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Fisiologia Coronaria

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  1. FisiologiaCoronaria Dr Raul Fernando Vasquez

  2. EnfermedadCoronaria • Cuando se manejanpacientes con enfermedadcoronaria el anestesiologodebe • Prevenir • Minimizar IsquemiaCoronaria • Factoresquedeterminaflujosanguineo miocardico • Sano • Enfermo Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  3. VasosCoronarios En condiciones de repososcerca de 45% a 50% de la resistencia vascular coronaria total reside en vasosmayores de 100 um de diametro Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  4. Pared Arterial Normal Endotelio - intima - lamina elasticainterna – media – lamina elasticaexterna – adventicia – vasa vasorum Normal human coronary artery of a 32-year-old woman. The intima (i) and media (m) are composed of smooth muscle cells. The adventitia (a) consists of a loose collection of adipocytes, fibroblasts, vasa vasorum, and nerves. The media is separated from the intima by the internal elastic lamina (open arrow) and the adventitia by the external elastic lamina (closed arrow). (Movat'spentachrome-stained slide, original magnification, ×6.6.) Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  5. Pared Arterial Normal • Intima • Tradicionalmenteconsiderada la capa mas importante de la pared arterial • Endoteliosencillo→ neointima • Radio intima/media 0.1 a 1 • Dos capasdistintas • Interna: proteoglicanos, musculolisoaislado, macrofagos • Externa o musculoelastica: musculoliso y fibraselasticas Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  6. Pared Arterial Normal • Media • Variassubpoblacionesespeciales • Homeostasis pared arterial • Relajacion – constriccion • Adventicia • Fibroblastos, microvasos, nervios y unaspocascelulasinflamatorias Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  7. ComunicacionTranscelular Brown AM, Birnbaumer L: Ionic channels and their regulation by G-protein subunits. Annu Rev Physiol 52:197, 1990 Steps in the process whereby hormone-receptor binding results in a change in cell behavior. In this example, the final result is the opening of an ion channel. A, A hormone or ligand (L) binds to a receptor (R) embedded in the cell membrane. The receptor-ligand complex interacts with G protein (G) floating in the membrane, resulting in activation of the α subunit (Gα). The activated α subunit can then follow different pathways (B). Effector enzymes in the membrane (E), such as adenylyl cyclase, cyclic guanosine monophosphate (cGMP), phospholipase C, or phospholipase A2, change the cytoplasmic concentration of their “messengers”: cyclic adenosine monophosphate (cAMP), cGMP, diacylglycerol(DAG), and inositol 1,4,5-triphosphate (IP3). These soluble molecules activate protein kinase A or C (PKA or PKC), or release Ca++ from sarcoplasmic reticulum (SR). Subsequently, cell behavior is changed by phosphorylation of an ionic channel on the cell membrane (CHAN) or by release of Ca++ from SR. B, Several pathways coupling receptor activation to final effect are illustrated. It is likely that multiple pathways are activated concomitantly, both facilitatory and inhibitory. In this way, the final response can be determined by the sum of the effects of several stimuli.

  8. ComunicacionTranscelular • Receptor B • EstimulaGs→ ↑AMPc • Receptor muscarinico • ActivaGi→ ↓AMPc • Vasopresina • Activafosfolipasa C → ↑IP3 : ↑Ca → ↑DAG: Activa PKC • Aperturacanalesionicos, contraccion o relajacionmusculoliso, actividadsecretora, division celular Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  9. Endotelio Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  10. FactoresRelajantesEndotelio Rubanyi GM: Endothelium, platelets, and coronary vasospasm. Coron Artery Dis 1:645, 1990 The production of endothelium-derived vasodilator substances. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  11. FactoresRelajantesEndotelio • PGI2 • Primerasubstanciaendotelialvasoactivadescubierta • NO • Molecula no prostanoidelipofilica • Vida media menor de 5 segundos • Se une con el grupoheme de guanilatociclasaaumentando 50 a 200 vecesGMPc • Causanrelajacion de musculoliso e inhiben la agregacionplaquetaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  12. FactoresRelajantesEndotelio • NO • Controlaantetodotono vascular en venas y arterias. No asi en arteriolas • Ejercicio→↑dilatacionmicrocirculacion→↑flujocoronarioepicardico→↑tension en la pared →↑NO →↑flujovasos de conductancia Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  13. FactoresRelajantesEndotelio Role of endothelium in the control of coronary tone. Intact endothelium has an important modulatory role in the effect of numerous factors on vascular smooth muscle. In the absence of a functional endothelium (mechanical trauma, atherosclerosis), many factors act directly on smooth muscle to cause constriction (left). Under normal conditions (right), the release of nitric oxide (NO; endothelium-derived relaxing factor [EDRF]) and prostacyclin (PGI2) stimulated by these same factors can attenuate constriction or cause dilation. PGI2 release is predominantly into the lumen, whereas EDRF release is similar on both the luminal and abluminal sides. Substances in parentheses elicit only vasodilation. 5-HT, serotonin; A, adenosine; ACh, acetylcholine; ADP, adenosine monophosphate; AII, angiotensin II; ATP, adenosine triphosphate; Bk, bradykinin; CGRP, calcitonin gene–related peptide; ET, endothelin; NA, norepinephrine; PAF, platelet-activating factor; SP, substance P; VIP, vasoactive intestinal polypeptide; VP, vasopressin. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  14. FactoresConstrictoresEndotelio • Prostaglandina H2 • Tromboxano A2 (via ciclooxigenasa= • Peptidoendotelina • 100 veces mas potenteque NE • Tresclasesrelacionadas de 21 a.a • Endotelina-1 (ET-1), ET-2, y ET-3. Endothelin (ET) released abluminally interacts with ETA and ETB receptors on vascular smooth muscle to cause contraction. Activators of ETB receptors on endothelial cells cause vasodilation. cAMP, cyclic Adenosine monophosphate cGMP, cyclic guanosine monophosphate; ECE, endothelin-converting enzyme; NO, nitric oxide; PGI2, prostacyclin. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  15. InhibicionPlaquetaria X Endotelio • La funcionprimaria del endotelioesmantener la fluidezsanguinea • Sintesis y liberacion • Anticoagulantes (trombomodulina, proteina C) • Fibrinoliticos (activadortisularplasminogeno) • Inhibidoresplaquetarios (PGI, NO) Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  16. InhibicionPlaquetaria X Endotelio Inhibition of platelet adhesion and aggregation by intact endothelium. Aggregating platelets release adenosine diphosphate (ADP) and serotonin (5-HT), which stimulate the synthesis and release of prostacyclin (PGI2) and endothelium-derived relaxing factor (EDRF; nitric oxide [NO]), which diffuse back to the platelets and inhibit further adhesion and aggregation, and can cause disaggregation. PGI2 and EDRF act synergistically by increasing platelet cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP), respectively. By inhibiting platelets and also increasing blood flow by causing vasodilation, PGI2 and EDRF can flush away microthrombiand prevent thrombosis of intact vessels. P2y, purinergic receptor. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  17. Determinantes del FlujoCoronario Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  18. PP y CompresionMiocardica • El flujosanguineoesproporcional al gradiente de presion a traves de la circulacioncoronaria • Presioncoronaria (downstream) – presion en la raiz de la aorta • Compresionextravascular sistole, 10%-25% Resistencia • Mayor en subendocardio • ↑Con presionsanguinea, FC, contractilidad y precarga Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  19. Presion de CierreCritico PFZ • Presion a la cual el flujocoronario se detiene • Excedepor mucho la presion a nivel del senocoronario • Discutida Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  20. Metabolismo Miocardico • El flujosanguineoestaapareado con los requerimientosmetabolicos • Tension de oxigenovenosocoronarioes 15 a 20mmHg • ↑MvO2 solo puedeocurrirsi se aumenta la entregaaumentando el flujosanguineocoronario Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  21. Control Neural - Hormonal • Neural • Dificilcuantificardebido a que la actividadsimpatica – parasimpaticacausacambios en PA, FC y contractilidad Inervacioncoronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  22. Control Parasimpatico • Estimulo vagal • Bradicardia • ↓Contractilidad • ↓Presionsanguinea VasoconstriccionCoronaria Mediadapormetabolismo ↓MvO2 Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  23. Control Neural • Dilatacion Beta adrenergica • Pequeños y grandesvasos • B1 y B2 • B1predomina en vasos de conductancia • B2 en vasos de resistencia • Constriccion Alfa adrenergica Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  24. Control Humoral • Vasopresina • Peptidonatriuretico auricular • Peptido intestinal vasoactivo • Neuropeptido Y • Peptidorelacionado con el gen de la Calcitonina • PGI2 • TxA2 Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  25. RelacionPresion-FlujoCoronaria • Autoregulacion PAM 60 – 140 mmHg • Flujoconstante a pesar de cambios en presion de perfusion arterial Autoregulation at two levels of myocardial oxygen consumption. Pressure in the cannulated left circumflex artery was varied independently of aortic pressure. When pressures were suddenly increased or decreased from 40 mm Hg, flow instantaneously increased with pressure (steep line, green triangles). With time, flow decreases to the steady-state level determined by oxygen consumption (purple and red circles). The vertical distance from the steady-state (autoregulating) line to the instantaneous pressure-flow line is the autoregulatory flow reserve. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  26. RelacionPresion-FlujoCoronaria • Autoregulacion PAM 60 – 140 mmHg • Tresteorias • Hipotesis de presiontisular • Cambios en PP alterapermeabilidadcapilarllevando a ↑resistencia extravascular que se opone a cambiosflujo • Teoriamiogenica • El musculoliso se contrae en respuesta al aumento de la presion intraluminal • Teoriametabolica • Balance de aporte y consumo de O2 Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  27. ReservaCoronaria • Isquemiacoronariacausavasodilatacionintensa • Despues de 10 – 30 segundos de oclusionrestauramientopresion de perfusion se acompaña de incrementomarcado en el flujocoronario • 5 a 6 veces el flujo en reposo • Hiperemiareactiva Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  28. ReservaCoronaria • No hay sobrepago de la deuda de oxigenoyaque la tasa de extracciondeclinadurante la hiperemia • La diferencia entre el flujosanguineocoronario en reposo y el flujopicodurante la hiperemiareactivarepresenta el flujo de reservaautoregulatorio • Capacidad del lecho arteriolar paradilatarse en respuesta a la isquemia Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  29. FlujoSanguineoTransmural • Distribuciontransmural de consumo de oxigeno, uso de substanciasoxidables, actividad de enzimasglicoliticas y mitocondriales, contenidoendogeno de sustratos, fosfatos de altaenergia, lactato, isoformas de proteinascontractiles y estres y acortmaiento de fibracardiaca 10%-20% Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  30. FlujoSanguineoTransmural Pressure-flow relations of the subepicardialand subendocardial thirds of the left ventricle in anesthetized dogs. In the subendocardium, autoregulation is exhausted and flow becomes pressure dependent when pressure distal to a stenosis declines to less than 70 mm Hg. In the subepicardium,autoregulationpersists until perfusion pressure declines to less than 40 mm Hg. Autoregulatorycoronary reserve is less in the subendocardium. Normal subendocardial/subepicardial or inner/outer (I/O) blood flow ratio is 1.10 Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  31. FlujoSanguineoTransmural • Tresmecanismos se hanpropuestoparaexplicar la reservacoronariaen el subendocardio • Presionsistolicaintramiocardicadiferencial • Presiondiastolicaintramiocardicadiferencial • Interaccionsistole - diastole Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  32. Ateroesclerosis Atherosclerotic human coronary artery of an 80-yearold man. There is severe narrowing of the central arterial lumen (L). The intima consists of a complex collection of cells, extracellular matrix (M), and a necrotic core with cholesterol (C) deposits. Rupture of plaque microvesselshas resulted in intraplaque hemorrhage (arrow) at the base of the necrotic core Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  33. Company Logo

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  35. Evaluacion US Intravascular • Angiografiacoronariaestandar • Representacionbidimensional del lumen • Enfermedadcoronaria • Invasion luminal • Remodelacion Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  36. EstenosisCoronariaRupturaPlaca • Mayor estenosis, mayor riesgo? mayor oclusion? Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  37. EstenosisCoronariaRupturaPlaca Our study indicates that the lesion that will be the site of the thrombotic occlusion frequently is not severe when evaluated by coronary angiography weeks to years before the infarct in patients with mild-to-modern artery disease; thus, coronary angiography was not able to accurately predict the time or subsequent myocardial infarction. Circulation 1988, 78:1157-1166

  38. Hemodinamia 75% Sources of energy loss across a stenosis. Equations that (accurately) predict the pressure gradient across a stenosis usually ignore entrance effects. Frictional losses are proportional to blood velocity but are usually not important except in very long stenoses. Separation losses, caused by turbulence as blood exits the stenosis, increase with the square of blood velocity and account for more than 75% of energy loss. F, friction coefficient (Poiseuille); S, separation coefficient; V, bloodvelocity. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  39. Hemodinamia Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  40. EstenosisCritica • Constriccioncoronariasuficienteparaprevenir un incremento en el flujosobre los valores en reposo en respuesta a aumento en la demandade oxigeno miocardico • Bloqueode la respuestahiperemiareactiva Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  41. EstenosisSignificativa • Angiograficamente se define comoreduccion en area transversa de 75% lo cualequivale a unadisminucion del 50% en el diametro de una lesion concentrica Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  42. ColateralesCoronarias • En el corazonhumanosano son pequeñas y tienenpoco o ningunrolfuncional. • En pacientes con EAC puedenprevenir la muerte– IAM • Variabilidadinterespecies Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  43. PatogenesisIsquemiaMiocardica • Isquemia: • Deprivacion de oxigenoacompañadoporremocioninadecuada de metabolitosconsecuente a perfusion reducida. • - Miocardica: • Disminucion del radio aporte/demanda (A/D) con alteracion de la funcion Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  44. Determinante A/D Relative importance of variables that determine myocardial oxygen consumption (Mvo2). Each line roughly approximates the effect of manipulating one variable without changing the others. Most interventions cause changes in several of the variables at the same time. The importance of contractility, which is difficult to monitor in practice, is apparent. Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  45. Determinante A/D • FC • Acorta diastole • ↓PA o ↑PFDVI • ↓Presion de perfusion coronaria • Isquemia • Retardarelajacion ventricular (↓tiempo de perfusion subendocardica) y ↓compliance diastolica (↑PFDVI) Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  46. Indices A/D Miocardica. MVO2 • DobleproductoFCxPAS • mmHg segundoporlatido/100gr • Buenestimador de MVO2 pero no correlacionabien en isquemia • Indicepresion-tiempodiastolico/presiontiemposistolico • Estima perfusion subendocardica • PAM/FC • Correlaciona con isquemiamiocardica Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  47. EstenosisDinamica • EAC tolerancia variable al ejercicio en el dia y entre dias • Excentrica 74% • Un acortamientomodesto del musculo en la region compliante del vasopuedecausarcambiosdramaticos en el calibre del lumen Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  48. RoboCoronario • Ocurrecuando la presion de perfusion de un lecho vascular vasodilatado (flujodependiente de presión) esdisminuidoporvasodilatacion en un lecho vascular paralelo • Ambos lechosusualmente son distales a la estenosis Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

  49. Gracias ! Raul Fernando Vasquez

  50. Hemodinamia Equation relating stenosis geometry to hemodynamic. where ΔP is the pressure decline across the stenosis, Q is the volume flow of blood, f is a factor counting for frictional effects, and s accounts for separation effects. Based on the Poiseuille law for laminar flow: where π is the blood viscosity, L is stenosis length, An is the cross-sectional area of the normal vessel, and As is the cross- sectional area of the stenosis. The separation or turbulence factor is: where ρ is blood density, and k is an experimentally determined coefficient. Thus, frictional losses are directly proportional to the first power of stenosis length but are inversely proportional to the square of the area (or fourth power of diameter). Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011