Advanced EKG/ECG Interpretation

Resting cardiac cells have a negative charge because sodium ions (outside) are more positively charged than potassium ions (inside). This polarized state means the cell is ready to fire. When stimulated, potassium leaks out, causing depolarization and a positive charge inside the cell. The electrical impulse then spreads through the heart. Recovery, or repolarization, occurs when sodium and potassium return to their original positions via the sodium-potassium pump (Klabunde, 2023).

Image 2: Cardiac Cycle

A P wave on an EKG/ECG represents atrial electrical release, or depolarization. This initiates a cascade or wave of electrical activity initiated by an impulse from the SA node and the following electrical spread (conduction) through the atria. The SA node is, physiologically, located in the right atrium, so the right atrium begins heart muscle constriction known as depolarization. This right atrium depolarization wave represents the first half of the P wave graphic. As depolarization spreads to and through the left atrium, we observe that process in the second half of the P wave graphic. The amplitude (height) is normally 0.05 to 0.25 mV (0.5 to 2.5 small boxes). Normal duration 0.06-0.12 seconds (1.5 to 2.75 small boxes). The shape of a P wave is usually smooth and rounded.

In leads I and II, the P waves should always be positive or above the baseline, whereas in lead aVR, in a normal sinus rhythm, they should be negative. And here is a teaser to whet your interest: when you see an abnormal P wave, consider strongly the presence of atrial changes, such as myocardial enlargement (Biology Insights, 2025).

AV conduction time is the PR interval. It is the time from the start of atrial depolarization, the P wave, to the beginning of the QRS, or ventricular depolarization. The normal PR interval is three to five small squares or 0.12 to 0.20 seconds. Long PR intervals may indicate the presence of a first-degree atrioventricular (AV) block, while short intervals are often associated with disorders of AV acceleration, such as Wolf-Parkinson-White (WPW) syndrome (Cardiovascular Medicine, n.d.).

Q+R+S represents the beginning of ventricular depolarization until the end of ventricular depolarization.

This brings us to the QRS complex, a crucial portion of the EKG/ECG that illustrates ventricular depolarization—the momentous electrical event that triggers the contraction of the heart’s powerful lower chambers. The QRS complex is typically much steeper and sharper than the P wave, reflecting the rapid spread of the impulse through the ventricles. Normally, its duration should measure no more than three small squares or 0.12 seconds, emphasizing the swiftness of ventricular activation. Widened QRS complexes can suggest issues like bundle branch blocks (BBB) or ventricular rhythms. Each component of the complex, the Q, R, and S waves, carries unique significance (Cardiovascular Medicine, n.d.).

The duration of the entire QRS is less than 120 ms or equivalent to three small squares. An extended QRS might indicate the presence of a BBB or hyperkalemia. Early ventricular contractions (premature ventricular contractions or PVCs) are frequently associated with a wide QRS length. So, remember to count boxes in the QRS when you see those annoying PVCs.

The delta wave is a slurred upstroke in the QRS complex, signifying a condition of pre-excitation in the ventricles. Typically, it arises at the end of the P wave, making for a shortened PR interval. Most commonly, it is associated with WPW syndrome, where an accessory pathway can allow early excitation of the ventricles (Cadogan & Buttner, 2022).

Delta Wave

Image 5: Delta Wave, Lead II

Note the upward slope beginning at the end of the P wave, overriding the Q, and climbing up the forepart of the R.

The Q wave is the initial, tiny, downward, or negative deflection of ventricular depolarization and contraction. To be more exact, Q represents depolarization of the intraventricular septum, the membranous and muscular partition separating the right from the left ventricles of the heart.

The normal Q wave is small and easily missed. It is less than 25% of the R wave amplitude and does not exceed 0.04 seconds in duration, which is equivalent to one small box. Abnormal Q waves are a strong indication of the presence of an old myocardial infarction (Burns & Buttner, 2024a).

The R wave is the first upward or positive deflection after the P wave and the tallest portion of the QRS complex (ACLS Medical Training, n.d.).

The S wave is the first downward or negative deflection after the R wave and represents the final depolarization of the Purkinje fibers in the ventricles (ACLS Medical Training, n.d.).

The ST segment is the electrical resting period after ventricular depolarization. It represents early repolarization of the left and right ventricles. This interval begins with the end of the QRS complex and ends with the onset of the T wave (Kashou et al., 2023). Its duration is two to three small squares, 80-120 ms, and its isoelectric charge should lie at the same height as the PR interval. This height comparison is important. ST-elevation can be an indication of acute myocardial infarction. Other heart conditions that are expressed in ST abnormalities include acute pericarditis, hyperkalemia, hypercalcemia, pulmonary embolism, ventricular aneurysm, left BBB, Prinzmetal angina, blunt trauma to the heart, Brugada syndrome, and even subarachnoid hemorrhage.

The T wave is the process of ventricular repolarization. T follows, after a short pause, the QRS complex (ACLS Medical Training, n.d.). The T should be less than two-thirds of the height of the R wave. T-wave morphology changes are seen in conditions such as hyperkalemia, hypercalcemia, endocrine changes, myocarditis, pericarditis, cardiomyopathy, pulmonary embolism, fever, generalized infections, anemia, acid-base disorders, and more.

U waves are small positive deflections that may be seen following the T wave. There is no clear consensus on what they represent; however, delayed repolarization of the tissue known as the papillary muscle or Purkinje fibers often occurs during the interval when they are seen (School of Health Sciences, n.d.).

The QT interval represents the total ventricular activity from ventricular depolarization to repolarization. There is no fixed “normal” for this period of length, though 400 to 440 ms has been suggested. It is measured from the beginning of the QRS complex to the end of the T wave, with slower heart rates having longer QTs (Lome, n.d.b).

Prolonged QT intervals indicate a lengthened relative refractory period, a vulnerable period for abnormal electrical mischief. Inside this vulnerable period, critical, life-threatening rhythms may attempt to establish themselves, such as torsades de pointes, ventricular tachycardia (VT), or ventricular fibrillation (VF).

Osborn waves or J waves are seen mostly during hypothermia. This wave presents a small deflection at the junction, “J,” of the QRS complex and the ST segment (Cadogan & Buttner, 2025).

Congratulations if you encounter one—Epsilon waves are rare. They are a regularly occurring, small positive deflection buried at the end of the QRS complex. Most frequently associated with inherited heart disease from arrhythmogenic right ventricular cardiomyopathy (ARVC). First described in 1977, this condition is responsible for 11% of sudden cardiac deaths (SCD) in athletes (McKenna, 2024).

Image 6: Cardiac Cycle Components

The standard heart monitor paper speed is 25 mm (five large squares)/sec. If the interval between two beats (R-R) is five large squares, the heart rate is 60 beats/min.

Rule of 300: Divide 300 by the number of the large squares between two heart beats (R-R), or, if the interval between two beats is one large square, the heart rate is 300 beats/min, two squares →150, three squares →100, four squares → 75, five squares → 60, six squares → 50 beats/min.

Image 8: Calculating Heart Rate

The six-second method: Count the number of complete R waves within six seconds and multiply that number by ten. This count is the one-minute heart rate. This method can be used when the rhythm is "regular” or “irregular" (Singh, 2025a).

The three-second method: Count the number of complete QRS complexes in three seconds and multiply that by twenty. This count is the one-minute heart rate.

Image 9: EKG/ECG Boxes

The eight-step system is a good starter system, and you will quickly learn what to look for.

Step One: Determine the Rate

• To determine the atrial rate, measure the distance between P-P and determine the rate by one of the methods listed earlier.
• What is the ventricular rate?
• To determine the ventricular rate, measure the distance between R-R.
• Note: The rate of a normal sinus rhythm is 60-100 bpm.

Step Two: Determine the Rhythm

• Is the rhythm regular? Regular? Regularly irregular? Irregularly irregular?

Step Three: Evaluate P Waves

• Are P waves present and uniform in appearance?
• Are P waves upright (positive) in lead II?
• Do P waves appear regularly before each QRS complex?
• Is there more than one P wave before a QRS complex?
• If irregular, is there an associated QRS?

Step Four: Evaluate the PR Interval

• If the PR interval is less than 0.12 or more than 0.20 seconds, conduction follows an abnormal pathway, or the electrical impulse is delayed at the AV node.
• The normal PR interval is 0.12 to 0.20 seconds.
• Is the PR interval consistent?

Step Five: Evaluate the QRS Complex

• Do the QRS complexes occur uniformly and look the same throughout the strip?
• If the QRS measures 0.10 seconds or less, it is considered narrow and is presumed to be supraventricular in origin.
• If the QRS complex is greater than 0.12 seconds or more, it is considered wide and presumed to be ventricular in origin until proven otherwise.
• The QRS normally measures 0.04 to 0.10 seconds in duration. Determine if they are married to the P waves.

Step Six: Evaluate T Wave

• Are T waves present?
• Are T waves smooth and rounded?
• Do they have a normal amplitude of 0.5 mV or less?
• Is the deflection the same as the preceding QRS?
• Is there a relationship between any ectopy to the T wave?

Step Seven: Evaluate the QT Interval

• Is the duration from 0.36 to 0.44 seconds?

Step Eight: Evaluate Other Components

• Is the ST-segment elevated? Depressed? Sloping or scooped?
• Are U waves present? Prominent?
• Are there other funny little beats detected?

Origin of the impulse plus the cardiac activity = rhythm name.

• Origin of the impulse - Is it sinus, atrial, junctional, or ventricular?
• Cardiac Activity: Normal (in rhythm), bradycardic (slow), accelerated (faster than normal), or tachycardic (greater than 100/min)?
• For example, sinus bradycardia, sinus tachycardia, junctional, or VT.

The normal electrical flow through the heart originates in the SA node > AV node > bundle of His > left and right bundle branches > Purkinje fibers with mechanical (muscle) cells stimulated along the way. Therefore, the primary pacemaker is the SA node and has an inherent rate of 60-100 bpm. The SA node has the highest level of automaticity; however, emergency “escape” pacemakers exist.

Escape pacemakers are cells that initiate a heartbeat when the faster normal pace fails to descend along the standard conduction pathway. Escape cells exist in the AV junction and the ventricles.

The AV junction is the AV node and the nonbranching portion of the bundle of His. The pacemaker cells in the AV junction are located near the non-branching portion of the bundle of His (Burns & Buttner, 2024b).

The AV node should only generate an impulse if the SA node does not function at its normal rate. The AV node fires electrical impulses at a slower rate of 40-60 bpm.

Ventricular pacemakers in the bundle branches and the Purkinje network will become the initiating pacemaker if the AV node cannot function or the depolarization wave fails to descend. The inherent ventricular rate is 20-40 bpm.

The industry standard in healthcare is the 12-lead EKG/ECG, of which there are 10 electrodes with wires, only 9 of which receive information. Have I made any engineering remarks yet? You do get 12 distinct readouts, however. The marvels of science.

Additionally, a 12-lead may not typically be used for monitoring a patient. For ongoing patient care, including pre-admission work by emergency responders, a three-lead configuration of foam-backed sticky electrodes is used, with limb lead II being considered the view of choice.

Back to 12-leads. One wire is a grounding wire and contributes only to patient safety in the process. The remaining leads, or more accurately, tracings, consist of ten wires, resulting in three standard leads (formerly known as limb leads), three augmented leads (also known as Goldberg leads), and finishing with six precordial leads (Wilson’s chest leads) for a complete 12-lead EKG/ECG report. Let me just mention that William Einthoven developed the practical EKG/ECG in 1902, earning a Nobel Prize. His triangle, now known as the limb leads and later as the standard leads, remains central to recording heart activity in leads I, II, and III (Lee, 2025).

Lead I:

• The electrode is often placed just below the left clavicle instead of the traditional left arm.
• Provides information about the left lateral wall of the chest.

Lead II:

• Electrode near the left leg (typically placed below the left pectoral muscle).
• Provides information about the inferior wall of the heart.
• Common in cardiac monitoring because the position of view for this lead is close to the heart’s actual conduction pathways.

Lead III:

• Provides information about the inferior wall of the heart.

STANDARD 12-LEAD SETUP

Image 11: Standard 12-Lead

Using the same placement of three-electrode pads and a little fancy math, we can get different views of the electrical activity in the heart. These are known as augmented limb leads, Goldberger leads, unipolar limb leads, or just unipolar leads. An EKG/ECG can create an augmented theoretical null point in the center of Einthoven’s triangle, allowing a view of the absolute potential in each electrode (Horoba, 2025).

Sounds a little esoteric? Well, it is all about the angle, or vector, from which you are looking at the heart. Think about standing at the end of an extremity, right arm, left arm, or feet, with the feet lying side by side. Now squint up at the heart along that axis. Electric waves moving away from your position will have a positive amplitude on the EKG/ECG strip. The waves are moving toward you, a negative deflection. Electrical events that do neither will be minimized, blended into the baseline (Horoba, 2025).

The augmented leads are named aVR, aVL, and aVF. “A” for “augmented,” “V” for “voltage,” then “Right,” “Left,” and “Foot.” The leading “A” can be lower case or capitalized, though the lower case is technically correct.

Lead aVR:

• The augmented unipolar right arm lead is oriented toward the cavity of the heart.
• Electrical current from the heart is traveling towards the right arm.
• All deflections of the EKG/ECG, P, QRS, and T should be negative in this lead.

Lead aVL:

• The augmented unipolar left arm leads oriented toward the heart, facing the anterolateral aspect of the left ventricle.
• Electrical current from the heart is traveling towards the left arm.

Lead aVF:

• The augmented unipolar left leg lead (feet). It is oriented toward the inferior surface of the heart.
• Electrical current from the heart is traveling toward the feet.

Standard leads, plus augmented leads, make up the first six of a 12-lead EKG/ECG. Surprise! These first six share one important characteristic: they all view the heart from the frontal plane, as though the patient is lying prone and their heart flat on the top of a table we are looking across. Oh, if we could only see the heart's activity from the horizontal plane, as though we were looking straight through our patient!

Well, with math, we can. Welcome to the six precordial leads.

The precordial, or chest leads, view the heart's electrical conduction from a straight face-to-face view. These leads, referred to as “V” leads, or Wilson’s chest leads, are horizontal plane, unipolar leads.

Lead V1:

• Anterior view of the right ventricle and right atrium.
• Faces the heart cavity.
• Provides an electrical view of the right ventricle.
• QRS is mostly negative in this lead.

Lead V2:

• Anterior view.
• Provides an unobstructed view of electrical activity in the right ventricle.
• QRS is mostly negative.

Lead V3:

• View of the heart's sternocostal surface.

Lead V4:

• Septal view and left ventricle.
• QRS is mostly positive.

Lead V5:

• Lateral view of the septum and left ventricle.
• QRS is mostly positive.

Lead V6:

• Lateral view of the septum and left ventricle.
• QRS is mostly positive.

There are additional uncommon, used for special situations, lead patterns out there. Just so you are aware.

Regularity is a fundamental factor for functional heart rhythms. The rate of conduction, whether it is too slow or too fast for adequate blood perfusion, is also essential for effective cardiac function. Additionally, the composition of each heartbeat is important; effective pumping ensures that blood moves forward efficiently, while ineffective efforts can reduce cardiac output. Assessment focuses on P waves, QRS complexes, and T waves to evaluate these functions quickly and effectively.

Regularity is measured using EKG/ECG graph paper. Typically, a single off-timing beat is notable but not usually concerning. Multiple irregular beats may indicate underlying issues and should prompt further evaluation. This applies to beats originating from the atrium, junctional region, or ventricles.

The heart's pumping ability depends on its rate. The standard is 60–100 bpm; rates below this range can reduce cardiac output, while higher rates can compromise consistency of blood flow. The origin of any rate abnormality is significant, as the heart attempts to compensate for impaired pumping capacity (King & Lowery, 2023).

Inadequate filling of the heart chambers can lead to a rapid decline before ventricular contraction fails, potentially resulting in congestion. Abnormal QRS complexes are indicative of incomplete contraction. What is observed electrically on the monitor corresponds to physiological outcomes that impact patient health. Early detection, investigation, and appropriate treatment are associated with improved outcomes.

Heart patterns involve rhythm, rate, and aberrancy (Nickson, 2024).

Image 12: Normal and Pathological EKGs/ECGs

Cardiac rhythms are controlled by the loci of the highest magnitude, fastest, and strongest cadence. This will be doubly important when we discuss pacemakers. At the core, there are three basic heart rhythms.

Basic Cardiac Rhythms

Image 13: Basic Rhythms, Lead II

Sinus rhythm (impulses are generated by the SA node). Junctional rhythm (impulses are generated by the AV junction). Ventricular rhythm (impulses are generated by Purkinje fibers in the ventricles).

Because the SA node generates impulses with the highest magnitude, it has overdrive suppression over all heart tissue. The SA node is referred to as the primary pacemaker, the cadence setter.

A normal heartbeat is triggered by the SA node in the upper right atrium, producing a regular rhythm of 60 to 100 bpm (King & Lowery, 2023). This normal sinus rhythm adjusts to the body's needs, increasing or decreasing with activity or rest.

Image 14: Normal Sinus Rhythm, Lead II and V1

Sinus Beats

Any beat is fine if it originates in the atrium of the heart, right?

Oh, you are not going to let me get by making a bold-faced provocation statement like that, are you?

Normal Sinus Beats

Image 15: Normal Sinus Rhythm

Regular P waves marching along.

Nice, full-heart contractions, beautiful heart-chamber filling times. There is nothing more satisfying than watching the parade of regular, well-formed cardiac cycles, of which each of us should experience one to two billion in our moderate-length, purposeful lives.

A Premature Atrial Contraction Beat

Image 16: Premature Atrial Contraction

Early QRS. Absent or malformed proceeding P. Note the following normal PQRS.

What is this! An early QRS means inadequate filling of the ventricular heart chambers. Should it happen too often, we face syncope, poor cardiac perfusion, anxiety, shortness of breath, and increased chances of provoking other less benign arrhythmias. More on that when we chat about supraventricular tachycardias.

Sinus bradycardia is a regular rhythm originating from the SA node that is slower than 60 bpm. In sinus bradycardia, the P vector on the EKG/ECG will be consistent with a SA node origin.

Atrium P Complex	EKG/ECG P Complex
Image 17A: Normal P Morphology, Lead II	Image 17B: Normal P Morphology, Lead II
P1 is right atrium. P2 is left atrium. Fires from SA node. P1 slightly faster.	P1 manifests first. P2 follows quickly. Lead II is being represented.

Just as a reminder, a normal SA-produced P wave will show right atrial depolarization followed rapidly by left atrial depolarization. A distinctive right-to-left, top-to-bottom atrial progression gives rise to the stereotypical upright P inflection in leads I, II, and aVL, with a negative P deflection in the aVR lead (Singh, 2024).

Image 18: Sinus Bradycardia, Lead II and V1

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The slower conduction of sinus bradycardia may be due to a normal response to sleep or deep breathing in a well-conditioned athlete. Abnormal drops in rate could be caused by diminished blood flow to the SA node, vagal stimulation, hypothyroidism, increased intracranial pressure, or pharmacologic agents, such as digoxin, propranolol, quinidine, or procainamide.

Consider a slow heart rate if dizziness, fatigue, or syncope occur. Sinus bradycardia may have no symptoms.

A 12-lead EKG/ECG or a wearable (Holter) heart monitor is considered diagnostic of sinus bradycardia.

Too fast a heart rate while at rest creates problems with heart filling. The large chambers of the heart, the ventricles, require a full second to fill with blood in anticipation of pushing it out on its voyage through the body. A contraction rate of greater than 100 bpm with the electrical stimulus arising from the SA node and the presence of evenly paired P with QRS waves qualifies as sinus tachycardia.

Image 19: Sinus Tachycardia, Lead II and V1

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There are several types of tachycardia. Sinus tachycardia is a regular cardiac rhythm that meets normal sinus rhythm standards, apart from being too fast. Greater than 100 bpm in a resting adult, faster than 150 bpm in infants, up to around six years old (Henning & Krawiec, 2023).

Do not be misled. Too quick a heart rate, even with a normal conduction mechanism, can be problematic. Strokes, heart failure, and the risk of heart attack from increased cardiac demands can accompany sinus tachycardia.

Be warned, sinus tachycardia is known as a secondary symptom. When seen, it is a sign that something else is awry. When sinus tachycardia is seen, begin searching for the cause, the irritant that provokes the fast pace.

Sinus tachycardia may result from stress, exercise, pain, fever, pump failure, hyperthyroidism, caffeine, nitrates, atropine, epinephrine, isoproterenol, nicotine, electrolyte imbalances, fatigue, blood loss, and other situations that place stress on the body.

Did you know some arrhythmias are healthy?

Healthy sinus arrhythmia occurs when a strong cardiac system, influenced by the vagal nerve, causes the heart rate to slow slightly during inhalation and speed up during exhalation (Soos & McComb, 2022). It is common in both children and adults, non-harmful, and does not require treatment.

Image 20: Sinus Arrhythmia, Lead II and V1

A distinct P wave will be associated with each QRS complex. Be sure to look at your patient’s overall condition and, if in doubt, a 12-lead EKG/ECG should clarify the situation.

A sinus pause differs from a sinus arrhythmia. It reflects SA node dysfunction, causing missed or paused heartbeats when electrical impulses fail to exit the SA node. While symptoms can vary from mild to severe, these pauses should not be ignored, as they may progress to a potentially dangerous sinus heart block.

To qualify as a sinus pause, the space between P waves should last at least two seconds (Miller, 2023). Sinus pauses and arrests are most frequently observed in older patients due to progressive SA node deterioration, though this is difficult to confirm without controlled studies. In younger individuals, sinus arrest typically results from a specific cardiac event or a severe electrolyte imbalance. Symptoms may include occasional missed beats, fatigue, dizziness, or angina.

Differentiate between a sinus pause and a sinus arrest by seeking a substitute rhythm intervention. A sinus pause will be followed by a substitute rhythm interposing. Sinus arrest has no substitute rhythm.

Image 21: Sinus Arrest, Lead II and V1

Sinus exit blocks occur when a depolarization wave leaves the SA node but is not conducted through the atria, so the ventricles are not stimulated. Delays in SA depolarization initiating the heartbeat can also appear as AV blocks, which are classified into three main types—these will be discussed later (Kashou et al., 2022).

SA node conduction failure is serious. It can cause abnormal P waves followed by normal QRS complexes, or a total absence of P waves (sinus arrest), where backup pacemaker cells take over. Sinus arrest may result in bradycardia, dizziness, fainting, or palpitations since escape beats are slower than normal impulses.

Sinus Exit Block - Sinoatrial Block

Image 22: Sinoatrial Block
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100	Irregular	P before every QRS	12-20 sec	< 10

Typically, this rhythm ranges from 60 to 100 bpm, but it can be slightly higher or lower. The pattern is irregular. Different cells in the SA node generate each impulse; however, some impulses are blocked before exiting the node. This leads to occasional missing PQRST complexes. The pause during these absences matches the interval between two P-P intervals of the underlying rhythm. Each PQRS appears uniform and upright in leads I, II, and aVL.

Expanding out into the heart atrium, we begin to see some common arrhythmias that present challenges to us as health professionals. Premature beats of any type can be problematic, and patients who report the feeling of skipped heartbeats need to be assessed for premature beats.

Premature atrial contractions (PACs) originate from early depolarization in the atrium outside the SA node, disrupting the normal heart rhythm (Heaton & Yandrapalli, 2023). These impulses often arise from irritation, inflammation, or unexplained triggers, causing an early atrial contraction. This results in a premature beat with an abnormal P wave and a mostly normal QRS complex.

Premature beats are classified by their origin: atrial, junctional, or ventricular. PACs happen when an atrial site fires before the SA node's scheduled discharge.

Image 23: Premature Atrial Complexes, Lead II and V1

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Aberrantly conducted PACs have a wide complex due to unusual conduction. PACs and other early beats can appear as couplets, bursts (premature atrial tachycardia), or bigeminy. Without other heart issues, the rate usually remains normal (60-100 bpm) with occasional PACs, but sinus tachycardia may increase their frequency. Early PACs make the rhythm irregular.

The P wave of a premature beat appears earlier and differs from those generated by the SA node, often appearing flattened, notched, or hidden in the preceding T wave detail, best seen on a 12-lead EKG/ECG. The PR interval varies from 0.12 to 0.20 seconds, depending on the pacemaker's proximity to the SA node; longer intervals suggest a higher initiation site, while shorter intervals indicate a site closer to the AV node. The QRS complex is typically less than 0.10 seconds but can be wider.

Tachycardia means fast. Supraventricular means the origin of the impulses is from above the cardiac ventricles, more accurately, above the bifurcation of the bundle of His. That means the entirety of both atria and the AV junction. High and fast, aberrant rhythms are typically grouped together because they exhibit similar features.

Supraventricular tachycardia (SVT) is a group of regular fast rhythms characterized by narrow QRS complexes and high heart rates. Please note that while atrial fibrillation and atrial flutter share a high conduction origin point and fast rate, they are typically irregular rhythms and will be discussed later.

According to Farkas (2025), women are at least twice as likely as men to experience SVT. The symptoms of SVT are often misinterpreted as panic attacks; employing EKG/ECGs may assist in confirming the diagnosis. Polyuria is noted as a less common symptom.

SVT may occur spontaneously or result from triggers like excessive energy drink intake, cocaine use, sepsis, dehydration, or elevated intracardiac pressures. Cardiac conditions such as heart failure, myocardial infarction, pulmonary embolus, and valve disorders can also induce SVT.

Treatments include vagal maneuvers (such as carotid massage, Valsalva maneuver, and cold immersion) and medications that reduce AV node sensitivity, including adenosine, verapamil, esmolol, calcium channel blockers, digoxin, amiodarone, beta-blockers, and diltiazem (Gugneja, 2024).

As we examine the anatomical structure of the heart and its electrical conduction pathways, we progress from simple cardiac arrhythmias to more complex and severe abnormalities. As electrical impulses follow the conduction system and initiate muscle contractions within the heart, conduction issues tend to increase in complexity and seriousness.

SVTs are categorized into two basic types: regular and irregular. SVT refers to the interval of QRS frequency. Fast, regular rhythms originating in the atrium of the heart are AVNRT, AVRT, and junctional tachycardia.

Of the regularly paced SVTs, AVNRT is the most common (Alvarado, 2025). Female patients comprise 70% of all AVNRT cases.

AVRT is a condition most common to young people and is the next most frequent of the SVTs. Typically, both SVTs occur due to circular electrical conduction between the atria and the ventricles. In AVNRT, two separate, parallel conduction pathways are present in the AV node: a slow conduction pathway and a fast one. When two pathways occur, there is a chance of a reciprocating re-entry stimulus occurring during cardiac stress. In AVRT, the AV node interacts with an accessory pathway that provides it with an untimely depolarization signal. This interplay establishes a circular trigger, keeping one depolarization working its way around through the AV node like a hula hoop of cardiac constriction.

Atrioventricular Nodal Reentrant Tachycardia

Image 24: Atrioventricular Nodal Reentrant Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
120-250	Regular	Absent, hidden by preceding QRS	Hard to see, 0.12-0.20	Narrow < 0.12

AVRTs are the second most common of the regular SVTs and share with the SVTs what is often referred to as a pre-excitation syndrome. That is regular, rhythmic, rapid-firing stimuli originating from above the ventricles and AV nodes.

Atrioventricular Reentry Tachycardia

Image 25: Atrioventricular Reentry Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
150-250	Regular	Non-sinus P waves occur after QRS retrograde II, III, AVF	Hard to see, 0.12-0.20	Narrow < 0.12

The direction of the circular conduction pathway can influence outcomes. The most frequently observed circuit is an antegrade conduction pathway through the AV node, referred to as orthodromic. Orthodromic typically presents with the RP interval being less than the PR interval, or with the RP interval greater than the PR interval in cases involving a slow-conducting accessory pathway. Retrograde P waves may be seen in leads I, II, III, aVF, and V1. If the heart rate is below 100 bpm, a delta wave can be present, but this occurs only at normal sinus rhythm rates, not during tachycardia. The image above demonstrates the more common presentation of orthodromic AVRT.

Image 26: Cardiac Electrical Conduction Chain of Events

Retrograde conduction through the AV node is referred to as antidromic AVRT.

The aberrant rapid conduction flows down from the atrium through the accessory pathway. At that point, it regurgitates back up into the atrium from the depolarizing ventricles, flowing in the wrong direction through the AV node. Then the atrium fires and sends another aberrant depolarization down through the accessory pathway to the ventricles, repeating the aberrant conduction. Antidromic AVRT is a much less common conduction issue that possesses a distinct set of characteristics, including a short RP interval (< 100 ms). A regular, wide QRS complex (≥ 120 ms). Delta waves, the upslurring of the R wave, can be seen at rates equivalent to normal sinus rhythm and tachycardia (Knight, 2025).

Let us look at antidromic AVRT on a 12-Lead.

Antidromic Atrioventricular Reentry Tachycardia

Image 27: Antidromic Reentry Tachycardia, 12-Lead
Heart Rate	Rhythm	P Wave	PR Interval	QRS
150-250	Regular	Retrograde and before QRS	Long	Wide > 0.12

Antidromic AVRT accounts for approximately 5% of all cases of AVRT. Delta waves are clearly visible in leads V4, V5, and V6 (Farkas, 2025). The P wave merges with the QR complex in leads I and II.

Additionally, WPW syndrome represents another form of accessory pathway reentrant rhythm. WPW is characterized by the presence of an accessory pathway and does not primarily involve the atrium; its detailed discussion will occur separately. On rare occasions, the accessory pathway in WPW may function such that the AV node serves as the retrograde pathway. These presentations typically feature a wide QRS complex, regular rhythm, and extremely rapid tachycardia (Farkas, 2025).

The bundle of His was mentioned earlier; however, time was not spent discussing what a great divider it is. Recall that the heart's electrical activity begins in the SA node (the heart's natural pacemaker), situated on the upper right atrium. The contraction stimulus travels around through the right atrium, then simultaneously through the left atrium, and finally triggers the AV node. From the AV node, the electrical impulse travels down the bundle of His, and here is the good part: it separates into the right and left bundle branches. The right bundle contains one fascicle (pathway, tract, nerve cable). The left bundle branch subdivides into two fascicles: the left anterior fascicle and the left posterior fascicle. Some academicians say that only some people possess the left septal (median) fascicle (Goldberger, 2024). The fascicles, however many you see in the heart, go on to fragment into millions of Purkinje fibers, which interrelate with cardiac myocytes (muscle cells), allowing rapid coordination and synchronous physiological depolarization and contraction of the ventricles.

So, what happens when a bundle branch gets constipated, stopped up, blocked? Welcome to the BBBs. In BBBs, the QRS complex will become wide, lasting more than 120 ms. This is due to whichever side is blocked; the depolarization stimulus to that ventricle will be delayed, as it is forced to propagate to that ventricle by means other than the nerve bundle leading into the ventricle from the bundle of His. As a rule, upward deflection on the EKG/ECG indicates the electrical impulse is heading towards the physical lead you are viewing it in. This means, diagnostic shortcut here, look at the V1 lead (V6 as the opposite view can be used to confirm). Should the abnormally wide QRS be deflected downward in direction, the left bundle is blocked. When the abnormally wide QRS in V1 is deflected upward, the right bundle is blocked.

Hint: Go over this in your head a few times, and trace it out. This will save you considerable time later in real life.

Bundle Branch Block Deflections in QRS

Image 28: Bundle Branch Block Deflections, Leads V1, V6

Wide QRS. Right BBB in V1 QRS has an “M” shape, with the second rabbit ear larger. Right BBB in V6 has a “fat” S wave (> 40 ms) with a QRS “W” shape.

Anatomical quirk here. The left side of our hearts is meatier and more muscular than the right. So, depolarization of the muscle has a greater influence on the EKG/ECG strip. When the left and right ventricles depolarize simultaneously, normally, a uniform R wave of less than 120 ms appears on the rhythm strip. BBBs force the QRS to widen.

BBBs can be considered complete or incomplete blocks, depending on the causative factors. In general, the QRS of a complete block will be wider than that of an incomplete block.

Junctional rhythms are impulses that originate from the AV node, also referred to as the junction (Hafeez et al., 2025). These rhythms occur when the SA node, which is typically the heart's primary pacemaker, does not function effectively. For classification purposes, rapid junctional rhythms are often grouped with SVTs. This section examines impulses that begin at the junction.

If necessary, the AV node can function as an alternative pacemaker when the SA node fails, with an inherent rate of 40–60 bpm, which is slower than the SA node. In some cases, the AV node may increase its rate above that of the SA node, resulting in junctional tachycardia, where the heart rhythm is governed by the fastest depolarization cycle.

Junctional Tachycardia

Image 33: Junctional Tachycardia, 12-Lead
Heart Rate	Rhythm	P Wave	PR Interval	QRS
> 200	Regular	P may be immediately before, follow, or be buried in QRS. May be inverted or retrograde.	Short	Narrow < 0.12

Note the P wave immediately before the Q as seen on lead II. This P-wave presentation is common for all junctional rhythms, as the depolarization pacing point originates within the AV node. The depolarization wave must travel upwards into the atria simultaneously, or at least concurrently, as the aberrant firing wave heads to the bundle of His and ventricles (Scanlon, 2025a).

Before moving on from the discussion of atrial anatomy, it is important to address several rapid atrial arrhythmias—specifically, the atrial tachycardias. These arrhythmias are frequently distinguished from other SVTs due to their characteristic irregular rates and rhythms. Nonetheless, they are classified as SVTs, despite some debate within the cardiology community regarding this categorization. The primary examples of these fast and irregular SVTs include atrial fibrillation (AFib), atrial flutter, and multifocal atrial tachycardia.

Atrial Tachycardia

Image 36: Atrial Tachycardia, Lead II

Stimuli originate from one point in the atria that is not the SA Node.

The name says it all. Multifocal, yes. There must be at least three different P-wave morphologies to qualify. Each differing P reflects an alternate or aberrant depolarization origin within the atrium. Atrial, yes. The depolarizations are initiated from within the heart atria. Whether from areas of inflammation, irritation, scarring, or from medication or chemical toxicities. Tachycardia, yes. Faster than 100 bpm. The speed may be driven by increased cardiac demand, as in chronic obstructive pulmonary disease (COPD) and other pulmonary conditions (Lucchetti, 2024).

Multifocal Atrial Tachycardia

Image 37: Multifocal Atrial Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
QRS rate usually > 100	Irregular	More than three distinct P waves	Varies	Narrow < 0.12

In lead II, arrows highlight different P wave morphologies, indicating irregular P-P intervals due to multiple electrical origins—not fibrillation or flutter. This tachycardia itself is not life-threatening, but its comorbidities often are. A rapid, irregular pulse may be the only sign, accompanied by symptoms such as shortness of breath, chest pain, palpitations, lightheadedness, or syncope.

Multifocal atrial arrhythmias can cause complications such as myocardial infarction, pulmonary emboli, and atrial thrombi, including stroke (Luchetti, 2024).

AFib is considered the most common type of treated cardiac arrhythmia, affecting 40 million people worldwide (Minneapolis Heart Institute Foundation, 2025).

Rhythmic atrial contraction contributes 20% to 30% of the heart's output (Scanlon, 2025b). Disruption of normal SA node function by irritation, inflammation, or other factors can lead to disorganized atrial depolarization, resulting in fibrillation or atrial quivering. AFib significantly compromises cardiac output, particularly in older adults or individuals with comorbidities, as effective atrial contractions are essential for optimal ventricular filling. Although many individuals with AFib remain asymptomatic, those who do experience symptoms may report sudden fatigue, dyspnea, dizziness, or chest pain, often remarking on the unexpected irregularity of their heartbeat.

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Complications of AFib can be serious (Johns Hopkins Medicine, n.d.).

• Blood clots – Due to ineffective pumping, blood can churn and pool in the atria, allowing thrombi, emboli, or clots to travel through the blood to various parts of the body.
• Stroke – Should an embolus reach the brain, a blood flow blockage or stroke may occur.
• Cognitive impairment or dementias – Studies support that AFib is associated with increased rates of cognitive impairment, Alzheimer’s, and vascular dementia.
• Heart attack – Women and African Americans show a considerable risk of heart attack associated with AFib.
• Heart failure – The fast and uneven beating of the heart raises the risk of heart failure.
• Sudden cardiac death – Sudden stoppage of cardiac function and AFib sadly walk hand in hand.

So please, do not think of AFib as just a quivering nuisance.

Atrial Fibrillation

Image 38: Atrial Fibrillation, 12-Lead
Heart Rate	Rhythm	P Wave	PR Interval	QRS
Atrial rate usually > 400	Irregular	No identifiable P waves	None	Narrow < 0.12

The QRS rate of AFib will be all over the scale. Fast, then slower, then well, chaotic. It is so unpredictable that there are, in some viewpoints, distinct types of atrial fibrillation (McDermott, 2025).

Atrial flutter is the quintessential atrial tachyarrhythmia. Not the most common, yet it is the one a clinician tends to point out to students and state, “Now this is an atrial arrhythmia!”

Flutter impulses traverse in the right atrium in a circular pattern. Each rotation creates a waveform on the EKG/ECG baseline—the distinctive saw-tooth pattern of the atrial flutter waves. While characteristically there are multiple P waves successfully constricting the atria, they only penetrate to the ventricular myocardium every second, third, or more atrial depolarizations. Pay special attention to leads II, III, aVF, and V1 to pick out the distinctive atrial flutter waves. Atrial rates typically range from 250 to 320 bpm. While ventricular rates typically range from 120 to 160 bpm, the most common ventricular rate in atrial flutter is 150 bpm, due to a phenomenon known as 2:1 AV block, which we will cover later.

Atrial Flutter

Image 41: Atrial Flutter, 12-Lead
Heart Rate	Rhythm	P Wave	PR Interval	QRS
The atrial rate is usually 250-320, and the ventricular rate 120-160	Regular	Sawtooth P waves	Varies	Narrow < 0.12

Here is a blowup of V1 from above. Note the choppy ocean waves of P in relation to the QRS complex. Most are 3:1, three P waves to each QRS. However, there is a variable ratio of P:QRS as we examine more of this lead. We would therefore call this atrial flutter with variable conduction (Prutkin, 2024).

Image 42: Atrial Flutter with Variable Conduction, V1

Atrial flutter is frequently associated with AV block, which refers to impaired conduction of electrical impulses from the atria to the ventricles. AV blocks can manifest as delayed depolarization and, in certain instances, may result in a total cessation of conduction. Etiologies range from benign factors, such as increased vagal tone during sleep, physical activity, pain, or carotid sinus stimulation, to pathological conditions including cardiac fibrosis, sclerosis, ischemic heart disease, alterations in myocardial tissue, certain medications, and hyperkalemia (Sauer, 2024).

AV block is classified according to the severity of the conduction disturbance, which is divided into three degrees: first-degree AV block; second-degree AV block, which includes type I (Wenckebach or Mobitz I) and type II (Mobitz II); and third-degree (complete) AV block (Sauer, 2024).

No talk on heart arrhythmia would be complete unless it meandered into this, the Where’s Waldo of heart arrhythmias—the wandering pacemaker.

A wandering atrial pacemaker is an arrhythmia originating in the atria where the pacing sources shift between the SA node, odd source spots within the atria themselves, and the AV node. These shifting, skipping-about, stimulus sites are best seen from lead II by looking for morphologic changes in the P waveform (Mond, 2024). It is most often seen in the young, the aging, or in fit athletes. It tends not to be symptomatic and rarely requires treatment, though the presence of the medication digoxin, or sometimes COPD, has been associated with it. A wandering atrial pacemaker is a favorite rhythm for instructors to use when teaching interns or learners, often saying, “What is wrong here?”

Wandering Atrial Pacemaker

Image 49: Wandering Atrial Pacemaker, Lead II
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100	May or may not be Regular	From at least three sources	Mostly Regular	Narrow

At least three diverse sources of atrial stimulation must be present. By sources, we mean three distinct pacing morphologies. So, yes, two different P sources might originate from the SA node yet follow different conduction paths, thus creating P waveforms that are distinct from each other. The QRS, however, should be consistent and narrow. If the cardiac strip above were faster, the arrhythmia would be considered multifocal atrial tachycardia.

Wandering Atrial Pacemaker

Image 50: Wandering Atrial Pacemaker, 12-Lead

Using the various leads, track the P waves. To fully fit the diagnosis of wandering atrial pacemaker, we need three (or more) distinct P wave sources (morphologies).

WPW displays intervals of abnormally fast heartbeats intruding on what otherwise would be a normally functioning heart rate. This rate is due to an additional abnormal electrical conduction pathway in the heart, which occasionally activates, leading to an extremely fast SVT. The accessory pathways or bypass tracts connect the atrium to the ipsilateral (on the same side) ventricle, allowing the ventricles a depolarization charge that pre-excites them, urging them to fire fast and often. Hence, the delta wave is a significant clue that a secondary, faster pathway is present that should not be there at all. 

This accessory pathway phenomenon, sometimes referred to as the Kent pathway, is shown by a short PR interval. By bypassing the AV node, the PR interval shortens. A delta wave becomes visible and represents early activation of the ventricles from the bypass tract. A form of fusion QRS results from two activation sequences, one from the bypass tract and one from the AV node. ST-T changes occur secondary to changes in the ventricular activation sequence (Hacking, 2025).

Image 51: Delta Wave, Lead II

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Short PR intervals and delta waves are best seen in leads V1-5. Pseudo-Q waves, seen in leads II, III, and aVF, are not Q waves but rather are negative delta waves. So do not be confused by the false Qs. There is no inferior myocardial infarction on this EKG/ECG.

For a diagnosis, WPW must be seen in more than one lead.

Wolff-Parkinson-White

Image 52: Wolff-Parkinson-White Syndrome
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100 or more	Regular	Slurs into Q	Short when using the accessory pathway	> 0.10

Rate: Usually 60-100 beats/min, but may be either faster or slower. WPW may be due to congenital pathways that allow rapid conduction of impulses. These pathways predispose the patient to atrial tachycardia since there is no blocking of impulses at the AV node.

PRI: If this interval is short, the sinus impulse partially avoids its normal delay in the AV node by traveling rapidly down the accessory pathway.

QRS: Often greater than 0.10 seconds since there is no delay in the AV node. Subsequent activation of the ventricles depends upon the intra-atrial conduction time from the sinus node to the accessory pathway, plus conduction time down the accessory pathway, compared with sinus node conduction time to the ventricles via conduction pathways.

Delta wave: Slurring occurs at the beginning of the QRS complex due to an aberrant entry pathway.

Secondary T-wave changes: Because ventricular depolarization is abnormal, repolarization will also be abnormal, resulting in ST and T-wave changes that are secondary to the degree and area of pre-excitation.

Abnormal Q waves: Q waves are considered abnormal when they have an amplitude of 25% of the succeeding R wave or a duration of 0.04 seconds or greater. Such Q waves are often seen in the presence of an accessory AV pathway and may be misdiagnosed as a myocardial infarction. These are negative delta waves, not Q waves, and they reflect pre-excitation and not myocardial necrosis (Hacking, 2025).

Ventricular impulses come from the ventricles. The large muscular chambers of the lower heart push a pulsing stream of blood out into the body. When a command to contract signals fails to arrive from the primary pacemaker, the sinus node, escape cells within the ventricles step up to emit electrical depolarization waves that contract the ventricular myocardium.

When blood flow feeding a part of the heart becomes blocked, myocardial tissue becomes distressed due to ischemia, the lack of metabolic oxygen. Should this condition persist, necrosis or tissue death occurs. EKG/ECG readings are one of the quickest ways to diagnose myocardial infarction. When ancillary symptoms arise (e.g., chest or shoulder pain, shortness of breath, arm or jaw pain, dizziness, heart rhythm disturbances), seek help and initiate active EKG/ECG monitoring as soon as possible (Reeder & Kennedy, 2025).

EKGs/ECGs show the presence of heart ischemia. Two main types of myocardial infarction stand out clearly with EKG/ECG monitoring: the ST-elevation myocardial infarction (STEMI) and the non-ST-elevation myocardial infarction (NSTEMI).

Fixed-rate pacemaker

It can be used on patients with significant or complete heart blocks. The rate is preset to a constant rhythm and rate, such as 70 bpm, although rate changes can be made using external magnetic control (most commonly).

Demand pacemaker

Only fires when the R-R interval of the patient's natural rhythm meets or exceeds a preset limit.

R-Triggered Pacemaker

When dealing with heart blocks that allow the occasional sinus rhythm, the ventricular-synchronized demand-type pacemaker, also known as the R-wave-triggered pacer, looks for the absence of R waves and stimulates the heart ventricles should they not appear, after a short delay.

R-Blocked Pacemaker

For patients with a sinus rhythm and only occasional heart blocks, the R-wave blocked pacemaker stops firing when it detects a natural R wave produced by the patient.

Atrial Triggered Pacemaker

When detecting natural atrial depolarization, the pacemaker stimulates the ventricles after a reasonable delay. This pacemaker provides the optimal cardiac output while maintaining normal atrial rate fluctuations.

Image 72: Atrial Single Chamber Pacemaker Spikes, Lead II and V1

Treats most sino-atrial conditions by providing both atrial and ventricular stimulation whenever needed.

Firing refers to the pacemaker's generation of an electrical stimulus. This impulse is seen as a narrow vertical spike on the EKG/ECG.

Atrial Demand Pacemaker (Single Chamber)

Image 73: Atrial Demand Pacing, Lead II

No pacer spike before the first P, as it is on time. Second P is late, so spike. Third P is late, so spike.

Capture refers to the presence of a P, a QRS, or both after a pacemaker spike. This capture indicates that the tissue in the heart chamber being stimulated has been depolarized. The term is that the pacemaker has "captured" the chamber being paced. Paced QRSs are wide and bizarre, resembling the morphology of PVCs.

Image 74: Ventricular Single Chamber Pacemaker, Lead II and V1