학술논문
Correlación clínica-ecocardiográfica-hemodinámica en los pacientes con derrame pericárdico severo sometidos a pericardiocentesis
Document Type
Dissertation/Thesis
Author
Source
TDX (Tesis Doctorals en Xarxa)
Subject
Language
Spanish; Castilian
Abstract
Introducción: El taponamiento cardiaco es el síndrome causado por la compresión del corazón por el derrame pericárdico a tensión. Previamente a la introducción del ecocardiograma solo se reconocían los taponamientos que tenían una clara repercusión clínica y que, por tanto, eran los más severos. Asimismo, la pericardiocentesis con monitorización de las presiones intrapericárdicas e intracavitarias ha permitido identificar grados de taponamiento poco severos que no se reconocen clínicamente. A pesar de la amplia difusión de estas técnicas existe poca información en la literatura sobre la correlación entre los hallazgos aportados por la exploración física, el ecocardiograma y el estudio hemodinámico en los pacientes con derrame pericárdico. Por otra parte el análisis de estos datos permite ampliar el concepto de taponamiento no como una situación de todo o nada sino como un cuadro que responde a un “continuum” de severidad clínica. Objetivo: Establecer la correlación existente entre los hallazgos clínicos, ecocardiográficos y del estudio hemodinámico en los pacientes afectos de derrame pericárdico severo sometidos a pericardiocentesis y cateterismo cardiaco. Método: Estudio observacional retrospectivo sobre 191 procedimientos de pericardiocentesis combinada con cateterismo cardiaco realizados en 168 pacientes con derrame pericárdico entre los años 1990 y 2010 en el Hospital Universitari Vall d’Hebron para establecer la relación existente entre los hallazgos clínicos, los datos del estudio ecocardiográfico y la severidad del taponamiento cardiaco establecida por criterios hemodinámicos. Se definió taponamiento clínico cuando existía pulso paradójico, ingurgitación yugular o hipotensión arterial; taponamiento ecocardiográfico-Doppler cuando existía al menos colapso de alguna cavidad cardiaca o variaciones patológicas de los flujos Doppler; y taponamiento hemodinámico si la presión transmural derecha era ≤2mmHg o existía pulso paradójico más incremento del índice cardiaco > 10% después de la pericardiocentesis. Resultados: 132 (69,1%) pacientes tenían criterios de taponamiento clínico, 137 (71,7%) taponamiento ecocardiográfico-Doppler y 150 (78,5%) tenían criterios de taponamiento hemodinámico. La edad mediana fue de 63.5 años (P25-75: 49.5-71.5). 103 pacientes eran mujeres (53,9%). Las etiologías más frecuentes del derrame pericárdico fueron: derrame pericárdico crónico idiopático (52 pacientes-25,2%), derrame pericárdico neoplásico (49 pacientes-23,8%) y el debido a pericarditis aguda idiopática o viral (38 pacientes-18,4%). Correlaciones: Pacientes con taponamiento clínico: taponamiento ecocardiográfico-Doppler: 85,6%, taponamiento hemodinámico: 81,8%. Pacientes sin taponamiento clínico: ausencia de taponamiento ecocardiográfico-Doppler: 33,9%, ausencia de taponamiento hemodinámico: 27,1%. Pacientes con taponamiento ecocardiográfico-Doppler: taponamiento clínico: 73,7%, taponamiento hemodinámico: 82,5%. Pacientes sin taponamiento ecocardiográfico-Doppler: ausencia de taponamiento clínico: 55,6%, ausencia de taponamiento hemodinámico: 37%. Pacientes con taponamiento hemodinámico: taponamiento clínico: 68%, taponamiento ecocardiográfico-Doppler: 84,7%. Pacientes sin taponamiento hemodinámico: ausencia de taponamiento clínico: 41,5%, ausencia de taponamiento ecocardiográfico-Doppler: 34,1%. Conclusiones: El estudio hemodinámico y el ecocardiograma-Doppler detectan grados subclínicos de taponamiento. De los enfermos sin criterios clínicos de taponamiento, el 66,1% tenían signos ecocardiográficos y el 72,9% tenían criterios hemodinámicos de taponamiento. Un 18,2% de los pacientes con diagnóstico de taponamiento clínico y un 17,5% de pacientes con signos de taponamiento en el ecocardiograma-Doppler no tenían datos hemodinámicos de taponamiento. Las discrepancias se pueden explicar por la baja sensibilidad y la baja especificidad de los criterios clínicos (especialmente de la ingurgitación yugular y de la hipotensión arterial), por las limitaciones de las técnicas de imagen, por una fisiopatología inhabitual del taponamiento como es la compresión de la vena cava superior, o bien, y no tanto, por las limitaciones del registro hemodinámico.
Introduction: Cardiac tamponade syndrome is caused by compression of the heart by pericardial effusion. Prior to the introduction of echocardiography only recognized the blockages that had a clear clinical impact and, therefore, were the most severe. Also, pericardiocentesis with intrapericardial pressure monitoring and intracavitary has identified some severe degrees of tamponade not recognized clinically. Despite the widespread diffusion of these techniques there is little information in the literature on the correlation between the findings provided by the physical examination, echocardiography and hemodynamic study in patients with pericardial effusion. Moreover, the analysis of these data allows to extend the concept of tamponade not an all or nothing situation but as a box that responds to a "continuum" of clinical severity. Objective: To establish the correlation between the clinical, echocardiographic and hemodynamic study in patients with severe pericardial effusion underwent pericardiocentesis and cardiac catheterization. Method: Retrospective observational study on 191 pericardiocentesis procedures combined with cardiac catheterization performed in 168 patients with pericardial effusion between 1990 and 2010 at the Hospital Universitari Vall d'Hebron to establish the relationship between the clinical, echocardiographic data and severity of cardiac tamponade hemodynamic criteria established by. Clinical tamponade was defined when there was paradoxical pulse, jugular venous distention or hypotension; Doppler echocardiographic tamponade when there was at least one heart chamber collapse or pathologic variations flow Doppler, and hemodynamic tamponade if right transmural pressure was ≤ 2mmHg or paradoxical pulse more increase in cardiac index> 10% after pericardiocentesis. Results: 132 (69.1%) patients had clinical tamponade criteria, 137 (71.7%) Doppler echocardiographic tamponade and 150 (78.5%) had tamponade hemodynamic criteria. The median age was 63.5 years (P25-75: 49.5-71.5). 103 patients were female (53.9%). The most common causes of pericardial effusion were: idiopathic chronic pericardial effusion (52 patients-25, 2%), neoplastic pericardial effusion (49 patients-23, 8%) and due to idiopathic or viral acute pericarditis (38 patients-18, 4%). Correlations: Patients with clinical tamponade: Doppler echocardiographic tamponade: 85.6%, hemodynamic tamponade: 81.8%. Patients without clinical tamponade: absence of Doppler echocardiographic tamponade: 33.9%, no hemodynamic tamponade: 27.1%. Patients with Doppler echocardiographic tamponade: clinical tamponade: 73.7%, hemodynamic tamponade: 82.5%. Patients without Doppler echocardiographic tamponade: absence of clinical tamponade: 55.6%, no hemodynamic tamponade: 37%. Patients with hemodynamic tamponade: clinical tamponade: 68%, Doppler echocardiographic tamponade: 84.7%. Patients without hemodynamic tamponade: absence of clinical tamponade: 41.5%, no Doppler echocardiographic tamponade: 34.1%. Conclusions: The hemodynamic and Doppler echocardiography detect subclinical degrees of tamponade. In patients without clinical tamponade criteria, 66.1% had echocardiographic signs and 72.9% had hemodynamic criteria of tamponade. 18.2% of patients diagnosed with clinical tamponade and 17.5% of patients with signs of tamponade on echocardiography-Doppler hemodynamic data were not plugging. Discrepancies can be explained by the low sensitivity and low specificity of clinical criteria (especially jugular venous distension and hypotension), by the limitations of imaging techniques, by an unusual pathophysiology of tamponade as compression the superior vena cava, or, rather, by the limitations of hemodynamic recording.
Introduction: Cardiac tamponade syndrome is caused by compression of the heart by pericardial effusion. Prior to the introduction of echocardiography only recognized the blockages that had a clear clinical impact and, therefore, were the most severe. Also, pericardiocentesis with intrapericardial pressure monitoring and intracavitary has identified some severe degrees of tamponade not recognized clinically. Despite the widespread diffusion of these techniques there is little information in the literature on the correlation between the findings provided by the physical examination, echocardiography and hemodynamic study in patients with pericardial effusion. Moreover, the analysis of these data allows to extend the concept of tamponade not an all or nothing situation but as a box that responds to a "continuum" of clinical severity. Objective: To establish the correlation between the clinical, echocardiographic and hemodynamic study in patients with severe pericardial effusion underwent pericardiocentesis and cardiac catheterization. Method: Retrospective observational study on 191 pericardiocentesis procedures combined with cardiac catheterization performed in 168 patients with pericardial effusion between 1990 and 2010 at the Hospital Universitari Vall d'Hebron to establish the relationship between the clinical, echocardiographic data and severity of cardiac tamponade hemodynamic criteria established by. Clinical tamponade was defined when there was paradoxical pulse, jugular venous distention or hypotension; Doppler echocardiographic tamponade when there was at least one heart chamber collapse or pathologic variations flow Doppler, and hemodynamic tamponade if right transmural pressure was ≤ 2mmHg or paradoxical pulse more increase in cardiac index> 10% after pericardiocentesis. Results: 132 (69.1%) patients had clinical tamponade criteria, 137 (71.7%) Doppler echocardiographic tamponade and 150 (78.5%) had tamponade hemodynamic criteria. The median age was 63.5 years (P25-75: 49.5-71.5). 103 patients were female (53.9%). The most common causes of pericardial effusion were: idiopathic chronic pericardial effusion (52 patients-25, 2%), neoplastic pericardial effusion (49 patients-23, 8%) and due to idiopathic or viral acute pericarditis (38 patients-18, 4%). Correlations: Patients with clinical tamponade: Doppler echocardiographic tamponade: 85.6%, hemodynamic tamponade: 81.8%. Patients without clinical tamponade: absence of Doppler echocardiographic tamponade: 33.9%, no hemodynamic tamponade: 27.1%. Patients with Doppler echocardiographic tamponade: clinical tamponade: 73.7%, hemodynamic tamponade: 82.5%. Patients without Doppler echocardiographic tamponade: absence of clinical tamponade: 55.6%, no hemodynamic tamponade: 37%. Patients with hemodynamic tamponade: clinical tamponade: 68%, Doppler echocardiographic tamponade: 84.7%. Patients without hemodynamic tamponade: absence of clinical tamponade: 41.5%, no Doppler echocardiographic tamponade: 34.1%. Conclusions: The hemodynamic and Doppler echocardiography detect subclinical degrees of tamponade. In patients without clinical tamponade criteria, 66.1% had echocardiographic signs and 72.9% had hemodynamic criteria of tamponade. 18.2% of patients diagnosed with clinical tamponade and 17.5% of patients with signs of tamponade on echocardiography-Doppler hemodynamic data were not plugging. Discrepancies can be explained by the low sensitivity and low specificity of clinical criteria (especially jugular venous distension and hypotension), by the limitations of imaging techniques, by an unusual pathophysiology of tamponade as compression the superior vena cava, or, rather, by the limitations of hemodynamic recording.