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New ECG Case Every Sundays Admin: @medicallegend
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ECG shows sinus rhythm with right bundle branch block (RBBB) and left axis deviation, the latter consistent with left anterior fascicular block.There are pathologic anterior Q waves V1-V3 with very slow R wave progression thereafter. The patient had severe coronary artery disease (CAD) with a trans-thoracic echo showing septal dyskinesis and apical akinesis. Note the rSr&39; morphology in V4. This polyphasic QRS phenotype in the left chest leads has been reported with ventricular aneurysm (El-Sherif sign). The patient was treated with amiodarone for ventricular tachyarrhythmias associated with chronic CAD with extensive scarring of left ventricle.
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Acute infero-lateral and probably posterior myocardial infarction (MI) with inferior Q waves and hyperacute ST-T complexes inferiorly and laterally with reciprocal ST depressions V1-V3. Tall initial R waves in V1-V3 with right bundle branch block. There is second degree AV block (Type 1) with 2:1 block initially and then 3:2 AV Wenckebach with underlying sinus rate of about 85/min. Left axis deviation is present. However, since this is an inferior MI, a pacemaker is not usually indicated: block here is in the AV node usually due to ischemia and increased vagal tone. In contrast, new right bundle with left axis with acute anterior-septal MI would be indication for prophylactic pacemaker. AV block in that setting is due to Type II mechanism associated with severe involvement of His-Purkinje system and carries ominous prognosis with high risk of complete heart block with slow (or no) escape rhythm.
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A 52-year-old man. What is his chief complaint? What is the rhythm disturbance? Look carefully at both ends of strip.
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ECG shows sinus rhythm with left ventricular hypertrophy (LVH), left atrial abnormality and tall peaked T waves best seen in the precordial leads (with non-specific infero-lateral ST depressions). (The QRS duration is slightly prolonged at 110-120 ms,) Also present are left axis deviation consistent with left anterior fascicular block and a long QTc (maximally about 470 ms) Putting it all together, the peaked T waves indicate increased K+ (6.3 mEq/L), with LVH consistent with renal failure associated with hypertension, which was the case here. The long QT, with a "stretched out" ST segment phase, is consistent with decreased serum calcium, seen with renal failure as well. ST depressions could be from LVH or primary ischemia, in addition to multiple other causes. So when you see the triad of "tented" T waves (hyperkalemia) with a long QT (due to ST segment prolongation consistent with hypocalcemia) and LVH (consistent with hypertension), the findings speak strongly for underlying renal failure, although other combinations are not excluded. Also, not all of the triad needs to be present to suggest renal failure (e.g., peaked T wave and LVH alone are suggestive. but could also be due to hypertension plus drug effects that tend to increase serum K+).
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This ECG "speaks" to some key clues about the underlying major medical condition in this 77-year-old woman. What does it say? What are the clues and what inference might you make by integrating these findings?
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The ECG shows sinus bradycardia with diffuse T wave flattening or inversions, and markedly prominent U waves. These are best seen in leads V2 and V3, but are essentially invisible in lead aVL. The two most common causes of this finding are 1) Hypokalemia (K+ here was 2.4 mEq/L) and 2) Drugs, especially the class 1A antiarrhythmics (like quinidine, procainamide, disopyramide) and related agents (like the phenothiazines and tricyclics), etc. Patients with hereditary (congenital) long QT syndromes due to "channelopathies" may show a similar finding (see Case 1). This ventricular repolarization prolongation pattern is of great importance because it identifies patients at high risk of torsade de pointes type of polymorphic ventricular tachycardia.
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A 38-yr-old woman with weakness. Previous ECG was normal and she was on no medications. What is the most likely diagnosis?
