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Biomedical subjects

P Fernández Bonetti

Publications and source records attributed to P Fernández Bonetti.

At least 19 recordsLinked to original sources
PubMedDate not supplied

[Respiratory changes in obesity. Functional and clinical aspects. Study of 26 cases].

A study was made, at the altitude of Mexico City, of the clinic aspects and of the pulmonary function of 26 obese subjects more than 45% overweight. This excess weight habitually produces severe disturbances in pulmonary and/or heart function. In 50% of the patients, clinic, radiologic and electrocardiographic manifestations were found which suggested the existence of pulmonary arterial hypertension. This provoked right heart failure in 19% of the cases. The most constant alterations in the pulmonary volumes was the decrease in the VER, which occurred in 96% of the cases. Most of the patients had hypoxemia (92.5), which was produced mainly by the increase in venoarterial shunts. Although the clinic manifestations were similar to those described in Pickwick's syndrome, alveolar hypoventilation was presented in only a minority of the cases. No relationship was found between the degree of obesity and alveolar hypoventilation. Altitudes of 2,200 meters or more apparently favor hypoxemia in obese patients, and "protects" them from the hypercapnea. The altitude of Mexico City may be one of the reasons why alveolar hypoventilation is observed in only 15% of the cases.

Adult↗
PubMedDate not supplied

[Alveolar-arterial oxygen gradient in cardiopulmonary patients breathing ambient air at rest and during exercise].

The alveolar to arterial difference of oxygen [(A-a)DO2] depends on variables such as ventilation, cardiac output, respiratory exchange ratio and arterial PO2. The arterial PO2 itself depends on the ventilation to perfusion ratio (V/Q) pulmonary shunt, (a-v) O2 difference, and the metabolic status of the patient. When the alveolar-ventilation is normal, the (A-a)DO2 reflects gas exchange abnormalities and when the alveolar-ventilation is increased, the (A-a)DO2 can increase because of a decrease in PaCO2. The factors capable of altering the alveolar to arterial oxygen difference were investigated in ninety patients with pulmonary disease: (pulmonary embolism, lung fibrosis and chronic obstructive lung disease), both at rest and during exercise. At rest when alveolar ventilation was increased, the (A-a)DO2 broadened due to the decrease in PaCO2. During exercise the (A-a)DO2 also increased and the PaCO2 was not significantly modified, therefore admixture it is the result of an increase in the proportion of venous. The difference between the mixed venous and arterial PO2 decreased due to alveolar hypoventilation reducing in consequence the (A-a)DO2. We conclude that in the group studied the increase in the (A-a)DO2 is mainly due to V/Q imbalance at rest and during exercise.

Air↗
PubMedDate not supplied

[The respiratory center in normal subjects at 2,240 meters above sea level. The ventilatory and occlusion pressure (P 0.1) responses upon CO2 stimulation].

Altitude hypoxia imposes acute changes and long term adjustments in the ventilation of human beings. Most of the present knowledge of the respiratory center behavior at high altitude derives from the studies of ventilatory response to both hypoxia and hypercapnea. Other indexes of respiratory center output such as the occlusion pressure (P 0.1) response to a variety of stimuli are at present being evaluated. We could not find, however, studies on the P 0.1 responses to CO2 at high altitude. In this study we analyze the ventilatory and P 0.1 responses to CO2 in a group of 32 normal subjects, all of them natives and residents of Mexico city (altitude of 2,240 meters) and we compared them with those reported at sea level. The slope of both, the ventilatory and P 0.1 responses to CO2 was found to be similar to that reported at sea level; 4.52 +/- 1.29 L. min. mmHg and 0.07 +/- 0.01 cm H2O/mmHg respectively. The crossing over of such responses, however, is shifted to the left of the reported at sea level. This means higher levels of both ventilation and P 0.1, for the same level of end-tidal PCO2, at high altitude. This finding might be explained in the basis of the so-called "acclimatization to hypocapnea".

Acclimatization↗
PubMedDate not supplied

[Pulmonary function in chronic ischemic cardiopathy].

Twenty patients with heart disease were prospectively studied. Seven of them had an old myocardial infarction and thirteen, ischemic symptoms without infarction. Pulmonary function was studied focusing on small airway disease and gas exchange abnormalities. Our results showed that a mild degree of abnormality exists as reflected by bronchial obstruction with origin in small airways, V/Q disturbed and hypoxemia. In 88% these seem to be related to left ventricular disfunction. Twenty four hours after pulmonary function test all patients underwent left heart catheterization with coronarography and ventriculography.

Coronary Disease↗
PubMedDate not supplied

[Pulmonary arterial hypertension of unknown etiology. Study of the cardiopulmonary function].

Thirty two cases of pulmonary arterial hypertension of unknown etiology (PAH-UE) were studied. The diagnosis was established by exclusion after the results of hemodinamics studies. Ninety percent of cases had severe PAH (100 mmHg). The end diastolic right ventricular pressure was elevated in 46% of cases. The total pulmonary vascular resistance was increased in the order of the 1700 dinas. seg. cm-5. The cardiac index was 3.3 1/m2 with a right ventricular work index of 3.96 K gm min. The total lung capacity (TLC) was normal, with a vital capacity (VC) of 78% of the predicted value. The residual volume was increased. The mean value of the maximal midexpiratory flow rate (MMFR) was 78%. The A-a gradient of O2 was 30 mmHg, with a venous mixture expressed as a percentage ratio of the cardiac output (Qva/Qt) of 26%. The mean paO2 mmHg and the anatomical pulmonary artery to vein shunt (Qs/Qt) was 9%, with a DLco normal. The clinical hemodinamic correlation was in good agreement. Our results suggested that PAH-UE "per se" has effect in pulmonary function changing slight lung mechanics, and in a moderate degree lung gas exchange. The hipoxemia results meanly from V/Q imbalance.

Adolescent↗
PubMedDate not supplied

[Effects of body posture on mechanical lung function in the obese patient].

The pulmonary mechanics of twelve obese patients were studied: the static and dynamic compliance, the maximum pressure of elastic recoil, and the expiratory flow curves breathing room air and a mixture of He-O2. Also analyzed were the closing capacity, the closing volume and the slope of the alveolar plateau (phase III), in the erect and supine positions. Our data confirm that the tests that explore the small airways are abnormal in the obese patients. The results obtained, allow us to assure that the pulmonary mechanics in the obese patients are affected by the change of position, as is shown by the closing volume and closing capacity when assuming the supine position when compared to orthostatism, as well as the decrease in vital capacity. These alterations were not found in non-obese patients which were used as controls.

Adult↗
PubMedDate not supplied

[Arteriovenous shunting in obesity, its relation to lung volume].

Thirty-five patients with an average overweight of 67.1% were studied. Pulmonary restriction of a variable degree was found in 68.6/; in 60% due to reduction of respiratory reserve volume. Bronchial obstruction was detected in 57% as measured by forced midexpiratory flow (25-75%). In addition, 14% showed a decrease of 75-85% in forced expiratory flow, which suggested that the pathology was located in the small respiratory airways. The PaO2 while breathing room air and in a resting state was of 52.6 +/- 9.42 mmHg, and after breathing it increased to 69.07 +/- 11.01 mmHg. The PaO2 breathing inspiratory fractions of 99.6% O2 in a resting condition was 309.34 +/- 70.07 mmHg, and after deep breathing it rose to 354.0 +/- 64.27 mmHg. The mechanisms which produce hypoxemia in the obese were analysed and it was concluded that they were due fundamentally to alterations of the ventilation perfusion ratio and to an increase of the venous-arterial shunt. In some cases, alveolar hypoventilation contributed (Pickwick syndrome). By increasing the pulmonary volume with deep breathing, the ventilation perfusion ratio improves or becomes normal, likewise, the venous-arterial shunt can improve or persist as the only cause of hypoxemia.

Adult↗