Makindo Medical Notes

Analysis

Axis

• X axis: Time at 25 mm/second: 1mm (small square) = 0.04 seconds 5mm (big square) = 0.2 sec
• Y axis: Millivolts: 1 mv = 1 cm unless the settings are changed e.g. 1 mV = 2cm. Always check calibration spike at beginning of reading

Rate

• Normal: Rate = 300 / number of large squares in between each consecutive R wave.
• Tachycardia: Rate = 1500 / number of small squares in between each consecutive R wave.
• Slow: Rate = number of complexes on the rhythm strip x 6 (this gives the average rate over a ten-second period).

Definition of Rates

• 60-100 beats/min: Normal
• >100 beats/min: Tachycardia
• <60 beats/min: Bradycardia

P waves

• The P wave is due to the depolarization of the atria. The wave of depolarization spreads from the right atrium to the left atrium. The P wave is therefore composed of the right atrial depolarization followed by that of the left.
• In normal practice happen so close that peaks cannot be differentiated easily. The entire P wave lasts less than 110 ms. The P wave is best seen in leads II and V1
• Upright in leads I, aVF and V3 - V6
• Normal duration of less than or equal to 0.11 seconds
• Polarity is positive in leads I, II, aVF and V4 - V6
• Diphasic in leads V1 and V3; negative in aVR
• Shape is generally smooth, not notched or peaked
• Pathological
  • Left atrial enlargement causes a "P mitrale" - with a bifid waveform. It may be seen best in lead II and may be due to mitral stenosis, systemic hypertension, valvular disease and cardiomyopathy.
  • Right atrial enlargement causes a "P pulmonale" - with a tall peaked P wave in lead II > 2.5 mm and positive in lead V1. Seen in COPD and pulmonary hypertension. There is a poor correlation poor between RA enlargement and P pulmonale.
  • Ectopic P wave where morphology differs with altered P wave axis. May be seen with what is called a coronary sinus rhythm. Occasionally associated with sinoatrial disease or ASD.
  • Absent P wave - Atrial fibrillation, Junctional rhythm, Sinoatrial block

PR interval: normally between 0.12 and 0.2 seconds

• PR interval is caused electrically by passage of the action potential from
  • Sinus Node to Atria: PA interval
  • Atria to His bundle: AH interval
  • His bundle to Ventricle: HV interval
• PR interval < 0.12 seconds
  • Causes are usually pre-excitation when the ventricular is depolarised by an accessory pathway
    • Wolff Parkinson white syndrome with a delta wave
    • Lown Ganong Levin syndrome
    • Ventricular ectopic immediately after p wave
    • Low atrial rhythm
    • Coronary sinus escape rhythm
  • PR interval > 0.2 seconds
    • This is first degree heart block
    • Usually asymptomatic but suggests conduction tissue disease

QRS complex

• The first negative deflection is a Q wave and the next positive deflection is an R wave
• If a negative deflection occurs after an R wave it is called an S wave
• If the first defection is positive it is called an R wave, if there is an S wave and then a 2nd positive wave this is called an R' wave
• An RSR' pattern in V1 in RBBB - the left ventricle depolarized first followed by the right ventricle
• An RSR' pattern in V6 is LBBB - the right ventricle depolarized first then the left ventricle
• There is widening and coarsening of the QRS complex with severe hyperkalaemia
• Duration less than or equal to 0.12 seconds, amplitude greater than 0.5 mV in at least one standard lead, and greater than 1.0 mV in at least one precordial lead. The upper limit of normal amplitude is 2.5 - 3.0 mV. small septal Q waves in I, aVL, V5 and V6 (duration less than or equal to 0.04 seconds; amplitude less than 1/3 of the amplitude of the R wave in the same lead).
• Represented by a positive deflection with a large, upright R in leads I, II, V4 - V6 and a negative deflection with a large, deep S in aVR, V1 and V2 in general, proceeding from V1 to V6, the R waves get taller while the S waves get smaller. At V3 or V4, these waves are usually equal. This is called the transitional zone.
• Wide QRS > 0.12 seconds (3 small squares)
  • Ventricular initiation of complex
  • Wolff Parkinson White syndrome
  • Intraventricular conduction defect - LBBB, RBBB
  • Hyperkalaemia
• Increased QRS voltage (height)
  • LVH S in V1 and R in V5/6 > 35 mm
  • RVH Dominant R wave in V1
  • Hypertropic cardiomyopathy
• Decreased QRS voltage (height)
  • Obesity
  • Pericardial fluid
  • Hypothyroidism
  • Emphysema
• QRS axis
  • Reflects net direction vector of ventricular depolarisation
  • Reflects muscle bulk and state of conduction pathways
  • Normal vector is between -30 to + 120 degrees. Zero is horizontal and points left.
  • Simply sum the net deflections of the ECG in lead I,II and III at 0, 60, 120 degrees
  • The axis is at right angles to any lead where the net value is 0 but then need to calculate vector direction
  • If lead I is positive then the vector points left. if lead II then is negative then LAD
  • If lead I is negative then the vector points right. if lead II then is negative then LAD

Normal Q wave

• Normally represents left to right septal depolarization seen in left-sided leads
• Normal < 2.5 mV (2.5 mm) in height and less than 1 mm (small square) wide
• Pathological Q wave
  • Pathological represents opposite R wave due to an electrical window caused by transmural infarction. It represents depolarisation away from the electrode of the opposing ventricular myocardium. Normal depolarisation passes from the internal endocardial surface to the external epicardial surface.
  • The lead with the Q wave usually identifies the territory damaged and the artery involved. They are usually deep and > 2.5 mm and often > 1 mm wide. Pathological Q waves can also be seen with LVH usually associated with hypertrophy and large R waves or occasionally in hypertrophic cardiomyopathy.
  • Where transmural infarction is incomplete the ECG marker is a loss of R wave height rather than the development of Q waves. This may be seen in the anterior leads as poor R wave progression. If there are additional T wave changes this is more indicative of previous infarction.
• A list of Causes of Pathological Q wave
  • Transmural infarction
  • Left ventricular hypertrophy
  • HOCM
  • Myocarditis
  • Dilated cardiomyopathy
  • Hyperkalaemia
  • Infiltrative muscle disease

ECG - ST Segment

• Definition
  • ST segment from ventricular depolarisation to repolarisation
• ST Elevation
  • Myocardial infarction > 1 mm in 2 contiguous chest leads or 1 mm in 2 limb leads
  • Myocardial ischaemia - reciprocal
  • Myocarditis/Pericarditis - saddle shaped concave upwards in all leads except aVR
  • LBBB/LVH in V1/2
  • Brugada syndrome
  • Coronary artery spasm - Printzmetal's angina
  • Left ventricular aneurysm
• ST Depression
  • Left ventricular Hypertrophy and strain pattern
  • Ischemia (typically best lead is V5 and 1-2 mm depression is significant). Downgoing > Flat > Upgoing in terms of significance
  • Digoxin - reversed tick
  • Hypokalaemia
• Changes with STEMI
  • Hyperacute T waves
  • ST elevation
  • T wave inversion
  • Loss of R wave height
  • Q waves develop

ECG - T waves

• Definition
  • The T wave is caused by ventricular repolarisation
• Abnormalities
  • Peaked T waves are seen classically in hyperkalaemia
  • Are generally in opposite polarity to the QRS complex
  • Amplitude can be altered in hypothyroidism - "low voltage" also seen in an obese person and in those with COPD

Differentials