Occult pneumothorax.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Julián Ortega-Carnicer.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The giant R wave syndrome is characterized by giant R wave accompanied by widening of the QRS complex, marked ST segment elevation, QRS axis deviation, and the formation of monophasic QRS-ST complex with obliteration of S wave in leads facing the ischemic zone. This report describes a 65-year-old-man with variant angina who had a transient giant R wave syndrome during an exercise treadmill test. Initially, at peak exercise, there was a convex ST segment elevation ending in a negative T wave in the same (inferior) leads which showed giant R waves. Later, in the recovery period and coinciding with an amelioration of myocardial ischemia, there was a less marked increase of R wave amplitude associated with concave ST segment elevation and positive T wave in the inferolateral leads. Subsequently, a ST segment depression in the inferolateral leads preceded the ECG normalization. The patient had also a concave ST segment elevation and positive T wave in inferolateral leads during a spontaneous episode of variant angina at rest. An emergency coronary arteriography showed a dominant right coronary artery with an 80% and a 75% diameter stenosis of the middle and distal segment, respectively; the other arteries and left ventriculogram were normal. The underlying mechanisms of the different shapes of ST segment elevation and T waveform in the setting of acute transmural myocardial ischemia are discussed.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The Brugada syndrome (BRS) is a hereditary cardiac condition (characteristically with a gene mutation affecting sodium channel function) identified by an elevated terminal portion of the QRS complex (prominent J wave) followed by a descending ST-segment elevation ending in a negative T wave in the right precordial leads, and malignant tachyarrhythmias in patients without demonstrable structural heart disease. We report a patient with a previous history of epilepsy treated with psychotropic drugs (with a sodium channel blocking effect) and chronic renal failure on haemodialysis who developed hyperkalaemia (6.6 mmol/l) and ECG findings resembling BRS. This condition was manifested by the prominent J wave, the coved-type ST-segment elevation and the negative T wave in the right precordial leads. These ECG changes disappeared after haemodialysis when the potassium became normal. Subsequently, a flecainide test did not reproduce ST-segment elevation. We conclude that hyperkalaemia associated with cardiac membrane active drugs may cause ECG changes mimicking the Brugada syndrome.