• LOW VOLTAGE ECG
  1. Definition
  2. Causes of Low Voltage

• INCREASED VOLTAGE ON ECG
  1. Left Ventricular Hypertrophy (LVH)
  2. Right Ventricular Hypertrophy (RVH)

• AXIS DEVIATION
  1. Causes of Axis Deviation
  2. Left Bundle Branch Block (LBBB)
  3. Right Bundle Branch Block (RBBB)
  4. Left Anterior Hemiblock
  5. Left Posterior Hemiblock (posteroinferior)
  6. Bifascicular Bundle Branch Block (Hemiblock associated with RBBB)
  7. Trifascicular Block
  8. Post-MI Bundle Branch Blocks (BBB)

• WAVE ABNORMALITIES
  1. P Wave Abnormalities
  2. Q Wave Abnormalities
  3. R Wave Progression
  4. S-T Segment Shifts
  5. T Wave Abnormalities
  6. U Waves
  7. ECG Changes and Myocardial Infarction (MI)

LOW VOLTAGE ECG

[Figure] "Normal Sinus Rhythm"

A. Definition

1. <15mm (15mV) in precordial leads OR
2. < 5mm (5mV) in limb leads
3. Determinants of Voltage on ECG
   1. Distance to electrodes
   2. Medium between muscle and electrodes (air attenuates less than fluid)

B. Causes of Low Voltage

1. Large Chest AP Diameter
   1. Normal Body Habitus
   2. COPD (Emphysema)
   3. Obesity
   4. Muscular Chest Wall
2. Poor Contractility of Heart
   1. Cardiomyopathy (Hypertension, Infection, Valvular Disease)
   2. Previous Myocardial Infarction with loss of muscle mass
   3. Hypothyroidism - poor muscle contraction (may cause effusion also)
   4. Addison's Disease (Hypoadrenalism)
3. Pericardial Effusion
   1. Infection
   2. Malignancy
   3. Hemorrhage (Tamponade)
   4. Hypothyroidism (must be severe for association with effusion)

1. Criteria on ECG
   1. Left axis deviation (-30°)
   2. High QRS voltage: V1-S + V5-R > 35mm and/or >11mm in I or aVL
   3. Left Atrial Enlargement (LAE) - prominent P wave in II
2. Secondary ST-T changes
   1. Left chest leads: I, aVL, V5-6
   2. S>R V1; R>S V6
   3. Inverted T waves in lateral leads
   4. Often called LV "Strain": looks like ischemia, but is a persistent finding
   5. "Strain" may be related to local ischemia with reperfusion abnormalities
3. Changes in second half of P wave
   1. Left atrial enlargement (abnormality): upright in II; downgoing in V1
   2. May be seen with dilated or hypertrophic LA
4. Causes
   1. Systolic Overload
   2. Hypertrophic Cardiomyopathy
   3. Diastolic Overload
5. Systolic Overload
   1. hypertension
   2. aortic valvular stenosis
   3. hypertrophic cardiomyopathy
   4. coarctation of the aorta
6. Hypertrophic Cardiomyopathy
   1. May see deep q waves inferiorly
   2. Loss of normal R wave progression in V2-V4
   3. LVH criteria in chest and/or limb leads
7. Diastolic Overload (LVH)
   1. aortic valvular regurgitation
   2. mitral regurgitation
   3. ventricular septal defect
   4. congenital abnormalities: eg. patent ductus arteriosus

B. Right Ventricular Hypertrophy (RVH)

1. Early R wave progression more common than right axis deviation (>90°)
2. Increased QRS in right chest leads (V1 and V2)
3. Decreased S in V1 with R>S; in V6 S > R
4. Positive deflections in V1 (usually), III, and possibly aVR.
5. Secondary ST-T changes, T inversion in aVF
6. Causes of RV Hypertrophy
   1. Mitral stenosis (overfill LA leads to increased Pulmonary Pressures)
   2. Pulmonic stenosis
   3. Tricuspid regurgitation
   4. Chronic pulmonary emboli or sleep apnea
   5. Other causes of increased pulmonary vascular resistance
7. Cor Pulmonale
   1. Right heart hypertrophy, then dilation, usually with failure
   2. Due to intrinsic lung disease which leads to increased pulmonary vascular resistance
   3. Pneumothorax and pulmonary embolism cause massive pulmonary vasoconstriction
   4. This leads to acute cor pulmonale, R heart failure, hypotension, death
8. Differential of R wave in V1
   1. Normal variant (or lead placement)
   2. Right Axis Deviation (L. Posterior Hemiblock more common than RVH, RBBB)
   3. Pulmonary Embolism or Hypertension
   4. Wolff Parkinson White Syndrome, usually R wave tall in V2>V1
   5. Posterior Extension of Infarction
   6. Duchenne Muscular Dystrophy

1. Change in muscle mass, Bundle Branch Blocks, Change in position of the heart
2. Left Axis Deviation:
   1. Left Bundle Branch Block (LBBB)
   2. Inferior Myocardial Infarction (MI)
   3. L anterior hemiblock (more negative than -30°)
   4. Wolff-Parkinson-White Syndrome
   5. Left Ventricular Hypertrophy (LVH) - less prominant unless conduction disease present
3. Right Axis Deviation
   1. Left Posterior Hemiblock (Axis > 120°)
   2. Right Bundle Branch Block (RBBB)
   3. RV Strain (pulmonary embolism) -acute setting
   4. Wolff-Parkinson-White Syndrome
   5. Right Ventricular Hypertrophy (COPD) - usually only with conduction delay

B. Left Bundle Branch Block (LBBB)

1. Left axis deviation is usually seen only in the presence of conduction disease
2. Generation of LBBB may be rate dependent
3. ECG Changes
   1. Increased QRS duration >0.12sec
   2. r wave in aVR
   3. Monophasic wide complexes
   4. ST/T abnormalities frequently seen
4. Very difficult to evaluate ischemic changes in patients with LBBB
5. Pacemaker rhythms usually have a LBBB pattern because pacemaker is usually in R heart
6. LBBB is an independent risk factor for early mortality [5,6]

C. Right Bundle Branch Block (RBBB)

1. Right axis deviation is rare (Left Posterior Hemiblock more common)
2. Increased QRS duration >0.12sec
3. Triphasic complexes, delayed ID in V1
4. Found in following conditions
   1. Common in lung disease including COPD, pulmonary hypertension, sleep apnea
   2. Right Ventricular Failure
   3. Pulmonary artery catheter complication
   4. Brugada Syndrome [7]
5. Complete RBBB is an independent risk factor (1.5X) for all-cause mortality [6]

D. Left Anterior Hemiblock

1. More common type of hemiblock; anterosuperior deviation
2. Left axis deviation (-60 )
3. Waves: q in I and aVL; r in II, III, aVF; rS in V6
4. High voltage QRS

E. Left Posterior Hemiblock (posteroinferior)

1. Right axis deviation (+120 )
2. q in II, III, aVF
3. r in I, aVL
4. No RVH (required for diagnosis for ECG)
5. Elevated QRS voltage

F. Bifascicular Bundle Branch Block (Hemiblock associated with RBBB)

1. Chronic intraventricular blocks
2. Lenegre's disease: degeneration of conducting paths
3. Leve's disease: calcification / fibrosis of conducting paths

G. Trifascicular Block

1. ECG diagnosis is only ~50% accurate
2. Combination of Primary Atrioventricular Block, LAH, and RBBB
3. This combination requires electrophysiological evaluation
   1. Confirmation of diagnosis
   2. High rate of progression to complete heart block, so pacemaker usually implanted

H. Post-MI Bundle Branch Blocks (BBB) [4]

1. New BBB (Left or Right) or RBBB and Left anterior hemiblock may accompany acute MI
2. Overall, ~13% of patients develop a new BBB, and prevalence of LBBB ~ RBBB
3. Blocks which occur with inferior MIs typically resolve
4. Blocks which occur with with anterior MIs may require permanent pacemaker
5. Development of a new BBB is associated with increased risk for in-hospital death
6. New LBBB had 34% increased risk, new RBBB had 64% increased risk for death in-hospital

1. Usually due to hypertrophy of one or both atria
2. L Atrial Hypertrophy (often due to mitral stenosis)
   1. P wave > 0.11 sec
   2. Notched upright P waves often in lead II (prolonged duration)
   3. P terminal force (negative) increase in V1
   4. Biphasic P waves in R sided leads
3. R Atrial Hypertrophy
   1. Tall, narrow P waves in II
   2. Prolonged upright ± tall P wave in V1 ± V2

B. Q Wave Abnormalities

1. Must be >0.04 seconds (1 block) for significance
2. Normal ("septal") Q waves
   1. Usually in L sided leads: I, aVL, V5, V6
   2. People with vertically rotated hypertrophic hearts, q's in inferior leads may occur
3. Old myocardial infarction (appears within hours of acute infarction)
4. Deep, narrow inferior lead (II, III, aVF) q waves may indicate significant LVH

C. R Wave Progression

1. Normal R wave Progression
   1. V2 should have small (r) wave
   2. R wave should increase in V1-V4, then smaller in V5-6
   3. V6 should have little or no S wave (except in RBBB)
2. Early R Wave Progression
   1. Abnormally large R waves (with R>S) in V1-V3
   2. Lead Placement
   3. Heart Orientation
   4. R sided domination: RVH, RBBB, WPW, Posterior Myocardial Infarction
3. Poor R Wave Progression
   1. Smaller than normal R waves V1-V3; r in V4
   2. Lead Placement
   3. Heart Orientation
   4. Loss (relative) of Heart Muscle Mass in anterior area: infarction, RVH
4. R Wave in V1
   1. Right Axis Deviation: RVH and RBBB
   2. RV Strain: Pulmonary Embolism, Pulmonary Hypertension
   3. Posterior Extension of Inferior MI
   4. Duchenne's Muscular Dystrophy

D. S-T Segment Shifts [9]

1. Normal Variants
   1. In women and ~10% of men, normal ST segment has no elevation (same as PR segment)
   2. ~90% of men have normal ST elevation primarily in precordial leads (V1-V3)
   3. Normal ST segment variant with elevation has a concave ST segment
   4. Black men have the most prominent ST segment elevation, up to 1-4mm midprecordium
   5. Early repolarization: usually in V2-V3, 1-2mm elevations and has notch at J point
   6. Junctional ST elevation: usually V1-V3; 2-3 mm elevation with smooth takeoff is normal
2. Significant ST Segment Shifts
   1. Required >1mm to be significant
   2. Pathologic changes usually have a sharp takeoff
   3. Normal variants usually have smooth takeoff from (QR)S wave
3. Elevation (above PR segment):
   1. Acute transmural infarction; see V2 lead
   2. Variant (Prinzmetal's, arterial spasm) angina: in affected leads
   3. Pericarditis: ST elevation throughout ECG (may have PR depression)
   4. Acute myocarditis can also cause ST segment elevation throughout)
   5. Pulmonary embolism - usually in both inferior and anteroseptal leads
   6. Aneurism (chronic): failure to resolve after acute transmural MI
   7. LBBB
   8. Hyperkalemia - usually with widened QRS and tall pointed T waves
   9. Hypomagnesemia
   10. Brugada Syndrome - congenital disease due to cardiac sodium channel mutations
   11. Arrhythmogenic right ventricular cardiomyopathy
   12. Acute pancreatitis, esophagitis, cholecystitis, splenic rupture [2]
4. Depression
   1. Shift >1mm below PR segment: posterior infarction; See lead V2
   2. May be caused by pure ischemia
   3. May be due to reciprocal changes

E. T Wave Abnormalities

1. Normal
   1. Caused by repolarization of the apex ahead of rest of heart
   2. Positive in all bipolar limb leads
   3. Negative in aVR
   4. Bipolar T wave is not uncommon in black men [9]
2. Inversion
   1. LBBB (left bundle branch block): lead I has T wave inverted
   2. RBBB: lead III has T wave inverted
   3. Subendocardial infarction
   4. Transmural infarction
3. Ischemia: increased duration of depolarization.
4. Biphasic T wave
   1. Digitalis toxicity
   2. Subendocardial Infarction
5. "Cerebral" T Waves [1]
   1. Cerebral events (usually ischemia, hemorrhage) lead to repolarization abnormalities
   2. Flat or inverted (highly peaked) T waves are most common abnormalities
   3. QTc prolongation or U wave abnormalities may also occur

F. U Waves

1. Occur following T waves, same direction as T waves
2. Unknown etiology
3. Causes
   1. Normal Variant
   2. Hypokalemia
   3. Ischemia will accentuate these waves
   4. Cerebral events may be associated with prominent U waves

G. ECG Changes and Myocardial Infarction (MI) [3,8]

1. Initial ECG is very useful for MI prognosis
2. Most typical ECG changes are associated with increased 30-day mortality (univariate)
3. Absolute ST deviation (depression + elevation) associated with 1.5X increased mortality
4. Increased QRS duration for anterior infarct associated with 1.5X increased mortality
5. ECG prior evidence of infarction had ~2.5X increased mortality risk

References

1. Pine DS and Tierney L. 1996. NEJM. 334(23):1530
2. Reymond J-M and Sztajzel J. 1996. Lancet. 348:1560
3. Halthaway WR, Peterson ED, Wagner GS, et al. 1998. JAMA. 279(5):387
4. Go AS, Barron HV, Rundle AC, et al. 1998. Ann Intern Med. 129(9):690
5. Fahy GJ, Pinski SL, Miller DP, et al. 1996. Am J Cardiol. 77:1185
6. Hesse B, Diaz LA, Snader CE, et al. 2001. Am J Med. 110(4):253
7. Naccarelli GV and Antzelevitch C. 2001. Am J Med. 110(7):573
8. Zimetbaum PJ and Josephson ME. 2003. NEJM. 348(10):933
9. Wang K, Asinger RW, Marriott HJL. 2003. NEJM. 349(22):2128