ECG 2

• Mean Vector


  Direction of the mean vector is from base to apex
• Axial Reference System


  Superimposing each limb of Einthoven's triangle over the heart
• ECG Rules


  • Depolarisation toward the (+) pole of a lead results in an upward (positive) deflection on the ECG recording of that lead
  • Depolarisation that heads away from the (+) electrode result in a downward deflection in that lead
  • The magnitude of the deflection, either upward or downward, reflects how parallel the net electrical vector is to the axis of the lead being examined
  • An electrical vector records zero magnitude in any lead perpendicular to it i.e. (a flat line on the recording)
• Axial Reference System


  • A wave of depolarisation traveling at +60° : the greatest positive deflection in lead II
  • A wave of depolarisation traveling at +90° relative to the heart : equally positive deflections in both lead II and III, no deflection in lead I because the depolarisation is heading perpendicular to the 0°, or lead I, axis
• Hexaxial Reference System


  Overlaying the unipolar limb leads : +ve electrode for aVL is at -30 degrees relative to the heart, +ve electrode for aVF is +90° relative to the heart, +ve electrode for aVR is -150° relative to the heart
• Sequence of Ventricular Depolarisation in the frontal plane as seen by Lead II


  • Vector 1: impulses are conducted down the L&R bundle branches on either side of septum, septum depolarises from left-to-right, vector heads slightly away from the positive electrode small negative deflection (Q wave)
  • Vector 2 (20 ms later): the mean electrical vector points downward toward the apex and is heading toward the positive electrode tall positive deflection (R wave)
  • Vector 3 (20 ms later): vector points towards LA and anterior chest, ventricle depolarizes from the endocardial to the epicardial surface small positive voltage
  • Vector 4: last regions to depolarise slight negative deflection (S wave)
• Quick Estimate


  1. Inspect limb leads I and II. If the QRS is primarily upward in both, then the axis is normal
• Estimation of the Mean Electrical Axis of the Ventricular QRS Complex


  Overlap of common "+" regions = -30 to +90 degrees, MEA falls in the "Normal" range
• Isoelectric QRS Complex


  When the upward and downward deflections of a QRS are of equal magnitude, it indicates that the mean electrical axis of the ventricles is perpendicular to that particular lead
• Estimation of the Mean Electrical Axis of the Ventricular QRS Complex


  The mean electrical axis averaged over the entire period of ventricular depolarisation is +59 degrees, usually estimated from the standard bipolar limb lead ECG's
• Causes of Electrical Axis Deviation - Left

  • Changes in heart position: left shift occurs at the end of a deep expiration, lying down, increased visceral adiposity
  • Hypertrophy of left ventricle (left axis shift) caused by hypertension, aortic stenosis, or aortic regurgitation, more muscle on hypertrophied side generation of electrical potential, normal ventricle becomes depolarised before the hypertrophied one vector from the normal side to hypertrophied side (+ve) axis deviation towards hypertrophied side ~ -15 degrees
• Left bundle branch block (LBBB) often causes a left axis shift


  QRS is prolonged (> 0.12 sec), Lead V1 has a wide, dominant negative S wave, Lead V6 has broad, notched ("rabbit ear" or " M" shaped) R wave, ~ -50 degrees
• Causes of Electrical Axis Deviation - Right


  Hypertrophy of right ventricle (right axis shift) is caused by pulmonary hypertension, congenital conditions eg. pulmonary valve stenosis, tetralogy of Fallot, interventricular septal defect, changes in heart position: right shift occurs at the end of deep inspiration, standing up, in tall individuals
• Left bundle branch block (LBBB)

  • QRS is prolonged (> 0.12 sec)
  • Lead V1 has a wide, dominant negative S wave
  • Lead V6 has broad, notched ("rabbit ear" or "M" shaped) R wave
• Left bundle branch block (LBBB) often causes a left axis shift
• Right bundle branch block (RBBB)


  • QRS is prolonged (> 0.12 sec)
  • Lead V1 has a positive secondary R wave, i.e. RSR' with T wave changes
  • Lead V6 has a wide slurred S wave
• Right bundle branch block (RBBB) often causes a right axis shift
• Sequence of conduction in RBBB

  1. Left ventricular activation via the left bundle (black arrow) occurs normally

  2. Septal depolarisation (yellow arrows) is thus unaffected, producing a normal early QRS complex

  3. Activation of the RV originates across the septum. The resultant depolarisation vector (red arrow) produces delayed R waves in leads V1-3, and S waves in lateral leads
• Increased voltages in standard bipolar limb leads


  If sum of voltages of leads I-III is greater than 4 mV, (normal ~ 0.5-2.0 mV) this is considered to be a high voltage ECG
• Decreased voltages in standard bipolar limb leads

  • Cardiac muscle abnormalities - (old myocardial infarctions causing decreased muscle mass & slow movement of the depolarisation wave though the ventricles low voltage ECG, and prolonged QRS)
  • Conditions surrounding heart (fluid in pericardium, pleural effusions, pulmonary emphysema)
  • Anterior–posterior rotation of apex of heart
• Low voltage QRS: QRS amplitude < 5mm in limb leads
• Acute Coronary Syndrome


  • Most common cause is occlusion due to thrombus from an atherosclerotic plaque
  • Coronary artery most commonly occluded (40–50%) is the LAD, followed by the RCA, and then the left circumflex
  • Earliest ECG changes are in the ST segment
• Myocardial Ischaemia - Ventricular Action Potentials


  1. Creation of ischaemia – induced depolarisation

  2. Effects of ischaemia – induced depolarisation (slow)
• Ischaemia hypoxia ATP KATP channels open K+ outflow


  • This might normally hyperpolarize the cell, but there is also an ECF [K+]
  • Na+ K+ pump inactivated
  • Together leads to a less negative (depolarised) resting membrane potential
• Myocardial Ischaemia - Changes in the ST segment- ST depression


  The ST segment is normally isoelectric (zero voltage)
• Myocardial Ischaemia - Current of injury - Subendocardial Ischaemia

  Subendocardial ischemia produces a region of depolarisation, which is recorded as a positive voltage because vectors generated at the boundary between depolarised and repolarised tissue (solid arrows) are directed toward the overlying recording electrode. This elevates baseline voltages observed before the QRS complex and after the T wave.

  
• Myocardial Ischaemia - Changes in the ST segment- ST elevation


  The ST segment is normally isoelectric (zero voltage)
• Myocardial Ischaemia - Current of injury - Transmural Ischaemia


  Transmural ischemia produces a region of depolarisation, which is recorded as a negative voltage by the overlying electrode. This occurs because vectors generated at the boundary between depolarised and repolarised tissue (solid arrows) are directed away from the overlying recording electrode when all but the ischemic tissue is repolarized. This depresses baseline voltages observed before the QRS complex and after the T wave.
• Myocardial Ischaemia - T wave


  Ischemic subendocardial cells have a depolarised resting membrane potential and a shortened action potential duration, which can cause repolarisation to occur before the subepicardial cells repolarise. This will lead to the repolarisation wave traveling toward the overlying recording electrode, which is generally the same vector orientation as depolarisation; this causes a negative deflection of the T wave.
• Pathologic Q Waves


  • Width ≥1 mm (1 small box) or depth >25% of the height of the QRS complex
  • Irreversible necrosis of the heart muscle served by occluded vessel, if there is no reperfusion of the vessel
  • Usually permanent evidence of an ST-elevation type of myocardial infarction with tissue necrosis
  • Must appear in lead grouping to indicate anatomic site of infarction

  
• Time-Dependent Changes during Acute ST-Elevation Myocardial Infarction