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REANIMACION CARDIOVASCULAR DIEGO
- 1. PARO CARDIO RESPIRATORIO DIEGO YANQUI MELENDEZ CARDIOLOGO ESSALUD RED SABOGAL
- 12. Paro Cardiaco: Formas de Presentación Fibrilación Ventricular Taquicardia ventricular sin pulso Actividad Eléctrica sin pulso Asistolia
- 16. Cada minuto que pasa disminuye en 7 a 10% la probabilidad de tener éxito con la RCP (ritmo FV)
- 20. FISIOLOGÍA DE LA VENTILACIÓN DURANTE PCR La distribución del gas entre los pulmones y el estómago durante la ventilación boca-boca o máscara será determinado por la impedancia relativa al flujo dentro de cada uno. Presión de apertura esofágica es de 20 cm H2O y de la compliance pulmón – tórax es menor Si la vía aérea permanece patente, compresiones torácicas causan substancial intercambio aéreo.
- 25. FIGURE 26–17 . External chest compression. Left, Locating the correct hand position on the lower half of the sternum. Right, Proper position of the rescuer, with shoulders directly over the victim's sternum and elbows locked. (From Standards and guidelines for cardiopulmonary resuscitation [CPR] and emergency cardiac care [ECC]. JAMA 255:2906, 1986. Copyright 1986, the American Medical Association.)
- 28. El corazón está pasivo TEORÍA DE LA BOMBA TORÁCICA La presión intratorácica propulsa la sangre En la entrada al tórax hay una válvula antireflujo El rellenado es pasivo AORTA VENA DIASTOLE: RELAJACION PASIVA SISTOLE : COMPRESIÓN VENA AORTA
- 30. Defibrilación Precoz: 5 minutos fuera de un Hospital 3 minutos en un Hospital
- 31. DESFIBRILACION SINDROME DE PURKINJE SEÑOR JESUS PASE LO QUE PASE QUE QUEDE ENTRE NOSOSTROS
- 36. Algoritmo Universal/Internacional de RCPA Adulto
- 44. Detención RCP Recuperación circulación y respiracion espontánea. Contraindicación RCP . Cuando el medico responsable determina que el PCR es irreversible. Criterios fiables en la determinación de la muerte
Notas del editor
- Assessing the Adequacy of Circulation During CPR Resucitación exitosa en modelos experimentales está asociado con flujo sanguíneo miocárdico de 15 a 30 ml/min/100g. Para obtener el flujo, compresiones torácicas cerradas deben generar adecuado gasto cardíaco y presión de perfusión coronaria. Durante CPR, perfusión coronaria ocurre primariamente durante la fase de relajación (diástole) de la compresión torácica. El flujo sanguíneo miocárdico crítico es alcanzado cuando la presión de diástole aórtica excede 40 mmHg y la presión de perfusión miocárdica (presión diastólica auricular derecha menos diástole aórtica) excede 20 – 25 mmHg. Monitoreo de presión invasiva, cuando está disponible durante el CPR, debe ser usado para guiar los esfuerzos de resucitación. Si la presión está bajo niveles críticos, debe realizarse ajustes para mejorar las compresiones torácicas y terapia vasopresora adicional debe ser considerada. Presiones vasculares bajo niveles críticos están asociados con pobres resultados incluso en pacientes que pueden ser salvables. Sin embargo , obtener presiones por encima de los niveles críticos no aseguran el éxito.. Daño al miocárdio por enfermedad subyacente puede evitar supervivencia, no importa cuan efectivo fue el esfuerzo. Successful resuscitation in experimental models is associated with myocardial blood flows of 15 to 30 ml/min/100g. 10 To obtain such flows, closed chest compressions must generate adequate cardiac output and coronary perfusion pressure. During CPR, coronary perfusion occurs primarily during the relaxation phase (diastole) of chest compression. The critical myocardial blood flow is reached when aortic 'diastolic' pressure exceeds 40 mm Hg and myocardial perfusion pressure (aortic diastolic minus right atrial diastolic pressure) exceeds 20-25 mm Hg. 10-13 Invasive pressure monitoring, when available during CPR, should be used to guide resuscitation efforts. If pressures are below the critical levels, adjustments should be made to improve chest compressions and additional vasopressor therapy should be considered. Vascular pressures below the critical levels are associated with poor results even in patients that may be salvageable. However, obtaining pressures above the critical levels does not ensure success. Damage to the myocardium from underlying disease may preclude survival no matter how effective the CPR efforts are. Although invasive pressure monitoring may be the ideal, exhaled end-tidal CO2 is an excellent noninvasive guide to the effectiveness of standard CPR. After intubation, CO2 excretion during CPR is dependent primarily on blood flow rather than ventilation. Since alveolar deadspace is large during low flow conditions, end-tidal CO2 is very low (frequently <10 mm Hg). If cardiac output increases, more alveoli are perfused and end-tidal CO2 rises (usually to >20 mm Hg during successful CPR). When spontaneous circulation resumes, the earliest sign is a sudden increase in end-tidal CO2 to greater than 40 mm Hg. Within a wide range of cardiac outputs, end-tidal CO2 during CPR correlates with coronary perfusion pressure, cardiac output, initial resuscitation and survival. 14-16 End-tidal CO2 measured during human CPR has been used to predict outcome. Two studies have demonstrated that no patient with an end-tidal CO2 <10 mm Hg could be successfully resuscitated. 16,17 In the absence of invasive pressure monitoring, end-tidal CO2 monitoring can be used to judge the effectiveness of chest compressions. 18 Attempts should be made to maximize the value by alterations in technique or drug therapy. Sodium bicarbonate administration results in the liberation of CO2 in the venous blood and a temporary rise in end-tidal CO2. Therefore, end-tidal CO2 monitoring will not be useful for judging the effectiveness of chest compressions for three to five minutes following bicarbonate administration.
- El mecanismo de bomba torácica fue descrito en los 80’s gracias a observaciones de la tos como favorecedor del flujo sanguíneo,10 y en estudios realizados en Johns Hopkins.11 “El masaje cardíaco aumenta la presión intratorácica de manera suficiente como para generar un flujo anterógrado a través de la vasculatura pulmonar, las cavidades cardíacas y la periferia”. La Teoría de la Bomba Torácica propone que la compresión torácica aumenta la presión intratorácica, forzando la salida de la sangre fuera del torax, con válvulas venosas y compresión venosa dinámica previniendo el retorno del flujo sanguíneo y la acción del corazón como un conductor pasivo El flujo sanguíneo total tiende a disminuir con el tiempo durante la compresión torácica cerrada. Casi todo el gasto cardíaco es dirigido a los órganos por encima del diafragma. El flujo sanguíneo cerebral es 50 a 90% del normal, el flujo sanguíneo miocárdico es 20 a 50% del normal, mientras que el flujo de las extremidades bajas y el flujo visceral abdominal es reducido a menos del 5%. Theory of the thoracic pump Developed in the years 1980, this theory supposes that it is not the compression direct of the heart that is responsible for the blood circulation, but the increase of the pressure inside the thorax [6]. Thus, when one compresses the thorax, the heart himself include like a passive duct and it is the whole cardiopulmonary volume, consisting of the heart and the big vessels, that constitute the blood reservoir. In this case, when the pressure in the thorax increases, blood cannot ebb in a retrograde manner, nor in the territory hollows superior, because there is a jugular venous collapse during the phase of compression of the MCE, nor in the territory hollows lower because the veins are there valvulées (face 3). This theory has been put in practice at the time of the Cough CPR (RCP by the cough) where the simple makes to make cough the patient to the starting of a ventricular fibrillation is sufficient to create a blood circulation [7]. Fig. 3. theory of the thoracic pump. What is the &quot;thoracic pump theory&quot;? As pressure is applied to the animal's thorax, it has been noted there is a correlation between the rise in intrathoracic pressure during compression and the apparent magnitude of carotid artery blood flow and pressure. For brain blood flow to occur during resuscitation, a carotid arterial-to-jugular pressure gradient must be present during chest compression. Experimental studies in large dogs have shown that thoracic compression during CPR results in an essentially equal rise in central venous, right atrial, pulmonary artery, aortic, esophageal, and lateral pleural space pressures with no transcardiac gradient being developed. Aortic pressure is efficiently transmitted to the carotid arteries, but retrograde transmission of intrathoracic venous pressure into the jugular veins is prevented by valves at the thoracic inlet and possibly by venous collapse. Thus, during &quot;artificial systole&quot; a peripheral arterial venous pressure gradient appears, and blood flow occurs consequent to this gradient. In such a system, there is no pressure gradient across the heart and thus the heart acts mearly as a passive conduit. Cineangiographic studies in large dogs confirm these observations by demonstrating partial right atrioventricular valve closure, collapse of the venae cavae, and opening of the pulmonary, left atrioventricular and aortic valves during thoracic compression. When thoracic compression is released (&quot;artificial diastole&quot;), intrathoracic pressures fall toward zero, and venous flow to the right heart and lungs occur. During &quot;diastole&quot;, a modest gradient also develops between the intrathoracic aorta and the right atrium providing coronary (myocardial) perfusion. In small dogs receiving vigorous chest compressions, intrathoracic vascular pressures are much higher than recorded pleural pressures. In these animals, the rise in vascular pressures likely is a result of compression of the heart during chest compression and is likely not a result of rising intrathoracic pressure. Théorie de la pompe thoracique Développée dans les années 1980, cette théorie suppose que ce n'est pas la compression directe du coeur qui est responsable de la circulation du sang, mais l'augmentation de la pression à l'intérieur du thorax [6] . Ainsi, lorsqu'on comprime le thorax, le coeur se comporte comme un conduit passif et c'est l'ensemble du volume cardiopulmonaire, comprenant le coeur et les gros vaisseaux, qui constitue le réservoir sanguin. Dans ce cas, quand la pression dans le thorax augmente, le sang ne peut pas refluer de manière rétrograde, ni dans le territoire cave supérieur, car il y a un collapsus veineux jugulaire pendant la phase de compression du MCE, ni dans le territoire cave inférieur car les veines y sont valvulées (figure 3) . Cette théorie a été mise en pratique lors de la Cough CPR (RCP par la toux) où le simple fait de faire tousser le patient au démarrage d'une fibrillation ventriculaire suffit à créer une circulation sanguine [7] . Theory of the thoracic pump Developed in the years 1980, this theory supposes that it is not the compression direct of the heart that is responsible for the blood circulation, but the increase of the pressure inside the thorax [6]. Thus, when one compresses the thorax, the heart himself include like a passive duct and it is the whole cardiopulmonary volume, consisting of the heart and the big vessels, that constitute the blood reservoir. In this case, when the pressure in the thorax increases, blood cannot ebb in a retrograde manner, nor in the territory hollows superior, because there is a jugular venous collapse during the phase of compression of the MCE, nor in the territory hollows lower because the veins are there valvulées (face 3). This theory has been put in practice at the time of the Cough CPR (RCP by the cough) where the simple makes to make cough the patient to the starting of a ventricular fibrillation is sufficient to create a blood circulation [7].