Hemodynamic profiles related to circulatory shock in cardiac care units / Perfiles hemodinámicos relacionados con el choque circulatorio en unidades de cuidados cardiacos

Abstract One-third of the population in intensive care units is in a state of circulatory shock, whose rapid recognition and mechanism differentiation are of great importance. The clinical context and physical examination are of great value, but in complex situations as in cardiac care units, it is mandatory the use of advanced hemodynamic monitorization devices, both to determine the main mechanism of shock, as to decide management and guide response to treatment, these devices include pulmonary flotation catheter as the gold standard, as well as more recent techniques including echocardiography and pulmonary ultrasound, among others. This article emphasizes the different shock mechanisms observed in the cardiac care units, with a proposal for approach and treatment.

Resumen Un tercio de la población de pacientes en unidades de cuidados intensivos se encuentran en choque circulatorio, el identificarlo y determinar su mecanismo de manera rápida y eficaz es de gran importancia. El contexto clínico y el examen físico son de gran utilidad, sin embargo existen situaciones de alta complejidad en las que se requiere del uso de las distintas modalidades de monitorización hemodinámica avanzada, tanto para determinar la causa, como para decidir el manejo y guiar respuesta al tratamiento, incluyendo el catéter de flotación pulmonar como gold standard, así como técnicas más recientes incluyendo ecocardiografía y ultrasonido pulmonar, entre otros. Este artículo enfatiza los distintos mecanismos de choque observados en las unidades de cuidados cardiacos, con propuesta de abordaje y tratamiento.

Utilidad del protocolo focused assessment with transthoracic echocardiography (FATE) en la evaluación del paciente con shock / The usefulness of the (FATE) protocol focused assessment with transthoracic echocardiography in patients with shock

Determinar la utilidad del protocolo FATE (Focused Assessment with Transthoracic Echocardiography) en la evaluación de los pacientes en shock. ingresados al Servicio de Cuidados Intermedios del Hospital Central Universitario Dr. "Antonio María Pineda", Barquisimeto, Venezuela en el período agosto-octubre 2019, Métodos: se realizó un estudio descriptivo transversal, de 30 pacientes, con promedio de edad de 56,86 ± 15,85 años, Resultados: predominó el grupo de 71-80 años (23,33%), de sexo masculino (63,33%). Según la clasificación del shock por Weil y Shubin el 50% presentó shock distributivo (todos por sepsis), 20% cardiogénico, 16,67% hipovolémico y obstructivo. 13,33% Los principales hallazgos ecocardiográficos fueron presencia de derrame pleural bilateral (33,33%), derrame pleural unilateral (30%) y derrame pericárdico (23,33%). Además, 26,67% presentaron espesor miocárdico patológico, 33,33% dimensiones de VD-VI aumentadas, 46,67% función sistólica ventricular alterada; sumado al hecho que 70% de la contractibilidad y 60% de la visualización pulmonar eran patológicas. El valor cualitativo del protocolo FATE resultó en: 43,33% soportaba la información disponible, 26,67% añadió información decisiva a la terapéutica, 23,33% agregó nueva información y 6,67% información fue pobre por mala ventana. La mortalidad a los 7 días fue de 43,33%, siendo más frecuente en pacientes con shock distributivo (61,54%), seguido de cardiogénico (23,08%) y obstructivo (15,38%), no hubo defunciones por shock hipovolémico. Los valores cualitativos del protocolo FATE en pacientes fallecidos; por shock distributivo 37,5%, soportó la información disponible y agregó nueva información, respectivamente. En cambio en 100% de los fallecidos por shock cardiogénico y obstructivo, el protocolo FATE añadió información decisiva a la terapéutica. Los resultados demuestran la importancia del Protocolo FATE en el manejo de pacientes con shock(AU)

To determine the usefulness of the FATE protocol (Focused Assessment with Transthoracic Echocardiography) in the evaluation of patients in shock admitted to the Intermediate Care Unit of the "University Hospital Antonio Maria Pineda" in Barquisimeto, Venezuela, during the period August-October 2019, Methods: A descriptive cross-sectional study was done, selecting 30 patients, with an average age of 56.86 ± 15.85 years; the most affected group was 71-80 years old (23.33%), with a predominance of the male sex (63.33%) Results: According to the classification of shock by Weil and Shubin, 50% were found to have distributive shock (all due to sepsis), 20% cardiogenic, 16.67% hypovolemic and obstructive 13.33%. The main echocardiographic findings were the presence of bilateral pleural effusion (33.33%), unilateral pleural effusion (30%) and pericardial effusion (23.33%). In addition, 26.67% presented pathological myocardial thickness, 33.33% increased RV-LV dimensions, 46.67% impaired ventricular systolic function; also, 70% of contractibility and 60% of pulmonary visualization were pathological. The qualitative value of the FATE protocol resulted in: 43.33% supported the available information, 26.67% added decisive information to the therapy, 23.33% added new information and 6.67% information was poor due to a bad US window. (Mortality at 7 days was 43.33%, being more frequent in patients with distributive shock (61.54%), followed by cardiogenic (23.08%) and obstructive (15.38%); there were no deaths due to hypovolemic shock. The qualitative values of the FATE protocol in patients with distributive shock who died, was that 37.5% In contrast, in 100% of those who died by cardiogenic and obstructive shock, the FATE protocol added decisive information to the therapy. Conclusion:The results demonstrate the importance of the FATE Protocol in the management of patients with shock(AU)

Cardiogenic shock with ST-segment elevation acute coronary syndrome (ReNa-Shock ST)

Cardiogenic shock (CS) in the setting of an ST-segment elevation myocardial infarction (STEMI) is a severe complication and constitutes one of the principal causes of death associated with this condition. The aim of this study was to describe the clinical characteristics, treatment strategies and hospital outcome of CS associated with STEMI in Argentina. The Argentine Registry of Cardiogenic Shock (ReNA-Shock) was a prospective and multicenter registry of consecutive patients with CS hospitalized in 64 centers in Argentina between July 2013 and May 2015. Only those with ST-segment elevation myocardial infarction (STEMI) were selected for this analysis. Of the 165 patients included in the ReNa-Shock registry, 124 presented STEMI. Median age was 64 years (IQR 25-75: 56.5-75) and 67% were men; median time from symptom onset to admission was 240 minutes (IQR 25-75: 132-720). 63% of the cases presented CS at admission. Eighty-seven percent underwent reperfusion therapy: 80% primary percutaneous intervention with a median door-to-balloon time of 110 minutes (IQR 25-75: 62-184). Inotropic agents were used in 96%; 79% required mechanical ventilation; a Swan Ganz catheter was inserted in 47% and 35% required intra-aortic balloon pumping. Most patients (59%) presented multivessel disease (MV). Hospital mortality was 54%. Multivariate analysis identified that time from symptom onset to admission (> 240 min) was the only independent predictor of mortality (OR: 3.04; CI 95%: 1.18-7.9). Despite using treatment strategies currently available, morbidity and mortality of STEMI complicated with CS remains high.

El shock cardiogénico (SC) en el síndrome coronario agudo con elevación del ST (SCACEST), es una complicación grave y constituye una de las principales causas de muerte. El objetivo del registro fue conocer las características clínicas, estrategias de tratamiento y evolución intrahospitalaria del SC secundario a un SCACEST en Argentina. El Registro Argentino de Shock Cardiogénico (ReNa-Shock) fue prospectivo, multicéntrico y consecutivo de pacientes internados con SC en el periodo 2013/2015 en 64 centros de Argentina. Fueron incluidos 165 pacientes, de los cuales124 presentaban SCACEST. La edad (mediana) fue de 64 [RIC25-75: 56-75] años, 67% hombres. La mediana de tiempo desde el inicio de los síntomas al ingreso hospitalario fue de 240 minutos [RIC25-75: 132-720]. Un 63% de los casos tuvo SC desde el ingreso. El 87% recibió tratamiento de reperfusión, con un 80% de angioplastia primaria y un tiempo puerta-balón (mediana): 110 minutos [RIC25-75: 62-184]. Requirieron inotrópicos un 96%, asistencia respiratoria mecánica el 79%, catéter de Swan Ganz 47%, balón de contrapulsación intraaórtico 35%. El 59% tenía lesión de 2 o 3 vasos. La mortalidad intrahospitalaria fue 54%. En el análisis multivariado, solo el tiempo de evolución al ingreso (345 min [RIC25-75: 135-720] vs. 180 min [RIC25-75: 85-420]; p: 0.03) fue la única variable predictora independiente de mortalidad. La morbimortalidad del SC complicando un SCACEST es elevada a pesar de la utilización de las estrategias de tratamiento actualmente disponibles.

Anesthetic and hemodynamic management of a rare case of Brucella multivalvular endocarditis in cardiogenic shock undergoing emergency aortic valve replacement and mitral valve repair.

We describe a very rare case of human brucella multivalvular endocarditis. Patient presented in a state of cardiogenic shock with low urine output and a history of breathlessness. Patient was diagnosed to have brucellosis 2 months back by blood cultures and agglutination tests and was receiving doxycycline and rifampicin therapy. Echocardiography showed severe aortic regurgitation, moderate mitral regurgitation, severe left ventricular dysfunction and a mobile vegetation attached to the aortic valve. Patient was scheduled for emergency surgery; while preparing for surgery hemodynamic monitoring, non‑invasive ventilation and inotropic supports were started. During surgery, the aortic valve was found perforated and the aortomitral continuity was disrupted. Aortic valve replacement and mitral valve repair were performed. Hemofiltration was used during cardiopulmonary bypass. Weaning from bypass was achieved with the help of inodilators, dual chamber pacing and intra‑aortic balloon pump.

Evolução hospitalar de pacientes com choque cardiogênico por infarto agudo do miocárdio com supradesnivelamento do segmento ST / In-hospital outcomes of patients with cardiogenic shock due to ST-elevation myocardial infarction

INTRODUÇÃO: O choque cardiogênico é uma condição clínica de inadequada perfusão tecidual devido à disfunção cardíaca. A etiologia mais comum é o infarto agudo do miocárdio com elevação do segmento ST (IMCSST) levando à insuficiência ventricular esquerda, mas também pode ser causado por complicações mecânicas, como insuficiência mitral aguda, ruptura do septo interventricular ou da parede livre do ventrículo esquerdo. Apesar dos avanços terapêuticos, a mortalidade continua elevada. MÉTODOS: Estudo retrospectivo, observacional, unicêntrico, incluindo pacientes consecutivos internados com o diagnóstico de IMCSST e choque cardiogênico, tratados por intervenção coronária percutânea (ICP), em hospital terciário especializado em cardiologia. O objetivo primário foi avaliar os desfechos clínicos hospitalares. RESULTADOS: Foram incluídos 78 pacientes, a maioria do sexo masculino (67,9%), com idade de 67,5 ± 13,4 anos e 41,0% diabéticos. ICP primária foi realizada em 46,2% dos pacientes, ICP de resgate em 25,6% e ICP eletiva em 28,2% dos casos. As artérias mais frequentemente acometidas foram a descendente anterior e a coronária direita, com 44,9% cada uma. O balão intra-aórtico foi utilizado em 32,1% e os inibidores da glicoproteína IIb/IIIa em 30,8% dos casos. A incidência de insuficiência renal aguda foi de 61,5%. A necessidade de reintervenção ocorreu em 9,0%, e a taxa de trombose aguda/subaguda foi de 3,8%. Óbito, no choque cardiogênico, ocorreu em 46,2%. CONCLUSÕES: O choque cardiogênico permanece uma entidade frequente e grave, com quase 50% de mortalidade hospitalar, apesar da evolução na terapêutica instituída atualmente.

BACKGROUND: Cardiogenic shock is a clinical condition of inadequate tissue perfusion due to cardiac dysfunction. The most common etiology is ST-segment elevation myocardial infarction (STEMI) leading to left ventricular failure, but it may also be caused by mechanical complications such as acute mitral regurgitation, ventricular septal rupture or rupture of the left ventricular free wall. Despite therapeutic advances, mortality rates remain high. METHODS: Retrospective, observational, single-center study, including consecutive patients admitted with a diagnosis of STEMI and cardiogenic shock treated by percutaneous coronary intervention (PCI) at a tertiary hospital specialized in cardiology. The primary objective was to evaluate in-hospital clinical outcomes. RESULTS: A total of 78 patients were included, most of them were male (67.9%), mean age was 67.5 ± 13,4 years and 41.0% were diabetic. Primary PCI was performed in 46.2% of the patients, rescue PCI in 25.6% and elective PCI in 28.2% of the cases. The most frequently involved arteries were the left anterior descending artery and the right coronary artery, with 44.9% each. Intra-aortic balloon pump was used in 32.1% of cases and glycoprotein IIb/IIIa inhibitors in 30.8% of the cases. The incidence of acute renal failure was 61.5%. The need for reintervention was observed in 9.0% and the rate of acute/subacute thrombosis was 3.8%. Death due to cardiogenic shock was observed in 46.2%. Conclusions: Cardiogenic shock remains a frequent and serious condition with almost 50% of in-hospital mortality despite the therapeutic advances.

Fisiopatología del shock: Nuevas perspectivas / Pathophysiology of shock: New perspectives

La actividad metabólica puede modificarse mediante la regulación de la población mitocondrial en distintas enfermedades críticas. A través de observaciones y ensayos clínicos examinamos esta adaptación metabólica en el shock cardiogénico, hemorrágico y séptico. La caída de la disponibilidad de O2 (DO2) llevaría a una reducción de la población mitocondrial y consecuentemente a una disminución del consumo de O2 (VO2). Esta secuencia permite atenuar y aun evitar la adquisición de una deuda de O2, considerada hasta hoy base fundamental de la fisiopatología del shock. El costo de esta adaptación mitocondrial es menor energía disponible y el déficit energético resultante ha sido relacionado con la falla orgánica múltiple (FOM), importante complicación de diversos procesos inflamatorios agudos y estados de shock. La FOM es mejor tolerada que el metabolismo anaeróbico y es potencialmente reversible si se revierten las causas desencadenantes y se reestablece el nivel energético por medio de la biogénesis mitocondrial.El desacople de la fosforilación oxidativa mitocondrial ocurre tanto en diversos modelos experimentales de shock como así también en el shock séptico en el hombre. Esta alteración mitocondrial puede ser detectada por un aumento desmesurado del VO2 en respuesta al incremento terapéutico de la DO2. Este aumento de la actividad metabólica puede ser equívocamente interpretado como la fase de repago de una deuda de O2.

Metabolic activity can be down-regulated throughout the reduction of mitochondrial population. Lowering O2 demand in cardiogenic, hemorrhagic and septic shock is here examined through clinical observations and trials. A decrease in the availability of O2 will be followed by reductions in mitochondrial population and, therefore, in a decrease in O2 demand. This response may lessen or prevent the acquisition of an O2 debt; until now, cornerstone in the pathophysiology of shock. The cost of this adaptation is less energy production, and the resulting energy deficit has been linked to multiple organ failure (MOF), a complication of acute inflammatory processes and shock. MOF is better tolerated than anaerobic metabolism and is potentially reversible if the triggering causes are reversed and the energy level is re-established through mitochondrial biogenesis.Decoupling of mitochondrial oxidative phosphorylation occurs in both experimental models and in clinical septic shock. In critical patients this phenomenon may be detected by an inordinate increase in VO2 in response to a therapeutically increased DO2. This hipermetabolic stage can be mistakenly interpreted as the repayment phase of an O2 debt.

Shock cardiogénico: [revisión] / Cardiogenic shock: [review]

El shock cardiogénico es un síndrome que comprende hipotensión y disminución de la perfusión tisular. Inicialmente los mecanismos de compensación neurohumoral mantienen la perfusión en los órganos vitales si el tratamiento adecuado no se instaura en forma temprana, estos mecanismos son sobrepasados, produciendo isquemia, daño celular, fallo multiorgánico y muerte. Las causas del shock cardiogénico incluyen: infarto agudo de miocardio y sus complicaciones agudas, arritmias agudas, contusión cardiaca, fármacos depresores, disección aórtica ascendente y embolia pulmonar. El determinante fisiológico del shock cardiogénico es un descenso brusco del volumen de la fracción de eyección cardíaca y de la presión arterial sistémica. La presión venosa central, la presión en la arteria pulmonar y la presión de enclavamiento pulmonar están elevadas.

Cardiogenic shock is a syndrome characterized by hypotension and decrease of the tissue perfusion. Initially the mechanism of neurohumoral compensation keeps the perfusion of the vital organs if the right treatment is not applied early. This mechanism is overrun producing ischemia, cell damage, multi-organic failure and eventually dead. Some of the causes for cardiogenic shock are: acute heart attack and its complications, acute arrhythmia, heart contusion, depression drugs, ascending aortic dissection and pulmonary embolism. The Physiological determinant of cardiogenic shock is a sudden drop in the volume of cardiac ejection fraction and the systemic arterial pressure. The central venous pressure, the pressure in the pulmonary artery and the pulmonary wedge pressure are raised.

Is persistent hypotension after transient cardiogenic shock associated with an inflammatory response?

We evaluated the recovery of cardiovascular function after transient cardiogenic shock. Cardiac tamponade was performed for 1 h and post-shock data were collected in 5 domestic large white female pigs (43 ± 5 kg) for 6 h. The control group (N = 5) was observed for 6 h after 1 h of resting. During 1 h of cardiac tamponade, experimental animals evolved a low perfusion status with a higher lactate level (8.0 ± 2.2 vs 1.9 ± 0.9 mEq/L), lower standard base excess (-7.3 ± 3.3 vs 2.0 ± 0.9 mEq/L), lower urinary output (0.9 ± 0.9 vs 3.0 ± 1.4 mL·kg-1·h-1), lower mixed venous saturation, higher ileum partial pressure of CO2-end tidal CO2 (EtCO2) gap and a lower cardiac index than the control group. Throughout the 6-h recovery phase after cardiac tamponade, tamponade animals developed significant tachycardia with preserved cardiac index, resulting in a lower left ventricular stroke work, suggesting possible myocardial dysfunction. Vascular dysfunction was present with persistent systemic hypotension as well as persistent pulmonary hypertension. In contrast, oliguria, hyperlactatemia and metabolic acidosis were corrected by the 6th hour. The inflammatory characteristics were an elevated core temperature and increased plasma levels of interleukin-6 in the tamponade group compared to the control group. We conclude that cardiovascular recovery after a transient and severe low flow systemic state was incomplete. Vascular dysfunction persisted up to 6 h after release of tamponade. These inflammatory characteristics may also indicate that inflammatory activation is a possible pathway involved in the pathogenesis of cardiogenic shock.

Hemodynamic impact of alveolar recruitment maneuver in patients evolving with cardiogenic shock in the immediate postoperative period of myocardial revascularization / Impacto hemodinâmico de manobra de recrutamento alveolar em pacientes evoluindo com choque cardiogênico no pós-operatório imediato de revascularização do miocárdio / Impacto hemodinámico de maniobra de reclutamiento alveolar en pacientes evolucionando con choque cardiogénico en el postoperatorio inmediato de revascularización del miocardio

JUSTIFICATIVA E OBJETIVOS: Manobras de recrutamento alveolar (MRA) utilizando pressões de 40 cmH2O nas vias aéreas são efetivas em reverter as atelectasias após revascularização cirúrgica do miocárdio (RM), contudo não existem estudos avaliando o impacto hemodinâmico dessa manobra em pacientes que evoluíram com choque cardiogênico. O objetivo foi testar a tolerância hemodinâmica à MRA em pacientes evoluindo com choque cardiogênico após RM. MÉTODO: Após admissão na UTI e estabilização hemodinâmica, foram estudados dez pacientes hipoxêmicos e em choque cardiogênico após RM. Os ajustes ventilatórios foram volume corrente de 8 mL.kg-1, PEEP 5 cmH2O, FR de 12 ipm e FiO2 de 0,6. Pressão contínua de 40 cmH2O foi aplicada nas vias aéreas por 40 segundos em três ciclos. Entre os ciclos, os pacientes foram ventilados por 30 segundos e após o último ciclo a PEEP foi ajustada em 10 cmH2O. Foram obtidas medidas hemodinâmicas após 1, 10, 30 e 60 minutos da MRA e colhidas amostras sangüíneas arteriais e venosas para mensuração de lactato e gases sangüíneos 10 e 60 minutos após. Dados analisados por meio de ANOVA e teste de Friedman. Valor de p fixado em 0,05. RESULTADOS: A MRA aumentou a relação PaO2/FiO2 de 87 para 129,5 após 10 minutos e 120 após 60 minutos (p < 0,05) e reduziu o shunt pulmonar de 30 por cento para 20 por cento (p < 0,05). Não foram detectadas alterações hemodinâmicas ou no transporte de oxigênio imediatamente ou em até 60 minutos após a MRA. CONCLUSÕES: Em pacientes que evoluíram com choque cardiogênico após RM e hipoxemia, a MRA melhorou a oxigenação e foi bem tolerada sob o ponto de vista hemodinâmico.

BACKGROUND AND OBJECTIVES: Alveolar recruitment maneuver (ARM) with pressures of 40 cmH2 O in the airways is effective in the reversal of atelectasis after myocardial revascularization (MR); however, there is a lack of studies evaluating the hemodynamic impact of this maneuver in patients who evolve with cardiogenic shock after MR. The objective of this study was to test the hemodynamic tolerance to ARM in patients who develop cardiogenic shock after MR. METHODS: Ten hypoxemic patients in cardiogenic shock after MR were evaluated after admission to the ICU and hemodynamic stabilization. Ventilatory adjustments included tidal volume of 8 mL.kg-1, PEEP 5 cmH2O, RR 12, and FiO2 0.6. Continuous pressure of 40 cmH2O was applied to the airways for 40 seconds in three cycles. Between cycles, patients were ventilated for 30 seconds, and after the last cycle, PEEP was set at 10 cmH2O. Hemodynamic measurements were obtained 1, 10, 30, and 60 minutes after ARM, and arterial and venous blood samples were drawn 10 and 60 minutes after the maneuver to determine lactate levels and blood gases. ANOVA and the Friedman test were used to analyze the data. A p of 0.05 was considered significant. RESULTS: Alveolar recruitment maneuver increased the ratio PaO2/FiO2 from 87 to 129.5 after 10 minutes and to 120 after 60 minutes (p < 0.05) and reduced pulmonary shunting from 30 percent to 20 percent (p < 0.05). Hemodynamic changes or changes in oxygen transport immediately after or up to 60 minutes after the maneuver were not detected. CONCLUSIONS: In patients who evolved to cardiogenic shock and hypoxemia after MR, ARM improved oxygenation and was well tolerated hemodynamically.

JUSTIFICATIVA Y OBJETIVOS: Maniobras de reclutamiento alveolar (MRA) utilizando presiones de 40 cmH2O en las vías aéreas son efectivas en revertir las atelectasias después de la revascularización quirúrgica del miocardio (RM), sin embargo, no existen estudios que evalúen el impacto hemodinámico de esta maniobra en pacientes que evolucionaron con choque cardiogénico. El objetivo fue probar la tolerancia hemodinámica a la MRA en pacientes que evolucionan con choque cardiogénico después de la RM. MÉTODO: Después de la entrada en la UCI y de la estabilización hemodinámica, se estudiaron 10 pacientes hipoxémicos y en choque cardiogénico después de RM. Los ajustes de ventilación fueron volumen corriente de 8 mL.kg-1, PEEP 5 cmH2O, FR de 12 ipm y FiO2 de 0,6. Presión continua de 40 cmH2O se aplicó en las vías aéreas por 40 segundos en tres ciclos. Entre los ciclos, los pacientes fueron ventilados por 30 segundos y después del último ciclo, la PEEP fue ajustada en 10 cmH2O. Fueron obtenidas medidas hemodinámicas después de 1, 10, 30 y 60 minutos de la MRA y recogidas muestras de sangre arteriales y venosas para la medida de lactato y de los gases sanguíneos 10 y 60 minutos después. Datos analizados a través de ANOVA y test de Friedman. Valor de p fijado en 0,05. RESULTADOS: La MRA aumentó la relación PaO2/FiO2 de 87 para 129,5 después de 10 minutos y 120 después de 60 minutos (p < 0,05) y redujo el shunt pulmonar de 30 por ciento para 20 por ciento (p < 0,05). No se detectaron alteraciones hemodinámicas o en el transporte de oxígeno inmediatamente o en hasta 60 minutos después de la MRA. CONCLUSIONES: En pacientes que evolucionaron con choque cardiogénico después de RM e hipoxemia, la MRA mejoró la oxigenación y fue bien tolerada hemodinámicamente.

Methylene blue improves hemodynamic shock but increases lipoperoxidation in severe acute pancreatitis pig model / Azul de metileno melhora as condições hemodinâmicas do choque circulatório, mas aumenta a peroxidação lipídica em um modelo suino de pancreatite aguda grave

PURPOSE: Study hemodynamic pattern and lipoperoxidation during methylene blue (MB) treatment on taurocholate - enterokinase induced acute pancreatitis (AP). METHODS: Thirty pigs were equally divided in control group; MB group; AP group; MB previous AP group; and MB after 90 min of induced AP group. MB was given iv in a bolus dose (2mg.kg-1) followed by maintenance dose (2 mg.kg-1.h-1). Hemodynamic parameters were recorded continuously during 180 min by Swan-Ganz catheter. Blood samples were taken every 60 min to determine arterial and venous nitrate, malondialdehyde (MDA) and amylase. Pancreatic tissue was removed for histopathologic study. RESULTS: In AP group MBP and CO decreased over time 33 percent (p<0.05) and 52 percent (p<0.05), respectively. In MB previous induced-AP group, there was 70 minutes delay (p<0.05) to decrease MBP and CO. In MB group arterial and venous nitrite decreased (p<0.05) over time. MB infusion increased (p>0.05) serum MDA when associated to AP. After induced AP, MB did not reverse MBP and CO decrease. There was no difference in serum amylase and necro-hemorrhagic findings with MB treatment. CONCLUSIONS: In this taurocholate-induced AP model MB treatment delayed hemodynamic shock and decreases serum nitrate levels but increases serum MDA levels. No volemic replacement was done and it may have been a mitigated factor to a poor tissue perfusion and impairment microcirculation. Further investigations are needed to elucidate MB treatment role during AP treatment.

OBJETIVO: estudar o perfil hemodinâmico e a lipoperoxidação durante o tratamento com azul de metileno (AM) de pancreatite aguda (PA) induzida por taurocolato-enteroquinase. MÉTODOS: Trinta porcos foram igualmente divididos em: grupo controle, grupo AM; grupo PA; grupo AM prévio à PA; grupo AM após 90 minutos após a indução da PA. O AM foi administrado sob a forma de bolus EV (2mg.kg-1) seguido por dose de manutenção (2 mg.kg-1.h-1). Os parâmetros hemodinâmicos foram registrados continuamente durante 180 min com auxílio de cateter de Swan-Ganz. Amostras sanguíneas foram colhidas a cada 60 min para a determinação arterial e venosa de nitrato, malondialdeido (MDA) and amilase. Removeu-se tecido pancreático para estudo histopatológico. RESULTADOS: No grupo PA a pressão arterial media (PAM) e o débito cardíaco (DC) diminuíram respectivamente 33 por cento (p<0.05) e 52 por cento (p<0.05) no decorrer do tempo. No grupo AM prévio à indução da PA ocorreu 70 minutes de demora (p<0.05) para as diminuições da PAM e DC. No grupo AM houve diminuição temporal do nitrato arterial e venoso (p<0.05). A infusão de AM aumentou os valores de MDA sérico quando associado a PA (p>0.05). Após a indução da PA a infusão de AM não reverteu as quedas da PA e DC. Não houve diferenças nos níveis de amilase sérica e achados histológicos com o tratamento com o azul de metileno. CONCLUSÕES: No presente modelo de PA induzida por taurocolato o AM retardou o desenvolvimento do choque circulatório, diminuiu os níveis de nitrato mas aumentou os níveis de MDA. Não se realizou nenhum tipo de reposição volêmica que poderia melhorar a perfusão tecidual e melhora da microcirculação. Investigações adicionais são necessárias para elucidar o papel terapêutico do AM no tratamento da PA aguda.

Choque / Shock

O choque é um colapso circulatório resultante de inúmeras etiologias. Pode ser classificado em hipovolêmico, cardiogênico, obstrutivo e distributivo. A hemorragia é a causa mais comum de choque hipovolêmico. Infarto agudo do miocárdio deve ser sempre investigado no choque cardiogênico. No choque obstrutivo, drenagem pleural ou pericárdica pode ser suficiente para estabilizar o paciente. Antibioticoterapia é fundamental na terapêutica da sepse, etiologia mais freqüente do choque distributivo. Atualmente novas tecnologias estão à disposição e outras seguem em estudo.

SHOCK: Enfoque diagnóstico y terapéutico en el adulto / SHOCK: diagnosis and treatment adult

El shock es un síndrome multifactorial, siempresecundario a una patología desencadenante que esclaramente evidente en la mayoría de los casos. Elcuadro de shock compromete la vida de los pacientesy se caracteriza por un conjunto de signos y síntomasque dependen de la enfermedad subyacente, más losoriginados por la insuficiencia circulatoria aguda, lahipoperfusión periférica y los trastornos funcionales ymetabólicos de los distintos órganos afectados...

Desenvolvimento de um coração artificial para suporte circulatório / Development of an artificial heart circulatory support

O presente trabalho descreve o desenvolvimento de uma bomba centrífuga magnética, portátil de fácil instalação e baixo custo, que pode ser utilizada em pacientes que precisam de suporte ciculatório temporário e que foi empregada em 65 pacientes submetidos a cirurgia cardíaca