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Edit Comment Close Premium member Presentation Transcript Slide 3: MYOCARDIAL PROTECTION Slide 4: Emptying of the heart- MVO2 ( 30-60% ) Myocardial Hypothermia Induction of cardiac arrest Cardioplegia : Cardioplegia Cardioplegia Composition : Cardioplegia Composition K = 10 – 40 m mol / lit Crystalloid and blood cardioplegia Critically ill patients {Energy-depleted hearts ( cardiogenic shock , acute MI before CPB ) }. To minimize myocardial stunning of blood cardioplegia Ca at 1 mEq/L to diminish myocyte Ca uptake , PH between 7.6 and 7.8 , osmolality between 340 and 360 mOsm to minimize edema-related myocardial dysfunction after reperfusion , hyperkalemia between 10 and 25 mEq/L to safely sustain electromechanical arrest CRYSTALLOID VERSUS BLOOD CARDIOPLEGIA : CRYSTALLOID VERSUS BLOOD CARDIOPLEGIA Crystalloid cardioplegia = low cost , simplicity of administration , and availability – bicarbonate added to provide buffering- Blood Cardioplegia =ability to carry oxygen , excellent buffering capacity – scavenge free radicals and minimize oxidative damage to the heart – decrease periop morbidity - Cardioplegia Temperature : Cardioplegia Temperature Myocardial temp. < 10 – 15 0C By : infusion of refrigerated cardioplegia ; external topical cooling ; Tepid (27-30 ); warm (37-38) Hypothermia: increased risk of myocardial edema ( through ion pump activity inhibition );impaired function of various membrane receptors; metabolic inhibition in the myocardium; increase in plasma viscosity; decrease in RBC deformability; leftward shift in the 02 hemoglobin dissociation cure( inhibiting the release of 02 into tissues ) Slide 12: The principal differences in cold versus warm cardioplegia result from the timing and route of delivery : Normothermic myocardium >> continuous cardioplegia ( retrograde ) Recovery of LV stroke work at 1 and 4 hours after surgery was optimal in the tepid group Retrograde cardioplegia limitations : Retrograde cardioplegia limitations RV and septum frequently receive inadequate delivery of cardioplegia ( because of shunting and blood flowing into the atrium and ventricles by thebesian veins and various arteriosinusoidal connections ) Persistent LSVC Retrograde cardioplegia is inefficient in producing arrest of the beating heart ; induction of arrest by a single antegrade infusion of cardioplegia before its institution Myocardial Injury : Myocardial Injury Mechanism=Ischemia Factors=abnormal perfusate composition(increasing titers of free fatty acids,denatured plasma proteins,vasoactive substances)-persistent ventricular fibrillation(manipulation of the heart,rapid myocardial cooling)-inadequate myocardial perfusion(CAD,emboli,altered lymph flow,myocardial edema,VF,distention or collapse,technical problems,hypothermia)-ventricular distention(inadequate venous drainage,AI,VF,infusion of cardioplegia,pulmonary venous flow,noncoronary collateral flow)-ventricular collapse(=beating heart,small hypertrophic ventricles)(appropriate management of venous drainage and vents)- coronary embolism(use of filters-venting of vein grafts-evacuation of intracardiac air) catecholamines-aortic cross clamping-reperfusion Myocardial protection strategies : Myocardial protection strategies Begins with preparation of the heart before arrest.(hydration-sufficient glucose-treate hypotension-vetricular distention must be avoided-HR<80 in IHD in pre bypass period-use beta blocker) Metabolic requirements should be reduced during the arrest interval. A favorable metabolic milieu during arrest helps provide a margin of safety with reduced metabolism. Reperfusion modification after an ischemic insult can minimize structural and functional damage to the myocardium. Pathophysiology Of Myocardial Injury : Pathophysiology Of Myocardial Injury Myocardial stunning = myocardial dysfunction that follows a brief ischemic event . Resolves over the 48 to 72 hours after the ischemic event . After aortic cross-clamping with cardioplegic arrest frequently is observed . Contributing Factors = Metabolic consequences of O2 deprivation , premorbid condition of the myocardium , Reperfusion injury , Acute alterations in signal transduction systems , Effects of circulating inflammatory mediators . Metabolic consequences of O2 Deprivation : Metabolic consequences of O2 Deprivation Apparent within seconds of coronary artery occlusion . Rapid depletion of high-energy phosphates Accumulation of lactate and intracellular acidosis in the myocytes Contractile dysfunction . Myocyte ATP levels decline to a critical level Inability to maintain electrolyte gradients requiring active transport ( eg., Na , k , Ca ) Cellular edema , intracellular Ca overload , loss of membrane integrity . Mechanisms For Myocardial Dysfunction ( STUNNING ) Of CPB : Mechanisms For Myocardial Dysfunction ( STUNNING ) Of CPB Free radical – dependent mechanism for Ca overload Free radical – independent mechanism for Ca overload Inflammatory response ( complement , leukotriene , Kallikrein , cytokines ) Acute desensitization and down-regulation of myocardial Beta-adrenergic receptors Myocardial Reperfusion : Myocardial Reperfusion Substrate for injurious free radical productionSTUNNING Free radical Impairment in Ca-activated excitation-contraction coupling , Injury to membranes through lipid peroxidation Increase intracellular Ca physiologic down-regulation of excitation-contraction coupling . Free radical-independent mechanism : Activation of the Na/H exchange ( by the cell to correct intracellular PH ) Increase intracellular Na Activate the Na/Ca exchanger Increasing Ca influx Increase intracellular Ca Ischemic preconditioning : Ischemic preconditioning IPC is endogenous myocardial protection triggered by exposure to brief ( 5 to 15 minutes) ischemia . IPC is a natural defense mechanism that permits the heart to better tolerate myocardial ischemia . Mechanisms : activation of several myocardial G protein-coupled receptors(eg; A1 adenosine and Alpha-1 adrenergic receptors)– PKC is a key cellular mediator of IPC , in part through activation of ATP-sensitive potassium channels . Before CPB by brief ischemia or pharmacologic means : Sevoflurane - Adenosine Myocardial Protection For Off-pump Revascularization : Myocardial Protection For Off-pump Revascularization Before the development of suction-based stabilizers, intermittent pharmacologic arrest and profound bradycardia were induced during the procedure with adenosine and short-acting beta-blockers . IPC not in routine use Maintenance of adequate systemic blood pressure ( optimizing preload conditions and the use of vasopressors ) (during target vessel occlusion is an important component of myocardial protection because perfusion to ischemic myocardium through collaterals is dependent on this perfusion pressure ) Slide 27: Careful use of traction sutures , apical heart positioners , and coronary stabilizers that provide adequate exposure ( can compressing the cardiac chambers and compromise hemodynamic ) Occlusion of the most highly collateralized target vessel first allows this territory to be perfused through collaterals during construction of the anastomosis . Construction of a prximal anastomosis before the first distal anastomosis allows immediate reperfusion of the ischemic territory after completion of the distal anastomosis . Slide 28: Intracoronary shunt ( range in size from 1 mm to 3 mm ) = provide significant flow and a near-bloodless field . Perfusion-assisted direct coronary artery bypass ( PADCAB ) = directly perfuses myocardium supplied by a bypassed coronary artery by providing a controlled flow down the conduit .( independent of systemic pressure ). IABP for patients at high risk for OPCAB failure ( severe proximal multivessel CAD , severe ventricular dysfunction , who have comorbid disease that makes the avoidance of CPB desirable ) . Slide 29: Cardioplegia , anesthetic agents , CPB , surgical techniques , and pre- and postoperative care all affect the ability of the myocardium to tolerate cardiac surgery THANKS : THANKS WHEN THERE IS A WILL , THERE IS A WAY Immunologic Inflammatory Response : Immunologic Inflammatory Response Whole-body inflammatory response(activation of the complement,fibrinolytic,kallikrein,and coagulation systems) Complement activation=Histamine release from basophil and mast cells,cell lysis,smooth muscle contraction,increased vascular permeability,and activation of phagocytic cells,neutrophil activation and migration,and secretory events. Activated factor XII (XIIa) results in plasmin generation{ plasmin activates complement by C1( classical pathway ), cleaves C3 ( alternative pathway ), and cleaves factor XII (activates the kallikrein-kinin systems)},[Reperfusion injury] Endotoxins : Endotoxins Bind to lipopolysaccharide-binding protein->this complex bind to specific receptors on macrophages->production of cytokinescardiovascular instability – pulmonary dysfunction – renal insufficiency – alterations in hemostasis – fever – excess extravascular fluid retention. Cytokines ( IL-1 -> IL-16 ) : Cytokines ( IL-1 -> IL-16 ) Immune-mediated signals -> variety of cells -> cytokines -> fever , hypotension , altered mental status , increased production of acute – phase proteins . Important intercellular regulators of cellular immune function. Stimulate proliferation and terminal differentiation of T cells , differentiation and secretion of immunoglobulins from B cells , neutrophil chemotaxis and transendothelial migration . 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myocardial protection-dr kianoosh saberi saberikn Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: (To copy code, click on the text box) Embed: URL: Thumbnail: WordPress Embed Customize Embed The presentation is successfully added In Your Favorites. Views: 346 Category: Entertainment License: All Rights Reserved Like it (1) Dislike it (0) Added: June 09, 2010 This Presentation is Public Favorites: 3 Presentation Description Myocardial protection during cardiac anesthesia Comments Posting comment... By: hariomshillong123 (22 month(s) ago) nice presentation Saving..... Post Reply Close Saving..... Edit Comment Close By: hariomshillong123 (22 month(s) ago) nice Saving..... Post Reply Close Saving..... Edit Comment Close Premium member Presentation Transcript Slide 3: MYOCARDIAL PROTECTION Slide 4: Emptying of the heart- MVO2 ( 30-60% ) Myocardial Hypothermia Induction of cardiac arrest Cardioplegia : Cardioplegia Cardioplegia Composition : Cardioplegia Composition K = 10 – 40 m mol / lit Crystalloid and blood cardioplegia Critically ill patients {Energy-depleted hearts ( cardiogenic shock , acute MI before CPB ) }. To minimize myocardial stunning of blood cardioplegia Ca at 1 mEq/L to diminish myocyte Ca uptake , PH between 7.6 and 7.8 , osmolality between 340 and 360 mOsm to minimize edema-related myocardial dysfunction after reperfusion , hyperkalemia between 10 and 25 mEq/L to safely sustain electromechanical arrest CRYSTALLOID VERSUS BLOOD CARDIOPLEGIA : CRYSTALLOID VERSUS BLOOD CARDIOPLEGIA Crystalloid cardioplegia = low cost , simplicity of administration , and availability – bicarbonate added to provide buffering- Blood Cardioplegia =ability to carry oxygen , excellent buffering capacity – scavenge free radicals and minimize oxidative damage to the heart – decrease periop morbidity - Cardioplegia Temperature : Cardioplegia Temperature Myocardial temp. < 10 – 15 0C By : infusion of refrigerated cardioplegia ; external topical cooling ; Tepid (27-30 ); warm (37-38) Hypothermia: increased risk of myocardial edema ( through ion pump activity inhibition );impaired function of various membrane receptors; metabolic inhibition in the myocardium; increase in plasma viscosity; decrease in RBC deformability; leftward shift in the 02 hemoglobin dissociation cure( inhibiting the release of 02 into tissues ) Slide 12: The principal differences in cold versus warm cardioplegia result from the timing and route of delivery : Normothermic myocardium >> continuous cardioplegia ( retrograde ) Recovery of LV stroke work at 1 and 4 hours after surgery was optimal in the tepid group Retrograde cardioplegia limitations : Retrograde cardioplegia limitations RV and septum frequently receive inadequate delivery of cardioplegia ( because of shunting and blood flowing into the atrium and ventricles by thebesian veins and various arteriosinusoidal connections ) Persistent LSVC Retrograde cardioplegia is inefficient in producing arrest of the beating heart ; induction of arrest by a single antegrade infusion of cardioplegia before its institution Myocardial Injury : Myocardial Injury Mechanism=Ischemia Factors=abnormal perfusate composition(increasing titers of free fatty acids,denatured plasma proteins,vasoactive substances)-persistent ventricular fibrillation(manipulation of the heart,rapid myocardial cooling)-inadequate myocardial perfusion(CAD,emboli,altered lymph flow,myocardial edema,VF,distention or collapse,technical problems,hypothermia)-ventricular distention(inadequate venous drainage,AI,VF,infusion of cardioplegia,pulmonary venous flow,noncoronary collateral flow)-ventricular collapse(=beating heart,small hypertrophic ventricles)(appropriate management of venous drainage and vents)- coronary embolism(use of filters-venting of vein grafts-evacuation of intracardiac air) catecholamines-aortic cross clamping-reperfusion Myocardial protection strategies : Myocardial protection strategies Begins with preparation of the heart before arrest.(hydration-sufficient glucose-treate hypotension-vetricular distention must be avoided-HR<80 in IHD in pre bypass period-use beta blocker) Metabolic requirements should be reduced during the arrest interval. A favorable metabolic milieu during arrest helps provide a margin of safety with reduced metabolism. Reperfusion modification after an ischemic insult can minimize structural and functional damage to the myocardium. Pathophysiology Of Myocardial Injury : Pathophysiology Of Myocardial Injury Myocardial stunning = myocardial dysfunction that follows a brief ischemic event . Resolves over the 48 to 72 hours after the ischemic event . After aortic cross-clamping with cardioplegic arrest frequently is observed . Contributing Factors = Metabolic consequences of O2 deprivation , premorbid condition of the myocardium , Reperfusion injury , Acute alterations in signal transduction systems , Effects of circulating inflammatory mediators . Metabolic consequences of O2 Deprivation : Metabolic consequences of O2 Deprivation Apparent within seconds of coronary artery occlusion . Rapid depletion of high-energy phosphates Accumulation of lactate and intracellular acidosis in the myocytes Contractile dysfunction . Myocyte ATP levels decline to a critical level Inability to maintain electrolyte gradients requiring active transport ( eg., Na , k , Ca ) Cellular edema , intracellular Ca overload , loss of membrane integrity . Mechanisms For Myocardial Dysfunction ( STUNNING ) Of CPB : Mechanisms For Myocardial Dysfunction ( STUNNING ) Of CPB Free radical – dependent mechanism for Ca overload Free radical – independent mechanism for Ca overload Inflammatory response ( complement , leukotriene , Kallikrein , cytokines ) Acute desensitization and down-regulation of myocardial Beta-adrenergic receptors Myocardial Reperfusion : Myocardial Reperfusion Substrate for injurious free radical productionSTUNNING Free radical Impairment in Ca-activated excitation-contraction coupling , Injury to membranes through lipid peroxidation Increase intracellular Ca physiologic down-regulation of excitation-contraction coupling . Free radical-independent mechanism : Activation of the Na/H exchange ( by the cell to correct intracellular PH ) Increase intracellular Na Activate the Na/Ca exchanger Increasing Ca influx Increase intracellular Ca Ischemic preconditioning : Ischemic preconditioning IPC is endogenous myocardial protection triggered by exposure to brief ( 5 to 15 minutes) ischemia . IPC is a natural defense mechanism that permits the heart to better tolerate myocardial ischemia . Mechanisms : activation of several myocardial G protein-coupled receptors(eg; A1 adenosine and Alpha-1 adrenergic receptors)– PKC is a key cellular mediator of IPC , in part through activation of ATP-sensitive potassium channels . Before CPB by brief ischemia or pharmacologic means : Sevoflurane - Adenosine Myocardial Protection For Off-pump Revascularization : Myocardial Protection For Off-pump Revascularization Before the development of suction-based stabilizers, intermittent pharmacologic arrest and profound bradycardia were induced during the procedure with adenosine and short-acting beta-blockers . IPC not in routine use Maintenance of adequate systemic blood pressure ( optimizing preload conditions and the use of vasopressors ) (during target vessel occlusion is an important component of myocardial protection because perfusion to ischemic myocardium through collaterals is dependent on this perfusion pressure ) Slide 27: Careful use of traction sutures , apical heart positioners , and coronary stabilizers that provide adequate exposure ( can compressing the cardiac chambers and compromise hemodynamic ) Occlusion of the most highly collateralized target vessel first allows this territory to be perfused through collaterals during construction of the anastomosis . Construction of a prximal anastomosis before the first distal anastomosis allows immediate reperfusion of the ischemic territory after completion of the distal anastomosis . Slide 28: Intracoronary shunt ( range in size from 1 mm to 3 mm ) = provide significant flow and a near-bloodless field . Perfusion-assisted direct coronary artery bypass ( PADCAB ) = directly perfuses myocardium supplied by a bypassed coronary artery by providing a controlled flow down the conduit .( independent of systemic pressure ). IABP for patients at high risk for OPCAB failure ( severe proximal multivessel CAD , severe ventricular dysfunction , who have comorbid disease that makes the avoidance of CPB desirable ) . Slide 29: Cardioplegia , anesthetic agents , CPB , surgical techniques , and pre- and postoperative care all affect the ability of the myocardium to tolerate cardiac surgery THANKS : THANKS WHEN THERE IS A WILL , THERE IS A WAY Immunologic Inflammatory Response : Immunologic Inflammatory Response Whole-body inflammatory response(activation of the complement,fibrinolytic,kallikrein,and coagulation systems) Complement activation=Histamine release from basophil and mast cells,cell lysis,smooth muscle contraction,increased vascular permeability,and activation of phagocytic cells,neutrophil activation and migration,and secretory events. Activated factor XII (XIIa) results in plasmin generation{ plasmin activates complement by C1( classical pathway ), cleaves C3 ( alternative pathway ), and cleaves factor XII (activates the kallikrein-kinin systems)},[Reperfusion injury] Endotoxins : Endotoxins Bind to lipopolysaccharide-binding protein->this complex bind to specific receptors on macrophages->production of cytokinescardiovascular instability – pulmonary dysfunction – renal insufficiency – alterations in hemostasis – fever – excess extravascular fluid retention. Cytokines ( IL-1 -> IL-16 ) : Cytokines ( IL-1 -> IL-16 ) Immune-mediated signals -> variety of cells -> cytokines -> fever , hypotension , altered mental status , increased production of acute – phase proteins . Important intercellular regulators of cellular immune function. Stimulate proliferation and terminal differentiation of T cells , differentiation and secretion of immunoglobulins from B cells , neutrophil chemotaxis and transendothelial migration .