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      "El poder cardíaco" un instrumento del pasado, posiblemente una herramienta moderna en la valoración: clínica, terapéutica y pronóstica del choque cardiogénico por síndrome isquémico coronario agudo Translated title: "Cardiac Power Output" an old tool, possibly a modern tool for assessing cardiac pumping capability, as well as for a short-term prognosis in cardiogenic shock due to acute myocardial infarction

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          Abstract

          Los registros de los parámetros hemodinámicos se han utilizado de una manera frecuente y habitual con el fin de establecer la estratificación y el riesgo de los enfermos con falla ventricular izquierda grave y en especial en aquellos que presentan el síndrome de estado de choque cardiogénico. Así mismo, se han aplicado con el propósito de guiar de manera más apropiada el tratamiento y conocer el pronóstico de los mismos a corto plazo. Sabemos que cada corazón tiene su propia capacidad de ejercer su función impulsora de la sangre al territorio sistémico. Este órgano es una máquina mecánica con la habilidad de generar tanto flujo como presión. El producto de multiplicar la presión arterial media sistémica por el flujo ejemplifica el trabajo útil desarrollado y es lo que conocemos como el "poder cardíaco" (PC). Esta capacidad impulsora de la bomba puede ser definida como el PC alcanzado durante la máxima motivación física o farmacológica y la reserva cardíaca es la que resulta a partir del punto del estado de reposo a la que se alcanza con la máxima estimulación física o farmacológica (RPC). El PC de reposo que se ha estimado para un adulto normal es aproximadamente de 1 watt. Sin embargo, durante las situaciones de estrés o durante el ejercicio máximo el corazón es capaz de desarrollar hasta 6 watts. En la disfunción ventricular izquierda aguda, el enfermo se torna en su hemodinámica inestable y la RPC se reduce con miras a tratar de sostener o de mantener la vida. Por lo tanto las determinaciones de PC en la insuficiencia cardíaca aguda o en el estado de choque cardiogénico en la condición de reposo representan la RPC que tiene el corazón en las situaciones agudas y su cuantificación refleja la severidad de la condición patológica imperante. Para la condición del estado de choque, el punto de corte para el PC se ha encontrado que es de 0.53 watts, límite que predice la mortalidad a corto plazo de forma bastante razonable. Para otros investigadores del tema, el límite del punto de corte es de 1 watt, dato que se debe de obtener bajo el efecto del máximo estímulo inotrópico. En nuestra experiencia en el choque cardiogénico por síndrome isquémico coronario agudo (SICA), el punto de corte del PC para predecir mortalidad a corto plazo es de 0.7 watts, pero su impacto en hacerlo es más claro, si el enfermo tiene un PC igual o mayor de 1 watt después de haberse realizado procedimientos coronarios intervencionistas y se ha obtenido éxito en la reperfusión del miocardio. De acuerdo a la revisión de la literatura acerca del tema del PC y sustentado en nuestra experiencia inicial, la cuantificación del PC en este escenario de los SICA, indica que esta determinación hemodinámica tiene un lugar preponderante en la valoración de estos enfermos, mas también pensamos que con la información que contamos hasta nuestros días, merece un análisis mucho más profundo y se debe de ser acreedor de investigaciones futuras, con miras a conocer su significado pronóstico exacto en el contexto del síndrome del estado de choque cardiogénico ocasionado por isquemia coronaria aguda.

          Translated abstract

          Hemodynamic monitoring has been used extensively during the last decades for risk stratification and guiding treatment of patients with cardiovascular destabilization, especially in the scenario of acute heart failure and cardiac shock. Every cardiac pump has its own maximum performance, which denotes its pumping capability. The heart is a muscular mechanical pump with an ability to generate both flow (cardiac output) and pressure. The product of flow output and systemic arterial pressure is the rate of useful work done, "or the cardiac power" (CP). Cardiac pumping capability can be defined as the cardiac power output achieved by the heart during maximal stimulation, and cardiac reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state (CPR). Resting CP for a hemodynamically stable average sized adult is approximately 1 W. However, during stress or exercise, CPR can be recruited to increase the heart's pumping ability up to 6 W. In acute heart failure, the patient becomes hemodynamically unstable, and most of the cardiac pumping potential is recruited in order to sustain life. Hence, cardiac power measurements in patients with acute heart failure or with cardiogenic shock at rest represent most of the recruitable reserve available during the acute event, and their measurement reflects the severity of the patient's condition. It has been found that a cutoff value for CP of 0.53 W accurately predict in-hospital mortality for cardiogenic shock patients. Others investigators observed cutoff for increased mortality of CP < 1 W, data that were obtained at doses of maximal pharmacologic support yielding the individual maximal CP. In our experience, the cutoff value for CP that accurately predicts in-hospital mortality for cardiogenic shock patients is 0.7 W but its impact on short-term prognosis is clearer if the patient achieves a CP equal or higher than 1 W after an optimal myocardial revascularization with interventional cardiac procedures. According to the data collected from the literature, CP deserves a place in the evaluation of the patient with cardiogenic shock due to an acute myocardial infarction, but a more profound analysis of this parameter an further evaluation are required in order to better understand its prognostic meaning in this acute cardiac syndrome.

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          Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry.

          We sought to analyze clinical, angiographic, and outcome correlates of hemodynamic parameters in cardiogenic shock. The significance of right heart catheterization in critically ill patients is controversial, despite the prognostic importance of the derived measurements. Cardiac power is a novel hemodynamic parameter. A total of 541 patients with cardiogenic shock who were enrolled in the SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) trial registry were included. Cardiac power output (CPO) (W) was calculated as mean arterial pressure x cardiac output/451. On univariate analysis, CPO, cardiac power index (CPI), cardiac output, cardiac index, stroke volume, left ventricular work, left ventricular work index, stroke work, mean arterial pressure, systolic and diastolic blood pressure (all p < 0.001), coronary perfusion pressure (p = 0.002), ejection fraction (p = 0.013), and pulmonary artery systolic pressure (p = 0.047) were associated with in-hospital mortality. In separate multivariate analyses, CPO (odds ratio per 0.20 W: 0.60 [95% confidence interval, 0.44 to 0.83], p = 0.002; n = 181) and CPI (odds ratio per 0.10 W/m(2): 0.65 [95% confidence interval, 0.48 to 0.87], p = 0.004; n = 178) remained the strongest independent hemodynamic correlates of in-hospital mortality after adjusting for age and history of hypertension. There was an inverse correlation between CPI and age (correlation coefficient: -0.334, p < 0.001). Women had a lower CPI than men (0.29 +/- 0.11 vs. 0.35 +/- 0.15 W/m(2), p = 0.005). After adjusting for age, female gender remained associated with CPI (p = 0.032). Cardiac power is the strongest independent hemodynamic correlate of in-hospital mortality in patients with cardiogenic shock. Increasing age and female gender are independently associated with lower cardiac power.
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            Cardiogenic shock complicating acute myocardial infarction: expanding the paradigm.

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              Systemic inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock.

              The role of inflammation in patients with coronary artery disease is emerging. We sought to assess the profile and outcomes of patients with a clinical syndrome of severe systemic inflammation that led to a diagnosis of suspected sepsis in the setting of acute myocardial infarction complicated by cardiogenic shock (CS). Patients enrolled in the randomized SHOCK (SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK) trial (n = 302) were divided into those with clinical signs of severe systemic inflammation (eg, fever [94%] or leukocytosis [72%]) that led to a diagnosis of suspected sepsis (n = 54 [18%]) and those without suspected sepsis (controls; n = 243 [80%]). The patients with suspected sepsis were then further subdivided into those who were considered to be potentially infectious (positive culture result ["culture-positive"]; n = 40) and those who were not (negative culture result ["culture-negative"]; n = 14). Severe systemic inflammation was diagnosed 4 and 2 days after the onset of CS in culture-positive and culture-negative patients, respectively. Patients who developed systemic inflammation tended to be younger (P = .05) and to have lower systemic vascular resistance (SVR) near the onset of CS (P = .006). Many culture-positive patients (40%) had undergone coronary artery bypass graft surgery. However, the lower the initial SVR, the higher the risk of developing culture-positive systemic inflammation (P = .01), even after controlling for age and coronary artery bypass graft surgery. A time-dependent model, adjusted for age, showed that culture-positive patients were at significantly higher risk for death than were controls (hazard ratio, 2.22; 95% confidence interval, 1.32-3.76; P = .008). Almost one fifth of patients with acute myocardial infarction complicated by CS showed clinical signs of severe systemic inflammation, and those who were culture-positive for sepsis had twice the risk of death. The observation of lower SVR at the onset of shock in patients who subsequently had culture-positive systemic inflammation suggests that inappropriate vasodilation may play an important role in the pathogenesis and persistence of shock and in the risk of infection.
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                Author and article information

                Journal
                acm
                Archivos de cardiología de México
                Arch. Cardiol. Méx.
                Instituto Nacional de Cardiología Ignacio Chávez (Ciudad de México, Ciudad de México, Mexico )
                1405-9940
                1665-1731
                March 2006
                : 76
                : 1
                : 95-108
                Affiliations
                [01] México, D.F. orgnameInstituto Nacional de Cardiología Ignacio Chávez
                Article
                S1405-99402006000100015 S1405-9940(06)07600100015
                6c2d4d23-ad22-41b5-8d3f-2cafe2cf28b4

                This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.

                History
                : 07 October 2005
                : 26 October 2005
                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 41, Pages: 14
                Product

                SciELO Mexico

                Categories
                Revisión de temas cardiológicos

                pronóstico,Cardiac power,cardiogenic shock,prognostic,Poder cardíaco,choque cardiogénico

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