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Biomedical subjects

G A Medrano

Publications and source records attributed to G A Medrano.

At least 19 recordsLinked to original sources

Electrocardiographic features in experimental subendocardial infarctions in canine hearts.

Chemical necrosis was produced with the infiltration of 96 degrees alcohol on the middle anterosuperior segment 5 (nomenclature of the International Society for Computerized Electrocardiology) of the free left ventricular (LV) wall in 45 dogs and on the apical segment 10 and middle posterolateral segment 11 in 30 others. In five animals from each group, a 10 bipolar arrow assembly was used to obtain Purkinje fiber potentials and to determine the degree to which QS complexes are recorded from the inner portions of the free LV wall. When transmural necrosis was present, QS complexes were generally obtained in both the epicardial and thoracic leads. Subendocardial necrosis was manifested by qrS complexes on the epicardium, as well as in the peripheral leads. When the posterolateral middle third of the LV wall was damaged, Rs or qRs complexes were recorded in leads II, III, and aVF, and an increase in the voltage of the R wave in leads V1 and V2 was observed. Intramural myocardial necrosis diminished the voltage of the R wave in the corresponding leads. Left peripheral blocks obscured the manifestation of myocardial necrosis.

Action Potentials

Interatrial conduction and STa in experimental atrial damage.

Right (RA) and left atrial (LA) damage was produced with a subepicardial infiltration of 96 degrees alcohol in two groups of dogs. In six other dogs the left or right portion of the interatrial band was also injured. Conventional ECG and supplementary unipolar leads were recorded using photographic and direct inscription polygraphs at paper speeds of 50 and 100 mm/sec. Control, immediate postinjury and late tracings were obtained. A-V block was provoked to determine QTac. Slowing of heart rate and slight widening of the P wave and P-R interval were observed with both types of atrial damage. In four cases low right atrial rhythm was detected: two showed anatomo-histological sinus node involvement in right atrial injury. Qp waves were registered over the left precordium with necrosis of both sides, but were more frequent with RA damage. Damage of the left portion of the interatrial band delayed left atrial activation and split P waves in the precordial leads. Damage of the RA distorts the initial vectors, magnifying the left ones and simulating LA enlargement. The Qp registered on the RA is also detected by surface leads. Contrary distorted LA depolarization increases the RA vector and delays the left, ones, giving rise to greater asynchronsim and bimodal P waves.

Animals

Experimental bases for diagnosis of left bifascicular and trifascicular block.

It seems to be justified to establish the diagnosis of fascicular blocks, in clinical tracings, on the basis of experimental findings. For this, we produced left bifascicular block as well as trifascicular block in the heart of 20 mongrel dogs. Because of left bifascicular block, the activation process is unequally delayed in high lateral and in posterior aspects of the free left ventricular wall. Nevertheless, it begins at normal time in middle left septal mass via intermediate strands of the left bundle. Consequently, left bifascicular block which resembles intermediate degree left truncular block, is recognizable by unequally delayed onset of intrinsicoid deflection in aVL, aVF and V6 and often by the manifestation of the first septal vector. Vectorcardiographic curves are diphasic and show initial and terminal slurrings. Trifascicular block delays the activation process in both ventricles. For this, the asynchronism between the electromotive forces of ventricles is lessened. The said conduction disturbance can be diagnosed by electrocardiographic and vectorcardiographic features suggesting intermediate degree RBBB as well as left bifascicular block.

Adult