The heart muscle receives its blood supply through a network of arteries known as the coronary circulation. This system is crucial for delivering oxygen and nutrients to the heart, allowing it to function properly.

Origin of Coronary Arteries:

• The arterial supply to the heart begins with two main arteries: the right coronary artery (RCA) and the left coronary artery (LCA).
• These arteries originate from the aorta, specifically from the root of the aorta, which is the section of the aorta closest to the heart.

Right Coronary Artery (RCA) and its Branches:

The right coronary artery travels along the surface of the heart and branches out to supply different areas. Key branches of the RCA include:

• Conus Artery: This is usually the first branch of the RCA.
• Acute Marginal Branches: These branches extend towards the acute margin (the sharper, lower border) of the heart.
• AV Nodal Artery: This artery supplies the atrioventricular (AV) node, a critical part of the heart's electrical conduction system.
• Posterior Descending Artery (PDA) or Posterior Interventricular Artery (PIV): This significant branch typically runs along the posterior interventricular groove, which is on the back surface of the heart between the ventricles.

Left Coronary Artery (LCA) and its Branches:

The left coronary artery, though shorter than the RCA, is generally larger in diameter and equally important. It quickly divides into two main branches:

• Left Anterior Descending Artery (LAD): This artery runs down the front of the heart in the anterior interventricular groove.
  • Septal Branches: These smaller branches penetrate into the interventricular septum, the wall separating the left and right ventricles.
  • Diagonal Branches: These branches extend diagonally across the front surface of the left ventricle.
• Left Circumflex Artery (LCx): This artery curves around the left side of the heart in the atrioventricular groove, which separates the atria and ventricles.
  • Obtuse Marginal Branches: These branches extend towards the obtuse margin (the smoother, rounded border) of the heart.

Dominance of Circulation:

The term "dominance" in coronary circulation refers to which artery, the RCA or the LCx, supplies the posterior descending artery (PDA). This is important because the PDA supplies a significant portion of the heart.

• Right-Dominant Circulation (Most Common): In approximately 80% of individuals, the PDA and at least one posterolateral branch originate from the RCA. This is termed right-dominant circulation.
• Left-Dominant Circulation: In about 15% of people, the PDA and at least one posterolateral branch arise from the LCx. This is known as left-dominant circulation.
• Balanced Circulation: In around 5% of cases, there is a dual supply to the posteroinferior part of the left ventricle from both the RCA and the LCx. This is called balanced circulation.

Blood Supply to the Nodes of the Conduction System:

The sinoatrial (SA) node and atrioventricular (AV) node are essential for initiating and coordinating the heart's electrical activity. Their blood supply is crucial.

• SA Node Blood Supply: The sinoatrial (SA) node is supplied by the SA nodal artery.
  • In approximately 60% of individuals, the SA nodal artery originates from the RCA.
  • In the remaining 40%, it arises from the LCA (typically the LCx branch).
• AV Node Blood Supply: The atrioventricular (AV) node receives its blood supply from the AV nodal artery.
  • The AV nodal artery arises from the RCA in about 90% of people (consistent with right dominance being common).
  • In the other 10%, it originates from the LCx (consistent with left dominance).

Venous Drainage of the Heart:

After circulating through the heart muscle, the deoxygenated blood needs to return to the heart's chambers to be pumped to the lungs for oxygenation.

• Coronary Sinus: The majority of the venous blood from the heart drains into the right atrium (RA) through a large vein called the coronary sinus.
• Thebesian Veins: A small amount of venous blood drains directly into all four chambers of the heart through small vessels called Thebesian veins.
• Physiological Right-to-Left Shunt: The drainage of deoxygenated blood directly into the heart chambers, particularly the oxygenated left chambers via Thebesian veins, contributes to a small physiological right-to-left shunt. This means a tiny amount of deoxygenated blood mixes with oxygenated blood, which is a normal physiological phenomenon.

The heart is a complex organ with distinct layers, valves, and a specialized conduction system that work together to pump blood throughout the body.

Layers of the Heart:

The heart wall is composed of several layers, each with a specific function:

• Endocardium: This is the innermost layer, lining the heart chambers and covering the valves. It is a thin, smooth layer that allows blood to flow easily.
• Myocardium: This is the thick muscular middle layer of the heart wall. It is responsible for the heart's contractions, pumping blood. The myocardium is composed of cardiac muscle cells.
• Epicardium: This is the outermost layer of the heart wall. It is also known as the visceral pericardium because it is the inner layer of the pericardium that is directly attached to the heart.
• Pericardial Cavity: This is a space between the epicardium (visceral pericardium) and the parietal pericardium. It contains a small amount of pericardial fluid, which lubricates the surfaces and reduces friction as the heart beats.
• Parietal Pericardium: This is the outer layer of the pericardium, forming a sac around the heart. It is a tough, fibrous layer that protects the heart and anchors it within the chest.

Heart Valves:

Heart valves are crucial for ensuring unidirectional blood flow through the heart, preventing backflow and maintaining efficient pumping action. There are two main types of heart valves:

• Semilunar Valves: These valves have three leaflets (cusps) and are located at the exit points of the ventricles, separating the ventricles from the great arteries (aorta and pulmonary artery).
  • Aortic Valve: This valve separates the left ventricle outflow tract (LVOT) from the ascending aorta. It has three cusps:
    • Noncoronary Cusp
    • Left Coronary Cusp (LCC)
    • Right Coronary Cusp (RCC)
    • Importantly, the RCC and LCC have coronary ostia located within them. These ostia are the openings to the coronary arteries, allowing blood to flow into the coronary circulation.
  • Pulmonary Valve: This valve separates the right ventricle outflow tract (RVOT) from the pulmonary artery (PA). It also has three cusps:
    • Anterior Cusp
    • Left Cusp
    • Right Cusp
• Atrioventricular Valves (AV Valves): These valves are located between the atria and ventricles. They have a subvalvular apparatus, which includes chordae tendineae and papillary muscles, to support the valve leaflets and prevent them from prolapsing back into the atria during ventricular contraction.
  • Mitral Valve: This valve separates the left atrium (LA) from the left ventricle (LV). It has two leaflets:
    • Anterior Leaflet: Larger, covering approximately 2/3 of the valve area and 1/3 of the valve circumference.
    • Posterior Leaflet: Smaller, covering about 1/3 of the valve area and 2/3 of the valve circumference.
  • Tricuspid Valve: This valve separates the right atrium (RA) from the right ventricle (RV). It has three leaflets:
    • Anterior Leaflet
    • Posterior Leaflet
    • Septal Leaflet

The heart has a specialized electrical conduction system that generates and transmits electrical impulses, coordinating the contractions of the atria and ventricles in a synchronized manner.

Sinoatrial (SA) Node:

• Location: Situated at the junction of the superior vena cava (SVC) and the roof of the right atrium (RA).
• Function: Known as the heart's natural pacemaker. It generates electrical impulses that initiate each heartbeat. The heartbeat originates here.
• Impulse Transmission within Atria: Electrical impulses from the SA node travel through the right atrium via three internodal tracts:
  • Anterior Internodal Tract
  • Middle Internodal Tract
  • Posterior Internodal Tract
• These tracts conduct impulses within the RA, and also via Bachmann's bundle to the left atrium (LA), ensuring both atria contract together. Atrial impulses converge at the AV node.

Atrioventricular (AV) Node:

• Location: Located within the triangle of Koch. This triangle is defined by:
  • Superior margin of the coronary sinus
  • Tendon of Todaro
  • Hinge of the septal leaflet of the tricuspid valve
• Function: The AV node acts as a gatekeeper for electrical impulses traveling from the atria to the ventricles. It slows down the impulse slightly, allowing time for the atria to contract and empty blood into the ventricles before ventricular contraction begins.
• Accessory Pathways: Under normal conditions, the AV node is the sole pathway for electrical impulses from the atria to the ventricles. However, in some individuals, there may be an accessory AV pathway (an abnormal electrical connection between the atria and ventricles, such as in Wolff-Parkinson-White (WPW) syndrome). These pathways can bypass the AV node and lead to abnormal heart rhythms.

Bundle of His:

• Connection: The AV node connects to the bundle of His.
• Function: The bundle of His is a pathway that transmits electrical impulses from the AV node to the ventricles. It is the beginning of the ventricular conduction system.
• Division: The bundle of His quickly divides into two main branches:
  • Left Bundle Branch (LBB)
  • Right Bundle Branch (RBB)

Left Bundle Branch (LBB):

• Further Division: The LBB further splits into two fascicles (smaller branches):
  • Anterior Fascicle
  • Posterior Fascicle

Right Bundle Branch (RBB) and Fascicles of LBB:

• Purkinje Fibers: The RBB and the anterior and posterior fascicles of the LBB branch out into a network of Purkinje fibers.
• Function: Purkinje fibers are specialized conducting fibers that rapidly spread electrical impulses throughout the ventricular myocardium (the muscular walls of the ventricles). This rapid and widespread distribution ensures synchronized contraction of the ventricles, leading to efficient pumping of blood to the body and lungs.

The heart and blood vessels are regulated by the nervous system, specifically the autonomic nervous system, which has two main branches: the sympathetic and parasympathetic nervous systems. These systems control heart rate, contractility, and blood vessel tone.

Sympathetic Nerves:

• Innervation: Sympathetic nerves innervate various parts of the cardiovascular system, including:
  • SA node
  • AV node
  • Ventricular myocardium (heart muscle of the ventricles)
  • Vasculature (blood vessels)
• Effects of Sympathetic Stimulation: When sympathetic nerves are activated, they release neurotransmitters (primarily norepinephrine) that bind to receptors in the heart and blood vessels.
  • Increased Heart Rate (Chronotropy): Increased sympathetic activity on the SA node, acting via beta-1 (ẞ1) receptors, leads to an increase in heart rate (HR). This occurs because the pacemaking cells in the SA node generate impulses more frequently. This effect is known as increased chronotropy.
  • Increased Contractility (Inotropy): In the cardiac muscle (myocardium), sympathetic stimulation, also acting through ẞ1 receptors, increases the force of contraction of the heart muscle. This is termed increased inotropy, which leads to an increased stroke volume (SV), meaning the heart pumps out more blood with each beat.
  • Vasodilation in Skeletal and Coronary Circulation: Stimulation of beta-2 (ẞ2) receptors and, to a lesser extent, ẞ1 receptors in the blood vessels of skeletal muscles and the coronary arteries causes vasodilation (widening of blood vessels). This increases blood flow to these areas, which is beneficial during physical activity or stress.

Parasympathetic Nerves:

• Innervation: Parasympathetic nerves, specifically the vagus nerve, primarily innervate:
  • SA node
  • AV node
  • Atrial myocardium (heart muscle of the atria)
  • They have fewer effects on most vascular beds (blood vessels throughout the body).
• Effects of Parasympathetic Stimulation: Parasympathetic nerves release acetylcholine, which acts on muscarinic receptors in the heart.
  • Dominance at Rest (Vagal Tone): At rest, vagal tone (the continuous activity of the parasympathetic nervous system) dominates the tonic (ongoing) sympathetic stimulation of the SA and AV nodes.
  • Decreased Heart Rate (Chronotropy): Parasympathetic stimulation of the SA node decreases heart rate.
  • Slowed AV Node Conduction (Dromotropy): Parasympathetic stimulation of the AV node slows down the conduction of electrical impulses through the AV node. This can lead to:
    • Prolonged PR interval on an electrocardiogram (ECG), which represents the time for atrial depolarization and conduction through the AV node.
    • In more pronounced cases, it can result in second-degree or third-degree AV block, where some or all electrical impulses from the atria are blocked from reaching the ventricles.
    • This effect on conduction velocity is termed reduced dromotropy (if it primarily affects AV node conduction).
  • Minimal Impact on Peripheral Vascular Resistance: Parasympathetic stimulation has very little impact on total peripheral vascular resistance. Its primary effects are on the heart itself, mainly slowing it down.

In summary, the sympathetic nervous system generally speeds up and strengthens heart activity and dilates blood vessels in muscles and the heart, while the parasympathetic nervous system slows down heart activity, particularly at rest, with minimal effect on most blood vessels. This balance between sympathetic and parasympathetic activity allows for precise regulation of cardiovascular function based on the body's needs.

This section outlines possible causes for common symptoms patients might present with, helping to guide diagnosis. It's crucial to remember that these are differential diagnoses, meaning a list of possibilities, and further investigation is needed to pinpoint the exact cause.

Chest pain is a common and concerning symptom. It is often described as pressure, heaviness, or discomfort. It's important to distinguish between different types of chest pain. Ischemic pain, related to reduced blood flow to the heart, is typically dull and diffuse, while chest wall pain or pericardial pain is often sharp, localized, and worsens with inspiration (pleuritic).

Possible causes of chest pain can be broadly categorized:

Loss of consciousness can be due to various reasons. It's crucial to differentiate between true syncope (caused by reduced blood flow to the brain) and other causes.

1. Causes of True Syncope (Impaired Cerebral Perfusion):

• Reflex Mediated/Reflex Dysfunction Syncope:
  • Vasovagal Syncope - Most Common cause of syncope (also known as reflex-mediated syncope or neurocardiogenic syncope; triggered by emotional stress, pain, prolonged standing, etc.)
  • Situational Syncope (triggered by specific situations):
    • Micturition syncope (during urination)
    • Cough syncope (during coughing)
    • Carotid Hypersensitivity (pressure on the carotid artery in the neck causing syncope)
• Autonomic Dysfunction Syncope (failure of the autonomic nervous system to regulate blood pressure, often associated with neurological diseases)
• Postural Hypotension (drop in blood pressure upon standing, can be due to):
  • Central nervous system disorders
  • Antihypertensive drugs (medications to lower blood pressure)
• Inadequate Circulating Volume (reduced blood volume):
  • Bleeding (hemorrhage)
  • Hypovolemia with orthostasis (dehydration with blood pressure drop upon standing)
• Obstruction to Blood Flow Syncope:
  • Tamponade (cardiac tamponade) - Life-threatening
  • Pulmonary Embolism (PE) - Life-threatening
  • Severe Pulmonary Hypertension (HTN)
  • Severe Obstructive Valve Disease:
    • Mitral Stenosis (MS) (narrowing of the mitral valve)
    • Aortic Stenosis (AS) (narrowing of the aortic valve)
  • Left Ventricular Outflow Obstruction (blockage of blood flow from the left ventricle):
    • Hypertrophic Cardiomyopathy (HCM) (thickening of the heart muscle, especially in the left ventricle)
• Cerebrovascular Events Syncope:
  • Cerebrovascular Accident (CVA) (stroke)
• Arrhythmia Leading to Sudden Loss of Cardiac Output (CO) Syncope: (abnormal heart rhythms causing reduced blood pumping) - Life-threatening
  • Tachyarrhythmia (fast heart rhythms):
    • Atrial Fibrillation (Afib)
    • Supraventricular Tachycardia (SVT)
    • Ventricular Tachycardia (VT)
    • Ventricular Fibrillation (Vfib)
  • Severe Bradycardia (slow heart rhythms):
    • Sinus Arrest (SA node stops firing)
    • AV Block (electrical signals blocked between atria and ventricles)

2. Loss of Consciousness NOT Due to Impaired Cerebral Perfusion:

(These are conditions that mimic syncope but are not due to reduced blood flow to the brain)

• Seizure (epileptic seizure)
• Hypoglycemia (low blood sugar)
• Severe Hypoxia or Hypercarbia (severe lack of oxygen or excess carbon dioxide in the blood)
• Psychiatric Causes (e.g., panic attack, conversion disorder)
• Head Trauma (concussion, etc.)

Local Edema

Local edema (swelling in a specific area) is often due to problems with venous or lymphatic drainage or inflammation.

• Venous or Lymphatic Obstruction:
  • Thrombophlebitis/Deep Vein Thrombosis (DVT) (blood clot in a vein)
  • Venous Insufficiency (veins not working properly to return blood to the heart)
  • Chronic Lymphangitis (chronic inflammation of lymphatic vessels)
  • Lymphatic Tumor Infiltration (tumor blocking lymphatic vessels)
  • Filariasis (parasitic infection affecting lymphatic vessels)
• Inflammation/Infection (local inflammation or infection causing swelling)
• Trauma (injury causing local swelling)

Generalized Edema

Generalized edema (swelling throughout the body) typically indicates a systemic problem affecting fluid balance.

• Increased Hydrostatic Pressure/Fluid Overload: (increased pressure in blood vessels pushing fluid into tissues)
  • Hypertension (HTN) (high blood pressure)
  • Pregnancy (increased blood volume)
  • Drugs (e.g., Calcium Channel Blockers (CCBs) can sometimes cause edema)
  • Iatrogenic (e.g., Intravenous (IV) fluids - excessive IV fluid administration)
• Decreased Oncotic Pressure/Hypoalbuminemia: (reduced protein (albumin) in the blood, reducing the blood's ability to hold fluid within vessels)
  • Liver Cirrhosis (liver disease reducing albumin production)
  • Nephrotic Syndrome (kidney disease causing albumin loss in urine)
  • Malnutrition (inadequate protein intake)
• Increased Interstitial Oncotic Pressure: (increased protein in the tissue spaces pulling fluid out of blood vessels)
  • Myxedema (severe hypothyroidism causing increased tissue protein)
• Increased Capillary Permeability: (capillaries becoming leakier, allowing fluid to move into tissues)
  • Severe Sepsis (severe infection causing systemic inflammation and capillary leak)
• Hormonal Causes:
  • Hypothyroidism (underactive thyroid)
  • Exogenous Steroids (steroid medications)
  • Pregnancy
  • Estrogens (hormone therapy)

Palpitations are the subjective sensation of an abnormal or irregular heartbeat. They can feel like fluttering, racing, pounding, or skipped beats.

Dyspnea, or shortness of breath, is a subjective sensation of breathing discomfort.

Electrocardiography (ECG or EKG) is a fundamental diagnostic tool in cardiology. It records the electrical activity of the heart over time, providing valuable information about heart rhythm, conduction, and structural abnormalities.

Description of Electrocardiography:

• Graphical Representation of Electrical Activity: An ECG is a graphical recording of the heart's electrical activity. It shows the amplitude (strength) of the electrical signals projected as vectors over time. In simpler terms, it's a tracing of the electrical impulses that make the heart beat.
• ECG Graph Axes: The ECG is recorded on graph paper with specific axes representing time and voltage.
  • Horizontal Axis (Time): Represents time. At the standard paper speed of 25 mm/second:
    • 1 small square (1 mm) = 40 milliseconds (msec) (0.04 seconds)
    • 1 large square (5 mm) = 200 milliseconds (msec) (0.20 seconds)
  • Vertical Axis (Voltage): Represents the voltage or amplitude of the electrical signal. At the standard gain setting of 10 mm/mV (millimeters per millivolt):
    • 1 small square (1 mm) = 0.1 millivolt (mV)
    • 2 large squares (10 mm) = 1 millivolt (mV)

  ECG Paper Basics (Standard Settings)

  • Speed: 25 mm/sec
  • Gain: 10 mm/mV
  • Small Square: 1 mm x 1 mm = 40 ms (0.04 s) x 0.1 mV
  • Large Square: 5 mm x 5 mm = 200 ms (0.20 s) x 0.5 mV
• Standard Leads of a 12-Lead ECG: A standard ECG uses 12 leads, which are different viewpoints of the heart's electrical activity. These leads are categorized into:
  • Limb Leads (Bipolar): These leads are placed on the limbs and provide views in the frontal plane (vertical plane of the body). They are:
    • Lead I
    • Lead II
    • Lead III
    • aVL (augmented Vector Left)
    • aVR (augmented Vector Right)
    • aVF (augmented Vector Foot)
  • Precordial Leads (Unipolar): These leads are placed on the chest and provide views in the horizontal plane (transverse plane of the body). They are labeled V1 to V6:
    • V1-V2: Primarily view the septal (interventricular septum) region of the heart.
    • V3-V4: Primarily view the anterior (front) region of the heart.
    • V5-V6: Primarily view the lateral (side) region of the heart.
• Additional ECG Leads: In specific clinical situations, additional leads can be used to get more detailed information:
  • Right-Sided Leads (V3R-V6R): These leads are placed on the right side of the chest, mirroring the standard precordial leads on the left. They are particularly useful in cases of:
    • Right Ventricular (RV) Infarction (heart attack affecting the right ventricle)
    • Dextrocardia (heart located on the right side of the chest instead of the left)
  • Posterior Leads (V7-V9): These leads are placed on the back, behind the standard precordial lead positions. They are helpful in detecting:
    • Posterolateral Infarction (heart attack affecting the back and side of the left ventricle)
• ECG Leads and Heart Regions: Different sets of ECG leads are more sensitive to electrical activity from specific regions of the heart:
  • Lateral Wall: Leads I, aVL, V5, V6 are best for assessing the lateral wall of the left ventricle.
  • Inferior Wall: Leads II, III, aVF are best for assessing the inferior (bottom) wall of the left ventricle.
  • Anterior Wall: Leads V1-V4 are best for assessing the anterior (front) wall of the left ventricle. (V1-V2 = septal, V3-V4 = anterior proper)

  Quick Guide: ECG Lead Groupings & Walls Viewed

  • Inferior: II, III, aVF (RCA territory*)
  • Lateral: I, aVL, V5, V6 (LCx or LAD diagonal territory*)
  • Anterior: V3, V4 (LAD territory*)
  • Septal: V1, V2 (LAD septal perforator territory*)
  • Posterior: Reciprocal changes V1-V3; Direct view V7-V9 (RCA or LCx territory*)
  • Right Ventricle: V1, V3R-V6R (RCA territory*)

  *Coronary artery territories are typical but can vary based on dominance and anatomy.

Indications for ECG Monitoring:

ECG monitoring can be brief (12-lead ECG, a snapshot in time) or prolonged (24 hours or more, using Holter monitors or event recorders). The indications depend on the clinical situation.

• Myocardial Injury, Ischemia, or Prior Infarction: To detect and monitor heart damage, reduced blood flow, or the effects of a previous heart attack.
• Conditions Associated with Palpitations or Risk of Serious Arrhythmias: For patients experiencing palpitations (heart racing, fluttering, etc.) or those at risk for dangerous heart rhythm problems, including conditions like:
  • Wolff-Parkinson-White (WPW) syndrome (accessory electrical pathway)
  • Long QT syndrome (electrical disorder predisposing to arrhythmias)
  • Hypertrophic Cardiomyopathy (HCM)
  • Heart Block (disruption of electrical conduction)
  • Bradycardia (slow heart rate)
• Conduction Abnormalities: To identify and monitor problems with the heart's electrical conduction system, such as:
  • Left Bundle Branch Block (LBBB)
  • Right Bundle Branch Block (RBBB)
• Electrolyte Abnormalities: Certain electrolyte imbalances can affect the heart's electrical activity, such as:
  • Hyperkalemia (high potassium)
  • Hypokalemia (low potassium)
• Investigation of Syncope, Near Syncope, or Palpitations ("Symptom/Rhythm Correlation"): To try and capture an ECG recording during episodes of fainting, near-fainting, or palpitations, to see if there is a rhythm disturbance causing the symptoms.

Uses of ECG:

ECG is a versatile tool with various applications in cardiology:

• Recording Cardiac Rhythm During Symptoms: To document the heart rhythm when a patient is experiencing symptoms like chest pain, palpitations, or dizziness.
• Antiarrhythmic Drug Monitoring: To assess the effectiveness of medications used to treat heart rhythm problems and to monitor for potential side effects (e.g., QT prolongation).
• Assessment of Cardiac Structure and Function: While not directly imaging the heart, ECG can provide clues about:
  • Right Ventricular Hypertrophy (RVH) (enlargement of the right ventricle)
  • Left Ventricular Hypertrophy (LVH) (enlargement of the left ventricle)
  • Cardiomyopathy (diseases of the heart muscle)
• Detection of Non-Sustained Arrhythmias Requiring Prophylactic Intervention: To identify brief episodes of abnormal heart rhythms that, although not sustained, may increase the risk of more serious arrhythmias or sudden cardiac events, and thus warrant preventive treatment.

Introduction to ECG Interpretation

There are different methods to analyze an ECG. We will discuss both the traditional method and a more recent approach called PQRSTU. While these methods may seem different in how they are structured, they are both thorough and lead to the same conclusion when interpreting an ECG.

The classical approach to reading an ECG involves systematically evaluating several key aspects. This structured method ensures a comprehensive analysis of the heart's electrical activity. The main components of this approach are:

• Heart Rate: Determining how fast or slow the heart is beating.
• Heart Rhythm: Identifying the regularity and pattern of heartbeats.
• Cardiac Axis: Assessing the overall direction of the heart's electrical activity.
• Conduction Abnormalities: Detecting any blocks or delays in the electrical signals as they travel through the heart.
• Hypertrophy/Chamber Enlargement: Identifying if any of the heart chambers are abnormally enlarged or thickened.
• Ischemia/Infarction: Looking for signs of reduced blood flow or heart muscle damage.
• Miscellaneous ECG Changes: Identifying any other relevant ECG findings, such as changes in the QT interval.

Heart Rate

Heart rate is measured in beats per minute (bpm).

• Normal Heart Rate: A normal heart rate typically falls between 60 and 100 bpm. (Some sources consider 50-100 bpm normal, especially at rest).
• Elevated Atrial Rates: When the atria (upper chambers of the heart) beat too fast, it can indicate specific conditions:
  • Paroxysmal Tachycardia: Atrial rates between 150 and 250 bpm are classified as paroxysmal tachycardia.
  • Atrial Flutter: Atrial rates ranging from 250 to 350 bpm suggest atrial flutter.
  • Atrial Fibrillation (Afib): When the atrial rate exceeds 350 bpm, it is generally considered atrial fibrillation. In AFib, the atrial electrical activity is so rapid and disorganized that a specific atrial "rate" cannot be accurately determined from the ECG.
• Calculating Heart Rate in Regular Rhythms: If the heart rhythm is regular (meaning the intervals between heartbeats are consistent), the heart rate can be calculated using these methods:
  • Large Square Method: Count the number of large squares between two consecutive QRS complexes (which represent the main pumping action of the ventricles). Divide 300 by this number to estimate the heart rate. This method is based on the fact that on standard ECG paper, each large square represents 0.20 seconds, and there are 300 large squares in one minute (300 squares x 0.20 seconds/square = 60 seconds).
  • Sequence Method: Use the number of large squares between two R waves and memorize this sequence:
    • 1 large square: 300 bpm
    • 2 large squares: 150 bpm
    • 3 large squares: 100 bpm
    • 4 large squares: 75 bpm
    • 5 large squares: 60 bpm
    • 6 large squares: 50 bpm

    You can approximate the rate by identifying which numbers in this sequence are closest to the number of large squares you count.

  Calculating Regular Heart Rate

  Methods:

  • 300 Method (Large Squares): Rate = 300 / (# Large Squares between R waves)
  • 1500 Method (Small Squares): Rate = 1500 / (# Small Squares between R waves) (More precise)
  • Sequence Method: Memorize 300, 150, 100, 75, 60, 50 for 1, 2, 3, 4, 5, 6 large squares.

  Only use these for REGULAR rhythms!

• Calculating Heart Rate in Irregular Rhythms: If the heart rhythm is irregular (intervals between heartbeats vary), the rate is estimated differently:
  • 6-Second Strip Method: Count the number of R-R intervals (or QRS complexes/heartbeats) in a 6-second ECG strip. Multiply this number by 10 to estimate the heart rate per minute. (A standard 12-lead ECG tracing often represents 10 seconds, so counting R waves and multiplying by 6 also works). For example, if you count 8 R-R intervals in 6 seconds, the estimated heart rate is 8 x 10 = 80 bpm.
• Escape Rhythms (Slow Heart Rates due to Pacemaker Failure): If the heart's natural pacemaker (the sinus node) fails, other areas of the heart can take over pacing function, but usually at a slower rate:
  • Atrial Escape Rhythm: If an area in the atria takes over, the heart rate is typically between 60 and 80 bpm.
  • Junctional Escape Rhythm: If the atrioventricular (AV) junction takes over, the heart rate is usually between 40 and 60 bpm.
  • Ventricular Escape Rhythm: If the ventricles take over pacing, the heart rate is generally very slow, between 20 and 40 bpm.

Heart Rhythm

Rhythm refers to the regularity of the heartbeat. Assessing the R-R interval (the time between consecutive heartbeats) on the ECG tracing is crucial for rhythm determination.

• Regular Rhythm: The R-R interval is consistent across the entire ECG tracing. This indicates a steady, predictable heartbeat.
• Irregular Rhythm: The R-R interval varies across the tracing. This indicates an unsteady or unpredictable heartbeat. Irregular rhythms can be further classified:
  • Regularly Irregular Rhythm: There is a repeating pattern to the variations in the R-R intervals. An example is atrial flutter with a variable block, where some atrial beats are conducted to the ventricles in a repeating pattern, but not all of them.
  • Irregularly Irregular Rhythm: The R-R intervals vary in an erratic and unpredictable manner with no discernible pattern. Atrial fibrillation is a classic example of an irregularly irregular rhythm.
• Normal Sinus Rhythm (NSR): This is the ideal and healthy heart rhythm. NSR is defined by specific ECG characteristics:
  • P Wave Precedes Each QRS Complex: A P wave represents atrial depolarization (electrical activation) and should always occur before the QRS complex, which represents ventricular depolarization. This indicates that the electrical signal is originating from the sinus node and traveling normally through the atria to the ventricles.
  • QRS Complex Follows Each P Wave: Following each P wave, there should be a QRS complex, confirming that the electrical signal has successfully conducted from the atria to the ventricles and triggered ventricular contraction.
  • Normal P Wave Axis: The P wave should have a normal axis, meaning it is positive (upward deflection) in at least two out of three specific ECG leads: Lead I, Lead II, and aVF. This normal axis indicates that the electrical activation of the atria is proceeding in the correct direction.
  • Heart Rate within Normal Range: The heart rate in normal sinus rhythm should be between 50 and 100 bpm. Although the notes mention 50-100 bpm, some sources consider 60-100 bpm as the typical range for NSR at rest in adults.

Cardiac Axis

The cardiac axis refers to the average direction of the heart's electrical activity during ventricular depolarization. It is typically described in the frontal plane (as if looking at the person from the front).

• Mean Axis: The mean axis represents the overall direction of the sum of all electrical vectors generated during ventricular depolarization. It can be determined for any waveform on the ECG, such as the P wave, QRS complex, or T wave. However, when "QRS axis" is mentioned in a standard ECG report, it almost always refers to the mean axis of the QRS complex in the frontal plane, reflecting the average direction of ventricular depolarization forces.
• QRS Axis in the Frontal Plane: The QRS axis in the frontal plane is categorized into three main ranges:
  • Normal Axis: A normal QRS axis is generally considered to be between -30° and +90°. This corresponds to a positive QRS complex (upward deflection) in both Lead I and Lead II on the ECG.
  • Left Axis Deviation (LAD): Left axis deviation is present when the QRS axis is less than -30° (more negative).
    • Differential Diagnosis for Left Axis Deviation: Conditions that can cause LAD include:
      • Normal Variant: In some individuals, LAD can be a normal physiological variation, sometimes related to age.
      • Left Anterior Hemiblock (LAHB): A block in the anterior fascicle of the left bundle branch.
      • Left Ventricular Hypertrophy (LVH): Enlargement of the left ventricle.
      • Inferior Myocardial Infarction (MI): Heart attack affecting the inferior (bottom) part of the heart.
      • Wolff-Parkinson-White (WPW) Syndrome: A condition with an extra electrical pathway in the heart.
      • Right Ventricular (RV) Pacing: Pacing from the right ventricle can alter the axis.
      • Elevated Diaphragm: Conditions that elevate the diaphragm (like pregnancy or ascites) can shift the heart's position.
      • Lead Misplacement: Incorrect placement of ECG leads can lead to axis deviation.
      • Congenital Heart Disease: Certain congenital heart defects, such as primum atrial septal defect (ASD) and endocardial cushion defect, can cause LAD.
      • Hyperkalemia: High potassium levels in the blood.
      • Emphysema: A lung condition that can affect heart position and ECG readings.
  • Right Axis Deviation (RAD): Right axis deviation is present when the QRS axis is greater than +90° (more positive).
    • Differential Diagnosis for Right Axis Deviation: Conditions associated with RAD include:
      • Normal Variant: A "vertical heart" position, which is a normal anatomical variant, can result in an axis around 90°.
      • Right Ventricular Hypertrophy (RVH): Enlargement of the right ventricle.
      • Left Posterior Hemiblock (LPHB): A block in the posterior fascicle of the left bundle branch.
      • Pulmonary Embolism (PE): A blood clot in the lung arteries.
      • Chronic Obstructive Pulmonary Disease (COPD): A lung disease that can cause changes in heart position and pressures.
      • Lateral Myocardial Infarction (MI): Heart attack affecting the lateral (side) part of the heart.
      • Wolff-Parkinson-White (WPW) Syndrome: Can sometimes present with RAD.
      • Dextrocardia: A rare condition where the heart is located on the right side of the chest instead of the left.
      • Septal Defects: Certain types of septal defects (holes in the walls between heart chambers).
• QRS Axis in the Horizontal Plane: The QRS axis in the horizontal plane (as if looking at a cross-section of the chest) is not routinely calculated in standard ECG interpretation. However, the transition zone, where the QRS complex changes from predominantly negative to predominantly positive in the precordial leads (V1-V6), is observed. Normally, this transition occurs around lead V3 or V4.

Conduction abnormalities refer to disruptions or delays in the normal electrical pathway through the heart. These abnormalities can be broadly categorized into bundle branch blocks and fascicular blocks.

Bundle Branch Blocks:

These occur when there is a block in one of the main branches of the bundle of His, which are responsible for conducting electrical signals to the ventricles.

• Right Bundle Branch Block (RBBB):
  • QRS Duration: The QRS complex is prolonged, with a duration greater than 120 milliseconds (ms) (> 3 small squares).
  • V1 Appearance: In lead V1, the QRS complex typically shows an rSR' pattern. This means there is a small initial upward deflection (r), followed by a large downward deflection (S), and then another large upward deflection (R'). In some cases, a broad R wave may be seen instead of rSR'. The overall QRS complex in V1 is predominantly positive.
  • V5-V6 and Lead I Appearance: In leads V5, V6, and Lead I, there are broad S waves, which are negative deflections lasting 40 ms or more.
  • Secondary T Wave Inversion: Often, there are secondary T wave inversions (T waves pointing in the opposite direction to the main QRS deflection) in leads V1 and V2. This is a "secondary" change because it's a consequence of the altered depolarization, not a primary issue with repolarization itself.
  • Frontal Axis Determination: When assessing for axis deviation in the presence of RBBB, it's important to focus on the first 60 ms of the QRS complex. This initial part of the QRS is less affected by the bundle branch block and more accurately reflects the underlying axis.
  • Summary of RBBB on ECG: In essence, RBBB is characterized by a positive complex in V1 (rSR' or broad R) and a broad S wave in V6 (and often I, V5).

  RBBB Key ECG Features

  • QRS Duration: > 120 ms
  • V1/V2: rSR' ("rabbit ears") or broad R wave
  • I, aVL, V5, V6: Wide, slurred S wave (>40 ms)
  • ST/T changes: Discordant (opposite direction to terminal QRS) T wave inversion in V1-V3
• Left Bundle Branch Block (LBBB):
  • QRS Duration: Similar to RBBB, the QRS complex is prolonged, with a duration greater than 120 ms.
  • Leads I, aVL, V5, V6 Appearance: In leads I, aVL, V5, and V6, the QRS complexes are broad and often notched R waves are observed. These leads typically show a predominantly positive QRS complex.
  • Leads V1-V2 Appearance: In leads V1 and V2, deep, broad S waves are seen. These leads are predominantly negative in LBBB.
  • Secondary ST-T Changes: Secondary ST-T wave changes are usually present in LBBB. Specifically, ST segment depression and T wave inversion are typically seen in leads with the broad notched R waves (like I, aVL, V5, V6) and also in leads V1-V2. These ST-T changes are secondary to the altered depolarization pattern.
  • Masking Myocardial Infarction (MI): LBBB can make it difficult to diagnose myocardial infarction on an ECG because the ST-T changes associated with LBBB can obscure the ST elevation that is a key sign of acute MI. (See Sgarbossa criteria for MI in LBBB).
  • Summary of LBBB on ECG: LBBB is characterized by a negative complex (broad S) in V1 and a positive, broad/notched complex in V6 (and often I, aVL, V5).

  LBBB Key ECG Features

  • QRS Duration: > 120 ms
  • I, aVL, V5, V6: Broad, notched, or slurred R waves; Absence of Q waves
  • V1, V2: Deep, broad S waves (negative complex)
  • ST/T changes: Discordant (opposite direction to main QRS) ST depression and T wave inversion in leads with upright QRS (I, aVL, V5, V6).
  • Note: New LBBB is often considered equivalent to ST-elevation MI (STEMI) in the context of ischemic symptoms.

Fascicular Blocks (Hemiblocks):

These are blocks in the fascicles (anterior and posterior) of the left bundle branch.

• Left Anterior Fascicular Block (LAFB) / Left Anterior Hemiblock:
  • Axis Deviation: Typically causes left axis deviation (axis more negative than -30°).
  • Lead I and aVL: Small Q waves and prominent R waves are often seen in leads I and aVL.
  • Lead II, III, and aVF: Small R waves and prominent S waves are often seen in leads II, III, and aVF.
  • Initial 60 ms of QRS: The first 60 ms of the QRS complex shows the pattern of LAFB (used for axis determination).
• Left Posterior Fascicular Block (LPFB) / Left Posterior Hemiblock:
  • Axis Deviation: Typically causes right axis deviation (axis more positive than +90°, generally between 110° and 180°). Note: LPFB is rare in isolation and is a diagnosis of exclusion.
  • Lead I and aVL: Small R waves and prominent S waves are often seen in leads I and aVL.
  • Lead II, III, and aVF: Small Q waves and prominent R waves are often seen in leads II, III, and aVF.
  • Initial 60 ms of QRS: The first 60 ms of the QRS complex shows the pattern of LPFB.

Bifascicular Block:

• Bifascicular block refers to impaired conduction in two of the three main fascicles of the ventricular conduction system (RBB, Left Anterior Fascicle, Left Posterior Fascicle). The most common combination is RBBB with left anterior hemiblock (LAHB).
• On an ECG, bifascicular block will show the criteria for both RBBB and the specific hemiblock (usually LAHB).

Nonspecific Intraventricular Block:

• QRS Duration: QRS duration is prolonged, greater than 120 ms.
• Diagnostic Criteria: It is diagnosed when the QRS is wide, but the ECG does not meet the definitive criteria for either LBBB or RBBB. It is essentially a wide QRS complex that is not clearly defined as a specific bundle branch block. (Often due to drugs, electrolytes, or diffuse myocardial disease).

Hypertrophy refers to the thickening of the heart muscle, while chamber enlargement refers to an increase in the size of a heart chamber. ECG criteria can help identify hypertrophy of the ventricles and enlargement of the atria.

Ventricular Hypertrophy:

• Left Ventricular Hypertrophy (LVH):
  • Voltage Criteria: Several voltage criteria are used to assess for LVH. These criteria are based on the amplitude (height) of the R and S waves in specific leads, which increase when the left ventricle is hypertrophied.
    • S wave in V1 + R wave in V5 or V6 > 35 mm: If the sum of the depth of the S wave in lead V1 and the height of the R wave in either lead V5 or V6 is greater than 35 mm (measured from the baseline), it suggests LVH in individuals over 40 years old. The threshold is adjusted for younger age groups: >40 mm for ages 31-40, and >45 mm for ages 21-30. (Sokolow-Lyon criteria)
    • R wave in aVL ≥ 11 mm: An R wave in lead aVL that is 11 mm or taller is another voltage criterion for LVH.
    • R wave in Lead I + S wave in Lead III ≥ 25 mm: If the sum of the height of the R wave in lead I and the depth of the S wave in lead III is 25 mm or greater, it is also suggestive of LVH. (Cornell criteria variation)
  • Strain Pattern: In addition to voltage criteria, a "LV strain" pattern can support the diagnosis of LVH. This pattern is characterized by:
    • ST segment depression: Specifically, asymmetric ST segment depression.
    • T wave inversion: T waves that are inverted (pointing downwards) and asymmetric.
    • Location of Strain Pattern: These ST-T wave changes are typically seen in leads I, aVL, and V4-V6, which are leads that "view" the left ventricle.
  • Left Atrial Enlargement: LVH is often associated with left atrial enlargement.
  • Note on Criteria: The more voltage criteria that are present, the higher the likelihood of LVH. If only one voltage criterion is met, it is considered "minimal voltage criteria for LVH" and may be a normal variant, particularly in younger, athletic individuals.

  Common LVH Voltage Criteria

  Presence of one or more suggests LVH (specificity increases with more criteria met):

  • Sokolow-Lyon: S_V1 + R_{V5 or V6} ≥ 35 mm (adjust for age < 40)
  • Cornell Voltage: R_aVL + S_V3 > 20 mm (female) or > 28 mm (male)
  • R in aVL: ≥ 11 mm
  • Other: R_I + S_III ≥ 25 mm

  LV Strain Pattern: Asymmetric ST depression and T wave inversion in lateral leads (I, aVL, V5-V6) supports LVH diagnosis, especially if voltage criteria are borderline.

• Right Ventricular Hypertrophy (RVH):
  • Right Axis Deviation: RVH is often associated with right axis deviation on the ECG.
  • R/S Ratio in V1: An R/S ratio greater than 1 in lead V1, or a qR complex in V1, is suggestive of RVH. Normally, in V1, the S wave is larger than the R wave (R/S ratio < 1). In RVH, the R wave becomes larger, sometimes exceeding the S wave. A qR complex means a small negative deflection (q) followed by a large positive deflection (R).
  • P wave in Lead II (P Pulmonale): A P wave in lead II that is taller than 2.5 mm (2.5 small squares) is called "P pulmonale" and can be associated with right atrial enlargement and RVH, especially in the context of pulmonary hypertension.
  • RV Strain Pattern: Similar to LV strain, RVH can have a "RV strain" pattern, characterized by:
    • ST segment depression
    • T wave inversion
    • Location of Strain Pattern: In RVH, the strain pattern is usually seen in leads V1-V3, which are leads that "view" the right ventricle.

Atrial Enlargement:

• Left Atrial Enlargement (LAE):
  • P Mitrale: In lead II, the P wave may be prolonged (>100 ms or 0.10 seconds) and notched. This is referred to as "P mitrale" and is often associated with mitral valve disease and LAE.
  • Biphasic P Wave in V1: In lead V1, the P wave may be biphasic (partly positive and partly negative). The negative (terminal) component of the P wave in V1 is particularly important. If this negative component is:
    • Width: ≥ 1 mm (0.04 seconds or one small square) wide.
    • Depth: ≥ 1 mm (0.1 mV or one small square) deep.

    This biphasic P wave in V1 with a prominent negative terminal component is a strong indicator of LAE.

• Right Atrial Enlargement (RAE):
  • P Pulmonale: In leads II, III, or aVF, the P wave may be tall, with a height of ≥ 2.5 mm (2.5 small squares). This is called "P pulmonale" and is indicative of RAE. The P wave is peaked and increased in amplitude but usually not prolonged.

Ischemia and infarction refer to conditions of reduced blood supply and tissue death in the heart muscle, respectively, usually due to coronary artery disease. ECG changes are crucial for diagnosing and localizing ischemia and infarction.

• Anatomical Distribution: When evaluating ECG changes for ischemia or infarction, it is essential to consider the anatomical distribution of these changes, meaning which areas of the heart are affected. Different coronary arteries supply different regions of the heart, and ECG leads reflect electrical activity from specific areas.
• Ischemia: Ischemia represents a temporary reduction in blood flow to the heart muscle, not severe enough to cause permanent damage initially. ECG signs of ischemia include:
  • ST Segment Depression: Downsloping or horizontal depression of the ST segment below the baseline.
  • T Wave Inversion: T waves become inverted (negative), most commonly seen in leads V1-V6, which are precordial leads that view the anterior and lateral aspects of the heart.
• Injury/Infarct: Injury and infarction represent more severe and prolonged ischemia, leading to potential or actual heart muscle damage.
  • Transmural Infarction: This type of infarction involves the full thickness of the heart muscle wall, from the endocardium (inner layer) to the epicardium (outer layer).
    • ST Elevation: The hallmark ECG sign of acute transmural injury/infarction is ST segment elevation. This elevation is seen in the ECG leads that are facing the injured or infarcted area of the heart. ST elevation indicates ongoing myocardial injury and is a critical sign of acute myocardial infarction (STEMI).
  • Subendocardial Infarction: This type of infarction involves the inner layer of the heart muscle (subendocardium).
    • ST Depression: In subendocardial ischemia or infarction, the ECG typically shows marked ST segment depression in the leads facing the affected area.
    • Enzyme Changes and Other MI Signs: Subendocardial infarction may be accompanied by elevated cardiac enzymes in blood tests (like troponin) and other clinical signs of myocardial infarction, even if ST elevation is not present. This type is sometimes referred to as non-ST elevation myocardial infarction (NSTEMI).
• Typical ECG Changes in Evolving Myocardial Infarction (MI): The ECG changes in myocardial infarction typically evolve over time through a sequence of stages:
  1. Hyperacute T Waves: In the very early stages (within minutes to hours) of acute MI, "hyperacute" T waves may appear in the leads facing the infarcted area. These are tall, symmetrically peaked T waves, often preceding or accompanying ST elevation.
  2. ST Elevation (Injury Pattern): ST segment elevation is the classic "injury pattern" in acute MI. It typically develops within the first few hours post-infarct and is seen in the leads facing the injured area.
     • Posterior MI: In acute posterior myocardial infarction, ST elevation is not directly seen in the standard 12-lead ECG because these leads do not directly view the posterior heart. Instead, "reciprocal" ST depression is observed in leads V1-V3. To better visualize posterior MI, additional posterior leads (like V7-V9) can be recorded, creating a 15-lead ECG, which may show ST elevation in the posterior leads.
  3. Significant Q Waves: Significant Q waves can develop hours to days after the onset of infarction. These Q waves represent electrically silent, necrotic (dead) heart muscle.
     • Criteria for Significant Q Waves:
       • Duration: Q wave duration > 40 ms (0.04 seconds or one small square).
       • Amplitude: Q wave amplitude > 1/3 of the total QRS amplitude.
       • Location: Present in at least two consecutive leads that correspond to the same anatomical territory (e.g., leads II and aVF for inferior territory).
     • Early Appearance: Q waves of infarction can sometimes appear very early, even with or without ST segment changes.
     • Non-Q Wave Infarction: In some cases, particularly in subendocardial infarction or non-transmural infarction, significant Q waves may not develop. These are referred to as "non-Q wave infarctions." In these cases, the ECG may only show ST segment or T wave changes despite clinical evidence of infarction.
  4. Inverted T Waves: T wave inversion typically develops one day to weeks after infarction. Inverted T waves in the context of MI usually indicate ischemia or a post-infarction state.
• Completed Infarction: In a completed or "old" infarction (months to years after the event), the ECG may show:
  • Abnormal Q Waves: Persistent, significant Q waves as described above. (Note: Small Q waves can be normal in lead III and aVL due to septal depolarization, but these are not typically wide or deep).
    • Duration Criteria: Q wave duration > 40 ms (>30 ms in aVF specifically for inferior infarction).
    • Amplitude Criteria: Q wave amplitude > 1/3 of the total QRS amplitude.
    • Location Criteria: Present in at least 2 consecutive leads in the same territory.
  • Abnormal R Waves in Posterior Infarction: In posterior infarction, abnormal R waves (R/S ratio > 1, R wave duration > 40 ms) may be found in leads V1, and sometimes V2. These are usually seen in association with signs of inferior and/or lateral infarction. The tall R wave in V1-V2 in posterior MI is a reciprocal change reflecting the Q waves that would be seen if we had leads directly over the posterior heart.
• ST Elevation Criteria: For diagnosing ST elevation myocardial infarction (STEMI), specific criteria for ST elevation are used:
  • New ST Elevation: New ST segment elevation at the J-point in two contiguous leads.
  • Magnitude:
    • ≥ 0.1 mV (1 mm) in all leads other than V2-V3.
    • For leads V2-V3: The criteria are gender- and age-specific:
      • ≥ 0.2 mV (2 mm) in men ≥ 40 years of age.
      • ≥ 0.25 mV (2.5 mm) in men < 40 years of age.
      • ≥ 0.15 mV (1.5 mm) in women.

  STEMI ECG Criteria Summary

  New ST elevation at J-point in ≥ 2 contiguous leads:

  • Leads V2-V3:
    • ≥ 2 mm (0.2 mV) in men ≥ 40 yrs
    • ≥ 2.5 mm (0.25 mV) in men < 40 yrs
    • ≥ 1.5 mm (0.15 mV) in women
  • Other Leads: ≥ 1 mm (0.1 mV)

  Note: New LBBB in context of ischemic symptoms is often treated as a STEMI equivalent. Reciprocal ST depression supports the diagnosis.

• Areas of Infarction/Ischemia and Corresponding ECG Leads: Different coronary arteries supply specific areas of the heart. Blockage of these arteries leads to infarction in those areas, which are reflected in specific ECG leads. (Assuming right dominant coronary anatomy, which is most common).

  Infarct Location, Vessel, and ECG Leads (Typical, Right Dominant)

  Vessel Usually Involved	Infarct Area	ECG Leads Showing Changes
  Left Anterior Descending (LAD) Artery	Anteroseptal	V1, V2
  LAD Artery	Anterior	V3, V4
  LAD and Left Circumflex (LCx) Arteries	Anterolateral	I, aVL, V3-V6
  LAD Artery (Proximal)	Extensive Anterior	I, aVL, V1-V6
  Right Coronary Artery (RCA)	Inferior	II, III, aVF
  RCA	Right Ventricle	V1, V3R, V4R (right-sided chest leads)
  RCA or LCx	Posterior MI (often with Inferior MI)	V1, V2 (prominent R waves, reciprocal changes); V7-V9 (ST elevation in posterior leads)
  Left Circumflex (LCx) Artery	Lateral	I, aVL, V5-V6
  LCx Artery	Isolated Posterior MI	V1, V2 (prominent R waves, reciprocal changes); V7-V9 (ST elevation)

  Note: LAD = Left Anterior Descending artery, LCx = Left Circumflex artery, RCA = Right Coronary Artery

Pacemakers are devices implanted to regulate heart rhythm in cases of slow heart rates or conduction problems. ECGs in patients with pacemakers will show characteristic "pacemaker spikes."

• Atrial Pacemaker:
  • Pacemaker Spike Timing: An atrial pacemaker spike will be visible on the ECG just before the P wave. This spike represents the electrical impulse delivered by the pacemaker to stimulate the atria to contract.
• Ventricular Pacemaker:
  • Pacemaker Spike Timing: A ventricular pacemaker spike will be visible on the ECG just before the QRS complex. This spike indicates the electrical impulse from the pacemaker stimulating the ventricles.
  • QRS Morphology: The QRS complex following a ventricular pacemaker spike is typically broad and has a left bundle branch block (LBBB) morphology. This is because ventricular pacing often starts from the right ventricle and spreads through the ventricles in a way that mimics LBBB on the ECG.