Myocardial Ischemia:
- One of the most important things to evaluate on EKG
- If severe narrowing/complete blockage of a coronary artery causes blood flow to become adequate, ischemia of the heart muscle develops
- Can be transient (angina pectoris) or more severe (necrosis & MI)
Myocardial Ischemia
- LV consists of an outer layer (epicardium/sub-epicardium) and inner layer (sub-endocardium)
- Can have limit of ischemia to the inner layer or can affect the entire thickness of the ventricular wall (transmural ischemia)
Myocardial Blood Supply
- RCA supplies both inferior (diaphragmatic) portion of the heart and RV
- Left main divides into the left anterior descending artery (LAD), which supplies the ventricular septum and large part of free LV wall, and LCx (lateral wall of the LV)
ST Elevation/Transmural Ischemia
- Ischemia & ultimately necrosis of a portion of the LV free wall
- Most patients w/ acute MI have underlying atherosclerotic disease
- Occlusion of coronary artery with a ruptured plaque leads to coagulation cascade (fibrin & platelets)
ST Elevation/Transmural Ischemia
- Other factors for acute STEMI: cocaine, coronary artery dissection, coronary artery emboli
- Acute phase: ST elevations, hyper-acute T-waves in multiple leads
- Evolving phase: Hours/days later with deep T-wave inversions replacing ST elevation
ST Elevation/Transmural Ischemia
- Anterior MI: infarct of anterior/lateral wall of LV
- Inferior MI: infarct of inferior wall of LV
- ST segment (& reciprocal) changes generally seen within minutes of blood flow occlusion
- Reperfusion therapy can decrease ST elevations
Thanks to these amazing website for the wonderful graphics:
Fascicular Blocks:
- Left bundle branch system: sub-divided into an anterior & posterior fascicle.
- Hemi-block does not widen the QRS complex markedly (compared to a RBBB or LBBB)
Left Anterior Fascicular Block (LAFB):
- Diagnosed by finding of a left axis deviation (-45 degrees or more negative)
- Delayed activation of more superior & leftward position of the LV
- Isolated finding is non-specific; can be seen w/ HTN, AV disease, CAD, and aging
LBBB:
- Similar to a RBBB, produces a wide QRS and affects the early phase of depolarization
- Septum will depolarize from (right to left; instead of normal left to right).
- Will see the loss of septal r-wave in V1 and septal q-wave in V6
LBBB:
- V1: Negative QRS complex b/c the LV is still electrically predominant (initial depolarization is negative and remains negative in the right-sided chest lead) (W-shape)
- V6: Entirely positive R-wave ('M'- Pattern)
Ventricular Conduction:
- Normal electrical stimulus reaches ventricles from the atria through the AV node & His-Purkinje systems
- First part of heart to be depolarized is the left-side of the septum; then spreads to RV and LV by right & left bundles
- Normal QRS < 0.10 sec
RBBB:
- 1st phase of depolarization: Left side of septum is stimulated first (branch of left bundle); on a normal ECG produces a septal r-wave in V1 and small septal q-wave in V6. No impact with RBBB.
- 2nd phase: Simultaneous depolarization of LV and RV. No impact with RBBB.
Atrial and Ventricular Enlargement:
- Both dilation & hypertrophy usually result in chronic pressure and volume overload on the heart muscle
- Pathological hypertrophy & dilation are often accompanied by fibrosis (scarring); can lead to arrhythmias and heart failure.
Right Ventricular Hypertrophy:
- Right chest leads show tall R-waves
- R-wave > S-wave in V1 is suggestive; not diagnostic of RVH
- Can see right-axis deviation and T-wave inversions in the right & mid-precordial leads
- RV hypertrophy can lead to variations in repolarization