EKG Interpretation



This page is for the exclusive use of those physicians for whom I perform EKG interpretation.


Please take note of the following disclaimer:

The information contained in this page is of a general nature only and must be interpreted in the context of the specific clinical situation of the individual for whom an EKG has been done.  At no time should clinical decision making be made based on the information contained on this page.

Okay, so now that we have got that out of the way, let's get to the salient points.  Basically what I have done on this web page is listed the (main) differential diagnoses of the most commonly encountered abnormalities that one sees on EKGs performed in day-to-day clinical practice.  I have not listed the diagnostic criteria for these abnormalities nor have I included those EKG abnormalities which are either exotic or esoteric.

 

Click on one of the following hyperlinks to be taken to the relevant section:

 

Sinus Tachycardia:

If mild, this is typically transient and unimportant.  If very rapid and/or sustained then it becomes important to determine the etiology.  Causes include:

  • Excess caffeine

  • Adrenergic stimuli (egs. exercise, stress, etc.)

  • Hyperthyroidism

  • Hypotension

 

Sinus Bradycardia:

If mild, this is typically transient and unimportant.  If very slow and/or sustained then it becomes more important to determine the etiology.

Causes include:

  • Increased vagal tone (egs. being physically fit, vasovagal response [as can be seen with coughing, micturition, defecation, etc.])

  • Hypothyroidism

  • Sick Sinus Syndrome

 

Premature Supraventricular (Atrial, Junctional) Beats:

These are seldom important and are often seen physiologically.

Causes include:

  • Excess caffeine

  • Adrenergic stimuli (egs. exercise, stress, etc.)

  • Alcohol consumption

  • Use of alpha agonists (eg. certain decongestants)

 

Premature Ventricular Beats:

If isolated (ie; not occurring in rapid succession) these are seldom important.  If very frequent or, more importantly, if occurring in runs (especially if sustained and/or symptomatic) then further evaluation is required.

Causes include:

  • Excess caffeine

  • Adrenergic stimuli (egs. exercise, stress, etc.)

  • Alcohol consumption

  • Use of alpha agonists (eg. certain decongestants)

  • Coronary Artery Disease

  • Myocardial Disease (eg. cardiomyopathy)

 

Low Voltages:

Low voltages can be unimportant, but certain pathological causes should be considered.

Causes include:

  • Technical error (ie; the EKG has been inadvertently performed at 1/2 voltage standardization; In my experience this is the most common cause!)

  • A large chest wall relative to cardiac size (egs. COPD, obesity)

  • Pericardial effusion

  • Severe myocardial injury (egs. cardiomyopathy, multiple MI's)

  • Hypothyroidism

  • Hypothermia

  • Hypopituitarism

  • Amyloidosis

 

High Voltages:

High voltages are typically pathologic, but with certain important exceptions.

Causes include:

  • Young age (in which case it is typically a physiologic finding)

  • Athletes (in which case it is typically a physiologic finding)

  • A small chest wall relative to cardiac size (eg. a thin individual)

  • Left Ventricular Hypertrophy

 

Shortened PR Interval:

The most important factors in helping determine if this is pathologic or not is the age of the individual and the presence or absence of symptoms (especially palpitations, pre-syncope or syncope).

Causes include:

  • Young age (in which case it is typically a physiologic finding)

  • Pre-excitation (egs; Wolff-Parkinson-White [in which case a delta wave is typically seen], Lown-Ganong-Levine [in which case a delta wave is not seen])

  • Low atrial pacemaker

  • Junctional rhythm

 

Poor R Wave Progression:

This is often meaningless and may be physiological or due to technical reasons (see below).  It is more likely to be significant if the R wave progression is markedly impaired (egs. QS complexes present in leads V1, V2 and V3 and/or there is a predominantly negative deflection all the way to lead V5).

Causes include:

  • Lead placement error

  • Rotation of the heart

  • Previous anterior wall MI

  • Left BBB

  • Chest wall deformity

  • COPD

  • WPW

  • Pneumothorax

 

Prominent (or Dominant) Right Precordial (ie V1 and/or V2) R Waves

This can be a simple matter of incorrect lead placement, but pathological causes may be responsible.

Causes include:

  • Normal variant

  • Right ventricular hypertrophy

  • Previous posterior MI

  • WPW

  • Right BBB

  • Rotation of the heart

  • Dextrocardia

 

ST Elevation:

In assessing the importance of ST elevation we need to look at the company it keeps (both in terms of correlating symptoms - such as chest pain - and other EKG abnormalities - such as which leads are affected and whether the T waves are abnormal).

Causes include:

  • Acute myocardial ischemia (+/-) acute myocardial infarction

  • Ventricular aneurysm

  • Pericarditis

  • Normal variant (especially in young men or black males)

  • LVH

  • Bundle Branch Block

 

QT Prolongation:

This is typically pathologic and, depending on the circumstances, can lead to life-threatening arrhythmias.

Causes include:

  • Drugs (egs; certain anti-arrhythmics, tri-cyclic antidepressants)

  • Electrolyte/Mineral disturbance (egs; hypokalemia, hypomagnesemia, hypocalcemia)

  • Acute CNS insult (egs; subarachnoid hemmorhage or other CVA, head trauma)

  • Acute myocardial ischemia

 

Peaked T Waves:

These may be physiological in healthy individuals, but can also be seen pathologically.  Peaked T waves are more likely to be pathological if the EKG shows accompanying abnormalities.

Causes include:

  • Acute myocardial ischemia

  • Hyperkalemia

  • Acute CVA

 

U Waves:

These are typically small and insignificant.  If large they are more likely to be meaningful.

Causes include:

  • Physiological (especially if sinus bradycardia is present)

  • Hypokalemia

  • Drugs (eg; certain anti-arrhythmics)

  • CNS disease

  • Left Ventricular Hypertrophy

  • MVP

  • Hyperthyroidism

 

Left Axis Deviation:

If borderline or slight or occurring in isolation, this is usually meaningless.  If more overt or associated with other EKG abnormalities, pathological causes should be considered.

Causes include:

  • Physiological (if slight or borderline)

  • Left Anterior Hemiblock

  • Previous inferior wall MI

  • Left Ventricular Hypertrophy (uncommon)

  • Left Bundle Branch Block (some cases; not all)

  • Atrial Septal Defect

  • WPW

 


Right Axis Deviation:

Except in young individuals, this is usually pathological.

Causes include:

  • Physiological (young individuals)

  • Left Posterior Hemiblock

  • Right Ventricular Overload (eg; pulmonary hypertension)

  • Previous high lateral MI

  • Right Bundle Branch Block

  • WPW

 

Complete Bundle Branch Block:

Rarely, complete right bundle branch block is seen in people with normal hearts.  Otherwise, complete BBB (right or left) is almost always pathological.

Causes include:

  • Coronary artery disease (including acute or previous myocardial infarction)

  • Hypertension

  • Rheumatic heart disease

  • Cardiac contusion

  • Right ventricular hypertrophy

  • Cardiomyopathy

  • Pulmonary embolism

  • Drug-induced

  • Hyperkalemia

 

RSR' Pattern (V1 and/or V2):

This is commonly seen in perfectly healthy young individuals and is mistakenly reported as "incomplete right bundle branch block" whereas it should have been reported as "RSR'" pattern (ie; purely descriptive, not assigning pathological nature to it) or, at most, as "incomplete right bundle branch block pattern" (ie; again, being primarily descriptive).  Only sometimes does this pattern actually represent incomplete right bundle branch block.

Causes include:

  • Physiological (as discussed above)

  • Chest wall deformities

  • (True) incomplete right bundle branch block

  • Right ventricular hypertrophy

  • Acute cor pulmonale (ie; acute right ventricular overload)

  • WPW