Cognisnap

Smarter Medicine in a Snap

Author: Anil Potharaju

  • Understanding Vectors in Electrocardiography: A Comprehensive Guide to the Heart’s Electrical Axis

    Learn how vectors apply to EKG interpretation, calculate the mean electrical axis using leads I, aVF, and II, and understand the clinical significance of axis deviations. This math isn’t needed for day to day reading of EKGs but if you love math like we do, here goes!

    One crucial aspect of EKG interpretation is understanding vectors and how they represent the direction and magnitude of electrical impulses in the heart. This guide starts from the basics of vectors and builds up to calculating the heart’s mean electrical axis, ensuring you gain a solid understanding of this essential concept.

    What Is a Vector?

    A scalar is a quantity that only has magnitude, or size. Examples of scalars include volume, density, speed, energy, mass, and time.

    e.g., the EKG strip is running at 25mm/ second or John is running at 5mph.

    A vector on the other hand is quantity that has both magnitude and direction. Examples of vectors include velocity, momentum, force, electromagnetic fields, and weight.

    e.g., The speed of the EKG paper is 25 mm per second (defining the magnitude) progressing from left to right on the paper (defining the direction). John is running 5mph North bound is another example.

    A vector is typically represented by an arrow:

    • Length of the Arrow: Indicates the magnitude.
    • Direction of the Arrow: Indicates the direction of the quantity.

    Vectors in the Context of an EKG

    In an EKG, vectors represent the electrical activity of the heart as it depolarizes and repolarizes:

    • Depolarization Vector: Shows the direction and magnitude of electrical impulses as heart muscle cells become electrically active. By convention, a wave of depolarization is considered to be in the direction of the positive electrode.
    • Repolarization Vector: Represents the return of heart muscle cells to their resting electrical state. By convention, a wave of repolarization is considered to be in the opposite direction of the positive electrode.

    The heart’s electrical activity can be visualized as a series of vectors (since the activity simultaneously spreads in multiple directions) that combine to form the mean electrical axis, reflecting the average direction of electrical depolarization during ventricular contraction. To simplify this, let us consider the following example: One wave of depolarization is left bound by 7mV (so -7mV in lead I) and another is right bound by 12mV (so +12mV in lead I). A electrode in the middle of these two forces would simply record 12 + (-7)= 5mV at an axis of 0 degrees (which is along lead I).

    Let us complicate this a lot!

    In the image, notice how lead I has a 7 mm positive deflection and 1 mm negative deflection. So the net amplitude is 6 mm positive deflection.

    Lead II on the other hand is at 60 degrees to lead I and has a 4 mm positive deflection and a 3 mm negative deflection. So the net amplitude is 1 mm positive deflection.

    So we now have two forces: 6 mm at 0 degrees and 1 mm at 60 degrees. So, how do we estimate the direction of depolarization and its amplitude?

    Step 1: Understand the Problem

    • Net QRS amplitude in Lead I (0°): +6 mm (positive amplitude indicates the depolarization wave is directed toward the positive electrode of Lead I).
    • Net QRS amplitude in Lead II (60°): +1 mm (positive amplitude indicates the depolarization wave is directed toward the positive electrode of Lead II).

    The goal is to calculate:

    1. Magnitude of the resultant depolarization vector (total QRS vector amplitude).
    2. Direction (angle) of the resultant depolarization vector relative to Lead I (0°).

    Step 2: Represent the Leads as Vectors

    Each lead measures the projection of the heart’s electrical depolarization vector onto its axis. To find the resultant vector, we must resolve these projections into their x (horizontal) and y (vertical) components and then combine them.

    Lead I (0 degrees)

    • Lead I aligns with the x-axis (horizontal).
    • The x-component of the depolarization vector is entirely determined by the amplitude in Lead I: XLead I=+6 mm.
    • The y-component of the vector in Lead I is zero: YLead I=0 mm.

    Lead II (60 degrees)

    • The amplitude in Lead II is a combination of both x- and y-components of the depolarization vector. Using trigonometry:
    • The x-component is: XLead II=AmplitudeLead II × cos⁡(60∘)=1 mm×0.5= 0.5 mm. How you ask?
      • Note that we know the hypotenuse and need to find out the adjacent side. The angle between the two is 60 degrees.
      • Recollect from math days that cos (short for cosine)= adjacent side/ hypotenuse. Cos 60 is 0.5
      • In this case, cos 60 (since the lead is at a 60 degree angle)= adjacent side (the x component)/ 1mm (the total amplitude on lead 2).
      • The value of Cos 60 is 0.5. So XLeadII/1= 0.5 or XLeadII is 0.5mm
    • The y-component is: YLead II=AmplitudeLead II × cos⁡(30)=1 mm×0.866=0.866 mm. How you ask?
      • Note that we know the hypotenuse and need to find out the adjacent side. The angle between the two is 30 degrees.
      • Cos 30 = 0.866
      • In this case, cos 30 (since the lead is at a 30 degree angle to Y-axis)= adjacent side (the Y component)/ 1mm (the total amplitude on lead 2).
      • The value of Cos 30 is 0.866. So YLeadII/1= 0.866 or YLeadII is 0.866 mm

    Step 3: Combine the Components

    The total x-component of the resultant depolarization vector is the sum of the x-components from Lead I and Lead II:

    Xtotalv=vXLead I + XLead II = 6+0.5 =6.5 mm.

    The total y-component of the resultant depolarization vector is the y-component from Lead II (since Lead I contributes no y-component):

    Ytotal=YLead II=0.866 mm.

    Step 4: Calculate the Resultant Vector’s Magnitude

    Since we have the X and Y axes, we can use the Pythagorean theorem:

    (Hypotenuse)^2= (Side 1^2)+ (Side 2^2)

    Hypotenuse= ((side 1^2)+(side 2^2))^(1/2)= ((6.5^2)+(0.866^2))^(1/2)= 6.56 mm

    Step 5: Calculate the Direction (Angle)

    Finally, we need to estimate the direction of the QRS vector: We can estimate this relatively easily since we already know the opposite side and the adjacent side of the vector.

    If you recollect, cot(θ) = adjacent side/ opposite side. In this case, θ is the angle to the QRS vector to lead I. So the opposite side is amplitude along the Y-axis and the adjacent side is the amplitude along the X axis.

    So, cot(θ)= 6.5/0.866=7.506

    So θ= about 7.6 degrees.

    Combining steps 4 and 5, we now know that the axis of the EKG is about 7.6 degrees and the amplitude is about 6.56 mm. Since 1mm is 0.1 mV, the voltage is 0.656 mV.

    If you are wondering where you get the numbers for cos, cot, etc. just google them!

    Finally, if we were to use an augmented limb lead in the calculation, the voltage will need to be adjusted since the augmented output is typically boosted by 50%. So, if we notice a 3mm net amplitude on aVF, then the actual amplitude is 3/(1+50%)= 2 mm along the Y axis and 0 along the X-axis.

    The good news is that if you’ve stuck around thus far, you now understand exactly what the axis means. The great news is that you rarely if ever need measurements this precise! As we go on, we will review how to intuitively get a good enough estimate for the axes!

  • Exploring Precordial Leads: Capturing the Heart’s Anteroposterior (Horizontal) Plane

    Precordial leads provide a window into the heart’s electrical activity from the Anterior-Posterior perspective. This post delves into how these leads are placed and what regions of the heart they examine.

    What Are Precordial Leads?

    Precordial leads are six chest leads (V1 to V6) placed on the anterior thoracic region. They capture the anteroposterior (front-to-back) flow of electrical impulses, offering a detailed view of the heart’s AP plane.

    Precordial leads on a standard EKG

    On a standard EKG, there are 6 precordial leads. Proper electrode placement is crucial:

    • V1: 4th intercostal space, right of the sternum.
    • V2: 4th intercostal space, left of the sternum.
    • V3: Midway between V2 and V4.
    • V4: 5th intercostal space at the midclavicular line.
    • V5: Horizontally aligned with V4 at the anterior axillary line.
    • V6: Horizontally aligned with V4 and V5 at the midaxillary line.

    Regions Viewed by Precordial Leads

    • V1 and V2: Septal leads, focusing on the heart’s septum.
    • V3 and V4: Anterior leads, viewing the front wall of the heart.
    • V5 and V6: Lateral leads, examining the side wall of the heart.

    Notice how none of these leads look at the right side of the heart (Right ventricle and its free wall): So, what do we do if we are concerned about a right sided pathology?

    Right Sided Leads

    We could simply place the leads in a “mirror image pattern”:

    • V1R: 4th intercostal space, left of the sternum.
    • V2R: 4th intercostal space, right of the sternum.
    • V3R: Midway between V2R and V4R.
    • V4R: 5th intercostal space at the midclavicular line on the right
    • V5R: Horizontally aligned with V4R at the anterior axillary line on the right.
    • V6R: Horizontally aligned with V4R and V5R at the midaxillary line on the right.

    Generally, on a EKG, we replace V3, V4, and V5 with V4R, V5R, and V6R when we need to evaluate the RV- This provides the information we need in most cases.

    How about if we are concerned about the posterior part of the heart?

    Posterior Leads

    On a standard EKG, there are no posterior leads. So, we use the anterior leads to evaluate the posterior wall of the heart! For instance, Q waves in the posterior wall imply that the net depolarization wave is moving away from the posterior wall. That means it is moving toward the anterior wall and so, R waves in V1 or V2 may signify the presence of Q waves posteriorly.

    We could also place leads on the back to better understand the flow of depolarization.

    Lead V7: Left posterior axillary line, in the same horizontal plane as V6.

    Lead V8: Left mid-scapular line (beneath the tip of the left scapula), same horizontal level as V6.

    Lead V9: Left paraspinal region, same horizontal level as V6.

    Finally note that the leads do not capture individual waves of depolarization: Instead they capture the net wave of depolarization. This leads us to the next interesting concept- vectors.

  • Exploring Limb Leads: Capturing the Heart’s Vertical Plane

    The six limb leads help us understand the electrical flow of impulses on the frontal plane. They detect vertical but not anteroposterior ones. These leads are generated by the six chest electrodes, with the EKG machine automatically assigning positive or negative charges to each electrode to form the leads.

    Standard Bipolar Limb Leads

    Among the six limb leads, three are standard- These are bipolar leads- they measure the voltage difference between two electrodes, one of which is positive and the other negative. A wave of depolarization toward a positive electrode would record a positive deflection. Repolarization would have the opposite effect.

    • Lead I is formed by making the left arm positive and the right arm negative (0° orientation).
    • Lead II is formed by making the legs positive and the right arm negative (60° orientation).
    • Lead III is formed by making the legs positive and the left arm negative (120° orientation).

    Augmented Unipolar Limb Leads

    The remaining three limb leads are augmented. Unlike the standard limb leads, these leads are unipolar- they measure the electrical potential at one electrode relative to a calculated central reference point, the central terminal.

    Central Terminal

    The central terminal is an average of the electrical potentials from the three limb electrodes: V central terminal=(RA+LA+LL)/3. This central terminal acts as a neutral reference point, approximating the heart’s electrical center.

    • Lead aVL is created by making the left arm positive and other limbs negative (-30° orientation).
    • Lead aVR is created by making the right arm positive and other limbs negative (-150° orientation).
    • Lead aVF is created by making the legs positive and other limbs negative (90° orientation).

    When using the central terminal as the reference, the voltages recorded by the unipolar limb leads are naturally smaller than those in the bipolar leads.To make these signals clinically useful, they are mathematically augmented (amplified) by approximately 50% in the EKG machine. This enhancement is why they are called augmented leads. If the amplitude of the recorded wave in aVF is 3mm, the actual voltage is only 2mm but to make it easier to see, the output is augmented.

    Limb Leads and the view they provide

    Based on their orientation, each lead provides a different view of the heart on the frontal plane:

    • Leads II, III, and aVF are known as inferior leads: As the direction of the vector of each lead suggests, they “look” at the inferior surface of the heart, composed primarily of the inferior aspect of the left ventricle. The Right Coronary Artery usually supplies this part of the heart.
    • Leads I and aVL are high lateral leads: They look at the high, left lateral side of the heart, primarily composed of the left ventricle.
    • Lead aVR is often overlooked but holds significant clinical importance. It views the heart from the right shoulder, essentially looking at the upper right side of the heart. Typically shows negative deflections because the heart’s overall electrical activity moves away from the right shoulder.

    A special focus on aVR, the most overlooked lead?

    Abnormalities in aVR are frequently overlooked. However, a few critical conditions may be diagnosed by looking at the lead that is frequently not looked at.

    • An ST-segment elevation in aVR with ST-depressions and T-wave inversions in other leads may signify global subendocardial ischemia or significant left main lesion or significant left anterior descending lesion.
    • Upright P-waves suggest severe right atrial abnormality.
    • In pericarditis, we note widespread ST elevation with PR depression, but ST elevation in aVR is typically absent
    • Differentiating Ventricular arrhythmia from Supra ventricular tachycardia with aberrant conduction: The Vereckei algorithm is a stepwise approach using lead aVR to differentiate VT from SVT with aberrancy. The following suggest VT as against SVT with aberrant conduction:
      1. Initial dominant R-Wave in aVR
      2. Initial q- or r-wave in aVR ≥40 ms
      3. Notching on the initial Downstroke
      4. Vt≥Vi in aVR is suggestive of VT: In SVT with aberrant conduction, the initial conduction happens via the Bundle of His: So, the vertical distance travelled by the QRS complex during the initial 40 msec (Vi) is greater than the terminal vertical distance travelled by the QRS complex during the last 40 msec (Vt) (i.e. Vi > Vt). However in VT, typically, the Bundle of His is the last to be depolarized- So the terminal vertical distance travelled by the QRS in the last 40 msec will be ≥ the total vertical distance travelled by QRS complex in the initial 40 msec.

  • Differentials for Common EKG findings

    EKG FindingDifferentials
    RAD (Right Axis Deviation)Normal Variation: vertical heart with an axis of 90º
    Right Ventricular Hypertrophy (RVH)
    Right heart strain (e.g. PE)
    Left Posterior Fascicular Block
    Pre-excitation Syndrome (Wolff-Parkinson-White)
    Lateral Wall Myocardial Infarction
    LAD (Left Axis Deviation)Normal Variation
    Left ventricular hypertrophy
    Left bundle branch block
    Left anterior fascicular block
    Pre-excitation syndromes (Wolff-Parkinson-White)
    Inferior wall myocardial infarction
    Early R-wave progressionPosterior MI
    RVH
    RBBB
    WPW
    Poor R-wave progressionAnterior MI
    LVH
    RVH
    Cor-pulmonale
    Important differentials for Q wavesMI
    LVH
    RVH
    Cor-pulmonale (Q waves in inferior and anterior leads)
    Cardiomyopathy
    Important ST-T changesNon-specific ST-T changes: < 1 mm ST elevation/ depression; flat T- waves or < 1 mm inversion of T- waves
    MI/ Angina
    Pericarditis
    Early repolarization
    Juvenile T waves
    LVH: ST depression and T- inversion, typically in I, aVL, V5, V6. Can be seen in other leads as well
    RVH: ST depression and T- inversion, typically in V1-3
    Bundle Branch blocks
    Persistent ST- elevation (Usually present for over 3 weeks): Consider ventricular aneurysm
    Peaked T-wavesHyperkalemia
    MI
    Intracranial bleed
    LVH/ RVH
    LBBB
    Deep T-wavesMI
    Intracranial bleed
    LVH/ RVH
    Takusubo cardiomyopathy
    Apical Hypertrophic cardiomyopathy
    Digoxin
    ST elevation in aVR with ST depression in multiple leads: suspect 3 vessel disease or left main disease
    Short QTcHypercalcemia, Hyperkalemia, Congenital
    Long QTcDrugs
    Antiarrhythmics: IA, IC, III
    Antipsychotics, tricyclics
    Methadone
    Antibiotics: Floroquinolones, Macrolides
    Fluconazole
    Most antiemetics
    Hypocalcemia (T- waves usually normal)
    Hypomagnesemia
    Hypokalemia
    Congenital
    Important differentials for U-wavesHypokalemia
    Hypothermia
    Bradyarrhythmias
    Drugs (e.g., digoxin, class IA, and class III anti-arrhythmics)
    Electrical alternansPericardial effusion
    Tachyarrhythmias
    Severe CHF/ CAD/ HTN
    Inverted P-QRS-T in I and aVL and upright in aVRDextrocardia (shows reverse R wave progression)
    LA/RA lead reversal (Shows normal R- progression)
    In WPW pattern, be cautious diagnosing the following on EKGVentricular hypertrophy
    MI and ischemia (since WPW can cause Q-waves and ST-T changes)
    Axis deviation
    Any other conduction abnormalities

  • T- and U- Wave Changes

    T-waves

    ConditionEKG Changes
    Normal Upright in all leads other than aVR and V1 with the amplitude normally being less than 5 mm in limb leads and 10 mm in precordial leads
    Hyperkalemia
    MI
    Tall T-waves
    Kids and young adultsT-wave inversions in V1-3 are normal in kids(Juvenile T-wave pattern).
    May persist into adulthood (Persistent Juvenile T-wave pattern)
    LBBB/ LVH/ Paced rhythm/RBBB/ RVHDiscordant T-waves
    PES1Q3T3 pattern. T-wave inversions in inferior leads and V1-V3.
    Hypertrophic cardiomyopathyDeep inverted T-waves in all precordial leads
    Raised Intracranial pressureDeep inverted T-waves
    Wellens SyndromeBiphasic (positive and then negative deflection- Type A) or inverted (deep symmetric inversion of T-waves- Type B) in V2 and V3. Suggests a LAD lesion.
    HypokalemiaT-waves may be biphasic (negative and then positive) and will progressively disappear while U waves become more pronounced. With U waves, the QU interval becomes prolonged.
    Double peaking T-wavesEither because of U-waves or because of P-waves getting superimposed on T-waves.
    Ischemia/ InfarctionIschemia: T-wave flattening/ inversion.
    In Infarction, “hyper acute T waves” (very tall T-waves) may be seen with reciprocal changes.

    U-waves

    ConditionEKG Changes
    Normalusually a small deflection after the T-waves, in the same direction as the T-wave. Usually seen at lower heart rates.
    Bradycardia
    Hypokalemia/ Hypomagnesemia/ Hypocalcemia
    Hypothermia
    Raised Intracranial Pressure
    LVH
    Drugs like Class Ia, III anti-arrhythmics, Digoxin
    Prominent U-waves (>1 mm or 25% of the height of the T wave.)
    Severe Heart Disease (ischemia/ valvular/ congenital/ cardiomyopathy,etc.)Inverted U-waves.

  • J-point, ST Segment, QT interval Changes

    J-point

    ConditionEKG Changes
    NormalThe point where QRS complex joins the ST segment. Often slightly above the baseline.
    Early Repolarization
    Pericarditis
    Myocardial ischemia/ Infarction
    J-point elevation
    HypothermiaJ-waves/ Osborne waves: long slow positive deflection just before the J-point.

    ST-segment

    ConditionEKG Changes
    Normalflat, isoelectric line between J-point and the start of T-wave
    1. Acute MI
    2. Printzmetal’s angina
    3. Takotsubo cardiomyopathy
    ST- elevation: Classically, STEMI has been associated with a “convex upwards” morphology- but the morphology may be convex/ concave/ oblique! Reciprocal changes are typically seen with MI and Printzmetal’s angina but usually absent with Takotsubo. Changes in Printzmetal’s angina are usually transient.
    PericarditisST-elevation- usually concave upwards. Reciprocal ST depression and PR elevation in leads aVR and V1.
    Early RepolarizationST-elevation- J-point notching is sometimes seen with early repolarization
    LBBB/ Paced rhythm/ LVHST- elevation/ depression: main vector of QRS and ST-T segments are usually discordant.
    Ventricular aneurysmPersistent ST segment elevation after an MI, along with Q-waves.
    Raised Intracranial Pressure (Intracranial bleed)ST-elevation/ depression with deep inverted T-wave inversions
    Brugada syndromeBrugada Sign: ST elevation with a coved morphology and a partial RBBB pattern in V1-V2.
    J-point elevationcan simulate ST elevation
    Sodium Channel Blocking DrugsQRS prolongation, tall R wave in aVR, QTc prolongation. can also cause ST elevation
    LAD lesionDe Winter pattern: Upsloping ST-depression at J point in precordial leads that is >1mm + reciprocal ST elevation in aVR + tall and symmetrical T waves in precordial leads (De Winter T-waves)
    Myocardial IschemiaHorizontal/ downsloping ST depression ≥ 0.5 mm at the J-point in ≥ 2 contiguous leads indicates myocardial ischaemia
    Diffuse ST depression with ST elevation in aVR is seen with LAD lesions as well as 3 vessel disease.
    Tachycardia (sinus/ supraventricular)widespread ST depression
    Digoxin effectDownsloping ST depression creating a “reverse check mark” appearance.
    HypokalemiaDownsloping ST depression with T-wave flattening or inversion and prominent U waves with increased QU interval.
    RVH, RBBBST depression and T-wave inversion in V1-V3.

    QT interval

    ConditionEKG changes
    NormalVaries with heart rate and so corrected QTc is used- A common way to correct it is using Bazett formula (QTC = QT / √ RR). QTC is usually 0.35-0.44 seconds in men and 0.35-0.46 seconds in women.
    Drugs: Class IA, IC, and III antiarrhythmics, Antipsychotics, Antiemetics, Tricyclic antidepressants, azaleas like fluconazole, antibiotics such as floroquinolones and macrocodes, etc.
    Hypokalemia/ Hypomagnesemia/ Hypocalcemia
    Myocardial Ischemia
    Hypothermia
    Raised ICT
    Congenital long QT syndromes
    Long QTC
    Congenital Short QT syndromes
    Digoxin
    Hypercalcemia
    Short QTC
  • QRS Complex Changes

    Q-wave

    ConditionEKG changes
    NormalSmall septal Q waves may be seen in I, AVL, V5, V6. Deep Q waves may be seen in III and aVR
    Pathological Q waves may be seen in MI, cardiomyopathies, lead placement errors, etc.Pathological Q-waves:
    Leads V2 to V3: Any Q wave ≥20 milliseconds or a QS complex.
    Other Leads (I, II, aVL, aVF, V4 to V6): Q wave ≥30 milliseconds and ≥0.1 mV deep in two contiguous leads or a QS complex.
    LBBBno Q-waves in LBBB

    R-wave changes

    ConditionEKG Changes
    Anteroseptal MI
    LVH/ RVH
    Cardiomyopathy
    lead misplacement
    Poor R wave Progression
    Posterior MI
    RBBB
    RVH/ Right heart strain
    Cardiomyopathy
    Dextrocardia
    Lead misplacement
    R>S in V1
    Tricyclic Antidepressant poisoning; other Na channel blocking drugsR in aVR > 3 mm
    Dextrocardia
    Ventricular tachycardia
    LA/ RA lead reversal
    Dominant R-wave in aVR

    QRS Complex

    ConditionEKG changes
    Normal
    Supraventricular origin without ventricular conduction defect
    QRS < 100 ms
    Ventricular origin of QRS including ventricular pacing
    Hyperkalemia
    Hypothermia
    Bundle Branch Block
    Sodium Channel Blockers
    WPW
    QRS > 100 ms
    WPWDelta Wave
    Pericardial effusion
    Infiltrative cardiomyopathies (amyloidosis, sarcoidosis, etc.)
    Lung diseases (COPD)
    Hypothyroidism
    Obesity
    Amplitude < 5mm in all limb leads or Amplitude < 10 mm in all precordial leads (Low voltage)
    Pericardial effusion/ tamponade
    PE
    CHF
    Severe tachycardia
    Ventricular tachycardia
    COPD
    Altering conduction pathways (intermittent change in velocity/ blockage)
    Changing morphology of QRS complexes (Electrical Alternans)
    LVH
    Biventricular Hypertrophy
    high amplitude QRS
    Arrhythmogenic right ventricular dysplasiaEpsilon wave
  • PR-segment and PR-Interval changes

    PR-Segment

    ConditionEKG changes
    Normalflat and isoelectric
    Pericarditisdepressed in all leads except aVR and V1 where it is elevated
    Atrial infarct/ ischemia (Liu’s Major criteria)Elevation of the P-Ta segment of over 0.5 mm in V5 and V6, with reciprocal depression of the same segment in V1 and V2.
    Elevation of the P-Ta segment exceeding 0.5 mm in lead I, with reciprocal depression of the same segment in leads II or III
    P-Ta segment Depression greater than 1.5 mm in the precordial leads and 1.2 mm in leads I, II, and III, particularly in the context of any atrial arrhythmia.

    PR Interval

    ConditionEKG Changes
    NormalPR interval = 0.12 to 0.2 seconds (3-5 small squares)
    First degree AV blockPR interval > 0.2 seconds
    Second Degree Type 1Progressively prolonging PR segment before a dropped QRS
    Preexcitation Syndromes: Wolff-Parkinson-White (WPW) and Lown-Ganong-Levine (LGL)
    Junctional Rhythm
    PR interval < 0.12 seconds
  • P-wave changes

    ConditionEKG Findings
    Normal P-waves– Upright in II, Biphasic in V1, and inverted in aVR with an axis of 0° to 75° and a duration < 120 msec (3 small squares)
    – II: < 2.5 mm tall and < 3 mm wide
    – V1: Positive component is < 1.5 mm tall and Negative component is < 1 mm wide and < 1mm deep.
    Right Atrial Abnormality– II: > 2.5 mm tall
    – V1: > Positive deflection is > 1.5 mm tall
    Left Atrial Abnormality– II: > 3mm wide ± notched p-wave
    – V1: > 1 mm wide or > 1 mm deep negative deflection
    Ectopic beats not from SA node– P-wave morphology changes based on origin.
    – PR interval is usually normal since the AV nodal delay is present.
    Junctional beats, AVNRT– P-waves are inverted
    – P-waves may be immediately before (so short PR), embedded within, or shortly after the QRS.
    – Multifocal Atrial Tachycardia (HR≥100)
    – Wandering Atrial Pacemaker (HR < 100)
    – ≥ 3 morphologies of P-waves
    Atrial Flutter– P-waves are replaced by F-waves, typically with a rate of around 300 beats per minute
    Atrial Fibrillation– No P-waves. Coarse Atrial fibrillation may show waves that are irregular with many different morphologies and a very high rate.
    Tachycardia, PACs, severe first degree heart block– P-waves may be embedded in T-waves and not be immediately obvious.
    Supra-ventricular tachycardia– P-waves may be embedded in QRS and not be immediately obvious.
    – Sinus Arrest, 3rd degree Sinoatrial exit block
    – Atrial Flutter (has F-waves)
    – Atrial Fibrillation
    – Absent P-waves

  • The Lead Reversal Nightmare

    Normal
    Leads
    RA/LARA/LLLA/LLRL/RARL/LARL/LLRA→ LA→ LL→ RARA→ LL→ LA→ RARA/RL + LA/ LLRA/LA + LL/RL
    I-I-IIIII-IIIIIIIII-II0-I
    IIIII-III 0IIII-I-III-IIIIII
    IIIII-I-IIIIII0III-III-IIIIII
    aVRaVLaVFaVRaVR=aVF-IIaVRaVLaVFaVR=aVLaVL
    aVLaVRaVLaVF-IIIaVL=aVFaVLaVFaVRaVR=aVLaVR
    aVFaVFaVRaVLaVR=aVFaVL=aVFaVFaVRaVL-IIIaVF
    V1-V6No Change in leads I, II, III, aVR, aVL, aVF. R/S wave amplitude change unexpectedly in the switched leads.