Alteraçöes cardiocirculatórias na sepse / Cardiovascular abnormalities in sepsis

O choque séptico é uma grave síndrome clínica, responsável, nos Estados Unidos, por aproximadamente 400 mil internaçöes em Unidades de Terapia Intensiva e 100 mil óbitos por ano. Em cerca de 15 'por cento' dos pacientes com hipotensão refratária constata-se quadro de depressão miocárdica, responsável por importantes alteraçöes hemodinâmicas. Vários estudos "in vitro" e "in vivo" demostraram que, após a introdução de endotoxinas existentes na parede de algumas bactérias, ocorre a indução de substâncias mediadoras e moduladoras presentes na circulação, desencadeando o processo séptico. O estudo anatomopatológico desses coraçöes demostrou diferentes graus de acometimento, variando desde inflamatória local até quadros de miocardite intersticial, abscesso intramiocárdico e necrose celular. As mais recentes pesquisas neste assunto são relacionadas às interaçöes do óxido nítrico com as estruturas celulares. O TNF, a IL-1 e outros mediadores atuam provavelmente de forma sinérgica, determinando as alteraçöes que acarretam a depressão do miocárdio nos pacientes sépticos. O uso de inibidores das enzimas formadoras de óxido nítrico tem sido motivo de estudos randomizados, com o intuito de avaliar seu benefício na reversão dessas alteraçöes cardiovasculares nos quadros sépticos.

Noncardiogenic pulmonary edema complicating diabetic ketoacidosis.

OBJECTIVE: To alert physicians to the possibility of pulmonary edema as a complication of diabetic ketoacidosis. METHODS: We report a case of adult respiratory distress syndrome after resuscitative efforts to compensate the first episode of diabetic ketoacidosis in a previously healthy young woman. RESULTS: In a 26-year-old woman with a 3-day history of malaise, polyuria, nausea, and vomiting, severe hypoxia and rales developed, and intubation and mechanical ventilation became necessary. Hemodynamic evaluation and striking electron microscopic findings on open-lung biopsy confirmed the diagnosis of adult respiratory distress syndrome. Despite adequate ventilatory support and hemodynamic management, death ensued and was attributed to irresponsive and progressive acute respiratory failure due to increased pulmonary capillary permeability edema. CONCLUSION: Clinicians should be aware of this possibly fatal pulmonary complication of diabetic ketoacidosis.

[Hemodynamic impact of thrombolytic therapy in acute pulmonary thromboembolism]. / Repercussões hemodinâmicas da terapia trombolítica no tromboembolismo pulmonar agudo.

PURPOSE: To evaluate pre and post-hemodynamic changes after thrombolytic therapy in patients with acute pulmonary embolism with multiple pulmonary segments compromised. METHODS: Nine patients, 5 females, aged between 27 and 83 (mean 62 +/- 16) years, with the onset of symptoms preceding 7 days, were submitted to thrombolytic therapy, administered after baseline perfusion-ventilation lung scan, echodopplercardiography (ECO) and hemodynamic measurements with a Swan-Ganz thermodilution catheter. The same procedures were done after the thrombolytic infusion. Streptokinase (SK) was used in 7 (78%) cases and recombinant human tissue-type plasminogen activator (rt-PA, alteplase) in 2 with the following doses: SK-250,000 i.u. infusion over 30 min, then 100,000 i.v/h over 24 to 72 h and rt-PA-20 mg in bolus infusion, then 80 mg over 6 h. Thrombolytic was infused in pulmonary artery trunk in 8 (88%) cases and a peripheral vein in 1 (12%) case, until mean pulmonary artery pressure (PAP) reached 20 mmHg. All patients received i.v. heparin and oral anticoagulation after thrombolytic therapy. RESULTS: A significant (p < 0.05) decrease in right atrial pressure (12 +/- 3 vs 8 +/- 2 mmHg), PAP (32 +/- 5 vs 19 +/- 2 mmHg), pulmonary vascular resistance (397 +/- 125 vs 87 +/- 24 dyne.s/cm5) and increase in cardiac output (3.4 +/- 0.5 vs 5.5 +/- 1.0 l/min) and stroke volume (30 +/- 5 vs 57 +/- 10 ml/beat) were observed after thrombolytic infusion. Two patients died as a result of pulmonary infection unrelated to the embolic event or thrombolysis. Minor bleeding complications occurred in two cases and major in one patient with orthopedic prosthesis. CONCLUSION: Thrombolytic therapy exert desirable effects on hemodynamic abnormalities, achieving lungs scan and ECO improvement in patients with acute pulmonary embolism.

[Diagnosis of papillary muscle rupture in acute myocardial infarction by transesophageal Doppler echocardiography]. / Diagnóstico da rotura do músculo papilar no infarto agudo do miocárdio através do ecodopplercardiograma transesofágico.

Three patients, two females, ages ranging from 62 to 78 years were studied, evolving with hypotension, acute pulmonary edema and cardiogenic shock. One had anterior myocardial infarction, and in two, infero-posterior. Due to severe hemodynamic instability and necessity of vasoactive drug therapy to maintain adequate arterial pressure, coronary angiography was performed in two, showing total occlusion of the circumflex artery and severe mitral regurgitation. In one case, angioplasty on the circumflex artery was successfully achieved. No hemodynamic improvement was observed, however. Doppler echocardiography depicted mild to moderate mitral regurgitation in the three cases. Transesophageal echo confirmed the clinical suspicion of papillary muscle rupture: total rupture of antero-lateral papillary muscle in one patient, as well as total and partial rupture of the postero-medial papillary muscle in the other two patients. Two patients were submitted to mitral valve replacement, and the surgical findings confirmed the transesophageal echo conclusions. One of them died in the immediate pos-operative period, whereas the other was discharged from the hospital and is doing well. The third patient died before operation. Differential diagnosis of acute mitral regurgitation due to papillary muscle dysfunction or rupture was not possible by left ventriculography or by transthoracic echo. Transesophageal echo was the only exam to clearly confirm papillary muscle rupture, as should be done promptly after clinical suspicion of this severe condition arises.

[Post infarction ventricular septal defect. Echocardiographic analysis of patients treated with positive end-expiratory pressure]. / Comunicação interventricular após infarto do miocárdio. Análise ecocardiografica de pacientes submetidos a pressão expiratória final positiva.

Interventricular septal rupture is a life-threatening complication occurring in 0.5 to 1.0% of patients following acute myocardial infarction and often results in right and left ventricular failure. This study aimed at evaluating the echocardiographic effects of PEEP on right (RV) and left (LV) ventricular dimension in three patients who developed a postinfarction septal defect and in whom acute respiratory failure was a preterminal event. The effects of PEPP on the heart remain controversial. We observed in all three patients a sudden large increase in RV dimensions and hence, probably through ventricular interdependence, a proportional decrease in LV dimensions. The progressive leftward septal displacement with increasing levels of PEEP probably contributed to reduce LV compliance. We concluded that PEEP therapy in this group of patients had no proven beneficial effects and probably contributed to further RV dilatation and failure.

Reliability of right atrial pressure monitoring to assess left ventricular preload in critically ill septic patients.

Right atrial pressure (RAP) can be used as a guide to fluid therapy in critical care settings. RAP and pulmonary capillary wedge pressure (WP) were measured in 27 septic patients without cardiac disease and on mechanical ventilation. An r of .61 was obtained with a regression line defined by the equation WP = 7.38 + (0.53 x RAP) +/- 3.15. However, a large SD of data points can invalidate the clinical usefulness of this equation. The reliability of various RAP interval values in predicting optimal WP was then studied in these patients. We concluded that RAP values less than or equal to 5 mm Hg were highly specific (97%) in predicting low or normal WP (less than or equal to 12 mm Hg).