EKG Fundamental Concepts and Interpretation

EKG Fundamentals and Basic Measurement

• Standard Grid Units: On a standard EKG tracing, speed and time are calculated based on grid boxes.

  • Small Box: Measures $0.04 \, \text{seconds}$.

  • Large Box (5 small boxes): Measures $0.2 \, \text{sec}$.

• Heart Rate Estimation: When the R-R interval is regular, the heart rate can be estimated using the sequence: $300$, $150$, $100$, $75$, $60$, $50 \, \text{bpm}$.

• Normal Sinus Rhythm (NSR) Criteria:

  • P-waves: Present and precede every QRS complex.

  • Polarity: P-waves must be upright in Lead I and II.

  • Regularity: R-R intervals must be constant and evenly spaced.

  • Rate: Normal range is between $60$ and $100 \, \text{bpm}$.

  • QRS Morphology: Typically narrow, measuring less than $3$ small boxes (< 0.12 \, \text{sec}).

QRS Axis Interpretation and Deviations

• Normal Axis: Polarity is positive ($+\text{ve}$) in Lead I and Lead aVF. The numerical range is $0^{\circ}$ to $+90^{\circ}$.

  • Nuance: An axis less negative than $-30^{\circ}$ is still considered technically normal. Ranging from $-1^{\circ}$ to $-29^{\circ}$ is classified as "leftward" but does not meet the threshold for Left Axis Deviation (LAD).

• Method of Perpendiculars (Biphasic Lead):

  • Lead I is Biphasic: The axis is perpendicular to Lead I ($\pm 90^{\circ}$). If aVF is positive, the axis is $+90^{\circ}$; if negative, it is $-90^{\circ}$.

  • Lead aVF is Biphasic: The axis is perpendicular to aVF ($0^{\circ}$ or $\pm 180^{\circ}$). If Lead I is positive, the axis is $0^{\circ}$.

  • Lead II or III is Biphasic: The axis is at $\pm 30^{\circ}$ or $\pm 150^{\circ}$. If Lead III is biphasic and Lead I and aVF are positive, the axis is $+30^{\circ}$.

  • Lead aVR or aVL is Biphasic: The axis is at $\pm 60^{\circ}$ or $\pm 120^{\circ}$. Quadrant confirmation via Lead I and aVF is required.

  • Indeterminate Axis: Occurs when no lead is clearly biphasic or multiple leads appear biphasic.

• Left Axis Deviation (LAD): Associated with Left Ventricular Hypertrophy (LVH), Left Bundle Branch Block (LBBB), Left Anterior Fascicular Block (LAFB), inferior wall MI, Wolff-Parkinson-White (WPW) syndrome, pregnancy, obesity, and Atrial Septal Defect (ASD).

• Right Axis Deviation (RAD): Associated with Right Ventricular Hypertrophy (RVH), Pulmonary Embolism (PE), lateral wall MI, COPD, WPW syndrome, and low potassium ($K^+$).

• Extreme RAD: Associated with severe RVH, ventricular rhythms, and high potassium ($K^+$).

Anatomical Localization: Cardiac Walls and Lead Correlation

• Inferior Wall: Leads II, III, and aVF.

• Lateral Wall (General): Leads I, aVL, V5, and V6.

  • High Lateral: Leads I and aVL.

  • Low Lateral: Leads V5 and V6.

• Septal Wall: Leads V1 and V2.

• Anterior Wall: Leads V3 and V4.

• Anteroseptal Wall: Leads V1, V2, V3, and V4.

• True Posterior Wall (MI Findings): Tall R-waves (R > S) and ST depression in leads V1 and V2.

• Apical Wall: Leads II, III, aVL, and any of leads V1 through V4. Note that these leads are more sensitive for ST-elevation than ST-depression.

• Right Ventricular (RV) Concerns: Use right-sided leads V1R through V6R (Right MI) and V7 through V9 for the posterior wall.

Chamber Enlargement Criteria (Atrial and Ventricular)

• Right Atrial Enlargement (RAE):

  • Lead II: Tall, narrow, peaked P-waves ($P \text{-pulmonale}$) with amplitude $\ge 2.5 \, \text{mm}$.

  • Lead V1: Biphasic P with a large initial component.

  • Axis: Shift of the P-wave axis to the right.

• Left Atrial Enlargement (LAE):

  • Lead II: Wide, notched P-waves ($P \text{-mitrale}$) measuring > 3 small boxes (> 0.12 \, \text{sec}).

  • Lead V1: Biphasic P with a terminal component > 1 \times 1 \, \text{small box} (deep and wide).

  • Axis: Shift of the P-wave axis to the left.

• Biatrial Enlargement: Exhibits criteria for both RAE and LAE.

• Left Ventricular Hypertrophy (LVH):

  • Voltage Criteria: R \, \text{wave in aVL} > 11 \, \text{mm}. S \, \text{in V1} + R \, \text{in V5 or V6} > 35 \, \text{mm}. Sum of any R + S \, \text{in precordial leads} > 45 \, \text{mm}.

  • Secondary Finding: Asymmetric T-wave inversion (strain pattern).

• Right Ventricular Hypertrophy (RVH):

  • Criteria: R > S depth in V1 ($R \ge S$) in the absence of RBBB or posterior MI.

  • Axis: Often presents with Right Axis Deviation (RAD).

Detailed Assessment of Cardiac Intervals

• PR Interval: Normal range is $0.12 - 0.20 \, \text{seconds}$.

  • Short PR ($\le 0.12 \, \text{sec}$): Retrograde junctional P-waves, Lown-Ganong-Levine syndrome, or Wolff-Parkinson-White (WPW) syndrome (associated with a Delta wave).

  • Long PR (> 0.20 \, \text{sec}): Indicates a fixed delay classified as 1st-degree AV block.

• QRS Complex Duration:

  • Normal: $2 - 3 \, \text{small boxes}$ ($0.06 - 0.10 \, \text{sec}$).

  • IVCD (Intraventricular Conduction Delay): $0.10 - 0.12 \, \text{sec}$.

  • BBB/Aberrant Conduction: > 0.12 \, \text{sec} (> 3 \, \text{small boxes}).

• QT Interval: Normal is < 0.42 \, \text{sec} (roughly $2$ big boxes).

  • Rule of Thumb: The QT should be < 1/2 the preceding R-R interval at heart rates of $65 - 90 \, \text{bpm}$. If the rate is outside this, the corrected QT (QTc) must be used.

  • Prolonged QT: Caused by CHF, MI, Hypocalcemia, Hypokalemia, Hypomagnesemia, and drugs like Quinidine or Procainamide. Risk of Torsades de Pointes.

  • Short QT: Caused by Digitalis use, Hypercalcemia, Hyperkalemia, or Hypermagnesemia.

Conduction Defects: Bundle Branch Blocks (BBB)

• Left Bundle Branch Block (LBBB):

  • Morphology: Broad, notched R-R' ("M" or "mu" shape) in leads I, aVL, V5, and V6.

  • Precordial Leads: May see a QS complex or rS in V1; tall R-waves in V6.

  • Clinical Pearl: A new LBBB in the presence of chest pain is a STEMI equivalent. LBBB makes diagnosing acute MI difficult.

• Right Bundle Branch Block (RBBB):

  • Morphology: R-S-R' ("rabbit ears") in leads V1 and V2.

  • Secondary Finding: Wide slurred S-wave in V5 and V6.

• Left Anterior Fascicular Block (LAFB):

  • Criteria: Left axis deviation (> -30^{\circ}) and S > R in leads II, III, and aVF in the absence of a previous MI.

Atrioventricular (AV) Blocks

• 1st-Degree AV Block: Fixed, consistent prolongation of the PR interval (> 0.20 \, \text{sec}) with no dropped QRS complexes.

• 2nd-Degree AV Block, Type I (Wenckebach/Mobitz I): Occurs at the AV node. Characterized by progressive PR interval prolongation until a QRS complex is dropped. Memory aid: "longer, longer, longer, drop."

• 2nd-Degree AV Block, Type II (Mobitz II): Occurs in the Purkinje system (Bundle of His/Branches). The PR interval remains fixed and constant, followed by a sudden, unexpected drop of a QRS complex. This is more dangerous than Type I.

• 3rd-Degree AV Block (Complete Heart Block): Total AV dissociation. P-waves and QRS complexes both "march out" regularly (regular P-P and R-R intervals) but have absolutely no temporal relationship. Atrial rate ($\approx 60-100 \, \text{bpm}$) is faster than the ventricular escape rate ($20-40 \, \text{bpm}$).

Arrhythmia Recognition

• Atrial Fibrillation (A-Fib): Organized by chaotic atrial foci. Rhythm is "irregularly irregular" with no discrete P-waves (chaotic baseline). Atrial rate is $350 - 450 \, \text{discharges/min}$.

• Atrial Flutter: Features a "sawtooth" pattern of flutter waves. Usually regular but can have variable block. Atrial rate is typically $\approx 300 \, \text{bpm}$. Ventricular rate depends on the block (e.g., $1:1 = 300, 2:1 = 150, 4:1 = 75 \, \text{bpm}$).

• Junctional Rhythm: Originates near the AV node. Rate is $40 - 60 \, \text{bpm}$. P-waves are either absent, inverted (retrograde), or follow the QRS. QRS is narrow.

• Ventricular Escape Rhythm: Rate is $20 - 40 \, \text{bpm}$. Features a wide QRS complex and no P-waves.

• Ventricular Tachycardia (VT): A wide-complex tachycardia with a rate > 100 \, \text{bpm}. Monomorphic VT shows uniform regular complexes.

• Ventricular Fibrillation (VF): Chaotic squiggles with no organized complexes or pulse.

• Multifocal Atrial Tachycardia (MAT): Features at least three morphologically different P-waves.

Myocardial Ischemia, Injury, and Infarction Patterns

• Ischemia: Characterized by symmetric T-wave inversion (TWI). Hallmark of Wellens syndrome (critical LAD stenosis) is deep TWI in V2 and V3.

• Injury: Identified by ST-segment elevation.

  • STEMI Thresholds: > 1 \, \text{mm} in limb leads or > 2 \, \text{mm} in precordial leads (in two contiguous leads).

  • Anterior MI: V1-V4 (LAD arterial involvement).

  • Inferior MI: II, III, aVF (RCA involvement).

  • Lateral MI: I, aVL, V5, V6 (LCX involvement).

  • Posterior MI: V7-V9 or reciprocal tall R/ST depression in V1-V2 (PDA involvement).

• Infarct (Completed): Confirmed by pathologic Q-waves (> 1 \, \text{small box wide} and depth > 1/3 height of R-wave).

• Sequence of Evolving MI:

  1. T-wave inversion ($1-2 \, \text{min}$) OR T-wave becomes hyperacute (upright and peaked).

  2. ST-segment elevation or depression.

  3. Pathologic Q-waves develop (permanent cell death).

ST Segment and T-Wave Morphology Analysis

• Reciprocal Changes: Acute MI in one wall causes ST-depression in the opposite leads.

  • Inferior MI (II, III, aVF) causes reciprocal ST-depression in high lateral leads (I, aVL).

  • Anteroseptal MI causes reciprocal ST-depression in inferior leads.

  • True Posterior MI causes reciprocal tall R and ST-depression in V1 and V2.

• T-wave Variations:

  • Hyperacute T-waves: Broad base, blunted/peaked, seen in early ischemia.

  • Hyperkalemia: Pointy T-waves with narrow base and sharp apical apex.

  • Hypokalemia: Flat T-waves and prominent U-waves (> 1-2 \, \text{mm} increase risk of lethal tachyarrhythmias).

• ST-Elevation Differential: Also includes early repolarization, pericarditis (diffuse elevation), ventricular aneurysm, PE, and brain hemorrhage (neuro-T's).

• ST-Depression Differential: MI, LVH, Angina, IV conduction defects, digitalis effects, or positive stress tests.

Professional Rapid Identification Summary