Summary Part 3 – CLINICAL PRESENTATIONS

  1. Disturbances in electrolyte balance
    • Potassium is the ion with greatest impact on the resting membrane potential. Hyperkalemia causes a less negative potential, retards phase 0 causing slower conduction and wider QRS complexes. The T wave becomes tall and peaked. Hypokalemia prolongs the action potential and hence the QT interval, and the T waves flatten. Both these changes facilitate arrhythmias
    • Calsium influences the plateau phase of the action potential (phase 2) Hypocalcemia prolongs, whereas hypercalcemia shortens QT the time
  2. Ischemia and infarction
    • In ischemia the resting membrane potential has a positive charge compared to that of the healthy myocytes, and there is a diastolic current of injury from ischemic toward healthy myocardium. Above ischemic tissue the ECG baseline is depressed. As QRST remains in place, we see an ST-elevation. Above healthy tissue, however, the baseline is elevated, and we see an ST depression
    • In ST elevation myocardial infarction (STEMI) the ECG changes indicate the localization of the infarction (which leads show the ST elevation), and the area at risk (number of leads with ST elevation and the sum (in millimeter) of ST elevations in all leads
      • Anterior wall: aVL, I, V1-V6
      • Inferior wall: II, aVF and III
      • Lateral wall: II, V5-V6 and aVL
      • Right ventricle: V1, v3R (intercept between the right-sided medioclavicular line and the 5th intercostal space
      • In posterior wall ischemia/infarction a precordial reciprocal ST depression is seen
    • Non-STEMI and angina can, unfortunately, not be reliably localized by ECG.
    • Infarct scars are suspected from pathological q waves: ≥(30) 40 ms duration, ≥1 mm deep and ≥1/4 of the following R wave. Pathological q waves in two neighbor leads are usually required.
    • The presence of a left bundle branch block complicates infarction diagnosis.
    • Inverted T waves and fragmented QRS suggest scar tissue/fibrosis
  3. Other conditions
    • Pericarditis presents with widespread ST elevation, independent from the coronary artery distribution
    • Lung embolism usually causes sinus tachycardia and frequently, a right-sided QRS axis
    • COPD: the ECG may present in different forms: tachycardia, small amplitudes (in emphysema), >70° P wave axis (vertical heart), right or left QRS axis deviation.
    • Left ventricular hypertrophy (LVH) results in larger QRS amplitudes, either anteriorly (Sokolow-Lyon: S i V1 + R i V5-6 ≥37 mm) or upward left posterior (Cornell: R i aVL + S i V3 ≥20 mm in females and ≥28 mm in males). Repolarization disturbances may result in permanent discordant ST deviation and T wave inversion.