blood flow but increased ventricular cooling. Ⅲ. SNUCH Approach : Ⅲ. SNUCH Approach 1. Principles : (1) Effective but simple (2) Liberal choice of cardioplegic solution for the non-energy depleted child myocardium. (crystalloid vs blood, high K vs low k, least additives, simplest one ) (3) Diluted high K cold blood cardioplegia for the energy- depleted myocardium. (4) Active resuscitation of myocardium with heavy possible damage. 2. Cardioplegic compositions : 2. Cardioplegic compositions (1) Crystalloid cardioplegia (2) Blood cardioplegia (1:1) Slide 41: (3) Characteristics SNUCH cardioplegia 1) cold high K(30mEq/L) diluted blood cardioplegia for induction 2) cold intermittent low K(15mEq/L) diluted blood cardioplegia for maintenance 3) hypocalcemic 4) more likely to ECF 5) Hb buffer 6) perfusion pressure at 80 mmHg (4) Occasional use of teminal hot shot with warm(37'C) high K(30mEq/L) substrate-enriched blood cardioplegia (5) Modified ultrafiltration (6) Avoidance of topical cooling with ice-slush (7) Cooling the room temperature

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