BASIC ECG FACTS EVERYONE SHOULD KNOW

The Language of the ECG: Waves, Intervals, and Segments

The standard ECG tracing is a graphical representation of voltage changes over time, displaying a repeatable sequence of deflections corresponding to the cardiac cycle. These deflections are categorized as waves, intervals, and segments.

Physiological Basis and Characteristics:

• Waves: Represent the electrical activity (depolarization or repolarization) of a mass of cardiac muscle cells.
  • P Wave:
    • Physiological Basis: Represents atrial depolarization, the electrical activation spreading from the sinoatrial (SA) node through both atria.
    • Appearance: A small, rounded, usually positive (upward) deflection preceding the QRS complex. It may be diphasic or inverted in certain leads (e.g., aVR, V1).
    • Normal Duration: Typically less than 0.12 seconds (or 120 milliseconds, corresponding to less than 3 small boxes on standard ECG paper).
  • QRS Complex:
    • Physiological Basis: Represents ventricular depolarization, the electrical activation spreading rapidly from the Bundle of His and bundle branches through the ventricular myocardium. This process is much faster and involves a larger muscle mass than atrial depolarization, resulting in a larger amplitude and shorter duration waveform. Atrial repolarization occurs simultaneously but is obscured by the larger QRS complex.
    • Appearance: Consists of up to three deflections:
      • Q wave: The first negative deflection following the P wave. A normal Q wave is small and narrow (less than 0.04 seconds duration and less than 25% of the succeeding R wave amplitude). Pathological Q waves are wider and deeper and indicative of prior myocardial infarction.
      • R wave: The first positive deflection following the P wave (or Q wave).
      • S wave: Any negative deflection following the R wave.
    • Normal Duration: Typically between 0.06 and 0.10 seconds (or 60 to 100 milliseconds, corresponding to 1.5 to 2.5 small boxes). A duration greater than 0.12 seconds indicates abnormal ventricular depolarization (e.g., bundle branch block).
  • T Wave:
    • Physiological Basis: Represents ventricular repolarization, the return of the ventricular muscle cells to their resting electrical state.
    • Appearance: A rounded, usually positive (upward) deflection following the ST segment. It is typically smoother, broader, and of lower amplitude than the QRS complex. It is normally inverted in lead aVR and may be inverted in V1. Its direction should generally be the same as the net QRS deflection in most leads.
    • Normal Duration: Variable and less precisely defined than other waves, but its significance is usually assessed within the context of the QT interval.
• Intervals: Include at least one wave plus the connecting segment. They represent the time taken for electrical conduction through specific areas of the heart.
  • PR Interval:
    • Physiological Basis: Represents the time taken for electrical activation to spread from the start of atrial depolarization (SA node firing) through the atria, the atrioventricular (AV) node, the Bundle of His, and the bundle branches, up to the start of ventricular depolarization. Crucially includes the physiological delay at the AV node, which allows atrial contraction to precede ventricular contraction.
    • Appearance: Measured from the beginning of the P wave to the beginning of the QRS complex.
    • Normal Duration: Typically between 0.12 and 0.20 seconds (or 120 to 200 milliseconds, corresponding to 3 to 5 small boxes). A shortened PR interval can indicate a bypass tract (e.g., Wolff-Parkinson-White syndrome), while a prolonged PR interval indicates slowed conduction through the AV node (first-degree AV block).
  • QT Interval:
    • Physiological Basis: Represents the total time for ventricular depolarization and repolarization. It corresponds to the duration of the ventricular action potential.
    • Appearance: Measured from the beginning of the QRS complex to the end of the T wave.
    • Normal Duration: Highly dependent on heart rate. It shortens at faster rates and lengthens at slower rates. A “corrected QT” (QTc) is often calculated using formulas (e.g., Bazett’s formula) to adjust for heart rate. Normal QTc is typically < 0.44 seconds (440 milliseconds). Prolonged QT intervals can increase the risk of certain life-threatening arrhythmias (e.g., Torsades de Pointes).
• Segments: Connect waves and represent periods of electrical isoelectricity (no net electrical activity being recorded, meaning all cells in that region are uniformly polarized or depolarized) or very slow conduction.
  • PR Segment:
    • Physiological Basis: Represents the time from the end of atrial depolarization to the beginning of ventricular depolarization. Corresponds primarily to the delay at the AV node and conduction through the Bundle of His and bundle branches before ventricular activation begins.
    • Appearance: The flat, isoelectric line connecting the end of the P wave to the start of the QRS complex.
  • ST Segment:
    • Physiological Basis: Represents the time when the ventricles are in their plateau phase of repolarization (Phase 2 of the action potential), during which there is minimal net electrical potential difference.
    • Appearance: The flat (normally isoelectric) line connecting the end of the QRS complex to the beginning of the T wave. Deviations from the isoelectric baseline (elevation or depression relative to the PR or T-P interval) are clinically significant, often indicating myocardial ischemia or injury.

Capturing the Electrical Activity: ECG Leads

ECG leads are not physical wires placed on the body, but rather hypothetical viewpoints or axes that measure the electrical potentialdifference between two points (bipolar leads) or between one point and a calculated average potential (unipolar leads). Standard ECG recordings use 12 leads to provide a multi-dimensional view of the heart’s electrical activity.

Types of Leads:

• Limb Leads (Frontal Plane): These six leads view the heart’s electrical activity in the frontal plane (superior-inferior and left-right). They are derived from electrodes placed on the limbs (Right Arm – RA, Left Arm – LA, Left Leg – LL).
  • Standard Bipolar Limb Leads (I, II, III): These measure the potential difference between two limbs.
    • Lead I: Measures the potential difference between the Left Arm and the Right Arm (LA – RA). Axis points horizontally to the left (0 degrees).
    • Lead II: Measures the potential difference between the Left Leg and the Right Arm (LL – RA). Axis points downwards and to the left (+60 degrees).
    • Lead III: Measures the potential difference between the Left Leg and the Left Arm (LL – LA). Axis points downwards and to the left (+120 degrees).
    • The ground electrode is typically placed on the Right Leg (RL).
  • Augmented Unipolar Limb Leads (aVR, aVL, aVF): These measure the potential difference between a single limb electrode and the average potential of the other two limbs (known as Wilson’s Central Terminal, which is ideally near zero potential). They are “augmented” because their signal is electronically amplified.
    • Lead aVR (augmented Vector Right): Measures potential at Right Arm relative to the central terminal (RA – Central Terminal). Axis points upwards and to the right (-150 degrees). Shows the heart from the upper right perspective. Typically shows inverted waveforms in a normal ECG.
    • Lead aVL (augmented Vector Left): Measures potential at Left Arm relative to the central terminal (LA – Central Terminal). Axis points upwards and to the left (-30 degrees). Views the heart from the upper left perspective.
    • Lead aVF (augmented Vector Foot): Measures potential at Left Leg relative to the central terminal (LL – Central Terminal). Axis points directly downwards (+90 degrees). Views the heart from an inferior perspective.
• Precordial (Chest) Leads (Horizontal Plane): These six leads (V1-V6) are unipolar leads placed directly on the chest wall, providing views of the heart’s electrical activity primarily in the horizontal plane (anterior-posterior and left-right). Like the augmented limb leads, they measure the potential difference between the chest electrode and Wilson’s Central Terminal. Their placement is standardized:
  • V1: Fourth intercostal space, right sternal border. Views the septum and anterior wall.
  • V2: Fourth intercostal space, left sternal border. Views the septum and anterior wall.
  • V3: Midway between V2 and V4. Views the anterior wall.
  • V4: Fifth intercostal space, midclavicular line. Views the anterior wall and apex.
  • V5: Fifth intercostal space, anterior axillary line (same horizontal level as V4). Views the lateral wall.
  • V6: Fifth intercostal space, midaxillary line (same horizontal level as V4 and V5). Views the lateral wall. These leads show a progression of the QRS complex as the electrical vector moves away from V1 towards V6 (typically small R, deep S in V1/V2; increasing R, decreasing S in V3/V4; larger R, small S or no S in V5/V6).

The Geometry of the Heart’s Electrical Field: Einthoven’s Principles

Willem Einthoven, the inventor of the string galvanometer ECG, developed foundational principles explaining the relationship between the standard bipolar limb leads.

• Einthoven’s Triangle: This is a conceptual model representing the three standard limb leads (I, II, III) as the sides of an equilateral triangle with the heart roughly at the center. The vertices of the triangle correspond to the electrical potentials sensed at the right arm (RA), left arm (LA), and left leg (LL) electrode sites. This triangle helps visualize the direction of the heart’s electrical vector in the frontal plane and its projection onto the axes of these leads.
• Einthoven’s Law: States that the sum of the electrical potentials (voltages) recorded in Lead I and Lead III is equal to the potential recorded in Lead II, assuming the heart is at the center of the triangle. Mathematically expressed as: Lead I + Lead III = Lead II. This law is derived from Kirchhoff’s voltage law applied to the theoretical circuit formed by the limb leads and holds true because the voltage measurement in Lead II (LL-RA) is electrically equivalent to the sum of the voltage in Lead I (LA-RA) and Lead III (LL-LA). (LA – RA) + (LL – LA) = LL – RA.

Deeper Dive into Specific ECG Features

• Physiological Basis of the Upright T Wave in Normal ECG: Ventricular repolarization follows depolarization. While depolarization spreads from the endocardium towards the epicardium, repolarization typically begins slightly earlier in the epicardial layers and spreads back towards the endocardium. Although the direction of repolarization propagation is opposite to depolarization, the electrical potential changes during repolarization are in the opposite direction relative to depolarization (returning to the polarized state, internal negativity). The combined effect of this sequence creates a net repolarization vector that generally points in the same direction as the net ventricular depolarization vector (the QRS axis). Therefore, in most leads where the QRS complex has a net positive deflection (meaning its vector is generally pointing towards that electrode), the T wave will also be upright, as its vector is similarly directed. Conversely, if the QRS is primarily negative, the T wave is likely to be inverted or biphasic. T wave inversion in leads other than aVR and V1 (and sometimes III) can be abnormal.
• Location and Significance of the J Point in ECG:
  • Location: The J point (junction point) is the precise point on the ECG tracing where the QRS complex ends and the ST segment begins. It represents the end of rapid ventricular depolarization and the beginning of the ventricular repolarization phase (specifically, the transition from Phase 0 to Phase 1 and the start of the Phase 2 plateau of the ventricular action potential).
  • Significance: The J point is crucial as the reference point for assessing ST segment deviation. ST segment elevation or depression, measured relative to the preceding PR segment or the T-P segment (the isoelectric line between the end of the T wave and the start of the next P wave), is a key indicator of myocardial ischemia, injury, or infarction. The height or depth of ST deviation is measured from the J point to the baseline segment.

The Physiological Basis of Current of Injury

The “current of injury” refers to a sustained electrical potential difference that exists between areas of injured myocardium and healthy myocardium. This difference results in a continuous current flow during certain phases of the cardiac cycle and is manifested on the electrocardiogram (ECG) primarily as deviations of the ST segment from the isoelectric baseline (ST elevation or depression). Understanding its physiological basis is crucial for interpreting acute myocardial injury.

Here is a breakdown of the physiological processes involved:

Step 1: Normal Cardiac Resting State (Polarization)

• In healthy myocardial cells during diastole (the heart’s resting phase), the cell membrane is polarized.
• This polarization is maintained by ion pumps (like the Na+/K+ ATPase) and selective ion channels, creating a negative resting membrane potential (typically around -90 mV) inside the cell relative to the outside.
• There is minimal net current flow between healthy cells during diastole, resulting in an electrically silent period represented by the TP or PR segment on the ECG, which defines the isoelectric baseline.

Step 2: Myocardial Injury Occurs (e.g., Ischemia or Infarction)

• Acute lack of oxygen (ischemia), leading to cellular injury or death (infarction), disrupts normal cellular metabolism and function.
• Reduced ATP production impairs the ion pumps responsible for maintaining the resting membrane potential and ion gradients.
• Cell membrane integrity can also be affected, altering the permeability to ions.

Step 3: Altered Resting Membrane Potential in Injured Tissue

• Due to pump failure and altered membrane permeability, the injured myocardial cells become electrically different from healthy cells.
• Specifically, injured cells often develop a less negative (partially depolarized) resting membrane potential compared to the healthy, fully polarized -90 mV state. In the case of infarction, the tissue may be electrically inactive or dead.

Step 4: Creation of a Potential Difference (Voltage Gradient) During Diastole

• Because the injured area has a different resting membrane potential than the surrounding healthy tissue, a voltage gradient now exists between these regions even during the diastolic resting phase.
• The injured area acts as a relatively positive pole compared to the negative interior of the surrounding healthy cells.

Step 5: Sustained Diastolic Current Flow

• This potential difference causes a continuous net current to flow between the injured area and the healthy myocardium during diastole. The direction of this current depends on the location and nature of the injury (e.g., transmural vs. subendocardial).
• This current flow disrupts the normal electrical silence of diastole.

Step 6: ECG Detection of the Diastolic Current

• The ECG machine measures the electrical potential difference between electrodes placed on the body surface.
• The diastolic current flowing within the heart creates an electrical field that extends to the body surface. The ECG electrodes detect this continuous current flow during the period that should normally be electrically silent (diastole).

Step 7: Manifestation as ST Segment Deviation

• The ECG machine defines the baseline (isoelectric line) based on a seemingly electrically quiet period, traditionally the TP segment (or sometimes the PR segment).
• However, with a current of injury, the TP segment is not truly isoelectric because of the sustained diastolic current flow. The machine records this electrical activity as the effective “baseline.”
• When the ventricles depolarize and repolarize (QRS and T waves), the electrical activity returns to the potential established by the injured area’s continuous current flow during diastole.
• The ST segment, which connects the end of ventricular depolarization (J point) to the beginning of repolarization (T wave), should normally align with the true isoelectric baseline (the absence of any current flow).
• Since the “baseline” recorded by the ECG is shifted due to the persistent diastolic current of injury, the ST segment (which attempts to return to this shifted baseline) appears elevated or depressed relative to where the true isoelectric line would be in the absence of injury.

Summary:

The current of injury is a physiological phenomenon where sustained electrical potential differences in injured myocardial tissue cause continuous current flow during diastole. This flow shifts the effective ECG baseline, leading to apparent ST segment elevation or depression when the ECG trace returns to this shifted potential during the ST segment phase. These ST segment changes are a critical ECG marker of acute myocardial ischemia or infarction.

ECG Changes in Angina Pectoris (Myocardial Ischemia)

Angina pectoris is the clinical symptom of reversible myocardial ischemia, typically caused by a temporary imbalance between myocardial oxygen demand and supply. ECG changes during angina reflect this transient lack of blood flow to the heart muscle. It is crucial to note that the ECG can be entirely normal during an episode of angina, especially if the ischemia is mild or non-transmural. However, when present, the characteristic changes are:

1. During an Anginal Episode:
   • ST Segment Depression: This is the most classic finding. The ST segment, normally isoelectric (at the level of the PR segment), becomes depressed below the baseline. The morphology of the depression can be:
     • Horizontal: A flat depression for at least 0.08 seconds. This is highly suggestive of ischemia.
     • Downsloping: The ST segment angles downwards from the J point. Also strongly suggestive.
     • Upsloping: The ST segment angles upwards from the J point. This is less specific for ischemia but can be associated, especially if significant (>1mm depression).
     • The depression is often diffuse, seen in multiple leads reflecting the area of ischemia.
   • T Wave Inversion: T waves, normally upright in most leads (except aVR and sometimes Lead III or V1), may become inverted. These inverted T waves are typically symmetrical and pointed, unlike the often asymmetrical normal T waves. They may accompany ST depression or occur in isolation. This also reflects myocardial ischemia affecting repolarization.
2. After the Anginal Episode Resolves:
   • The ECG changes typically revert back to normal or to their baseline appearance as blood flow is restored and ischemia resolves. This transient nature is a key feature distinguishing angina from infarction.

Important Considerations for Angina:

• A normal ECG does not rule out angina.
• Changes are most likely to be captured if an ECG is recorded during an episode of chest pain.
• Exercise stress testing or pharmacological stress testing is often used to induce ischemia and record ECG changes when the patient is asymptomatic at rest.

ECG Changes in Myocardial Infarction (MI)

Myocardial infarction, or heart attack, occurs when prolonged or severe ischemia leads to irreversible damage (necrosis) of myocardial tissue. The ECG changes in MI evolve over time and can indicate the location and extent of the damage. Classic changes reflect the process of injury and necrosis.

The ECG evolution in ST-Elevation Myocardial Infarction (STEMI) often follows a pattern:

1. Hyperacute Phase (Minutes to Hours):
   • Hyperacute T Waves: T waves in the affected leads may become abnormally tall, peaked, and symmetrical before significant ST elevation occurs. This is an early, often transient sign of severe transmural ischemia.
   • Subtle ST Elevation: The ST segment may begin to subtly elevate.
2. Acute Phase (Hours to Days):
   • ST Segment Elevation: This is the hallmark of transmural injury and STEMI. The ST segment is elevated above the baseline (J point elevation) in two or more contiguous leads. The morphology is often convex or coved upwards (like a tombstone). The amount of elevation required for diagnosis varies by lead (e.g., >1-2 mm in limb leads, >2 mm in precordial leads).
   • Reciprocal Changes: ST depression and/or T wave inversion may be seen in leads opposite the area of infarction. This reflects electrical forces pulling away from the infarct site or concurrent ischemia in a different region.
   • Onset of Pathological Q Waves: Small or absent Q waves in the affected leads begin to deepen and widen. A pathological Q wave is generally defined as being >/= 40 ms (0.04 seconds) in duration AND >/= 25% of the amplitude of the subsequent R wave in the same QRS complex. They signify necrotic tissue that is electrically silent.
3. Subacute Phase (Days to Weeks):
   • ST Segment Begins to Return to Baseline: The significant ST elevation gradually resolves.
   • Deep T Wave Inversion: As the ST segment normalizes, deep, symmetrical T wave inversion often develops in the infarct-related leads. This reflects persistent electrical abnormalities surrounding the necrotic area (ischemic “memory”).
   • Pathological Q Waves Persist: Q waves usually solidify and often remain permanently, reflecting the chronic scar tissue.
4. Chronic Phase (Weeks to Months/Years):
   • ST Segment is Isoelectric: Returns fully to baseline.
   • T Waves May Remain Inverted or Gradually Normalize: T wave inversion can persist for months or years, or may eventually become upright again.
   • Pathological Q Waves Persist: Q waves are typically permanent markers of a prior transmural MI.

ECG in Non-ST Elevation Myocardial Infarction (NSTEMI):

In NSTEMI, the infarction is typically subendocardial (partial thickness), and the characteristic ECG findings are:

• Persistent ST Segment Depression: Often horizontal or downsloping, similar to angina but persistent after symptoms subside.
• Prominent T Wave Inversion: Deep, symmetrical T wave inversion.
• Absence of Pathological Q Waves: Because the infarction is not transmural, pathological Q waves usually do not develop.

Important Considerations for MI:

• The specific leads showing changes help localize the infarct (e.g., inferior leads II, III, aVF; anterior leads V1-V4; lateral leads I, aVL, V5, V6).
• A new Left Bundle Branch Block (LBBB) in the setting of chest pain is highly suspicious for acute MI, as it can obscure typical STEMI changes.
• ECG findings must always be interpreted in the context of clinical presentation, cardiac enzyme levels, and imaging studies.

Plotting the Mean Cardiac Axis

The mean electrical axis of the heart represents the predominant direction of electrical activity during ventricular depolarization (the QRS complex). It is determined using the frontal plane leads (I, II, III, aVR, aVL, aVF). The standard normal axis range is generally considered to be between -30 and +90 degrees. Various methods exist, but a common approach using Leads I and aVF is described below:

Steps to Plot the Mean Cardiac Axis (Using Leads I and aVF):

1. Understand the Reference System: Envision the hexaxial reference system, where Lead I is at 0 degrees (horizontal), aVF is at +90 degrees (vertical), and other leads are positioned at 30-degree intervals. For this method, we primarily use Lead I (0-180 degrees) and Lead aVF (+90 to -90 degrees).
2. Analyze QRS Complex in Lead I: Examine the QRS complex in Lead I. Measure the net deflection. This is calculated as the sum of the positive deflections (R wave amplitude) minus the sum of the negative deflections (Q wave and S wave amplitudes). Note if the net deflection is positive or negative.
3. Analyze QRS Complex in Lead aVF: Examine the QRS complex in Lead aVF. Measure the net deflection similarly (R wave amplitude minus Q + S wave amplitudes). Note if the net deflection is positive or negative.
4. Plot the Net Deflections: Imagine a graph where the horizontal axis represents Lead I and the vertical axis represents Lead aVF, with the origin (0,0) at the center.
   • On the hypothetical horizontal axis (Lead I), move right for a positive net deflection or left for a negative net deflection. Mark this point.
   • On the hypothetical vertical axis (Lead aVF), move downwards for a positive net deflection or upwards for a negative net deflection. Mark this point.
5. Draw Perpendiculars: From the point marked on the Lead I axis, draw a line segment perpendicular to the Lead I axis (i.e., a vertical line). From the point marked on the Lead aVF axis, draw a line segment perpendicular to the Lead aVF axis (i.e., a horizontal line).
6. Determine the Axis Endpoint: The intersection of these two perpendicular lines represents the endpoint of the mean cardiac vector.
7. Draw the Vector and Determine the Angle: Draw a line segment from the origin (center of the graph) to the intersection point. This vector represents the mean electrical axis. The angle of this vector relative to the positive horizontal axis (Lead I) is the mean cardiac axis angle.
   • If Lead I is positive and aVF is positive, the axis is in the Normal Quadrant (0 to +90 degrees).
   • If Lead I is positive and aVF is negative, the axis is in the Left Axis Deviation Quadrant (-0 to -90 degrees).
   • If Lead I is negative and aVF is positive, the axis is in the Right Axis Deviation Quadrant (+90 to +180 degrees).
   • If Lead I is negative and aVF is negative, the axis is in the Extreme Axis Deviation (or Northwest) Quadrant (-90 to -180 degrees).
8. Refine with Other Leads (Optional but helpful): The exact angle can be estimated more precisely. Find the lead in the frontal plane where the QRS complex has the smallest net deflection (most isoelectric). The mean electrical axis is approximately perpendicular to this lead’s axis on the hexaxial system. The precise direction (positive or negative) is determined by looking at the QRS in the perpendicular lead.

Clinical Significance of Axis Determination:

• Assesses the overall direction of ventricular depolarization.
• Deviations from the normal range can indicate various underlying conditions affecting ventricular mass, conduction pathways, or spatial orientation of the heart.

Physiological and Pathological Causes of Right Axis Deviation (RAD)

Right axis deviation (RAD) occurs when the mean electrical axis is greater than +90 degrees.

Physiological Causes:

• Children and Infants: The right ventricle is relatively dominant at birth.
• Tall, Thin Individuals: The heart may hang more vertically in the chest cavity.
• Inspiratory Maneuvers: Deep inspiration can shift the heart’s position slightly, causing transient RAD.

Pathological Causes:

• Right Ventricular Hypertrophy (RVH): Increased muscle mass of the right ventricle leads to increased electrical forces directed towards the right. Common causes include pulmonary hypertension, chronic lung disease (cor pulmonale), valvular stenosis (pulmonic, tricuspid).
• Pulmonary Embolism (PE): Acute right heart strain can cause sudden RAD (sometimes with S1Q3T3 pattern – S wave in I, Q wave in III, inverted T wave in III).
• Chronic Lung Disease (e.g., COPD, Emphysema): Can lead to chronic hypoxia, pulmonary hypertension, and secondary RVH.
• Inferior Wall Myocardial Infarction: Necrosis in the inferior wall (often affecting the posterior fascicle of the left bundle) can leave unopposed electrical forces leading predominantly downwards and to the right.
• Left Posterior Fascicular Block: A type of fascicular block in the left bundle branch system.
• Dextrocardia (Rare): Heart located on the right side of the chest.
• Ventricular Arrhythmias originating from the Left Ventricle: Electrical activation proceeds towards the right ventricle.
• Electrolyte Imbalances: Severe hyperkalemia.

Physiological and Pathological Causes of Left Axis Deviation (LAD)

Left axis deviation (LAD) occurs when the mean electrical axis is less than -30 degrees.

Physiological Causes:

• Obesity: The diaphragm is elevated, pushing the heart upwards and horizontally.
• Pregnancy: Similar to obesity, elevated diaphragm shifts the heart.
• Expiratory Maneuvers: Deep expiration can shift the heart’s position slightly.
• Older Age: Less common physiological cause, possibly related to changes in cardiac position and conduction.

Pathological Causes:

• Left Ventricular Hypertrophy (LVH): Increased muscle mass of the left ventricle leads to increased electrical forces directed towards the left. Common causes include hypertension, aortic stenosis, aortic regurgitation, hypertrophic cardiomyopathy.
• Inferior Wall Myocardial Infarction (Sometimes Early in Evolution): Though often causing RAD when pathological Q waves develop, early inferior MI can sometimes shift forces leftward.
• Left Anterior Fascicular Block (LAFB): The most common cause of LAD. Block in the anterior fascicle of the left bundle branch.
• Left Bundle Branch Block (LBBB): Often associated with LAD, as conduction is delayed through the left bundle.
• Certain Congenital Heart Defects: E.g., Atrioventricular canal defects.
• Ventricular Arrhythmias originating from the Right Ventricle: Electrical activation proceeds towards the left ventricle.
• Dilated Cardiomyopathy: Enlargement of the heart chambers, though axis is variable.

Abnormalities of the T Wave and Their Causes

The T wave represents ventricular repolarization. Its morphology, amplitude, and direction can be altered by various conditions. Normally, the T wave is asymmetrical, rounded, and upright in most leads (Head III can be inverted normally, V1 can be inverted/flat normally, aVR is normally inverted). Abnormalities include:

1. Tall, Peaked T Waves (“Hyperacute T Waves”):
   • Description: Abnormally tall (amplitude > 5 mm in limb leads, > 10 mm in precordial leads), narrow base, symmetrical T waves.
   • Causes:
     • Early Myocardial Ischemia/Infarction: Often the earliest sign of acute transmural ischemia (as discussed in Section 2).
     • Hyperkalemia: Significantly elevated potassium levels critically affect repolarization, causing tall, peaked T waves, often with a narrow base, particularly visible in precordial leads. This is a critical sign of electrolyte imbalance.
     • CNS Events: Intracranial hemorrhage, stroke, or head trauma (“cerebral T waves”) can cause Tall, inverted, or otherwise bizarre T waves, often with associated QT prolongation.
2. Flat T Waves:
   • Description: T wave amplitude is significantly reduced or the T wave appears almost absent.
   • Causes:
     • Hypokalemia: Low potassium levels impair repolarization, leading to flattened T waves and often a prominent U wave (a small positive deflection appearing after the T wave, most visible in precordial leads).
     • Myocardial Ischemia: Can cause flattened or mildly inverted T waves.
     • Myocarditis: Inflammation of the heart muscle.
     • Pericarditis: Inflammation of the sac surrounding the heart (often global low voltage and PR depression as well).
     • Hypothyroidism: Reduced metabolic state can affect repolarization.
     • Non-Specific: Can be seen in otherwise healthy individuals or due to minor physiologic effects.
3. Inverted T Waves:
   • Description: T wave deflects below the isoelectric line. Can be symmetrical or asymmetrical, shallow or deep.
   • Causes:
     • Myocardial Ischemia/Infarction: As discussed in Sections 1 & 2. Symmetrical, deep T wave inversions are highly suggestive of ischemia or post-infarction changes.
     • Ventricular Hypertrophy with “Strain” Pattern: Severe LVH or RVH can cause asymmetrical T wave inversion (and reciprocal ST depression) in leads overlying the hypertrophied ventricle. This is a repolarization abnormality distinct from ischemia, though it can coexist.
     • Bundle Branch Blocks: LBBB or RBBB can cause secondary T wave inversions in certain leads (discordant with the terminal deflection of the QRS).
     • Pulmonary Embolism: Can cause T wave inversion, especially in anterior leads (V1-V3) with associated RAD and S1Q3T3.
     • Certain Drugs: E.g., Digoxin (causes characteristic “scooping” ST depression and flattened/inverted T waves, but often symmetrical inversion as well), antiarrhythmics.
     • CNS Events: “Cerebral T waves” can be deeply inverted, often widespread and symmetrical, with prolonged QT interval.
     • Electrolyte Imbalances: Severe hypokalemia can cause inversions.
     • Pericarditis/Myocarditis: Diffuse, non-specific T wave inversions.
     • Normal Variants: Persistent juvenile T wave pattern (inversion in anterior leads V1-V3, especially common in young black individuals) is a normal finding. Inversion in Lead III or aVR is also normal.

Conclusion

Understanding these specific ECG findings for angina, myocardial infarction, cardiac axis, and T wave abnormalities is crucial for accurate interpretation and diagnosis. ECG is a dynamic test, and changes often evolve over time, particularly in acute coronary syndromes. Determination of the cardiac axis provides insight into potential underlying structural or conduction abnormalities. T wave morphology offers critical clues about ventricular repolarization, affected by a wide range of cardiac and systemic conditions. While this guide details key patterns, comprehensive ECG interpretation requires knowledge of all waveform components, intervals, segments, and rhythm analysis, always integrated with the patient’s clinical presentation and other diagnostic information.