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Biomedical subjects

S R Vieira

Publications and source records attributed to S R Vieira.

At least 19 recordsLinked to original sources
PubMed2001

[Multiple recurrences of cardiac myxomas with acute tumoral pulmonary embolism].

We report the case of a 42-year-old female with a second recurrence of cardiac myxoma. Her first diagnosis was at the age of 24 years, when cardiac tumors were withdrawn from her right ventricle and left atrium. Her first recurrence was at the age of 36 years, when tumors were removed from the left and right atria, and the right ventricle. Six years later, the patient was admitted to the Hospital das Clínicas de Porto Alegre complaining of sudden dyspnea, dry cough, and pain in the right hypochondrium, which bore no relation to breathing. The transesophageal echocardiography showed a small tumor in the interatrial septum, close to the superior vena cava, and 2 larger tumors in the right ventricle, 1 close to the outflow tract and the other almost completely obstructing the right branch of the pulmonary artery. The patient was referred to surgery, in which myxomas were removed from the right atrium and ventricle with extension to the right pulmonary artery. The postoperative period was uneventful.

Acute Disease↗
PubMed1999

A simple automated method for measuring pressure-volume curves during mechanical ventilation.

Measurement of respiratory compliance is advocated for assessing the severity of acute respiratory failure (ARF). Recently, the administration of an automated constant flow of 15 L/min was proposed as a method easier to implement at the bedside than supersyringe or inspiratory occlusions methods. However, pressure-volume (P-V) curves were shifted to the right because of the resistive properties of the respiratory system. The aim of this study was to compare the P-V curves obtained using two constant flows-3 and 9 L/min-during volume-controlled mechanical ventilation with those obtained with the supersyringe and the inspiratory occlusions methods. Fourteen paralyzed patients with ARF were studied. The supersyringe and the inspiratory occlusions methods were performed according to usual recommendations. The new automated method was performed during volume-controlled mechanical ventilation by setting the inspiratory:expiratory ratio at 80%, the respiratory frequency at 5 breaths/min, and the tidal volume at 500 or 1,500 ml. These peculiar ventilatory settings were equivalent to administering a constant flow of 3 or 9 L/min during a 9.6-s inspiration. Esophageal and airway pressures were recorded. P-V curves obtained by the 3-L/min constant-flow method were identical to those obtained by the reference methods, whereas the P-V curve obtained by the 9-L/min constant flow was slightly shifted to the right. The slopes of the P-V curves and the lower inflection points were not different between all methods, indicating that the resistive component induced by administering a constant flow equal to or less than 9 L/min is not of clinical relevance. Because the 3-L/min constant-flow method is not artifacted by the resistive properties of the respiratory system and does not require any other equipment than a ventilator, it is an easy-to-implement, inexpensive, safe, and reliable method for measuring the thoracopulmonary P-V curve at the bedside.

Acute Disease↗
PubMed1999

A scanographic assessment of pulmonary morphology in acute lung injury. Significance of the lower inflection point detected on the lung pressure-volume curve.

The goal of this study was to assess lung morphology in patients with acute lung injury according to the presence or the absence of a lower inflection point (LIP) on the lung pressure-volume (P-V) curve and to compare the effects of positive end-expiratory pressure (PEEP). Eight patients with and six without an LIP underwent a spiral thoracic CT scan performed at zero end-expiratory pressure (ZEEP) and at two levels of PEEP: PEEP1 = LIP + 2 cm H2O and PEEP2 = LIP + 7 cm H2O, or PEEP1 = 10 cm H2O and PEEP2 = 15 cm H2O in the absence of an LIP. The volumes of air and tissue within the lungs were measured from the gas-tissue ratio and the volumes of overdistended and normally, poorly, and nonaerated lung areas were determined by the analysis of the frequency histogram distribution. In the ZEEP condition, although total lung volume, volume of gas, and volume of tissue were similar in both groups, the percentage of normally aerated lung was lower (24 +/- 22% versus 55 +/- 12%, p < 0.05) and the percentage of poorly aerated lung was greater (40 +/- 12% versus 23 +/- 8%, p < 0.05) in patients with an LIP than in patients without an LIP. Lung density histograms of patients with an LIP showed a unimodal distribution with a peak at 7 Hounsfield units (HU). Lung density histograms of patients without an LIP had a bimodal distribution, with a first peak at -727 HU and a second peak at 27 HU. Total respiratory system and lung compliances were lower in patients with an LIP whereas all other cardiorespiratory parameters were similar in the two groups. In both groups, PEEP induced an alveolar recruitment that was associated with lung overdistension only in patients without an LIP. The amount of lung overdistension was related to the volume of lung parenchyma, characterized by a CT number less than -800 HU before PEEP implementation (y = 0.52x + 4, R = 0.87, and p < 0.0001). This study shows that the presence or the absence of an LIP on the lung P-V curve is associated with differences in lung morphology. In patients without an LIP on the lung P-V curve, normally aerated lung areas coexist with nonaerated lung areas and increasing levels of PEEP result in lung overdistension rather than in additional alveolar recruitment. In patients with an LIP, air and tissue are more homogeneously distributed within the lungs and increasing levels of PEEP result in additional alveolar recruitment without lung overdistention.

Acute Disease↗
PubMed1999

Expiratory washout versus optimization of mechanical ventilation during permissive hypercapnia in patients with severe acute respiratory distress syndrome.

The aim of this study was to compare three ventilatory techniques for reducing PaCO2 in patients with severe acute respiratory distress syndrome treated with permissive hypercapnia: (1) expiratory washout alone at a flow of 15 L/min, (2) optimized mechanical ventilation defined as an increase in the respiratory frequency to the maximal rate possible without development of intrinsic positive end- expiratory pressure (PEEP) combined with a reduction of the instrumental dead space, and (3) the combination of both methods. Tidal volume was set according to the pressure-volume curve in order to obtain an inspiratory plateau airway pressure equal to the upper inflection point minus 2 cm H2O after setting the PEEP at 2 cm H2O above the lower inflection point and was kept constant throughout the study. The three modalities were compared at the same inspiratory plateau airway pressure through an adjustment of the extrinsic PEEP. During conventional mechanical ventilation using a respiratory frequency of 18 breaths/min, respiratory acidosis (PaCO2 = 84 +/- 24 mm Hg and pH = 7.21 +/- 0.12) was observed. Expiratory washout and optimized mechanical ventilation (respiratory frequency of 30 +/- 4 breaths/min) had similar effects on CO2 elimination (DeltaPaCO2 = -28 +/- 11% versus -27 +/- 12%). A further decrease in PaCO2 was observed when both methods were combined (DeltaPaCO2 = -46 +/- 7%). Extrinsic PEEP had to be reduced by 5.3 +/- 2.1 cm H2O during expiratory washout and by 7.3 +/- 1.3 cm H2O during the combination of the two modes, whereas it remained unchanged during optimized mechanical ventilation alone. In conclusion, increasing respiratory rate and reducing instrumental dead space during conventional mechanical ventilation is as efficient as expiratory washout to reduce PaCO2 in patients with severe ARDS and permissive hypercapnia. When used in combination, both techniques have additive effects and result in PaCO2 levels close to normal values.

Acidosis, Respiratory↗
PubMed1998

A lung computed tomographic assessment of positive end-expiratory pressure-induced lung overdistension.

The aim of this study was to assess positive end-expiratory pressure (PEEP)-induced lung overdistension and alveolar recruitment in six patients with acute lung injury (ALI) using a computed tomographic (CT) scan method. Lung overdistension was first determined in six healthy volunteers in whom CT sections were obtained at FRC and at TLC with a positive airway pressure of 30 cm H2O. In patients, lung volumes were quantified by the analysis of the frequency distribution of CT numbers on the entire lung at zero end-expiratory pressure (ZEEP) and PEEP. In healthy volunteers at FRC, the distribution of the density histograms was monophasic with a peak at -791 +/- 12 Hounsfield units (HU). The lowest CT number observed was -912 HU. At TLC, lung volume increased by 79 +/- 35% and the peak CT number decreased to -886 +/- 26 HU. More than 70% of the increase in lung volume was located below -900 HU, suggesting that this value can be considered as the threshold separating normal aeration from overdistension. In patients with ALI, at ZEEP the distribution of density histograms was either monophasic (n = 3) or biphasic (n = 3). The mean CT number was -319 +/- 34 HU. At PEEP 13 +/- 3 cm H2O, lung volume increased by 47 +/- 19% whereas mean CT number decreased to -538 +/- 171 HU. PEEP induced a mean alveolar recruitment of 320 +/- 160 ml and a mean lung overdistension of 238 +/- 320 ml. In conclusion, overdistended lung parenchyma of healthy volunteers is characterized by a CT number below -900 HU. This threshold can be used in patients with ALI for differentiating PEEP-induced alveolar recruitment from lung overdistension.

Adult↗
PubMed1989

Improvement in wall motion after pindolol: a mechanism for the preservation of left ventricular function in coronary artery disease.

1. In order to evaluate the mechanism by which beta blockers with intrinsic sympathomimetic activity preserve left ventricular systolic function at rest, 46 patients with coronary artery disease were studied by right and left heart catheterization and left ventriculography. Patients were studied using a double-blind, randomized protocol before and after a single intravenous dose of 3 mg propranolol (N = 22) or 0.5 mg pindolol (N = 24). 2. Mean right atrial pressure increased similarly after both drugs. Mean pulmonary artery pressure, left ventricular end-diastolic pressure, mean aortic pressure, and peripheral vascular resistance did not change significantly after either drug. Cardiac index (before: 3.0 +/- 0.7 (mean +/- SEM); after: 2.8 +/- 0.2 1 min-1 m-2) and heart rate (before: 78 +/- 15; after: 72 +/- 12 bpm) decreased only after propranolol administration. 3. Ejection fraction decreased only after propranolol (48 +/- 16 to 41 +/- 15%). Improvement in segmental wall motion abnormalities was noted (23 of 47 segments) only after pindolol. The total left ventricular wall motion score improved after pindolol and worsened after propranolol (P less than 0.05). In patients with impaired left ventricular function, pindolol administration resulted in improved resting ejection fraction. 4. Thus, the acute hemodynamic consequences of pindolol administration differ from those of propranolol owing to the preservation of left ventricular systolic function which seems to be related to the intrinsic sympathomimetic effect of pindolol on areas of reversible wall motion abnormality.

Adult↗