Wednesday, 10 February 2016

ECG Module on Myocardial Infarction & Ischaemia

Acute Inferoposterior MI Examples

R-wave Progression

  • normal R-wave progression in the praecordial leads 
    • normal chest lead ECG shows an rS-type complex in lead V1 with a steady increase in the relative size of the R-wave toward the left chest and a decrease in the S wave amplitude. Leads V5 and V6 generally show a qR-type complex, with R-wave amplitude in V5 often taller than V6 because of the attenuating effect of the lungs. Normal variations include: narrow QS and rSr patterns in V1 and qRs and R patterns in V5 and V6
    • at some point, generally around the V3 or V4 position, the QRS complex changes from predominately negative to predominately positive and the R/S ratio becomes>1. This is known as the transition zone. In some normal individuals, the transition may be seen as early as V2. This is called early transition. At times, transition may be delayed until V4 to V5. This is called delayed transition
    • normal R-wave height in V3 is usually greater than 2 mm 
    • if the height of the r wave in leads V1 to V4 remains extremely small, we say there is "poor R-wave progression" In the literature, definitions of poor R-wave progression have been variable, using criteria such as R-wave less than 2-4 mm in leads V3 or V4 and/or the presence of reversed R-wave progression defined as R in V4
  • poor R wave progression secondary to previous anterior myocardial infarction 
    • in anterior myocardial infarctions, this produces Q waves in the right and midprecordial leads (V1-V4) 
      • however, in a significant number of patients the Q waves do not persist
      • with previously documented anterior myocardial infarction, the reported estimate of poor Rwave progression on subsequent ECGs varies between 20% and 30%
      • average length of time for the complete disappearance of the abnormal Q waves is 1.5 years
      • the magnitude of the subsequent leftward forces is less than in patients with poor Rwave progression from other causes
      • on the ECG, this results in a diminuation of R-wave amplitude in standard lead I 

ST Segment Elevation Morphologies

  1. Obliquely straight
  2. Concave
  3. Non concave (CONVEX)

ST depression & T wave inversion causes

  1. LVH with strain pattern
  2. WPW with pre-excitation
  3. Right Ventricular Hypertrophy (RVH)
  4. Digitalis
  5. Subarachnoid Hemorrhage/CVA
  6. Posterior STEMI
  7. Ischemia (lead with upright QRS)
  8. Ischemia (wellen's patterns)
  9. Right Bundle Branch Block (RBBB)
  10. Left Bundle Branch Block (LBBB) 

Types of T-waves

How to calculate the QTc (Bazett's Formula)

LVH by voltage criteria - (Sokolow-Lyon Index)

P wave Abnormalities

  1. Right Atrial Enlargement (RAE) or (p Pulmonale)
  2. Left Atrial Enlargement (LAE) or (p Mitrale)
  3. Right + Left Atrial Enlargement (p Biatriale)

Cardiac Axis Made Easy

Normal Axis = QRS axis between -30 and +90 degrees.

Left Axis Deviation = QRS axis less than -30 degrees.

Right Axis Deviation = QRS axis greater than +90 degrees.

Extreme Axis Deviation = QRS axis between -90 and 180 degrees.

Posterior ECG Lead Placement

Heart Blocks

First Degree AV Block

Second Degree AV Block - Type 1 (wenckebach)

Second Degree AV Block - Mobitz Type 2

3rd Degree AV Block (Complete Heart Block)

Ventricular Ectopics

NSR with isolated PVC

Multifocal PVC's

NSR with Ventricular Couplets

Ventricular Triplets (salvo)

Ventricular Bigeminy

Ventricular Trigeminy

Ventricular Quadrigeminy

Ventricular Pentageminy

Ventricular Hexageminy

Ventricular Rhythms

Idioventricular Rhythm

Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm is ventricular rhythm with a rate of between 40 and 120 beats per minute. Idioventricular means "“relating to or affecting the cardiac ventricle alone“ and refers to any ectopic ventricular arrythmia. Accelerated idioventricular arrhythmias are distinguished from ventricular rhythms with rates less than 40 (ventricular escape) and those faster than 120 (ventricular tachycardia). Though some other references limit to between 60 and 100 beats per minute. It is also referred to as AIVR and "slow ventricular tachycardia."

It can be present at birth. However, it is more commonly associated with reperfusion after myocardial injury.

Polymorphic Ventricular Tachycardia

Polymorphic ventricular tachycardia, on the other hand, has beat-to-beat variations in morphology. This may appear as a cyclical progressive change in cardiac axis, previously referred to by its French name torsades de pointes ("twisting of the spikes"). However, at the current time, the term torsades de pointes is reserved for polymorphic VT occurring in the context of a prolonged resting QT interval.

Ventricular Flutter

Ventricular Tachycardia (VT)

Monomorphic ventricular tachycardia means that the appearance of all the beats match each other in each lead of a surface electrocardiogram (ECG).Scar-related monomorphic ventricular tachycardia is the most common type and a frequent cause of death in patients having survived a heart attack or myocardial infarction, especially if they have weak heart muscle.

Ventricular Fibrillation (VF)

Ventricular fibrillation (V-fib or VF) is a condition in which there is uncoordinated contraction of thecardiac muscle of the ventricles in the heart, making them quiver rather than contract properly. Ventricular fibrillation is the most commonly identified arrhythmiain cardiac arrest patients. While there is some activity, the lay person is usually unable to detect it by palpating (feeling) the major pulse points of the carotid and femoral arteries. Such an arrhythmia is only confirmed by electrocardiography. Ventricular fibrillation is a medical emergency that requires prompt Advanced Life Support interventions. If this arrhythmia continues for more than a few seconds, it will likely degenerate further into asystole ("flatline"). This condition results in cardiogenic shock and cessation of effective blood circulation. As a consequence, sudden cardiac death (SCD) will result in a matter of minutes. If the patient is not revived after a sufficient period (within roughly 5 minutes at room temperature), the patient could sustain irreversible brain damage and possibly become brain-dead, due to the effects of cerebral hypoxia. On the other hand, death often occurs if sinus rhythm is not restored within 90 seconds of the onset of VF, especially if it has degenerated further into asystole.