Enfermedad Coronaria Cuando se manejan pacientes con enfermedad coronaria el anestesiologo debe Prevenir Minimizar
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Factores que determina flujo sanguineo miocardico Sano Enfermo Vasos Coronarios Grandes Vasos Conduccion Pequeos vasos de resistencia Venas Angiografia coronaria 10-250 um de diametro Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Anatomia y Fisiologia En condiciones de reposos cerca de 45% a 50% de la resistencia vascular coronaria total reside en vasos mayores de 100 um de diametro Pared Arterial Normal Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Anatomia y Fisiologia Coronaria Endotelio - intima - lamina elastica interna media lamina elastica externa 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's pentachrome-stained slide, original magnification, 6.6.) Pared Arterial Normal Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Anatomia y Fisiologia Coronaria Intima Tradicionalmente considerada la capa mas importante de la pared arterial Endotelio sencillo neointima Radio intima/media 0.1 a 1 Dos capas distintas Interna: proteoglicanos, musculo liso aislado, macrofagos Externa o musculoelastica: musculo liso y fibras elasticas Pared Arterial Normal Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Anatomia y Fisiologia Coronaria Media Varias subpoblaciones especiales Homeostasis pared arterial Relajacion constriccion
Adventicia Fibroblastos, microvasos, nervios y unas pocas celulas inflamatorias
Comunicacion Transcelular Anatomia y Fisiologia Coronaria
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 subunit (G). The activated 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. Comunicacion Transcelular Anatomia y Fisiologia Coronaria Receptor B Estimula Gs AMPc Receptor muscarinico Activa Gi AMPc Vasopresina Activa fosfolipasa C IP3 : Ca DAG: Activa PKC Apertura canales ionicos, contraccion o relajacion musculo liso, actividad secretora, division celular Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Endotelio Anatomia y Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Factores Relajantes Endotelio Anatomia y Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Rubanyi GM: Endothelium, platelets, and coronary vasospasm. Coron Artery Dis 1:645, 1990 The production of endothelium-derived vasodilator substances. Factores Relajantes Endotelio Anatomia y Fisiologia Coronaria PGI2 Primera substancia endotelial vasoactiva descubierta NO Molecula no prostanoide lipofilica Vida media menor de 5 segundos Se une con el grupo heme de guanilato ciclasa aumentando 50 a 200 veces GMPc Causan relajacion de musculo liso e inhiben la agregacion plaquetaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Factores Relajantes Endotelio Anatomia y Fisiologia Coronaria NO Controla antetodo tono vascular en venas y arterias. No asi en arteriolas Ejercicio dilatacion microcirculacion flujo coronario epicardico tension en la pared NO flujo vasos de conductancia Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Factores Relajantes Endotelio Anatomia y Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
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 generelated peptide; ET, endothelin; NA, norepinephrine; PAF, platelet- activating factor; SP, substance P; VIP, vasoactive intestinal polypeptide; VP, vasopressin. Factores Constrictores Endotelio Anatomia y Fisiologia Coronaria Prostaglandina H2 Tromboxano A2 (via ciclooxigenasa= Peptido endotelina 100 veces mas potente que NE Tres clases relacionadas de 21 a.a Endotelina-1 (ET-1), ET-2, y ET-3.
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
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. Inhibicion Plaquetaria X Endotelio Anatomia y Fisiologia Coronaria La funcion primaria del endotelio es mantener la fluidez sanguinea Sintesis y liberacion Anticoagulantes (trombomodulina, proteina C) Fibrinoliticos (activador tisular plasminogeno) Inhibidores plaquetarios (PGI, NO) Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Inhibicion Plaquetaria X Endotelio Anatomia y Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
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 microthrombi and prevent thrombosis of intact vessels. P2y, purinergic receptor. Determinantes del Flujo Coronario Anatomia y Fisiologia Coronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
PP y Compresion Miocardica Determinantes del Flujo Coronario PP: Presion de Perfusion El flujo sanguineo es proporcional al gradiente de presion a traves de la circulacion coronaria Presion coronaria (downstream) presion en la raiz de la aorta Compresion extravascular sistole, 10%-25% Resistencia Mayor en subendocardio Con presion sanguinea, FC, contractilidad y precarga
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Presion de Cierre Critico PFZ Determinantes del Flujo Coronario
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Presion a la cual el flujo coronario se detiene Excede por mucho la presion a nivel del seno coronario Discutida
Metabolismo Miocardico Determinantes del Flujo Coronario
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
El flujo sanguineo esta apareado con los requerimientos metabolicos Tension de oxigeno venoso coronario es 15 a 20mmHg MvO2 solo puede ocurrir si se aumenta la entrega aumentando el flujo sanguineo coronario
Control Neural - Hormonal Determinantes del Flujo Coronario
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Neural Dificil cuantificar debido a que la actividad simpatica parasimpatica causa cambios en PA, FC y contractilidad Inervacion coronaria
Simpatico Parasimpatico Terminaciones neurales a nivel de musculo liso Arterias y venas Ganglio simpatico sup, med, inf y los primeros 4 ganglios toracicos Terminaciones neurales en la adventicia de vasos coronarios Arterias y venas Nervio vago X PC Control Parasimpatico Determinantes del Flujo Coronario Control Neural
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Vasoconstriccion Coronaria Mediada por metabolismo
Control Neural Determinantes del Flujo Coronario
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Dilatacion Beta adrenergica Pequeos y grandes vasos B1 y B2 B1 predomina en vasos de conductancia B2 en vasos de resistencia
Constriccion Alfa adrenergica
Control Humoral Determinantes del Flujo Coronario
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Vasopresina Peptido natriuretico auricular Peptido intestinal vasoactivo Neuropeptido Y Peptido relacionado con el gen de la Calcitonina PGI2 TxA2 Relacion Presion-Flujo Coronaria Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Autoregulacion PAM 60 140 mmHg Flujo constante 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. Relacion Presion-Flujo Coronaria Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Autoregulacion PAM 60 140 mmHg Tres teorias Hipotesis de presion tisular Cambios en PP altera permeabilidad capilar llevando a resistencia extravascular que se opone a cambios flujo Teoria miogenica El musculo liso se contrae en respuesta al aumento de la presion intraluminal Teoria metabolica Balance de aporte y consumo de O2 Reserva Coronaria Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Isquemia coronaria causa vasodilatacion intensa Despues de 10 30 segundos de oclusion restauramiento presion de perfusion se acompaa de incremento marcado en el flujo coronario 5 a 6 veces el flujo en reposo Hiperemia reactiva Reserva Coronaria Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
No hay sobrepago de la deuda de oxigeno ya que la tasa de extraccion declina durante la hiperemia La diferencia entre el flujo sanguineo coronario en reposo y el flujo pico durante la hiperemia reactiva representa el flujo de reserva autoregulatorio Capacidad del lecho arteriolar para dilatarse en respuesta a la isquemia Flujo Sanguineo Transmural Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Distribucion transmural de consumo de oxigeno, uso de substancias oxidables, actividad de enzimas glicoliticas y mitocondriales, contenido endogeno de sustratos, fosfatos de alta energia, lactato, isoformas de proteinas contractiles y estres y acortmaiento de fibra cardiaca Flujo Sanguineo Transmural Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Pressure-flow relations of the subepicardial and 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,autoregulation persists until perfusion pressure declines to less than 40 mm Hg. Autoregulatory coronary reserve is less in the subendocardium. Normal subendocardial/subepicardial or inner/outer (I/O) blood flow ratio is 1.10 Flujo Sanguineo Transmural Fisiologia Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Tres mecanismos se han propuesto para explicar la reserva coronaria en el subendocardio Presion sistolica intramiocardica diferencial Presion diastolica intramiocardica diferencial Interaccion sistole - diastole Ateroesclerosis PAtofisiologia
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
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 microvessels has resulted in intraplaque hemorrhage (arrow) at the base of the necrotic core
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Company Logo www.themegallery.com Evaluacion US Intravascular Ateroesclerosis
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Angiografia coronaria estandar Representacion bidimensional del lumen Enfermedad coronaria Invasion luminal Remodelacion Estenosis Coronaria Ruptura Placa Patofisiologia del Flujo Coronario
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Mayor estenosis, mayor riesgo? mayor oclusion?
Estenosis Coronaria Ruptura Placa Patofisiologia del Flujo Coronario
Circulation 1988, 78:1157-1166 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. Hemodinamia Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
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, blood velocity. Hemodinamia Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Constriccion coronaria suficiente para prevenir un incremento en el flujo sobre los valores en reposo en respuesta a aumento en la demanda de oxigeno miocardico Bloqueo de la respuesta hiperemia reactiva
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Angiograficamente se define como reduccion en area transversa de 75% lo cual equivale a una disminucion del 50% en el diametro de una lesion concentrica Colaterales Coronarias Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
En el corazon humano sano son pequeas y tienen poco o ningun rol funcional. En pacientes con EAC pueden prevenir la muerte IAM Variabilidad interespecies Patogenesis Isquemia Miocardica Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Isquemia: Deprivacion de oxigeno acompaado por remocion inadecuada de metabolitos consecuente a perfusion reducida. - Miocardica: Disminucion del radio aporte/demanda (A/D) con alteracion de la funcion Determinante A/D Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
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. Determinante A/D Flujo Coronario - Estenosis Coronaria. PFDVI Presion de fin de diastole VI
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
FC Acorta diastole PA o PFDVI Presion de perfusion coronaria Isquemia Retarda relajacion ventricular (tiempo de perfusion subendocardica) y compliance diastolica (PFDVI) Indices A/D Miocardica. MVO2 Flujo Coronario - Estenosis Coronaria. PFDVI Presion de fin de diastole VI
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Doble producto FCxPAS mmHg segundo por latido/100gr Buen estimador de MVO2 pero no correlaciona bien en isquemia Indice presion-tiempo diastolico/presion tiempo sistolico Estima perfusion subendocardica PAM/FC Correlaciona con isquemia miocardica
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
EAC tolerancia variable al ejercicio en el dia y entre dias Excentrica 74% Un acortamiento modesto del musculo en la region compliante del vaso puede causar cambios dramaticos en el calibre del lumen Robo Coronario Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Ocurre cuando la presion de perfusion de un lecho vascular vasodilatado (flujo dependiente de presin) es disminuido por vasodilatacion en un lecho vascular paralelo Ambos lechos usualmente son distales a la estenosis
Raul Fernando Vasquez Hemodinamia Flujo Coronario - Estenosis Coronaria
Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011
Equation relating stenosis geometry to hemodynamic. where P 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 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 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).