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Biomedical subjects

H Romaldini

Publications and source records attributed to H Romaldini.

At least 19 recordsLinked to original sources
PubMed1995

Hemodynamic improvement in hemorrhagic shock by aortic balloon occlusion and hypertonic saline solutions.

The initial treatment of uncontrolled hemorrhage shock from an abdominal source is controversial. The hemodynamic effects of transfemoral diaphragmatic aortic occlusion with a balloon followed by a single bolus of hypertonic saline solutions have been evaluated in 28 dogs. The animals were submitted to pressure-driven hemorrhage for 90 min, according to mean arterial pressure in the abdominal aorta and randomized into four groups, according to the treatment employed at 34 min after hemorrhage. Group 1 dogs (controls) received isotonic NaCl (0.9%, 208 mOsm/l, 4 ml/kg) without aortic occlusion; group 2 underwent aortic occlusion and received isotonic NaCl (0.9%, 308 mOsm/l, 4 ml/kg): group 3 were occluded and received hypertonic NaCl (7.5%, 2400 mOsm/l, 4 ml/kg); group 4 were occluded and received hypertonic sodium acetate (10.5%, 2400 mOsm/l, 4 ml/kg). There were no significant differences between groups at basal measures and also after 30 min of continuous bleeding, when animals presented with severe shock, and significant decreases in mean arterial pressure, cardiac index, systolic index and cardiac filling pressures; the systemic vascular resistance index was increased. Control animals remained in severe shock throughout the experiment and three died. The recovery of mean arterial pressure in aortic-occluded dogs given isotonic NaCl was associated with a marked increase in systemic vascular resistance index, without improvements in cardiac index, systolic index and cardiac filling pressures. In occluded dogs given hypertonic NaCl and NaAc the mean arterial pressure recovery lasted longer, with lower increases in systemic vascular resistance index, while the cardiac index, systolic index and cardiac filling pressures showed a marked albeit transient increase. Injection of hypertonic saline following aortic occlusion produced significantly better hemodynamic profiles and should be seriously considered for the first treatment in severe uncontrolled hemorrhagic shock from an abdominal vascular source.

Analysis of Variance↗
PubMed1995

Effects of almitrine on the ventilatory control, breathing pattern and maximal exercise tolerance in hypoxemic patients with chronic obstructive pulmonary disease.

Almitrine bismesylate improves arterial blood gases in patients with chronic obstructive pulmonary disease (COPD), but side effects such as increase of ventilatory drive and dyspnea have been reported in some studies. We studied 18 COPD patients (mean age = 59.1 years; mean FEV1 = 0.92 1; mean PaO2 = 58.6 mmHg) in a double-blind randomized study using placebo or almitrine 50 mg twice a day by mouth, for 60 days. In contrast to the placebo group, 40% of the patients in the almitrine group presented a significant increase in PaO2 and a decrease in P(A-a)O2 > or = 5 mmHg during submaximal exercise after 60 days of treatment. Ventilatory drive and the breathing pattern were measured at rest and during submaximal exercise. Both groups showed high levels of ventilatory drive and a tachypneic breathing pattern before drug treatment and no modification was found 30 and 60 days after treatment. Metabolic, cardiovascular and ventilatory variables were studied during an incremental to maximum exercise symptom-limited test (cycloergometry). Maximal VO2 ranged from 46 to 52% and heart rate from 76 to 78% in relation to the predicted values. The percent ratio of ventilation at maximal exercise to maximal voluntary ventilation at rest ranged from 86 to 94%. These results show that the reduction of ventilatory capacity was the main factor decreasing the aerobic performance of our COPD patients. Maximal exercise tolerance (VO2 max) did not change after almitrine treatment. Negative factors like an increase in neuromuscular drive did not occur, and positive factors like an increase in PaO2 and oxygen transport had no critical influence on exercise performance in our ventilatory-limited COPD patients.

Adult↗
PubMed1995

[Effect of dopamine in dopaminergic doses on pulmonary circulation of dogs in normoxia and hypoxia].

PURPOSE: To study if dopamine in dopaminergic doses (1.5 and 4.0 micrograms/kg/min) had some effect on the pulmonary vasoconstriction mechanism, and if in those doses the drug had some action on systemic and pulmonary hemodynamic variables, as well as in the pulmonary gas exchange. METHODS: Seventeen normal mongrel dogs, anesthetized and paralized under mechanical ventilation were submitted to two different gas mixtures: room air (F1O2 = 0.2093 -10 dogs) and hypoxic mixture (F1O2 = 0.125 -7 dogs). Dopamine was infused in both groups during 15 min in the two doses 1.5 and 4.0 micrograms/km/min, separated by a period of 30 min. RESULTS: Pulmonary hemodynamics and gas exchange variables after infusion of dopamine at 1.5 and 4.0 micrograms/km/min in dogs in normoxia and hypoxia. [table: see text] CONCLUSION: Dopamine in the used doses had no action on the pulmonary circulation and on the hypoxic pulmonary vasoconstriction mechanism; pulmonary gas exchange was not affected by dopamine in both doses during normoxia and hypoxia; in the experimental model there was no evidence of dopaminergic receptors in the pulmonary vessels.

Animals↗
PubMed1991

[The effect of nifedipine on hemodynamics and gas exchange in dogs with experimental acute respiratory insufficiency].

PURPOSE: Evaluate the action of nifedipine, a calcium channel blocking agent, on the hemodynamics and gas exchange experimental acute respiratory failure. METHODS: Lung injury was provoked in sixteen mongrel dogs with intratracheal instillation of hydrochloric acid (HC1) (0.1N; pH = 2.0; 2.0 ml/kg body weight). As steady state was achieved after HC1 instillation (maintenance of a stable arterial PO2), saline 1 ml (six dogs) or nifedipine (ten dogs) 30 micrograms/kg for body weight were intravenously injected. The hemodynamic variables and gas exchange parameters were analyzed before HC1, after HC1 and 10 and 30 minutes after nifedipine or saline. RESULTS: The intratracheal instillation of HC1 provoked significant drop of PaO2, of systemic oxygen transport index (ITO2S), and increase of venous admixture (QVA/Q). Nifedipine provoked significant reduction of the mean systemic arterial pressure (Pas), and of the systemic (IRVS) and pulmonary vascular resistance index (IRVP), with significant increase of cardiac (IC) and systolic index (IS), with no changes ot the mean arterial pulmonary (Pap) and capillary pressures (Pcap). After nifedipine there was a significant increase of PaO2, PvO2, and ITO2S, with no significant variations of QVA/Q and alveolar arterial O2 difference (P(A-a)O2). CONCLUSION: Nifedipine promoted systemic vasodilation, and probably by increasing the venous return and/or by a reflex mechanism, the cardiac output increased, augmenting the ITO2S. The IRVP decreased in the nifedipine group, with no significant alterations of Pap and Pcap, probably consequent to the systemic vasodilation provoked by the drug. The arterial PO2 augmented in the nifedipine group, as a consequence of mixed venous PO2 increase, since no changes occurred in QVA/Q, P(A-a)O2, inspired fraction of O2 and alveolar ventilation.

Acute Disease↗
PubMed1989

[The role of angiotensin-converting enzyme inhibitor (captopril) on the mechanism of hypoxic pulmonary vasoconstriction. Experimental study in dogs].

In order to evaluate the action of an angiotensin converting enzyme inhibitor (Captopril) on the pulmonary hypoxic vasoconstriction, twenty one mongrel dogs were studied in two groups: group I with hypoxia, group II with normoxia. The dogs were anesthetized, intubated, and had their femoral vein and artery cannulated for blood-gas sampling and pressure records. They were mechanically ventilated with hypoxic gas mixtures (12.3% O2-87.7% N2)--group I and room air group II, at random. In both groups we measured, before and after administration of captopril 3 mg/kg intravenously, gas exchange and hemodynamic variables, as well as plasmatic levels of renin and angiotensin converting enzymes (ACE). Our results showed that the group I dogs decreased the systemic and pulmonary vascular resistances with small changes in pulmonary arterial pressures and no significant variations of pulmonary systemic resistances ratio. There were no significant variations of the same variables in the group II dogs. The gas exchange has not changed in either group of animals. In the group I dogs Captopril provoked systemic and pulmonary vasodilatation, with no gasometric and ventilation/perfusion ratio changes. In our experimental model we could not conclude that Captopril inhibited the hypoxic pulmonary vasoconstriction and/or that the angiotensin II had some action on the hypoxic pulmonary vasoconstriction mechanism, but there are some evidences favoring that hypothesis.

Analysis of Variance↗
PubMed1989

[Effects of captopril on hemodynamics, gas exchange and exercise capacity in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease].

Captopril, a potent inhibitor of angiotensin converting enzyme, was tested in patients with COPD (means forced expired volume in the first second--FEV1 = 0.73 l) and pulmonary hypertension (PAP = 41.3 mmHg). In the first phase of the experiment, patients underwent and incremental exercise test to the limit of tolerance. These were double blind, randomized, cross-over studies, where the patients received oral placebo (Pl) or captopril (Cp) 25 mg, on different days. In a second phase, the patients were submitted to hemodynamic and gasometric studies in the supine position, before placebo, the 60 min after and immediately after exercise (cycling-like leg movements). After 30 min of rest the same protocol was repeated with oral administration of 25 mg of captopril. In the metabolic evaluation (cycloergometry) captopril increased significantly exercise tolerance (means VO2-uptake at maximal exercise: CP = 0.81 vs Pl = 0.73 1/min), associated with a slower heart rate and higher O2-pulse at maximal exercise. In the hemodynamic study, when the effects of Cp and Pl were compared, the mean values of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were similar at rest, but significantly lower during exercise, after captopril (means PAP Cp = 41.3 vs Pl = 51.2 mmHg; XPVR Cp = 278 vs Pl = 392 dyn. sec. cm5). There were similar systemic hemodynamic effects after Cp, but these were more intense in the pulmonary circulation (lower PVR/SVR ratio post-Cp in relation to post-Pl, during exercise). The cardiac index, systemic O2 transport and arterial and mixed venous blood gases were similar at rest and during exercise, with Pl or Cp.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Central venous blood composition and the pulmonary ventilation during hemodialysis.

The elimination of CO2 across the dialyzer has been reported as the cause of pulmonary hypoventilation during hemodialysis. There are some evidences that the venous line blood composition could influence the central venous blood and this one the pulmonary ventilation. Our purpose was to analyze (1) the influence of the changes in composition of the venous line blood on the central venous blood and (2) the possible role of the central venous blood composition on the pulmonary ventilation of 10 chronic renal failure patients during hemodialysis performed twice in the same patients in two different conditions: acetate dialysate without (condition I) and with (condition II) constant addition of 100% CO2 bubbling into the dialysis bath. During condition I the venous line blood pH was kept in a normal range, and the PCO2 was low, whereas during condition II the pH was very low and the PCO2 extremely high. The patients during condition I decreased their pulmonary ventilation and lost CO2 across the dialyzer as the central venous blood pH and HCO3- increased, and PCO2 did not change. The same patients during condition II increased their pulmonary ventilation and absorbed CO2 across the dialyser as the central venous blood pH decreased and PCO2 increased. Thus, the venous line blood has influence on the central venous blood composition, and this plays a role on the control of pulmonary ventilation of these patients.

Adolescent↗
PubMed1985

Lung inhalation scintigraphy: development of a new aerosol system.

A new technique for lung inhalation scintigraphy is reported, developing a new aerosol system, based on the original system of Taplin [1]. With two small compact polypropylene reservoirs, this 99Tcm DTPA technique allowed continuous breathing during the inhalation period. This system proved to be a useful alternative to that using radioactive gases and the system of Taplin, due to its low cost and the ease with which several projections may be obtained.

Adult↗
PubMed1984

The mechanisms of arterial hypoxemia during hemodialysis.

Hypoxemia during hemodialysis has variously been attributed to worsening ventilation-perfusion (VA/Q) relationships, alveolar hypoventilation combined with a reduced respiratory quotient, increased right-to-left shunting, and diffusion impairment. It is difficult to separate out these various effects, which explains lack of agreement in the literature. To more critically evaluate the causes of hypoxemia during hemodialysis, we used a multiple inert gas elimination technique to determine the distribution of ventilation-perfusion ratios during hemodialysis in 8 patients with chronic renal failure. Measurements were made before, during (at 60, 120, and 210 min), and after hemodialysis. Whereas arterial PO2 fell from 87 to 74 mmHg by 120 min, ventilation-perfusion relationships actually improved. Cardiac output fell from 5.3 to 4.0 L/min over the same time. Alveolar ventilation, respiratory quotient, and alveolar PO2 all fell, and the alveolar arterial PO2 difference remained essentially unchanged. These findings suggest that the hypoxemia observed during hemodialysis is primarily due to a decrease in alveolar ventilation and respiratory quotient associated with removal of metabolic CO2 in the dialyzer. Secondary factors affecting arterial PO2 were the slight improvement in ventilation-perfusion relationships tending to increase it, and the decrease in cardiac output tending to decrease it. There was no evidence for diffusion impairment because the measured VA/Q inequality accounted for the degree of hypoxemia.

Arteries↗
PubMed1983

Enhancement of hypoxic pulmonary vasoconstriction by almitrine in the dog.

In order to test the hypothesis of enhancement of hypoxic pulmonary vasoconstriction by Almitrine, 12 anesthetized and paralyzed dogs with normal lungs were studied under controlled ventilation. They were ventilated in random sequence with air, 12% O2, and 100% O2, and almitrine (0.1 mg/kg body weight) was infused over 30 min during each O2 mixture. The multiple inert gas elimination technique was used to detect alterations in ventilation-perfusion (VA/Q) mismatching before and during the interventions and to measure cardiac output (QT). Arterial, mixed venous and expired gases, inert gas concentrations, and hemodynamic measurements were made while the dogs were breathing the different O2 mixtures before infusing the drug, near the end of 30 min of infusion and 30 min after infusion had ended. There were no significant changes in pH, PaO2, PaCO2, QT, oxygen uptake, oxygen delivery index, systemic vascular resistance, mean systemic arterial pressure, heart rate, stroke volume index, or VA/Q distribution during the experiment. Significant increases in: (a) pulmonary artery pressure (PA), (b) the pressure difference between PA and pulmonary capillary wedge pressure (PCw), and (c) pulmonary vascular resistance (PVR) occurred when the drug was infused during 12% O2 and air, but not during 100% O2. The PVR increased 59.7% with almitrine infusion during 12% O2 and 38.4% during air breathing (p less than or equal to 0.01), but there was no significant change during 100% O2. Vascular responses were not dependent on the order in which the different O2 mixtures were administered. These data strongly suggest that almitrine enhances hypoxic vasoconstriction in the lung, and this effect may explain reported improvement in PaO2 in hypoxic patients given the drug.

Almitrine↗
PubMed1982

Pulmonary ventilation during hemodialysis.

During hemodialysis a decrease in pulmonary ventilation has been reported. The elimination of CO2 across the dialyzer has been suggested as the cause of the pulmonary hypoventilation. Our purpose was to analyze the factors that could have influenced the pulmonary ventilation of 7 patients with chronic renal failure during hemodialysis, performed against an acetate dialysate with constant addition of CO2, bubbling into the dialysis bath. In spite of the large volume of CO2 mainly as bicarbonate, eliminated across the dialyzer there was no significant decrease of ventilation. The values of pH in the venous line were extremely low and the values of PvCO2 were artificially maintained around 35.0 mm Hg. Thus, the total CO2 delivered to the lungs, but mainly the levels of pH and PCO2 in the venous line play an important role in the control of pulmonary ventilation of these patients.

Bicarbonates↗
PubMed1982

Pulmonary gas exchange and ventilation during hemodialysis.

Hemodialysis-induced hypoxemia has been explained by several mechanisms: pulmonary microembolization, decreased pulmonary diffusing capacity, fall in alveolar oxygen tension, hypoventilation and ventilation/perfusion abnormalities. The objective of this study was to analyze the factors influencing pulmonary ventilation and gas exchange of 20 patients with chronic renal failure during hemodialysis performed under the following conditions: Group 1 (9 patients) dialyzed against an acetate dialysate with a cuprophan membrane; Group 2 (7 patients) dialyzed against acetate bubbled with CO2 with a cuprophan membrane; Group 3 (4 patients) similar to Group 1, but using a polyacrylonitrile membrane. Arterial and venous blood samples were obtained from the respective lines during the predialysis period (zero), at 30, 60, 120 180 and 240 min of hemodialysis, and 60 min post dialysis (300 min) for the measurement of pH, PCO2, PO2, HCO-3 and total CO2. The minute expired volume (VE), expired fractions of O2 (FEO2) and CO2 (FECO2), O2 consumption (VO2), CO2 elimination through the lungs (VCO2) and dialyzer, respiratory exchange ratio (R), dead space to tidal volume ratio (VD/VT), alveolar ventilation (VA) and alveolar-arterial O2 difference (delta AaPO2) were measured and a leukocyte count was performed for each period of hemodialysis. The patients in Groups 1 and 3 showed a significant drop in ventilation and PaO2, a slight decrease in PAO2 and a significant increase in delta AaPO2. The patients in Groups 1 and 2 showed a significant leukopenia at 30 min of hemodialysis. The volume of CO2 eliminated across the dialyzer was very similar for the three groups of patients. Group 2 did not show any drop in ventilation or PaO2. For Group 2 venous line pH was very low and PCO2 was within the normal range, in contrast to the normal or high pH and low PCO2 shown by Groups 1 and 3. This study indicates that the drop in PaO2 was partially the consequence of a slight decrease in PAO2, but mainly due to the increase in delta AaPO2. Thus the most likely cause of the decrease in PaO2 was the VA/Q imbalance brought about by a drop in ventilation. The drop in ventilation was linked not only to the volume of CO2 eliminated across the dialyzer, but also to the amount of CO2 delivered to the lungs, and to the pH and PCO2 of the venous line.

Adult↗