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Biomedical subjects

E Lupi

Publications and source records attributed to E Lupi.

34 records · Page 2Linked to original sources
PubMedDate not supplied

[Electrocardiogram in interstitial pneumonia. Electrocardiographic-hemodynamic correlation].

Twenty four patients with interstitial pulmonary disease from the Cardiopulmonary Service of the Instituto Nacional de Cardiología were studied. Surface electrocardiograms and pulmonary hemodynamic studies were registered to all patients in order to obtain the pulmonary vascular resistances and pressures to find out the electrocardiographic-hemodynamic correlation. Three groups were made according to the pulmonary artery sistolic pressure: Group I, 30 to 45 mm Hg (6 patients); Group II, 46 to 70 mm Hg (12 patients) and Group III more of 60 mm Hg (6 patients). Also, arterial gaseous partial pressures were determined, among other pulmonary test parameters. Electrocardiographically, the rhythm, A=V node conduction, AQRSF, APF, atrial and ventricular hypertrophy, intraventricular conduction and ventricular repolarization were studied in leads II, III, aVF, aVR, V1, V2, V3 and V6. The characteristics of the ventricular repolarization and depolarization processes of each group are described, in order to discuss the mechanism of the anormalities. Finally, the electrocardiographic findings were correlated with the different degrees of pulmonary arterial hypertension; the conclusions are: I. The electrocardiogram allows us to differenciate the patients with III degree of arterial pulmonary hypertension, from those of I and II degrees. II. Patients with I and II degrees of pulmonary arterial hypertension determine nearly the same electrocardiographic alterations; the mean differences to establish the differential diagnosis is the AQRSF, shifted to the right and upwards, in the II degree of pulmonary arterial hypertension.

Adult↗
PubMedDate not supplied

[Effect of hypoxia on atrio-ventricular conduction in severe respiratory insufficiency].

The role of hipoxia on A-V conduction was studied in the patients with severe respiratory insufficiency. Intervals of A-V conduction were measured under basal conditions, breathing room air and with increasing atrial rates. Results are compared with those obtained after the administration of 99% oxygen. A-V conduction times were normal in all the patients while breathing room air and in response to atrial pacing. With oxygen administration most patients had a decrease in A-V conduction at the expense of a prolonged A-H time, without significant alteration of the other time intervals. A-V conduction in chronic hipoxia with a PaO2 above 28 mm Hg is not delayed. Intranodal conduction delay with oxygen administration may be due to a decrease in sympathetic nerve stimulation.

Aged↗
PubMedDate not supplied

[Active and passive factors in the genesis of pulmonary arterial hypertension in various cardiopathies and pneumopathies].

The role of active and passive factors involved in the genesis of Pulmonary Arterial Hypertension (PAH) is analyzed in a group of eighty patients with several cardiopathies and pneumopathies. The group include: 20 patients with Chronic Obstructive Lung Disease (NODC), 20 with Diffuse intersticial pneumopathy (NI), 12 with Cardiorespiratory Syndrome of the grossly obese (OB), 6 with Pulmonary Embolism (TEP), 6 with Mitral Stenosis (CRI), 5 with Hypertensive Ventricular Septal Defect (CIV + HAP) and 11 patients with Pulmonary Arterial Hypertension of Unknown etiology (HAP-ED). For the analysis, the Harvey and Enson's formulas were used. The conclusions of the study are: 1) The compliance of the elastic arteries of the lung in the groups of NOC, NI and OB is normal but in the other groups seems to be modified. 2) In the groups of NI and OB the interrelationship of factors such as alveolar hypoxia and pulmonary wedge pressure (PWP) play the major role in the genesis of PAH, although the role of the PaCO2 in the OB group remains to be established. 3) In the groups of NOC, CRI and TEP the PWP is not determinant. The absence of a significant correlation between arterial oxygen unsaturation and pulmonary diastolic pressure in the NOC group suggests other factors. 4) The vascular structural damage seems to be the most important factor in the genesis of PAH in the HAP-ED and CIV + HAP groups.

Carbon Dioxide↗
PubMedDate not supplied

[Exercise tests in pneumopathy patients].

In this prospective work eleven pneumopathes patients were studied, ten of them with HAP, which were subjected to effort prove in endless band, in order to know the electrocardiographic alterations presented during the exercise. The VO2 máx was determined simultaneously in four patients. In the four, the value of this parameter was found under the normal value, which showed us a poor increase of the cardiac expense for the demands in the exercise. If the effort proves had not been practiced, this fact could not have been known. Related to the electrocardiographic alterations, cellular diastolic depolarization signs (cellular damage), product of the cellular damage, were found. The mechanics of this cellular damage, as well as the one of the poor increase of cardiac expense, are mentionned in the discussion.

Adolescent↗
PubMedDate not supplied

[Acute myocardial infarction related to cocaine use. Report of a case].

Cocaine use has been associated with ischemic syndromes, especially angor pectoris, myocardial infarction, cardiac arrhythmias and sudden death. A significant number of persons suffering from myocardial infarction associated with cocaine abuse do not have significant coronary atherosclerosis, and the mechanism for infarction in these patients have remained obscure. This report describes a young man with angiographically normal coronary arteries in whom cocaine abuse probably produced coronary artery spasm leading to coronary thrombosis and infarction.

Adult↗
PubMedDate not supplied

[Hemodynamic effects of oral captopril in patients with critical aortic stenosis].

OBJECTIVES: To analyse the hemodynamic and ventricular function effects of oral captopril in severe aortic stenosis. PATIENT POPULATION: inclusion criteria: patients older than 18 years with critical aortic stenosis. EXCLUSION CRITERIA: angiotensin-converting enzyme inhibitor used previously contraindication to right catheterisation aortic insufficiency, valvular prosthesis in aortic position, or other valvulopathy. As well as the need for immediate valvular aortic replacement arrhythmia, A-V conduction alterations, or ventilatory support. PROTOCOL: prospective, no randomized. Swan-Ganz catheter was used. Basal hemodynamic measurements were made on 1, 2, 4, 6 and 8 hours during 48 hours. Captopril was administered 12.5 mg first and then 8 mg tid (6 doses). STATISTICAL ANALYSIS: Neuman-Keuls test was used for multivariate comparisons. Statistical significance was determined with P < 0.05. RESULTS: 22 patients were analyzed. Systemic vascular resistance fell from 1750 Dyn/seg/cm-5 to 1200 (P-0.001), cardiac output increased from 4.1l/min to 5.8 (P-0.001), cardiac index increased from 2.4 l/min/m2 to 2.9 (P-0.009), stroke volume from 47 ml to 64 (P-0.04) and stroke volume index from 27 ml/m2 to 36 (P-0.002). In patients with heart failure (n = 7) the systemic vascular resistance fell from 2050 Dyn/seg/cm-5 to 1463 (P-0.04), cardiac output increased from 2.8l/min to 4.1 (P-0.04), cardiac index from 2.07 l/min/m2 to 2.75 (P-0.04), stroke volume from 46 ml to 64 (P-0.03), pulmonary capillary wedge pressure fell from 19 mmHg to 16 (0.04) and the systolic pulmonary arterial pressure fell from 63 mmHg to 42 (P-0.009). CONCLUSIONS: captopril improves the hemodynamic parameters in patients with critical aortic stenosis, principally in those with heart failure.

Administration, Oral↗