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Fisiologia Coronaria Dr Raul Fernando Vasquez. Enfermedad Coronaria Cuando se manejan pacientes con enfermedad coronaria el anestesiologo debe Prevenir.

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Presentación del tema: "Fisiologia Coronaria Dr Raul Fernando Vasquez. Enfermedad Coronaria Cuando se manejan pacientes con enfermedad coronaria el anestesiologo debe Prevenir."— Transcripción de la presentación:

1 Fisiologia Coronaria Dr Raul Fernando Vasquez

2 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

3 Vasos Coronarios Grandes Vasos Conduccion Pequeños vasos de resistencia Venas Angiografia coronaria 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

4 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.)

5 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

6 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

7 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 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 Comunicacion Transcelular Anatomia y Fisiologia Coronaria Receptor B Estimula G s AMPc Receptor muscarinico Activa G i AMPc Vasopresina Activa fosfolipasa C IP 3 : 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

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

10 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.

11 Factores Relajantes Endotelio Anatomia y Fisiologia Coronaria PGI 2 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

12 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 NOflujo vasos de conductancia Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

13 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 gene–related peptide; ET, endothelin; NA, norepinephrine; PAF, platelet- activating factor; SP, substance P; VIP, vasoactive intestinal polypeptide; VP, vasopressin.

14 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.

15 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

16 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.

17 Determinantes del Flujo Coronario Anatomia y Fisiologia Coronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

18 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

19 Presion de Cierre Critico P FZ 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

20 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

21 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 SimpaticoParasimpatico 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

22 Control Parasimpatico Determinantes del Flujo Coronario Control Neural Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011 Estimulo vagal Bradicardia Contractilidad Presion sanguinea Vasoconstriccion Coronaria Mediada por metabolismo

23 Control Neural Determinantes del Flujo Coronario Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011 Dilatacion Beta adrenergica Pequeños y grandes vasos B 1 y B 2 B 1 predomina en vasos de conductancia B 2 en vasos de resistencia Constriccion Alfa adrenergica

24 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 PGI 2 TxA 2

25 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.

26 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 aresistencia 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

27 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 acompaña de incremento marcado en el flujo coronario 5 a 6 veces el flujo en reposo Hiperemia reactiva

28 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

29 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

30 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

31 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

32 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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35 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

36 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?

37 Estenosis Coronaria Ruptura Placa Patofisiologia del Flujo Coronario Circulation 1988, 78: 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.

38 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.

39 Hemodinamia Flujo Coronario - Estenosis Coronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011

40 Estenosis Critica Flujo Coronario - Estenosis Coronaria 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

41 Estenosis Significativa Flujo Coronario - Estenosis Coronaria 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

42 Colaterales Coronarias Flujo Coronario - Estenosis Coronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011 En el corazon humano sano son pequeñas y tienen poco o ningun rol funcional. En pacientes con EAC pueden prevenir la muerte – IAM Variabilidad interespecies

43 Patogenesis Isquemia Miocardica Flujo Coronario - Estenosis Coronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011 Isquemia: Deprivacion de oxigeno acompañado por remocion inadecuada de metabolitos consecuente a perfusion reducida. - Miocardica: Disminucion del radio aporte/demanda (A/D) con alteracion de la funcion

44 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.

45 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)

46 Indices A/D Miocardica. MVO 2 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 MVO 2 pero no correlaciona bien en isquemia Indice presion-tiempo diastolico/presion tiempo sistolico Estima perfusion subendocardica PAM/FC Correlaciona con isquemia miocardica

47 Estenosis Dinamica Flujo Coronario - Estenosis Coronaria 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

48 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 presión) es disminuido por vasodilatacion en un lecho vascular paralelo Ambos lechos usualmente son distales a la estenosis

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50 Hemodinamia Flujo Coronario - Estenosis Coronaria Edward R.M. O'Brien. Coronary Physiology and Atherosclerosis. Kaplan Anesthesia 2011 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).


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