Electrocardiogram (EKG)

Normal Cardiac Cycle

CARDIAC CYCLE


Normal Cardiac Conduction

Electrical Correlates of the Normal EKG

  • PR Interval
    • Depolarization of Atrium (P-Wave)
    • Conduction Through AV Node
    • Conduction Through His Bundle
    • Conduction Through Bundle Branches
    • Conduction Through Fascicles
    • Conduction Through Terminal Purkinje Fibers
  • QRS
    • Ventricular Depolarization
  • T-Wave
    • Ventricular Repolarization

CARDIAC CONDUCTION


Technical Aspects of the Electrocardiogram

  • Paper Speed: 25 mm/sec
  • Calibration: 1 mV/cm deflection
  • Time: 1mm = 0.04 sec = 40 msec

Electrical Correlates of the Normal EKG

  • PR Interval
    • Depolarization of Atrium (P-Wave)
    • Conduction Through AV Node
    • Conduction Through His Bundle
    • Conduction Through Bundle Branches
    • Conduction Through Fascicles
    • Conduction Through Terminal Purkinje Fibers
  • QRS
    • Ventricular Depolarization
  • T-Wave
    • Ventricular Repolarization

Waves and Intervals

P-Wave

  • Normal P-Wave Duration: <0.12 sec (120 msec = 3 boxes)
  • Normal P-Wave Amplitude: <3 mm
  • P-Wave is Normally Positive in Leads I/II/III/AVF
  • Measure P-Wave in Leads II/III/AVF

PR Interval

  • Normal PR Interval: 0.12-0.20 sec (120-200 msec = 3-5 small boxes)

  • Normal PR Interval (P-Wave + PR Segment): 0.12-0.20 sec (120-200 msec)

  • PR Interval Shortens with Increased Heart Rate: due (in part) to rate-related shortening of the cardiac action potential

Q-Wave

  • Normally absent, although septal Q’s may be seen in I/II/V5/V6
  • Pathologic Q: 1 box wide or >1/3 of amplitude of entire QRS

QRS

  • Normal duration <0.12 sec (3 small boxes)
  • Measure QRS in II/III/AVF
  • Negative deflection usually in V1/AVR

Q-T Correction for HR

  • HR Upper Limit for Q-T
  • 50 0.47 sec
  • 60 0.43 sec
  • 70 0.41 sec
  • 80 0.39 sec
  • 90 0.37 sec
  • 100 0.35 sec
  • 110 0.33 sec

T-Wave

  • T-Wave is Normally Positive in All Leads Except AVR (and Sometimes V1)

S-T Segment

  • ST Segment is Normally Isoelectric to P-Segment (Between T and P-Waves)
  • Significant S-T Depression
    • All Leads: at least 1 mm
  • Significant S-T Elevation
    • Limb Lead: at least 1 mm
    • Chest Lead: at least 2 mm

Chamber Enlargement

  • RAE
    • P>2.5 mm in II,III,AVF
  • LAE
    • Biphasic P in V1
  • RVE
    • Tall R in V1 (with inv T) + RAD + Deep S in V4-V6
  • LVE
    • R in I + S in III > 25 mm
    • R in V5 or V6 + S in V1 > 35 mm
    • R in AVL >11 mm
    • LAE

Axis

            -90    

    -120            -60     

+180                    0    

    +120            +60     

            +90
  • Normal Axis: -30 to +105
  • LAD: >-30
  • RAD: >+105
  • Indeterminate Axis:

QRS Prolongation

  • Right Bundle Branch Block (RBBB)
  • Left Bundle Branch Block (LBBB)
  • Junctional or Ventricular Focus of Rhythm
  • Paced Rhythm
  • Ventricular Preexcitation Due to Wolf-Parkinson-White Syndrome
  • LV Dysfunction
  • Hyperkalemia (see Hyperkalemia, [[Hyperkalemia]])
  • Drugs
    • First-gen Antihistamines: effect myocyte sodium channel
    • Tricyclic Antidepressant Intoxication (see Tricyclic Antidepressants, [[Tricyclic Antidepressants]])
    • Lidocaine (see Lidocaine, [[Lidocaine]])
    • Flecainide (see Flecainide, [[Flecainide]])
    • Thioridazine Intoxication (see Thioridazine, [[Thioridazine]])

Shortened Q-T Interval

Etiology


U Wave

  • Hypokalemia
  • Hypercalcemia
  • Thyrotoxicosis
  • Digoxin
  • Epinephrine
  • Class 1A and 3 Antiarrhythmics
  • Congenital Long QT Syndrome
  • Intracranial Hemorrhage

Peaked T Waves

  • Hyperkalemia
    • Tall, peaked T waves occur due to hyperkalemia. If the tall T waves are seen throughout the ECG, general hyperkalemia is present. P waves will be small, PR interval short.
  • Hyperacute MI
    • When typical tall, peaked T waves are seen only within a specific set of cardiac leads, it suggests impending infarction. The tall Ts are due to potassium leak through damaged membranes in the area of the infarct

T-Wave Inversion

  • “Cerebral T-Waves”: dramatic T-wave inversions seen in mid-precordial (as well as inferior and lateral leads) in patients with severe CNS events (intracerebral bleed, SAH, large CVA)
    • Caused by massive sympathetic outflow due to cerebral damage
    • In acute cerebral disease, such as intracranial hemorrhage, elongated or bizzare T waves may be seen. These Ts are often biphasic or deeply and sharply inverted. The QT interval is often dramatically lengthened (0.5 to 0.7 seconds).
  • Evolving infarction
    • Inverted T waves are seen during the evolution of myocardial infarction. The T inversion appears in the leads “looking at” the infarcted area. Several hours after an infarct, T waves begin to invert. T wave inversion may persist for months.
  • Chronic pericarditis
    • In chronic pericarditis, T waves show wide-spread inversion, not corresponding to any coronary artery distribution. General inversion of T waves can also be due to an evolving global subendocardial infarct.
  • Conduction block
    • Left bundle branch block can cause ST depression and inverted T waves in leads I, L, and V5-V6. The ST depression is usually not great. The T wave tends to be oriented opposite the QRS in LBBB.
  • Ventricular hypertrophy
    • Left ventricular hypertrophy or strain commonly causes T wave inversion. In “strain” pattern, the ST segment slopes down to an inverted T in the leads “looking at” the affected ventricle
    • Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2. The T wave will be inverted over right heart leads showing evidence of hypertrophy and strain.
  • Acute cerebral disease
  • Other cardiac disease

T-Wave Flattening

  • Ischemia
  • Cardiac scar
  • Evolving infarction
  • Electrolyte abnormality
    • Hypokalemia

S-T Depression

  • Ischemia
    • When ST segment depression is transient, it’s almost always due to acute myocardial ischemia. The ECG signs of ischemia may come and go fairly quickly — over a matter of minutes.
    • ST segment depression is MOST specific for ischemia if the ST segment slopes down from the J point. Horizontal or flat STs are also quite suspicous for ischemia. Upsloping ST depression is only about 60% accurate for diagnosing ischemia.
    • “J point” depression at the beginning of the QRS complex is not significant if the location of measurement (two boxes past the QRS) finds the ST segment has risen back to the baseline.
  • Non Q-Wave MI/NSTEMI
    • ST depression can also be seen in infarction, typically in non Q-wave infarction, often called subendocardial infarction. This type of infarct does not extend through the ventricular wall (non-transmural). Subendocardial infarctions involve small areas of injured tissue, with larger areas of overlying ischemia. These infarctions may show ST segment depression (rather than elevation) because of the larger areas of ischemia.
    • ST depression can also be seen as a “mirror” of what’s happening on the other side of the heart. For example, the inferior leads may show ST depression as a reflection of what’s happening in the upper lateral side of the heart.
  • Hypothermia
    • Hypothermia and severe hypokalemia routinely cause ST segment depression in multiple leads
    • Hypothermia will tend to lengthen all ECG intervals, including the PR and QT, while
  • Hypokalemia
    • hypokalemia will often lengthen the PR while shortening the ST segment slightly.
  • Tachycardia
  • Reciprocal ST elevation
  • Ventricular Hypertrophy
    • Left ventricular hypertrophy or strain commonly causes ST segment depression, often with T wave inversions. These changes are seen in the “lateral” leads — those that record activity over the left ventricle. In LVH, ST and T wave abnormalities are commonly seen in leads I, L, and V4-V6.
    • Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2.
  • Bundle branch block
    • Left bundle branch block produces ST depression and inverted T waves in leads I, L, and V5-V6. In general, the ST will slope away from the direction of the QRS: a large wide R wave will have a down-sloping ST ending in an inverted T, while a deep wide S wave will have an upsloping ST segment ending in an upright T.
  • Digoxin
    • Patients on digitalis often show mild ST depression. This depression is usually less than 1 mm, and produces a “scooped” appearance — the “Salvador Dali mustache” ST. These ST abnormalities are seen in multiple leads
  • Non-Specific S-T Depression
    • ST segment depression is called “nonspecific ST abnormality” rather than “ST segment depression” if the ST segments are less than 1 mm depressed and are accompanied by a normally-oriented T wave.

S-T Elevation

  • Early Repolarization
    • “Early repolarization” is a cause of ST elevation
    • This innocent condition typically occurs in young healthy males
    • The T wave begins early, adding elevation to the ST segment
    • Usually, early repolarization shows elevation of the J point (the junction between the end of the QRS and the ST segment) and a concave upward curve towards the T wave. (“Concave upward” means the hollow portion of the curve is on top.)
    • Early repolarization is usually seen in the anterior precordial leads of the ECG, but can be seen in limb leads to a lesser degree
    • Early repolarization cannot always be differentiated from myocardial infarction. In the chest pain patient, it’s safest to assume ST elevation to be infarction until proven otherwise by reviewing a previous ECG or by obtaining serial ECGs.
    • Infarction
    • In transmural infarction, ST segment elevation will be among the first manifestations. The ST segment elevation will be seen in those leads involved in impending infarction.
    • ST segment elevation decreases as T wave inversion begins. ST segments may remain elevated when ventricular aneurysm develops.
    • ST segment elevation that persists beyond three months following myocardial infarction suggests ventricular aneurysm. ST elevation will be present in about 1/3 of ventricular aneurysms. When the patient with ventricular aneurism presents with acute chest pain, a baseline ECG may help avoid misdiagnosis of impending infarction (and use of non-needed thrombolytic drugs).
  • Pericarditis
    • Pericarditis, an inflammation of the space between the pericardial sack and outer surface of the heart, causes widespread ST segment elevation. Physical damage and irritation of the heart’s surface produces a “current of injury” in virtually all ECG leads
    • Generalized ST segment elevation, unrelated to the distribution of any coronary artery, implies pericarditis. One must be very cautious in diagnosing pericarditis from the ECG. For example, an inferolateral transmural infarction with pre-existing junctional ST elevation in the anterior leads, could produce widespread ST elevation that could be confused with pericarditis.
    • Later in the course of pericarditis, ST segment elevation resolves, without development of Q waves. After days to months, ST elevation is replaced by widespread T wave inversions.
  • Propofol Infusion Syndrome (see Propofol, [[Propofol]])
  • Vasospastic Angina
    • ST segment elevation can be seen in a severe type of ischemia called vasospastic or Prinzmetal’s angina. While exercise angina involves the subendocardium, vasospastic angina causes severe transmural loss of blood flow. ST elevation simply indicates injury, whether due to coronary thrombosis with impending infarction, or coronary spasm (Prinzmetal’s angina). At this point, the injury is reversible.

Conduction Delays

  • Churg-Strauss Syndrome (see [[Churg-Strauss Syndrome]])
  • xxx
  • xxx

References

  • A prolonged QRS duration on surface electrocardiogram is a specific indicator of left ventricular dysfunction. J Am Coll Cardiol, 1998; 32:476-482
  • Relationship between QRS duration and left ventricular mass and volume in patients at high cardiovascular risk. Heart. 2011 Nov;97(21):1766-70. Epub 2011 Aug 11