ECG Flashcards
Right axis deviation
• RVH (including pulmonary embolism)
• Lung disease even without RVH
• Left posterior fascicular block (LPFB) (usually associated with right bundle‐branch block [RBBB])
• Lateral MI: Q wave is seen in lead I. Instead of a Q wave, a diminutive small r wave (rS pattern) sometimes appears in leads I–aVL. In this case, the Q waves in leads V5–V6 and the frequently seen T‐wave inversion in I–aVL allow the diagnosis (≠ RVH)
• Normal variant: vertical heart with a 90–100° axis in young individuals
• Arm electrodes misplacement: P wave will also be negative in lead I, and upright in lead aVR
Left axis deviation
• LVH
• Left anterior fascicular block (LAFB)
• Left bundle branch block (LBBB)
• Inferior MI
Early transition causes
• RVH (which also leads to right‐axis deviation).
• RBBB.
• Posterior wall infarction: large, and more importantly, wide R wave in V1 , reciprocal of a posterior Q wave. Often, Q waves are present in V7–V9 and in the inferior leads.
• WPW: short PR and delta wave are present.
• Septal hypertrophic cardiomyopathy (thick septum, thicker than the lateral wall, projects as big R in V1–V2 and big Q in the lateral leads) ; or Duchenne muscular dystrophy (posterior wall fibrosis).
• However, the most common cause of early transition is a normal variant. It is more common in young individuals, where the heart is swung more anteriorly than older individuals. A low malposition of electrodes V1–V2 is also a common cause of early transition.
Poor R wave progression
• LAFB.
• LVH.
• LBBB.
• High misplacement of electrodes V1–V2 or low heart/low diaphragm position (thin and tall individuals); or heart swung posteriorly, away from V1–V2 (older subjects). Normal R‐wave progression may be seen when the chest leads are placed one interspace lower.
• COPD, in which case the heart is pushed down and posteriorly, away from the precordium: COPD leads to poor R‐wave progression with right‐axis deviation. Poor R‐wave progression with right‐axis deviation may also be seen when anterior MI is associated with a high lateral MI. The overall size of the QRS allows the distinction between COPD and anterior MI (QRS voltage is often reduced in COPD). Also, in COPD, recording the chest leads one interspace lower often corrects R‐wave progression, at least partially.
RVH
- Right‐axis deviation (net QRS [–] in lead I, [+] in lead aVF)
and - Big R wave in the right lead V1 (≥7 mm), or big S wave in the left leads V5–V6 (≥7 mm)
Or big R > S in V1 , big S > R in V6 , or small S in V1 ≤ 2 mm
Or R in V1 + S in V6 > 10.5 mm
In the absence of RBBB, a monophasic R wave in V1 or a qR pattern in V1 signifies severely increased RV pressure (higher than systemic pressure in the case of qR pattern).
Differential diagnosis of RVH
Posterior MI may lead to a prominent R wave in V1 . In posterior MI, R wave is not only high but is also wide > 1 mm (≠ RVH), T wave is positive in V1–V2 (vs. inverted in RVH), the axis is not right, and there are often Q waves in V7–V9 and in the inferior or lateral leads.
An incomplete RBBB pattern with RSR’ may be seen along with RVH. In fact, incomplete RBBB with right axis is frequently secondary to RVH, more specifically a volume overload pattern of RVH, with prolonged right bundle conduction related to the RV size rather than right bundle disease. RVH is definitely diagnosed if the axis is right and R’ > 10 mm. As RVH progresses, R’ becomes taller and a monophasic R may develop, particularly with pressure overload patterns.
Lung disease, such as COPD, is characterized by: (1) right‐axis deviation in the frontal plane as the heart is pushed down and made more vertical; (2) deep S wave in all precordial leads, V1 through V6 , as the heart rotates posteriorly; (3) reduced overall QRS voltage in all leads, especially limb leads, because of increased chest air; while dominant, S wave is not particularly deep in the precordial leads. This chronic lung disease pattern simulates an old anterolateral MI, wherein R is diminished across all precordial leads and in the lateral leads I and a VL (rS pattern throughout all those leads). The presence of true RVH in conjunction with lung disease is characterized by one of the following: large R or small S in V1 (≤2 mm), RSR’ pattern, or T‐wave inversion in V1–V2 . P pulmonale may be seen with lung disease even without RVH.
Biv enlargment
- Voltage criteria for both LVH and RVH. This usually implies tall R waves in V5–V6 (LVH) with a small S wave in V1 , or R > S in V1 (R is not usually large in V1 , but is larger than S).
- LVH with right‐axis deviation.
- LVH with right atrial or biatrial enlargement.
- LVH with T inversion in V1–V2 (T going in the same direction as QRS). This T inversion can be secondary to RV strain or anterior ischemia.
- Tall R wave and tall S wave in the mid‐precordial leads V3–V4 (Katz–Wachtel sign).
LBB
- Wide notched R wave in leads I, aVL, and V5–V6 (M‐shaped or slurred, plateaued R wave).
- QRS is negative in leads V1 , V2 , V3 with an rS or QS pattern. QS pattern may also occur in leads III and aVF, simulating an inferior MI, but not in lead II. QR pattern does not occur with LBBB and always implies an associated MI
- The septal q wave should be absent in the left leads I and V5–V6 . A narrow q wave may be seen in aVL.
- The ST segment and T wave should be directed opposite to QRS. Unlike LVH, RBBB, and RVH, secondary ST–T changes are mandatory in LBBB.
- Two less usual features may be seen in LBBB and do not preclude the diagnosis of LBBB:
• q wave in aVL.
• RS pattern (rather than a plateaued R pattern) in leads V5–V6 . This occurs in patients with delayed QRS transition, such as patients with enlarged LV or LV depolarization that spreads from apex to base; the frontal QRS axis is leftward in both of these cases.
LVH and LBBB
LVH cannot be formally diagnosed in the presence of complete LBBB, but can be diagnosed in the presence of incomplete LBBB. In fact, LVH with QRS 110–119 ms and with loss of septal q waves and delayed R peak in leads I and V5–V6 is a combined LVH + incomplete LBBB. Outside LBBB, septal q waves are prominent in patients with LVH and may be of pathological dimension. In some patients, LBBB is due to a block across the left bundle, but in many other patients, LBBB is due to diffuse slowing across a diseased, enlarged LV. In the latter patients, there is a progression from LVH to incomplete LBBB then complete LBBB over months to years, as cardiomyopathy progresses, and LBBB tends to have more left‐axis deviation
Wide QRS causes
Pre‐excitation (WPW). In that case, the wide QRS starts with a “slur” (= delta wave = slow QRS upslope). This slur is riding the P wave (= short PR). Unlike bundle branch block, where QRS has a steep initial portion and a slow terminal portion, the QRS complex of WPW is widened at its initial uptake (Figure 31.27).
Hyperkalemia.
Drugs (class Ic antiarrhythmic drugs, tricyclics, phenothiazines).
Non‐specific intraventricular conduction delay
LAFB
• LAFB is defined as “an unexplained left‐axis deviation” with QRS axis between –45° and –90°. In other words, LAFB manifests as left‐axis deviation beyond –45° without LBBB or inferior MI.
• A qR pattern is seen in lead I and particularly lead aVL, while rS pattern is typically seen in the inferior leads II, III, and aVF (net QRS is nega tive in the latter leads). Beside being positive in I and negative in aVF, the net QRS is larger in aVF than in I, which defines axis ≤ –45°.
• Additional notes :
LVH does not preclude LAFB diagnosis. In fact, LVH with left‐axis deviation over –45° usually implies LVH + LAFB.
Inferior MI makes LAFB diagnosis more difficult. Inferior MI may lead to a QS pattern in leads II, III, and aVF and a left axis over –45°, whether LAFB coexists or not. If LAFB coexists, R wave will peak in aVL earlier than in aVR. LAFB does not, by itself, produce QS waves in leads III and aVF and should not mimic inferior MI.
While the ACC guidelines mandate the presence of a small septal q wave in lead aVL for the definition of LAFB, a study has suggested that up to 27% of patients with LAFB do not have a q wave in leads I and/or aVL. These may be patients who have a horizontal heart, in whom the septal depolarization is orthogonal to lead I ± aVL, or patients who have a degree of septal conduction block.
LAFB is common with and without underlying heart disease and does not portend an independent prognostic significance. LAFB does not lead to secondary ST–T abnormalities.
Differential diagnosis of small QRS voltage
• Pericardial effusion. Electrical alternans may also be seen.
• Any “shield” around the heart: COPD, obesity, large pleural effusion, and notably hypothyroidism (“low” and “slow”).
• Constrictive pericarditis; some restrictive infiltrative cardiomyopathies (such as amyloidosis and hemochromatosis, but not Fabry disease).
Electrical alternans
is an every‐other‐beat alternation of two different but equally wide and equidistant QRS complexes Electrical alternans may also involve the P and T waves, in which case it is called total alternans and is very specific for pericardial effusion
Causes of electrical alternans
• Severe HF, where it is mechanically induced by an alternate change in cardiac contraction (like pulsus alternans).
• SVT, especially AVRT or any fast SVT, wherein a slight variation in ventricular conduction occurs alternately.
• Acute myocardial ischemia or PE, where again there is a conduction alternans.
• Intermittent pre‐excitation or intermittent conduction block, such as LAFB or bundle branch block, occurring in an alternat ing fashion. This is rather a mimic than a true electrical alternans
The inferior RCA injury is looking rightward, while the inferior LCx injury is looking leftward. Features supportive of RCA:
Lateral ST depression in lead I (vs. lack of ST depression or ST elevation with LCx)
ST elevation ≥ 0.5 mm in lead V1 or V4R (implies RV infarct, and thus, RCA).This is a very specific finding
ST elevation in lead III > II (lead III is more parallel to the slightly rightward RCA current of injury, whereas lead II is parallel to the leftward LCx current of injury)
No or minimal (<1mm) ST depression in aVR implies RCA. The LCx current of injury is directly opposite to the right arm, thus LCx injury leads to ≥ 1 mm ST depression in aVR
