Comprehensive Guide to EKG Interpretation and Cardiac Pathophysiology

Introduction to Electrocardiography

• Basic Questions and Goals:

  • Define what an electrocardiogram ($ECG$) is.

  • Understand how an $ECG$ is obtained.

  • Identify what individual wave segments and intervals represent on the recording.

  • Learn the systemic method for interpreting an $ECG$.

• Terminology and History:

  • $Wilhelm \, Einthoven$ was a Dutch scientist who created the first electrocardiogram in $1903$.

  • In Dutch, the word is spelled "Elektrokardiogram," which is where the abbreviation $EKG$ originates.

  • In English, the term is "Electrocardiogram," resulting in the abbreviation $ECG$ because of the "C" in "Cardio."

  • The terms $ECG$ and $EKG$ are $100\%$ interchangeable; preference of nomenclature is often based on habit.

• Professional Advice for Students:

  • Be patient with the learning process; $ECG$ interpretation is a career-long skill, not just a fact to be memorized.

  • There is entire subspecialty of Cardiology dedicated to this subject.

  • Personal wellness is encouraged during study: take breaks, go outside, and take care of yourself. Chance, a retired service dog, serves as a reminder to take walks.

Origins and Physiology of the ECG

• Inherent Automaticity:

  • All cardiac cells possess an inherent ability for automaticity.

  • Normally, this automatic ability is suppressed unless the dominant cells fail to take control.

• Hierarchy of Automaticity Rates:

  • The heart follows a specific hierarchy for electrical dominance: $SA \, node \rightarrow AV \, node \rightarrow Atria \rightarrow Ventricles$.

  • When the hierarchy is intact, the automaticity of lower centers is suppressed.

  • Deviations from this hierarchy lead to abnormal rhythms.

• Normal Conduction Pathway ($Normal \, Sinus \, Rhythm$):

  • $1.$ The impulse starts in the $Sinoatrial \, (SA) \, node$.

  • $2.$ Electrical impulses travel around the atrial cells to the $Atrioventricular \, (AV) \, node$.

  • $3.$ The $AV \, node$ pauses to hold the energy until all impulses arrive.

  • $4.$ The impulse travels down the $Bundle \, of \, His$.

  • $5.$ It proceeds through the right and left $Bundle \, Branches$.

  • $6.$ It moves into the $Purkinje \, fibers$, resulting in a coordinated muscular contraction for pumping.

• The $AV \, Nodal$ Delay:

  • Slowing of electrical conduction occurs at the $AV \, node$ to allow energy buildup.

  • This is followed by rapid conduction through the bundle branches and $Purkinje \, fibers$, which is what produces the narrow $QRS$ complex.

Physical Principles and Lead Placement

• Types of Electrical Leads:

  • $Bipolar \, Leads$: These have two poles (one positive, one negative) and are labeled with Roman numerals $I$, $II$, and $III$. The positive electrode is the "viewpoint" from which the electrical impulse is watched as it travels toward the observer.

  • $Augmented \, Limb \, Leads$: These provide a view within the frontal plane and use the same electrodes as bipolar leads but are unipolar. They reference a single positive electrode against a combination of others called $Wilson \, Central \, Terminal \, (WCT)$. They include $aVR$ (right), $aVL$ (left), and $aVF$ (foot/floor).

  • $Precordial \, (Chest) \, Leads$: Labeled $V_1$ through $V_6$ (sometimes $C_1$ through $C_6$). These are unipolar and calculate activity against the $WCT$. Placement of these leads is more critical than limb leads because of the central terminal calculation.

• Lead Configuration and the $12$-Lead System:

  • A full $12$-lead $ECG$ only requires $10$ actual stickers or wires.

  • $Limb \, Setup$: Right Arm ($RA$), Left Arm ($LA$), Left Leg ($LL$), and a Ground lead on the Right Leg ($RL$).

  • $Einthoven's \, Triangle$: Formed by the connections between the right arm, left arm, and left foot to calculate leads $I$, $II$, and $III$.

  • $3D \, Perspective$: Limb leads provide a view in the frontal plane, while precordial leads look at the horizontal plane, creating a three-dimensional view of the heart.

Standard ECG Paper and Measurements

• Axes of Measurement:

  • $X \, axis$: Represents time, measured in seconds ($s$).

  • $Y \, axis$: Represents voltage, measured in millivolts ($mV$).

• Grid Units:

  • One small box on the horizontal axis equals $0.04 \, s$.

  • One large box (comprising $5$ small boxes) equals $0.2 \, s$.

  • One small box on the vertical axis equals $0.1 \, mV$.

  • One large box equals $0.5 \, mV$.

• Technical Standards:

  • Standard paper speed is fixed at $25 \, mm/s$.

  • Adjustments in speed may be required for exceptionally fast or slow rhythms.

  • The rhythm strip at the bottom of the page is typically $6 \, s$ long.

  • There are small tick marks on the rhythm strip every $3 \, s$, which constitute $15$ large boxes ($0.2 \, s \times 15 = 3 \, s$).

Basic Waveform Analysis

• Individual Waves:

  • $P \, wave$: Represents atrial depolarization. Duration is typically $0.08 \, s$ to $0.1 \, s$.

  • $QRS \, complex$: Represents ventricular depolarization. Normal duration is less than $0.12 \, s$ (fewer than $3$ small boxes).

  • $T \, wave$: Represents ventricular repolarization.

• Intervals and Segments:

  • $PR \, interval$: Includes the $P$ wave and the space before the $QRS$. It represents atrial depolarization plus the $AV \, nodal$ delay. Normal range is $0.12 \, s$ to $0.2 \, s$.

  • $ST \, segment$: The isoelectric period after the ventricle has depolarized but before it repolarizes. It occurs between the $S$ wave and the start of the $T$ wave.

  • $QT \, interval$: Total time for depolarization and repolarization, corresponding to the total action potential duration. Normal range is $0.2 \, s$ to $0.4 \, s$.

• Directional Deflections:

  • Depolarization moving toward a positive electrode creates an upward deflection.

  • Depolarization moving away from a lead creates a downward deflection.

  • Repolarization moving toward a positive electrode creates a downward deflection.

  • Repolarization moving away from a positive electrode creates an upward deflection.

• $QRS$ Nomenclature Variations:

  • $Q \, wave$: Any initial downward deflection.

  • $R \, wave$: The first upward deflection.

  • $S \, wave$: Any downward deflection following an $R$ wave.

  • $R' \, (R \, prime)$: Any subsequent upward deflection after an $S$ wave.

  • A complex is still called a $QRS$ complex even if specific components like the $S$ or $Q$ are missing.

Interpretation Workflow and Heart Rate Calculation

• The Systematic Approach:

  • Standardized steps must be followed every time: $Rate \rightarrow Rhythm \rightarrow Axis \rightarrow Individual \, Waves/Intervals/Segments$.

  • Analyze consistency: Are waves present? is shape/size/duration normal? What is the position?

• Rhythm Strip Specific Analysis:

  • $1.$ Heart Rate.

  • $2.$ Regularity.

  • $3.$ $P$ wave morphology (Presence and consistency).

  • $4.$ $PR$ interval (Consistency and duration).

  • $5.$ $QRS$ morphology (Consistency, width - narrow vs. wide).

• Calculating Heart Rate (Option $1$ - The $6$-Second Method):

  • Count the number of $R$ waves on a $6$-second strip and multiply by $10$.

  • This is highly beneficial for irregular rhythms as it provides an average.

• Calculating Heart Rate (Option $2$ - The Sequence Method):

  • Find an $R$ wave on a bold line and count the large boxes to the next $R$ wave using the sequence: $300$, $150$, $100$, $75$, $60$, $50$.

  • Detailed math for specificity: Subtract the two sequence values, divide by $5$ (number of small boxes) to find the "value" of each small box. For example, between $75$ and $60$, each small box is worth $3 \, bpm$.

• Rate Variability Significance:

  • Variation in tachycardic patients (e.g., $140 \, bpm$ vs. $150 \, bpm$) is only about $6\%$ and is less clinically significant.

  • Variation in bradycardic patients (e.g., $40 \, bpm$ vs. $50 \, bpm$) is a $20\%$ difference and significantly impacts care decisions.

Sinus Node Rhythms

• Normal Sinus Rhythm ($NSR$):

  • Rate: $60$ to $100 \, bpm$.

  • Regularity: Regular.

  • $P$ waves: Present, normal shape, same direction as $QRS$, consistent morphology.

  • $PR$ interval: Normal ($3$ to $5$ small boxes).

  • $QRS$: Normal (< 3 small boxes).

• Sinus Arrhythmia:

  • Characterized by irregular spacing between beats, often due to respiratory changes.

  • Inhalation increases blood flow and $SA \, node$ firing; exhalation slows it down.

  • Common in anesthetized patients on ventilators.

• Sinus Bradycardia:

  • Rate: < 60 \, bpm. All other characteristics are normal.

• Sinus Tachycardia:

  • Rate: > 100 \, bpm. Usually caused by physiologic or psychological stress rather than being a primary arrhythmia.

• Sinus Arrest:

  • The $SA \, node$ stops firing, leading to a pause.

  • Often followed by "escape beats" from other centers to maintain output.

Ectopic Beats: Escape vs. Premature

• Escape Beats and Rhythms:

  • An escape is a response to a pause or failure of the $SA \, node$. It serves as a safety mechanism.

  • $Atrial \, Escape$: Rate $60$ to $80$. Features a different $P$ wave shape ($P'$).

  • $Junctional \, (AV \, Node) \, Escape$: Rate $40$ to $60$. No $P$ wave, or an inverted (retrograde) $P$ wave.

  • $Ventricular \, Escape$: Rate $20$ to $40$. No $P$ wave, and the $QRS$ is wide and bizarre (> 3 small boxes).

  • An "Escape Rhythm" is defined as $3$ or more consecutive escape beats.

• Premature Beats:

  • These occur preemptively due to an irritable focus; they do not follow a pause.

  • $Premature \, Atrial \, Contraction \, (PAC)$: Irritable atrial focus; different $P$ wave shape, normal $QRS$. Often followed by a pause to allow the $SA \, node$ to repolarize.

  • $Premature \, Junctional \, Contraction \, (PJC)$: Irritable junctional focus; no $P$ wave, normal/narrow $QRS$.

  • $Premature \, Ventricular \, Contraction \, (PVC)$: Most recognizable; no $P$ wave and wide $QRS$.

    • $\text{Monomorphic (Uniform)}$ : Same shape, same focus.

    • $\text{Polymorphic (Multiform)}$: Multiple shapes, multiple foci.

  • PVCs can be triggered by stimulants, caffeine, stress, or medications.

• Social Metaphor:

  • Premature beats are like a friend with a big personality who interrupts a conversation (irritable).

  • Escape beats are like a quiet, subdued friend who steps in to help only when someone else stops talking (response to failure).

Atrial and Junctional Dysrhythmias

• Wandering Atrial Pacemaker ($WAP$):

  • Impulses originate from multiple different locations in the atria rather than a single focus.

  • Requires at least $3$ different $P$ wave morphologies. Heart rate is typically normal (< 100 \, bpm).

• Multifocal Atrial Tachycardia ($MAT$):

  • Similar to $WAP$ but with a heart rate greater than $100 \, bpm$.

  • Commonly associated with patients suffering from Chronic Obstructive Pulmonary Disease ($COPD$).

• Atrial Flutter:

  • Characterized by rapid, organized atrial depolarization created by a reentrant circuit (often in the right atrium near the cavotricuspid isthmus).

  • Produces "sawtooth" or flutter waves with no baseline between them.

  • Atrial rate is usually $250$ to $350 \, bpm$. The ventricular rate depends on the conduction ratio (e.g., $2:1$, $3:1$, $4:1$).

  • Usually regular, but can be irregular if the conduction block is variable.

• Atrial Fibrillation ($AFib$):

  • Extremely disorganized, chaotic electrical activity with many foci firing simultaneously.

  • Described as looking like "a pool in a rainstorm" (many small disruptions, no coordination).

  • Clinical Signs: Loss of $P$ waves, a fuzzy/varying baseline, and an $Irregularly \, Irregular$ rhythm.

  • Treatment: Synchronized cardioversion to restore organized rhythm.

Atrioventricular Blocks

• First-Degree $AV \, Block$:

  • Delayed conduction through the $AV \, node$. Every impulse gets through, but the $PR$ interval is consistently prolonged (> 0.2 \, s or $5$ small boxes).

• Second-Degree $AV \, Block, \, Type \, 1 \, (Mobitz \, I \, or \, Wenckebach)$:

  • Progressive lengthening of the $PR$ interval until a $QRS$ beat is dropped.

  • Poem: "Longer, longer, longer, drop! Then you have a $Wenckebach$!"

  • Usually results from a benign $AV \, nodal$ problem.

• Second-Degree $AV \, Block, \, Type \, 2 \, (Mobitz \, II)$:

  • The $PR$ interval is constant and normal, but beats are dropped randomly without warning.

  • Poem: "If some $P\text{'s}$ don't get through, then you have a $Mobitz \, II$."

  • Indicates severe disease below the $AV \, node$ and is a high risk for complete heart block.

• Third-Degree ($Complete$) $AV \, Block$:

  • Total dissociation between atria and ventricles. No communication occurs.

  • Both atria and ventricles fire at their own regular but independent rates.

  • Poem: "If $P\text{'s}$ and $Q\text{'s}$ don't agree, then you have a $Third \, Degree$."

Bundle Branch Blocks

• Mechanism:

  • Electrical impulses are slowed in one of the bundle branches (right or left), causing the ventricles to depolarize sequentially rather than simultaneously.

  • This creates a wide $QRS$ (> 0.12 \, s) and the appearance of two overlapping $R$ waves, often called "bunny ears" ($RSR'$).

• Right Bundle Branch Block ($RBBB$):

  • Check leads $V_1$ and $V_6$.

  • In $V_1$: Presence of the $RSR'$ (bunny ears) pattern.

  • In $V_6$: Slurred $S \, wave$ (a deep, slow-sloping downward deflection).

• Left Bundle Branch Block ($LBBB$):

  • Always considered pathologic.

  • Check leads $V_1$ and $V_6$.

  • In $V_1$: A large, deep, wide $S \, wave$. It can look like a "$W$."

  • In $V_6$: A notched, wide "bunny ear" $R \, wave$ ($M$ shape).

  • $Incomplete \, LBBB$: Signs are present, but the $QRS$ duration is still within the normal range ( < 0.12 \, s).

Ventricular Arrhythmias and Accessory Pathways

• Ventricular Tachycardia (V$-Tach):

  • Rapid heart rate (> 100 \, bpm) with wide, bizarre $QRS \, complexes$ and no visible $P$ waves. It is a regular rhythm originating in the ventricles.

• $\text{Torsades de Pointes}$:

  • French for "twisting of points." A polymorphic ventricular tachycardia where the $QRS$ complexes appear to twist around an imaginary baseline.

  • Atrial rate is high ($250$ to $350 \, bpm$). Associated with a prolonged $QT \, interval$.

  • Treatment: Immediate synchronized cardioversion if unstable; treat underlying causes like electrolyte imbalances or drugs like $Ondansetron$.

• Ventricular Fibrillation (V$-Fib):

  • Chaotic quivering of the ventricles with no coordinated contraction or pulse. Appears as a wavy baseline on the $ECG$.

• Wolf-Parkinson-White ($WPW$) Syndrome:

  • An accessory pathway called the $Bundle \, of \, Kent$ bypasses the $AV \, node$.

  • Features a short $PR \, interval$ (< 0.12 \, s) and a slow, slurring upstroke of the $QRS$ called a $Delta \, wave$.

  • Risk: Reentrant tachycardias ($AVRT$) and dangerously high heart rates if the patient develops $AFib$.

• Pacemaker Rhythms:

  • Visible as short electrical "spikes."

  • $\text{Atrial pacing}$: Spike before the $P$ wave.

  • $\text{Ventricular pacing}$: Spike before the $QRS$.

  • $\text{Sequential pacing}$: Spikes before both the $P$ wave and the $QRS$.

Determination of the Mean Electrical Axis

• Definition:

  • The mean electrical axis is the average direction of all electrical activity (vector) during ventricular depolarization.

• Clinical Influences:

  • Tall, slender people may have a more vertical heart (rotation to the right).

  • Obese patients may have the heart pushed up and to the left by the diaphragm.

  • Hypertrophy (building muscle muscle) shifts the axis toward the more muscular side.

• Axis Segments:

  • Normal Axis: $0^{\circ}$ to $+90^{\circ}$ (though some sources say $-30^{\circ}$ to $+90^{\circ}$).

  • Left Axis Deviation ($LAD$): $-30^{\circ}$ to $-90^{\circ}$.

  • Right Axis Deviation ($RAD$): $+90^{\circ}$ to $+180^{\circ}$.

• The Lead $I$ and $aVF$ Method:

  • If both Lead $I$ and $aVF$ are positive (upward): Normal Axis ("Double thumbs up").

  • If Lead $I$ is positive and $aVF$ is negative: Possible $LAD$.

  • If Lead $I$ is negative and $aVF$ is positive: $RAD$.

• Refining the Axis (The Isoelectric Lead):

  • Identify the limb lead that is most isoelectric (equal deflection up and down).

  • The axis is $90^{\circ}$ perpendicular to that lead.

  • Confirm by finding the lead with the highest $R \, wave$; the axis should be parallel to it.

Chamber Enlargement and Hypertrophy

• Basic Concept:

  • Hypertrophy refers to muscle fiber thickening (usually in ventricles).

  • Enlargement refers to chamber dilation (usually in atria).

  • Both result in increased duration (longer route), increased amplitude (more voltage), and potential axis shifts.

• Atrial Enlargement (Look at Lead $V_1$):

  • $V_1$ sits perpendicular to the current, resulting in a biphasic $P$ wave.

  • $\text{Right Atrial Hypertrophy/Enlargement}$: The initial part of the biphasic $P \, wave$ is larger.

  • $\text{Left Atrial Hypertrophy/Enlargement}$: The latter part of the biphasic $P \, wave$ is larger and deeper.

• Ventricular Hypertrophy:

  • $\text{Right Ventricular Hypertrophy (RVH)}$: Characterized by a large $R \, wave$ in $V_1$ (> 6 \, mm) and a lot of $R \, wave \, progression$. Often accompanied by $RAD$.

  • $\text{Left Ventricular Hypertrophy (LVH)}$: Diagnosed using the $Sokolow-Lyon \, Criteria$.

    • $\text{Formula}$: S(V_1) + R(V_5 \, \text{or} \, V_6) > 35 \, mm.

    • Another criterion: $R \, wave$ in aVL > 11 \, mm.

Myocardial Ischemia and Infarction

• Ischemia:

  • Deprivation of oxygen to tissue. Usually reversible if caught early.

  • $ECG \, Signs$: $ST \, segment \, depression$ and/or symmetrical, narrow, deep $T \, wave \, inversion$.

• Myocardial Infarction ($MI$):

  • Irreversible damage to the muscle. "Time is muscle."

  • $STEMI \, (ST \, Elevation \, MI)$: Transmural (full-thickness) damage. Signified by a $J-point$ elevation of at least $0.1 \, mV \, (1 \, mm)$ in two contiguous leads.

  • $NSTEMI \, (Non-ST \, Elevation \, MI)$: Subendocardial or intramural damage. Diagnostics rely on $ST \, depression$ and positive clinical labs like $Troponin$.

• $\text{Evolution of a STEMI (Stages)}$:

  • $Stage \, 1$: Hyperacute (peaked) $T \, waves$ (ischemia).

  • $Stage \, 2$: $ST \, segment \, elevation$ ($0$ to $12 \, hours$).

  • $Stage \, 3$: Development of pathological $Q \, waves$ (necrosis).

  • $Stage \, 4$: $ST \, elevation$ resolves, but the $T \, wave$ remains inverted for weeks.

  • $Stage \, 5$: Final recovery. The inverted $T \, wave$ corrects, and only the permanent $Q \, wave$ remains as evidence of the old infarct.

• $\text{Pathological Q Waves}$:

  • A significant $Q \, wave$ must be at least $1/3$ the height of the entire $QRS \, complex$ (or appearing in two contiguous leads).

Localization of Infarcts and Correlating Coronary Arteries

• Determining the Affected Area:

  • $\text{Anterior Wall}$: Leads $V_3, \, V_4$. Vessel: $Left \, Anterior \, Descending \, (LAD)$.

  • $\text{Septal}$: Leads $V_1, \, V_2$. Vessel: $LAD$.

  • $\text{Lateral Wall}$: Leads $I, \, aVL, \, V_5, \, V_6$. Vessel: $Circumflex \, artery$.

  • $\text{Inferior Wall}$: Leads $II, \, III, \, aVF$. Vessel: $Right \, Coronary \, Artery \, (RCA)$.

  • $\text{Posterior Wall}$: Often presents as reciprocal $ST \, depressions$ in $V_1, \, V_2$. To confirm, use posterior leads $V_7, \, V_8, \, V_9$ or the "mirror test" (invert the tracing and look in a mirror).

• Reciprocal Changes:

  • Electrical changes on one side of the heart produce opposite deflections on the other side.

  • An inferior infarct (elevation in $II, \, III, \, aVF$) will show reciprocal depression in leads $I$ and $aVL$.

Clinical Pathologies: Pericarditis, Electrolytes, and Brugada

• Pericarditis:

  • Inflammation of the pericardium. Shows $ST \, elevations$ in nearly every lead (diffuse), with no reciprocal changes. Often features $PR \, segment \, depression$.

• Potassium Disorders:

  • $\text{Hyperkalemia}$: Tall, peaked, pointy $T \, waves$. Can progress to flat $P \, waves$ and a wide $QRS$.

  • $\text{Hypokalemia}$: Flattening of $T \, waves$ and appearance of $U \, waves$. If the $U \, wave$ is taller than the $T \, wave$, it is a "prominent $U \, wave$."

• Calcium Disorders:

  • $\text{Hypercalcemia}$: Shortened $QT \, interval$.

  • $\text{Hypocalcemia}$: Prolonged $QT \, interval$ and flat $T \, waves$.

• Hypothermia:

  • Causes severe bradycardia, prolonged intervals, and the $Osborn \, wave$ ($J \, wave$ or camel hump) at the $J-point$.

• Brugada Syndrome:

  • Genetic (autosomal dominant) condition affecting sodium channels. Poses a high risk for sudden cardiac death during sleep.

  • $\text{Brugada Pattern}$: Look for an $RSR'$ in $V_1, \, V_2$ with $ST \, elevation$ going into a negative $T \, wave$.

  • $\text{Brugada Syndrome}$: The aforementioned pattern plus clinical symptoms (e.g., syncopal episodes, polymorphic $V-Tach$). Requires an Internal Cardioverter Defibrillator ($ICD$).