•PART III: DETERMINATION OF PRECISE ELECTRICAL AXIS
Normal Limits of QRS Axis in Adults: -30° to +90°.
Quadrant Method (I and aVF; can also be approximated using I and III).
• Both leads have primarily positive QRS deflections = normal axis.
• QRS in I is primarily positive and QRS in aVF is primarily negative = LAD.
• QRS in I is primarily negative and QRS in aVF is primarily positive = RAD.
• Both leads are primarily negative = extreme axis; equivocal.
Perpendicular Rule (all frontal leads)
• Mean QRS vector is perpendicular (_|_) to the axis of the lead with the most equiphasic complex in the
pre-selected quadrant using quadrant method .
• Lead _|_ to the most equiphasic QRS lead = axis.
• Numerical value of axis is determined by following _|_ lead toward pole that is in the preselected quadrant.
E.g., quadrant method shows LAD [0°-90°].
Lead II is most equiphasic.
aVL is _|_ to II.
Therefore a LAD of -30° is present.
Parallel Rule (look at all frontal leads).
• Used to confirm quadrant and/or perpendicular rule.
• Find lead with largest (+ or -) QRS deflection.
• If the QRS is positive, follow that lead to its positive, pole thus giving you the numerical axis.
• If the QRS is negative, follow that lead to its negative pole to obtain numerical axis.
LAD — Etiology:
• May occur normally in obese person [fat pushes diaphragm up;] also in elderly.
Abnormal LAD Etiology (in descending order of occurrence):
• Left anterior fascicular block (LAFB).
Axis -45° to -90° (possibly < -30°).
Criteria: qR in aVL, with onset of Q to peak of R 45 msec (R-peak time).
Clinical correlations: seen in hypertensive heart disease, coronary artery disease, or idiopathic conducting system disease.
• Acute MI — inferior (q 30 msec in aVF).
• Posteroseptal accessory pathway (W-P-W [Wolff-Parkinson-White] pattern).
• COPD (uncommon - 10%).
RAD — Etiology
• May occur normally in slender person and in infants.
Abnormal LAD Etiology (in descending order of occurrence):
• R ventricular hypertrophy (RVH) [more muscle Æ more electrical activity so axis moves toward area of hypertrophy]; the MOST COMMON CAUSE of RAD; however, one must first exclude inferior or posterior MI or acute inferior injury causing LPFB in addition to #'s 2 and 3 below.
• Acute MI (no electrical activity in area of necrosis; therefore the axis moves away from MI site.)
Anterior
Anterolateral
Lateral
• Left ventricular free wall accessory pathway (W-P-W pattern)
• L posterior fascicular block
Criteria include: axis > +90° to +150° with qR complex in III with onset of Q to peak of R 45 msec (R-peak time)
ETIOLOGY OF AXIS DEVIATIONS
Left anterior fascicular block (LAFB)
Right ventricular hypertrophy
Left bundle branch block Acute MI:
Hypertensive heart disease
Coronary artery disease
Idiopathic conducting system disease
Acute MI — inferior LV free wall accessory pathway (W-P-W)
Posteroseptal accessory pathway (WPW)
L posterior fascicular block
COPD (uncommon - 10%)
Other conduction defects:
L ventricular hypertrophy
RBBB
Elevated diaphragm: R anterior hemiblock
Pregnancy
Pacing of R ventricle
Abdominal mass
Pulmonary conditions
Ascites
Pulmonary hypertension
Tumor
COPD
Conduction defects: Emphysema/bronchitis
R ventricular (apical) pacing
Pulmonary emboli/infarcts
Systemic hypertension, esp. chronic
Congenital defects
Valvular lesions
Rheumatic heart disease
Pulmonic stenosis
Aortic regurgitation
Mitral regurgitation
Mitral stenosis
Coarctation of the aorta
Tricuspid regurgitation
Hyperkalemia
Pulmonic stenosis
Normal variant in obese and in elderly
Pulmonic regurgitation
FASICULAR BLOCKS (HEMIBLOCKS)
Anterior Hemiblock — a block of the anterior superior division of the left bundle branch.
More common and less serious than posterior hemiblock.
Anterior fascicle of the LBB is long, thin, and has only one blood supply as does the RBB.
Located in the outflow tract of the LV and is, therefore, subjected to mechanical stresses.
Impulse activates the ventricles via the posterior inferior fascicle producing LAD.
Rate, rhythm, and PR interval are normal.
QRS complex — normal. Lengthens by only 0.02 sec.
Distinguishing features — LAD of > -45°; increased QRS voltage in the limb leads; a terminal R wave in aVR and aVL; R wave in aVR is later than the R wave in aVL; q wave in I and aVL, r wave in II, III, and aVF.
Causes — aortic valve calcification, cardiomyopathy, ischemic heart disease, acute MI, cardiac catheterization, hyperkalemia, otherwise normal hearts.
Prognosis — depends on underlying cause.
Treatment — usually none. A pacemaker may be indicated if LAFB develops after an acute (anteroseptal) MI.
Posterior Hemiblock — a block of the posterior inferior division of the LBB.
Implies compromise of the right and left coronary arteries and damage to a broad inferior conduction system in the LV.
Impulse gets into the ventricles via the anterior superior fascicle producing a RAD.
Rate — may be normal, accelerated, or slow.
Rhythm and PR interval — normal.
QRS complex — normal. Lengthens by only 0.02 sec.
Distinguishing features — RAD of > + 120°; increased QRS voltage in the limb leads; q wave in II, III, and aVF; r wave in I and aVL.
Causes — aortic valve calcification, cardiomyopathy, ischemic heart disease, acute MI, cardiac catheterization, hyperkalemia.
Notify M. D. immediately it posterior hemiblock develop in the setting of acute anteroseptal MI in which case it is usually associated with RBBB (possibly intermittent) and a poor prognosis.
Complete subnodal AV block develops in approximately 90% of cases.
Treatment — a pacemaker is usually indicated if LPFB develops after an acute anteroseptal MI.
Trifasicular Block — complete or incomplete pathologic conduction impairment in the RBB and both divisions of the LBB.
Implies compromise of the left anterior descending branch (LAD) of the left coronary artery (LCA)and the right posterior descending artery (PDA).
If all three fascicles are simultaneously blocked a complete AV block with a ventricular escape rhythm will result.
Rate — < 40 bpm.
QRS complex — broad.
Incomplete trifasicular blocks may manifest as:
RBBB plus left anterior hemiblock plus 1° or 2° AV block.
RBBB plus left posterior hemiblock plus 1° or 2° AV block.
LBBB plus 1° or 2° AV block.
Various combinations of the above.
PART II: 12-LEAD ECG INTERPRETATION
To ensure consistency, develop a systematic method of assessing 12-lead ECGs and rhythm strips.
• Read name, date, and time on ECG.
Make sure you have the correct ECG.
Use the computer interpretation as a learning tool rather than a substitute for thinking.
• Get old ECG for comparison.
Are those Q waves, if present, new? Is it LVH with stain or lateral ischemia? A prior ECG is needed to tell with certainty.
Temporal change is more significant than constant, isolated findings.
Comparison of serial changes is necessary for proper ECG interpretation.
• Is the ECG recorded at full-amplitude?
Is the calibration mark a full 10 mm in height?
• Ventricular Rate — slow, normal, or fast?
An ECG record is 10 seconds long; therefore if there are 17 or more complexes across the page the rate is fast and if there are 6 or less the rate is slow.
Know the 300, 150, 100, 75, 60 rule:
If the QRS complexes (R-R intervals) are 1 large box (thick line) apart the ventricular rate is 300.
2 large boxes = 150. 5 large boxes = 60. 8 large boxes = 37.
3 large boxes = 100. 6 large boxes = 50. 9 large boxes = 33.
4 large boxes = 75. 7 large boxes = 43. 10 large boxes = 30.
As the marks on the upper or lower border of the ECG or monitor paper fall every 3 sec, with regular rhythms the complexes occurring in a six second interval can be counted and multiplied by 10.
• QRS Duration (of dominant QRS complex) — is QRS narrow or wide?
• Best leads to look at = I and V1. Should be less than 3 small boxes wide.
Narrow QRS means the impulse originated from a supraventricular focus (sinus, atrial, AV nodal, or AV reciprocating).
Causes of wide QRS:
• Rhythm supraventricular in origin with a bundle branch block (BBB).
• Rhythm supraventricular in origin with aberrant conduction.
• Rhythm supraventricular in origin with pre-excitation (in patients with an accessory AV pathway, termed Wolff-Parkinson-White or W-P-W syndrome).
• Ventricular in origin (the wider the complex, the more likely rhythm is to be ventricular in origin).
If QRS is wide (_120 msec or 0.12 sec or 3 small boxes) see the criteria for diagnosis of bundle branch blocks below.
Bundle Branch Blocks (BBB)
• If QRS duration 120 msec, but typical waveforms of either RBBB or LBBB are not present, diagnosis is intraventricular conduction delay or IVCD.
• Incomplete BBB = waveform typical of RBBB or LBBB but QRS duration is < 120 msec.
Incomplete LBBB — septal Q wave normally present in leads I and V6 is absent.
• Right and left bundle branch blocks cannot be diagnosed from lead II. Much of the wide QRS complex during BBB is isoelectric in lead II, often producing a narrow, normal-looking complex.
Right Bundle Branch Block — characteristic triphasic QRS morphology; best observed from a right precordial lead (MCL1 or V6) because the exploring electrode is located near the RV free wall. Consequently, delayed RV activation which occurs in the right bundle branch produces a primarily positive, wide QRS complex with a large R' in these leads.
ECG Characteristics in RBBB:
• Wide QRS complex (> 0.11 sec.); often 0.12-0.14.
• Triphasic rsR' or rR' in MCL1/V1; triphasic qRS in MCL6/V6.
• S-T segment and T wave slope away from major deflection (i.e., negative in MCL1/V1 and positive in MCL6/V6).
• If the QRS complex has the typical RBBB contour, but measures 0.09-0.11 sec., the diagnosis of incomplete RBBB is made. (We don't know what else to call it and are not sure exactly what is happening in heart.)
Left Bundle Branch Block — characteristic monophasic QRS morphology can be observed in a right or left precordial lead; delayed LV activation which occurs in the LBB produces a negative, wide QRS complex in the right precordial leads (MCL1 or V1) and a positive, wide complex in the left precordial leads (MCL6, V6, or lead I).
The left bundle branch splits into two divisions or fascicles. Blocked conduction in a fascicle (a partial block in the left bundle branch or hemiblock), however, alters the electrical axis in the frontal plane rather than widening the QRS complex. Fascicular blocks are discussed further in the sections on axis deviation. (See pages 14 and 29-31.)
• QRS Rhythmicity (R-R Intervals) — regular? or irregular?
"Irregular" is defined as any change in R-R intervals.
Irregularly irregular suggests atrial fibrillation.
Regularly irregular suggests a bigeminal or trigeminal rhythm or Wenckebach cycles.
• Is the rhythm a sinus rhythm (does it originate in the SA node)?
_ Can you see upright P waves in I, II, and aVF? If so, the rhythm is sinus in origin.
A "rhythm" = 3 or more of anything in a row.
Rate of normal sinus rhythm = 60-100 bpm.
Sinus bradycardia = rate < 60.
Sinus tachycardia = rate > 100.
Sinus arrhythmia = P-P interval varies > 10%. (See page 32 for discussion of sinus arrhythmia and other arrhythmias originating in the SA node.)
Normal Sinus Rhythm (NSR):
• SA node is the pacemaker .
• P wave is rounded, symmetrical, identical and a QRS follows each P.
• PR interval is 0.12-0.20 sec and constant.
• QRS complex will be positive or negative (depending on lead) and 0.10 sec or less.
• ST segment is slightly concave, sloping into T wave.
• T wave is rounded, slightly asymmetrical.
• Rate = 60-100 bpm.
Rhythm not of diagnostic significance unless the rate is inappropriate for the clinical setting.
Sinus rhythm is physiologic in that it tracks the body's requirements.
Sinus Tachycardia:
Due to increased automaticity of the SA node.
Rate is 100-180 beats per minute (bpm). Differs from NSR only in that the rate is >100 bpm.
(Some books say > 90 bpm = tachycardia.)
Rhythm regular.
PR interval normal.
One QRS for each P.
Onset and termination of the rhythm is gradual and regular, but may vary from minute to minute.
Not paroxysmal; it doesn't start and stop abruptly except for a rare type called sinus nodal reentrant tachycardia.
Almost always a secondary arrhythmia so the underlying cause should be determined and treated if necessary.
Usually harmless except in patients with heart disease — increased oxygen demand causes symptoms.
Often a poor prognostic sign in patients with heart disease.
Causes of sinus tachycardia in normal situations — exercise, emotional stress, stimulants.
Abnormal, non-cardiac causes of sinus tachycardia — fever, hemorrhage, infection, hypoglycemia,
anxiety, pain, thyrotoxicosis, shock, hypoxemia, hypovolemia.
Causes of sinus tachycardia in cardiac patients — any of the above; poor LV function (cardiogenic shock, CHF, pulmonary edema); sympathomimetic drugs (Isuprel, dopamine, dobutamine, epinephrine); vagolytic drugs (atropine); vasodilators (nitroglycerine), especially if the patient is volume-depleted.
Management of sinus tachycardia includes — none; treating the underlying cause, sedation, and possibly digitalis (if the patient has CHF).
Sinus Bradycardia:
Due to depressed SA node automaticity.
Rate < 50-60 bpm. Differs from NSR only in that the rate is below 60 bpm.
Rhythm is regular but may vary minute to minute.
PR interval is normal.
One QRS for each P (1:1 ratio).
Decreased HR may decrease cardiac output (CO) and cause ischemia.
Bradycardia is usually harmless unless it is associated with a low CO that is followed by sensorium changes, diaphoresis, skin color and temperature changes, chest pain, or dysrhythmias.
Causes of sinus bradycardia in normal situations — athletic heart, vasovagal reactions (Valsalva maneuver results in first bradycardia, then tachycardia), sleep.
Non-cardiac causes of sinus bradycardia — ocular pressure (glaucoma and drugs to treat glaucoma which have b-blockers in them like Timoptic which contains timolol); increased intracranial pressure; obstructive jaundice (bile salts effect on SA node); vagal stimulation from nausea and vomiting; hypothermia; and hyperkalemia.
Causes of sinus bradycardia in cardiac patients — any of the above; b-blockers; vagal stimulation from carotid sinus massage; digitalis; morphine; some Ca++-channel blockers such as verapamil and diltiazem; SA node ischemia (inferior or posterior MI).
Acute sinus bradycardia may be extremely dangerous in a patient with an acute MI or poor LV function because stroke volume (SV) cannot be increased to maintain cardiac output (CO = HR x SV).
Other more malignant arrhythmias may surface.
Treat only if symptomatic (syncope, decreased BP, chest pain, or SOB); don't treat for "dizziness" alone.
Treatment should be prompt — atropine 0.5 mg IV push; put head of bed flat or Trendelenburg to increase blood to SA node and increase BP.
• Is there one P wave for every QRS complex (a 1:1 ratio)?
Lack of a 1:1 ratio implies A-V dissociation, either complete or incomplete (presence of capture or fusion complexes). A-V dissociation refers to a group of three categories of rhythms in which the atrial and ventricular rhythms are unrelated to each other. Four major causes:
• Slowing of the primary pacemaker (e.g., sinus block [page 33] with junctional escape rhythm).
Speeding of a subsidiary pacemaker (e.g., ventricular [page 53] or junctional tachycardia [page 49]).
• Third degree A-V block. (See page 46.)
• Combinations of the first two above (e.g., some sinus slowing with accelerated junctional rhythm or junctional tachycardia.)
• What is the PR interval and is it constant?
_ Use Lead II to measure the PR interval.
If it is less than 1 large box it is not prolonged. (Normal range = 0.12-0.20 sec.)
PR > 0.20 sec with 1:1 A-V ratio = first degree (1°) A-V block.
First Degree Block — This refers to an excessively long PR interval only.
Not really a block; conduction is just delayed at the AV junctional area. Every impulse eventually reaches ventricle.
Whether the rate and rhythm are regular depends upon the underlying rhythm.
P is upright, uniform and has a 1:1 ratio with the QRS.
PR interval is greater than 0.20, but constant.
May result from disease in the AV node, high vagal tone, or medication that increase conduction through the AV node. Seen with digitalis, quinidine, and procainamide toxicity; hyperthyroidism, anterior MIs, cardiac surgery, coronary artery disease, and myocarditis.
Usually no treatment is necessary, although the medications may be discontinued if they are causing the problem. The patient should be observed for 2nd or 3rd degree block.
All P waves are conducted through the AV node to the ventricle.
By itself, it is a benign condition.
Short PR Intervals
A short PR interval, less than 0.12 seconds, is associated with accessory pathways between the atria and ventricles — the Wolff-Parkinson-White syndrome (see page 42) and Lown-Ganong-Levine syndrome.
A short PR interval may also result from junctional or low atrial ectopic rhythms.
• Is there evidence of atrial enlargement? Look at leads II, V1, and V2.
Thicker muscle mass in atria increase distance traveled by the depolarizing impulse and increase current flow in the areas of hypertrophy.
Criteria for Left Atrial Enlargement (LAE) or P Mitrale = any one of the following:
P wave takes on appearance of an "m" in limb leads in LAE because of difference in depolarization of the two sides of the heart. Look at leads V1 and II.
_ Negative portion of the P wave is wider and/or deeper than normal in V1. Depth (of negative portion of P) in mm x width (of negative portion) = _ 0.04. (Depolarization moves away from lead V1 creating a terminal negative deflection.)
_ The space between the peaks of the P wave is more than 0.04 sec in any lead.
_ The P wave in lead II is taller than 3 mm or wider than 0.12 sec.
_ The P wave is 1.6 or more times wider than the P-R segment.
Often 2° to LV hypertrophy, coronary artery disease, or mitral valve disease.
Criteria for Right Atrial Enlargement (RAE) or P Pulmonale = any one of the 3 criteria below:
_ QRS axis > +90°.
_ R/S ratio _ 1 in V1. (In RVH, but not in RBBB or post MI.)
_ Upright P wave in V1-2 _ 1.5 mm. (V2 is best lead to look at.)
_ Pronounced positive portion of P wave in V1.
_ Tall, peaked P waves in II, III, and aVF.
_ ?? negative P wave in aVL (P wave axis is to the right of +60°.)
Tall, peaked P waves are indicative of possible RAE, but more commonly are due to COPD and/or increased sympathetic tone, not RAE.
See in pulmonic stenosis in children and in tricuspid stenosis and tricuspid regurgitation.
Diseases affecting the left atrium produce P waves which look like P mitrale and diseases affecting the right atrium produce P waves which look like P pulmonale.
• What is the electrical axis of the QRS complexes?
Axis represents the major direction of the total electrical forces of the heart, a summation of all vectors.
The main thing to determine is whether or not is it is normal. This determination is much more important than calculation of the numerical axis.
_ Look at leads I and II.
• If both I and II have upright QRS complexes, the axis is normal.
• If I is upright and II is negative, left axis deviation (LAD), the most common axis deviation, is present.
• If I is negative (and the P wave in I is upright) with a upright QRS in II, right axis deviation (RAD) is present. If both the P wave and the QRS are negative in lead I, the right arm and left arm electrodes are reversed — they were attached in the wrong places.
Other leads that are commonly reversed are V1 with V3 and V6 with V4.
• If both I and II have negative QRS complexes, an extreme axis deviation is present (left upper quadrant).
• If the QRS is equiphasic in both leads, the axis cannot be determined. i.e., an indeterminate axis is present.
• Is the QT interval normal, prolonged, or short?
_ Q-T interval should be roughly less than half the preceding R-R interval.
If a patient develops a wide QRS complex (which is a problem with depolarization) such as a bundle branch block, the QT interval will be increased. Thus, a long QT interval is not thought of as abnormal in patients with a wide QRS complex unless you have subtracted the extra width of the QRS from the QT interval and still found it prolonged.
_ If the rhythm is irregular, measure the QT relative to the rate of the prior R-R interval.
_ Causes of prolonged QT (> 50% of R-R interval) — congenital, hypomagnesemia, hypocalcemia, type IA anti-arrhythmic agents such as quinidine, ischemia, myocarditis, phenothiazines, tricyclics, subarachnoid hemorrhage, torsades de pointes.
_ Causes of short QT (< 50% of R-R interval) — hypercalcemia, digoxin, thyrotoxicosis, hyperkalemia, and hypermagnesemia.
• Is there evidence of ventricular hypertrophy?
Ventricular enlargement alters the QRS and T waves. The thicker muscle mass increases the distance traveled by the wave of depolarization as well as the amount of current that flows from hypertrophied cells (amplitude is therefore increased). LVH causes eightfold increase in mortality.
_ Especially important to look for evidence of left ventricular hypertrophy (LVH) in preoperative screening ECG as there is increased incidence of perioperative cardiac events.
Criteria for Left Ventricular Hypertrophy (LVH) in Adults:
Do not diagnose LVH in the presence of W-P-W pattern or LBBB. LVH is assumed to be present with LBBB.
The most important ECG feature is enormously tall QRS complexes in leads situated over the left ventricle — I, aVL, V4, V5, and V6.
_ Height of R wave in aVL > 9 mm (females) or > 11 (males); OR
_ Height of R in aVL + S in V3 > 20 mm (females), or > 25 mm (males); OR
_ Height of R in aVL + S in V3 times the QRS duration (msec) >1847 (females) or > 2530 (males); OR
_ S in V1 + R V5 or V6 > 35 mm (age > 35); OR
_ R wave in lead I plus S wave in lead III > 25 mm.
_ Left atrial enlargement and ST segment "strain" pattern in a patient not taking digitalis.
LVH may show repolarization abnormalities with evidence of "strain" — the ST and T wave are directed opposite the dominant QRS waveform.
LVH is seen with systemic hypertension, aortic stenosis, aortic regurgitation, and coarctation of the aorta. Left atrial hypertrophy often occurs concomitant with LVH.
The QRS voltage is decreased, there is ST depression and T inversion.
In leads I, V5, V6, the T wave is inverted and the ST is depressed.
There may be a LAD. LVH is the most common cause of left anterior fascicular block (LAFB).
Conduction delay or altered pathways of conduction in ventricles result in increased QRS interval (the total duration of ventricular depolarization) and ventricular activation time (interval from the beginning of QRS to the peak of the R wave). Injury and fibrotic changes in the involved myocardial cells depress the ST segment.
Ischemia occurs first, probably due to the increased oxygen demand in the hypertrophied cells, followed by injury and fibrotic changes as the disease progresses. The altered duration and pathways of repolarization produce T wave inversion in the leads with R waves of the greatest amplitude.
Axis shift, which may accompany enlargement, alters direction and amplitude of QRS complex.
Left Ventricular Dilation — see smaller QRS in limb leads and taller QRS in precordial leads (leads closer to heart demonstrate the increased size).
Criteria for Right Ventricular Hypertrophy (RVH):
_ Right axis deviation >90°.
_ An R/S ratio _ 1 in lead V1 (in the absence of posterior MI or RBBB), OR
_ An R wave > 7 mm tall in V1 (not R' of RBBB), OR
_ An rsR' complex in V1, with a QRS duration of < 0.12 sec (incomplete RBBB), OR
RVH may show repolarization abnormalities in leads V1-3 and III.
_ An S wave > 7 mm deep in leads V5 or V6; OR
_ "Incomplete RBBB" pattern in V1 (rSR' < 0.12 sec.)
_ RBBB with either RAD (first 0.06 sec of the QRS; may be +90° or more). Consider RVH in RBBB if the R/S ratio in lead I is less than in II.
RVH produces a false positive sign for left posterior fascicular block (LPFB). LPFB give right axis deviation; RAD is most commonly due to RVH. Before making the diagnosis of RVH, you must exclude the LPFB.
Main causes of RVH are chronic lung diseases, pulmonary hypertension, tricuspid regurgitation, and congenital lesions such as tetralogy of Fallot, pulmonic stenosis, ASD, and VSD.
Other causes of tall R waves in V1 are: W-P-W Syndrome (type A), RBBB, true posterior MI, wrong ECG lead placement — these must not be misdiagnosed as RVH.
Right Ventricular Dilation — see poor R wave progression as dilated RV pushes LV posteriorly resulting in loss of anterior forces.
Ventricular Strain
Strain is often associated with ventricular hypertrophy as the ventricle is straining against some kind of resistance (e.g., increased vascular or valvular resistance) and becomes hypertrophied in an attempt to compensate.
Characterized by moderate depression of the ST segment; generally curves upward or humps gradually in the middle of the segment.
• Is there low QRS voltage?
_ Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial leads.
_ Chronic causes — pulmonary disease, hypothyroidism, obesity, cardiomyopathy.
_ Acute causes — pleural and/or pericardial effusions
• Are prominent U waves evident?
_ Usually suggests digitalis or hypokalemia. Also seen in bradycardias or with antiarrhythmic drugs.
• Are there signs of myocardial injury, ischemia, or infarction?
Right chest (or anterior) leads — V1, V2; also aVR.
Septal leads — V1 to V3 — located over interventricular septum.
Left chest (or lateral) leads — V5, V6; also I and aVL.
V1 and V2 mirror changes occurring from the posterior side of the heart.