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4ta Clase F Isiopatolopgia De La Circulacion Sistemica
- 1. FISIOPATOLOGIA DE LA CIRCULACION SISTEMICA Dr. Alfredo Dávalos Tapia Jefe de la División de Medicina del Hospital Nacional PNP
- 4. Paredes capilares Vena Capilares Arteria Corazón Venas pulmonares Arterias pulmonares Traquea Salida de CO2 Entrada de O2 Alveolos Tejido celular Bronquios Pulmones
- 8. Cerebral Coronaria Renal Digestiva Músculo Esqueletico Piel Aurícula Derecha Aurícula Izquierda Ventrículo Derecho Ventrículo Izquierdo Pulmones V Tricúnspide V. Mitral Vena Cava Arteria Aorta Arterias Venas Válvula Pulmonar Hemicardio derecho Hemicardio Izquierdo 15% 5% 25% 25% 5% 25% 100% 100% 100%
- 13. Circulación coronaria Vea un by pass coronario
- 26. Vea como se bloquea la circulación cerebral
- 38. Progresi ó n de la Aterosclerosis Una amenaza latente en 3 etapas/f ases
- 39. Ateroesclerosis en la linea del tiempo Libby P. Circulation . 2001;104:365-372. años
- 40. Aterosclerosis : Una enfermedad si st é mic a que afecta todas las a rteri a s mayores o principales Virmani R et al. Arterioscler Thromb Vasc Biol. 2000;20:1262-1275. Libby P. Circulation. 1995;91:2844-2850. Renal dysfunction Stroke CAD Coronary arteries Peripheral ischemia Carotid arteries Abdominal aorta Iliac arteries
- 42. F R C Disfunción Endotelial Lesión Vascular Placa Eventos CV Estable Inestable
- 45. Fisiopatología Aunque la Arteriopatia Obstructiva es la causa subyacente ,principal, la baja presión de perfusion activa un numero de complejas respuestas microcirculatorias locales ,las cuales son la causa final determinantes del dolor de reposo y los cambios troficos.El resultado es un circulo vicioso automultiplicador.Por eso aunque el objetivo final del tratamiento es la Arteriopatia Obstructiva ,los intentos de tratar y normalizar farmacologicamente los cambios microcirculatorias pueden mejorar los resultados de la revascularizacion y ser la mejor opción en pacientes en quienes la revascularizacion es imposible o ha fallado. Sin embargo, el manejo de las ulceras o la gangrena en el Pie Diabético es mas difícil que en los no Diabéticos, lo que se evidencia en la mayor incidencia de amputación en los primeros.
- 46. Palpación Pulsos
- 67. Regulación metabólica Reserva coronaria
- 70. Flujo en reposo y esfuerzo según grado de estenosis Flujo máximo Flujo en reposo
- 72. Stress
Notas del editor
- The figure depicts the progression of atherosclerosis over many decades. The left-hand images show the initiation of atherosclerosis where lipid is deposited in intima and promotes endothelial dysfunction and an inflammatory response. As depicted in the middle images, early atherosclerosis is often accompanied by compensatory enlargement of the artery in an effort to preserve the artery lumen. Although this may not limit blood flow to cause angina, progressive development of the vulnerable plaque may lead to plaque rupture and thrombus formation. Plaque rupture may lead to artery occlusion and an acute coronary syndrome or healing, and the development of a stenosis. The key features of endothelial dysfunction, inflammation, and thrombosis are illustrated in the figure. Libby P. Current concepts of the pathogenesis of the acute coronary syndromes. Circulation . 2001;104:365-372.
- Stable plaque can cause systemic complications related to vascular occlusion. Complications include stable angina, stroke, renal dysfunction, myocardial infarction, and peripheral ischemia. Virmani R, et al. Arterioscler Thromb Vasc Biol. 2000;20:1262-1275. Libby P. Circulation. 1995;91:2844-2850.
- FIGURE 13-22A Effect of coronary resistance on coronary blood flow reserve. A, At rest, flow is driven by the pressure head (P) at the proximal end of the system. R1 refers to resistance offered by the large epicardial conductance vessels. R2 represents the coronary arteriolar resistance, which predominantly regulates coronary blood flow. R3 represents the resistance provided by wall tension in the subendocardium. At rest in the normal vessel, some vasoconstrictor resistance is present. In the setting of an epicardial coronary stenosis, blood flow at rest can be maintained, as coronary resistance can be lowered downstream (R2 decreased) by autoregulatory dilation. Thus, with lower resistance, flow may be maintained despite the lower pressure head at the distal end of stenosis. B, With a demand stress or with the administration of coronary arteriolar vasodilators, perfusion increases substantially in the area supplied by the normal epicardial artery as R2 decreases. However, there is blunted flow reserve in the area supplied by the stenosis because most vasodilator reserve at the R2 level has been used to maintain resting flow. (Adapted from Follansbee WP: Alternatives to leg exercise in the evaluation of patients with coronary artery disease: Functional and pharmacologic stress modalities. In Gerson MC [ed]: Cardiac Nuclear Medicine. New York, McGraw-Hill, 1997, pp 193-236.)
- FIGURE 13-22B Effect of coronary resistance on coronary blood flow reserve. A, At rest, flow is driven by the pressure head (P) at the proximal end of the system. R1 refers to resistance offered by the large epicardial conductance vessels. R2 represents the coronary arteriolar resistance, which predominantly regulates coronary blood flow. R3 represents the resistance provided by wall tension in the subendocardium. At rest in the normal vessel, some vasoconstrictor resistance is present. In the setting of an epicardial coronary stenosis, blood flow at rest can be maintained, as coronary resistance can be lowered downstream (R2 decreased) by autoregulatory dilation. Thus, with lower resistance, flow may be maintained despite the lower pressure head at the distal end of stenosis. B, With a demand stress or with the administration of coronary arteriolar vasodilators, perfusion increases substantially in the area supplied by the normal epicardial artery as R2 decreases. However, there is blunted flow reserve in the area supplied by the stenosis because most vasodilator reserve at the R2 level has been used to maintain resting flow. (Adapted from Follansbee WP: Alternatives to leg exercise in the evaluation of patients with coronary artery disease: Functional and pharmacologic stress modalities. In Gerson MC [ed]: Cardiac Nuclear Medicine. New York, McGraw-Hill, 1997, pp 193-236.)