Note: these are transcriptions of a search on ekg on MDCHALLENGER

They are for study purposes only. The reader is advised to cross check these notes against their own reading and study.

 

Normal QRS duration

    1. infants: 0.005-0.07 seconds
    2. children: 0.06-0.09 seconds
    3. adults :0.08-0.10 seconds

 

QTc (corrected QT interval)

    1. less than : 0.45 seconds
    2. calculated as the measured QT interval divided by the square root of the RR interval measured in seconds.

 

QT interval

    1. caused by Ventricular polarization
    2. measured from beginning of ventricular depolarization to the completion of repolarization.
    3. from the beginning of the QRS to the terminus of the T wave.

 

Pericardial effusion

    1. low voltage EKG
    2. Electrical Alternans

 

Acute Pericarditis

    1. ST segment elevations which are diffuse
    2. T wave inversions which are diffuse
    3. T waves invert after ST segments return to baseline
    4. pr interval baseline is often depressed.

 

Constrictive Pericarditis

    1. low voltage QRS
    2. T wave flattening or inversion

 

Early Repolarization Variant

    1. in leads V5, V6, and 1, the ratio of the height of the initial ST segment to the height of the T wave peak is less than 0.25

 

Intracranial lesions

    1. QT prolongations
    2. T wave inversions
    3. ST elevation or depressions
    4. Sinus bradycardia due to Cushing's Reflex
    5. arrhythmias

 

Pulmonary embolism

    1. non-specific ST segment changes
    2. new right heart strain pattern due to pulmonary hypertension
    3. ischemic changes on EKG suggestive of multiple areas of infarction.

      4.  

    4. most often EKG is normal however
    5. S1, QIII, TIII
    6. part of differential of syncope, shock, hypoperfusion

 

Primary Adrenal Insufficiency

    1. low voltage EKG
    2. prolonged QT, PR, or QRS interval
    3. St depressions
    4. Changes of hyperkalemia

 

Hypothyroidism

    1. low voltage EKG

 

Myxedema coma

    1. low voltage EKG
    2. flattened or inverted T waves
    3. PR interval prolongation

 

High Altitude Pulmonary Edema

    1. EKG may show ischemic changes
    2. right heart strain

 

Hyporthermia

    1. Sinus Bradycardia
    2. Osborn J waves ( a short broad positive wave appended to the S wave of the qRS especially in lead II
    3. slowed conduction with prolonged PR and QT interval
    4. atrial fibrillation or atrial flutter
    5. AV blocks or nodal rhythm
    6. PVC's, Ventricular fibrillation or asystole
    7. "never" V.Tach

 

Esophageal colicky pain

    1. may show EKG changes (diagnosis of exclusion of more emergent causes)

 

Hypercalcemia (eg malignancy)

    1. shortened QT interval
    2. increased PR interval
    3. diminished T waves
    4. depressed ST segment
    5. normal QRS duration
    6. widened T wave

 

Anaphylactic shock

    1. Conduction blocks
    2. ST changes
    3. arrhythmias
    4. premature ventricular contractions
    5. ventricular tachycardia
    6. ventricular fibrillation

 

non coronary ischemia causes of chest pain that can cause EKG changes (usually cause ST depression or ST segment elevation or depression and/or inverted T waves):

    1. Pericarditis
    2. esophageal spasm
    3. cerebrovascular accident
    4. hyperventilation
    5. pulmonary embolism
    6. aortic dissection

 

Variant (Prinzmetal's Angina)

    1. transient ST elevation

 

EKG changes of ischemia heart disease (angina or infarction)

    1. new q waves
    2. ST depressions
    3. ST elevations
    4. hyperacute T waves
    5. inverted T waves

Ichemic cardiac causes of ST segment depressions:

    1. angina pectoris
    2. subendocardial MI

 

Ischemic cardiac causes of ST segment elevations:

    1. Transmural infarction

 

Paroxysmal Atrial tachycardia

1. Atrial Rate = 160-350

 

 

Childhood aortic stenosis

    1. Left Ventricular Hypertrophy (LVH)

 

Cyclic Antidepressant Overdose

    1. ST- T changes
    2. QT and QRS prolongation
    3. bundle branch blocks and AV blocks
    4. ventricular arrhythmias and electromechanical dissociation (EMD-PEA)
    5. "rightward axis deviation of the terminal 40 millisecons (T40ms) of the QRS complex of 120 to 270 degrees with a negative T40ms in Lead I and a positive T40ms in leac aVr has a sensitivity of 83% and a specificity of 63% for TCA and CAD (cyclic antidepressant overdose)

 

Organophosphate/Carbamate pesticide poisoning

    1. Sinus tach
    2. Sinus brad
    3. conduction blocks or asystole
    4. idioventricular rhythm
    5. premature ventricular contraction
    6. ventricular tachycardia
    7. torsades de points
    8. ventricular fibrillation
    9. ST-T changes
    10. conduction delays
    11. prolonged QT interval

 

Phenothiazines

    1. quinidine like membrane stabilizing effects
    2. prolonged PR and QT intervals
    3. ST-T changes

 

Dig toxicity

    1. anorexia, nausea and vomiting
    2. changes in color perception
    3. mental status changes (rare)
    4. virtually any arrhythmia and all degrees of heart block
    5. scooping of st segment, shortening of QT interval
    6. or slow regular ventricular response with atrial fib
    7. PVC's, Ventricular bigeminy,
    8. bidirectional V.Tach, the QRS's alternate in direction from beat to beat (Goldberger)
    9. V Tach, V Fib
    10. AV Junctional (Nodal) Rhythms are frequently seen
    11. Sinus bradycardia, SA block
    12. PAT with block
    13. AV block and AV dissociation
    14. First degree, Second degree and complete heart block

 

Lithium Overdose (at levels above 4 mEq/L)

    1. T wave changes
    2. AV blocks
    3. arrythmias

 

Premature Ventricular Contractions (PVC's):

    1. T waves and ST segment elevations are directed opposite the QRS axis.

 

Characteristics of PVC's thought to be associated with increase risk of ventricular tachycardia or fibrillation:

    1. increased frequency of VPC's
    2. close coupling or R on T phenomenon
    3. multifocal
    4. couplets or triplets

 

Idioventricular rhythm

    1. QRS duration greater thant 0.16 seconds
    2. rate less than 40

 

Accelerated Idioventricular rhythm

    1. Rate is greater than 40

 

atrial flutter

    1. atrial rate of 250-350 in adults
    2. 500 in children
    3. seen best in inferior leads

Paroxysmal Supraventricular Tachycardia (W-P-W syndrome)

    1. in most cases there is antegrade conduction down the AV node with retrograde rentry up the bypass tract
    2. in these case there are normal QRS complexes without delta waves.

 

PSVT with antegrade conduction down the bypass tract and retrograde AV nodal reentry

    1. less common
    2. PSVT with QRS having delta waves may occur
    3. atrial fib and flutter with rates of 300 or greater in adults
    4. different treatment strategies apply to these cases of PSVT

 

Definitions in WPW Syndrome:

    1. Delta waves are initial QRS distortions due to antegrade conduction down the bypass tract during normal sinus rhythm and in certain cases of PSVT in WPW syndrome
    2. Kent bundles: myocardial fibers which bridge the atria to the ventricles
      1. produce complexes with short pr intervals and delta waves in sinus rhythm.
    1. Mahaim Bundles: muscle bundles arising from the AV node and inserting into the ventricular septum

      2. a. produce complexes with normal pr intervals and QRS's with delta waves.

    2. James Fibers: accessory pathways which directly connect the atrial conduction system to the His Bundle bypassing the AV node
      1. produce complexes with decreased pr interval and NORMAL QRS during sinus rhythm
      2. Lown-Ganong-Levine (LGL) Syndrome: Reentrant SVT with James Fibers.

 

Ventricular Tachycardia

    1. widened QRS complexes
    2. rate usually 140 to 200 and regular
    3. rate in children 120-360

 

 

 

Torsades de Pointes

    1. polymorphic v. tach
    2. atypical v.tach
    3. long QT syndrome
    4. sinusoidal oscillation of QRS height

 

Action potential - phase 0

    1. corresponds to QRS (ventricular depolarization)
    2. rapid upstroke of action potential
    3. caused by
      1. rapid influx of sodium (Na+) and some calcium (Ca++)
      2. there is a slow Ca++ influx in all cardiac cells
      3. fast Na+ influx occurs in all except sinoatrial and atrioventricular node cells.
      4. the fast sodium influx is limited by increase in intracellular sodium concentration.
    1. begins when phase 4 reaches threshold

 

Action potential - phase 1

    1. seen as a descent of the sharp peak of the leading edge of the action potential in those tissues with rapid Na+ influx. (SA and AV node cells)
    2. occurs when fast sodium influx of phase 0 ceases.
    3. possibly due to chloride influx causing a slight amount of repolarization.
    4. calcium influx continues during phase 1 of action potential

 

Action potential - phase 2

    1. the plateau of the action potential
    2. maintained by calcium influx (Ca++) through slow Ca++ channels.
    3. reflected in action potential duration

 

 

Action potential - phase 3

    1. responsible for T wave and ventricular membrane repolarization.
    2. Potassium (K+) efflux restores the resting potential (repolarizes the membrane)

 

Effect of Hypocalcemia on the action potential

    1. increases the action potential duration
    2. causes prolongation of QT interval

 

Ischemic changes in the action potential:

    1. less negative intracellular resting potential (greater absolute transmembrane potential
    2. a slower rate of rise of the action potential
    3. a shorter plateau of the action potential
    4. a shorter action potential duration
    5. i.e. with actual infarction the action potential duration becomes prolonged and then finally disappears.

 

Causes of Right Axis Deviation:

    1. Left Posterior Inferior Fascicular block
    2. massive pulmonary embolism with right ventricular strain
    3. cor pulmonale or other causes of right ventricular hypertrophy
    4. lateral MI

 

Causes of Left Axis Deviation (greater than negative 30 degress QRS axis)

    1. Left Anterior Superior Fascicular Block
    2. Hyperkalemia
    3. inferior myocardial infarction
    4. ventricular ectopy or excitation
    5. unusual body habitus

 

Left Bundle Branch Block

    1. QRS duration greater that 0.12 seconds
    2. loss of initial q waves in leads I, V5, V6
    3. broad R waves in leads I, aVL, V5, V6
    4. displacement of the St segments and T waves in the direction opposite the major QRS deflection

 

Right Bundle Branch Block

    1. initial 0.04 seconds of the QRS in unaffected (should appear normal)
    2. QRS duration greater than 0.12 seconds
    3. RSR' (RSR prime) in V1
    4. wide terminal S waves in the lateral leads (1, V5, V6)

 

 

 

unifascicular blocks

    1. Right Bundle Branch Block
    2. Left posterior inferior fascicular block

 

Bifascicular blocks

    1. Left Bundle Branch Block:
      1. Left Posterior Inferior Fascicular Block (LPIFB) plus Left Anterior Superior Fascicular Block
    1. RBBB plus LPIFB

 

EKG change of Left Anterior Superior Fascicular Block

    1. QRS is normal or only mildly prolonged
    2. frontal QRS axis is left of negative 45 degress
    3. larger R wave in lead I than in lead II or III
    4. large S waves in inferior leads

 

Left Posterior Inferior Fascicular Hemiblock

    1. occurs in emphyzema, RVH, Acute MI
    2. normal or mildly prolonged QRS duration
    3. Frontal plane QRS axis is positive 80 degrees to positive 140 degrees
    4. small Q waves in inferior leads II III aVf
    5. R in lead III greater than in lead II

 

causes of peaked T Waves

    1. Hyperkalemia (K+ = 7.5)
    2. MI and CVA

 

Hyperkalemia

    1. (7.0-7.5) peaked T Waves
    2. at higher potassium levels
      1. QRS widens
      2. QRST Slurs
      3. Sine Wave at about K+ of 10

 

Hypocalcemia- prolonged QT interval

 

Hypercalcemia- shortened QT interval

 

Hypomagnesemia

    1. increased or prolonged PR interval
    2. ST depressions
    3. T wave inversions
    4. increased or prolonged QT interval
    5. QRS widening

 

Hypokalemia

    1. low voltage
    2. QT prolonged
    3. diminished or inverted T waves
    4. ST segment depression
    5. ST segment elevation
    6. arrhythmias
      1. increase in AV block
      2. increased dig toxicity

 

Traumatic

    1. interventricular septal rupture causes anteroseptal infarct pattern

 

Stepwise EKG interpretation with normals (Goldberger)

    1. Standardization-standardization mark should be 10mm=1mv.
    2. heart rate
    3. rhythm
    4. PR interval (beginning of P wave to beginning of QRS = 0.12-0.20 normally)
    5. P wave size (2.5mm amplitude, less than 3mm wide in all leads
    6. QRS width
    7. QT interval
    8. QRS voltage
    9. Mean QRS electrical axis (normal= minus 30 to positive 100 degrees)
    10. R wave progression in chest leads
    11. Abnormal Q waves in II, III, aVf or I, aVL, V1 to V6)
    12. ST segment
    13. T wave (normally positive in leads with +qrs, V3 to V6 in adults, negative in aVr, and positive in lead II
    14. U wave

 

Bibliography

 

MD Challenger programmed learning aid (Challenger Corporation)

Goldberger- Clinical Electrocardiography A Simplified Approach 3rd Ed

 

 

 

 

 

transcribed by J Ferrara MD