The Basics of EKG/ECG Interpretation

Activities on the right side of the heart and the left side of the heart occur simultaneously.

The heart's ability to perform its vital functions relies on its highly specialized structure and intricate coordination of impulses. This coordination begins in the sinoatrial (SA) node, often referred to as the heart's natural pacemaker, located in the upper wall of the right atrium. The SA node generates electrical signals that initiate each heartbeat. These signals travel through the atria, causing them to contract and push blood into the ventricles (Kashou et al., 2022).

From there, the impulses reach the atrioventricular (AV) node, which briefly delays the signal to ensure the ventricles are filled completely before contracting. The signals are then transmitted via the bundle of His and Purkinje fibers to the ventricular muscles, causing them to pump blood either to the lungs or throughout the body. This flawless communication between the components allows the heart to maintain a rhythm that adapts seamlessly to the body's varying demands (Heaton & Goyal, 2023).

The right side of the heart receives deoxygenated blood from the body via the vena cava into the right atrium. Blood is ejected from the right atrium into the right ventricle. Blood is pumped to the lungs from the right ventricle via the pulmonary artery. The left side of the heart receives oxygenated blood from the lungs via the pulmonary vein into the left atrium. Blood is ejected from the left atrium to the left ventricle. Blood is pumped to the body from the left ventricle via the aorta. The right side of the heart pumps blood into the lungs. The left side pumps blood into the body.

Image 2: Posterior View

• The tricuspid valve is located between the right atrium and the right ventricle.
• The pulmonary (pulmonic) valve is between the right ventricle and the pulmonary artery.
• The mitral valve is between the left atrium and left ventricle.
• The aortic valve is between the left ventricle and the aorta.

Each valve has a set of "flaps" (also called leaflets or cusps). The mitral valve normally has two flaps; the others have three.

Image 3: Anterior View

Our heart supplies or pushes oxygenated blood to the cells throughout the body. Given the workload, it is not surprising that the heart itself also needs oxygenated blood delivered to its busy muscle cells!

Yes, coronary arteries, the ones frequently implicated in myocardial infarctions, are the delivery arm for oxygen to myocardial cells.

There are two basic cardiac cell types (Ripa et al., 2023).

Myocardial muscle cells (mechanical cells) are the myocardium or the body of the heart. These contain contractile filaments that shorten when the cells are electrically stimulated. Their primary function is contraction and relaxation. Their primary property is contractility.

Electrical cells (pacemaker cells) are electrical impulse-generating cells that are found in the electrical conduction system. They conduct impulses very rapidly, and their primary property is automaticity and conductivity.

Cardiac cells are surrounded by, and filled with, a solution that contains ions. Three key ions are sodium, potassium, and calcium. In the resting period of the cell, the inside of the cell membrane is considered negatively charged, and the outside of the cell membrane is positively charged. The movement of these ions inside and across the cell membrane constitutes a flow of electricity that generates the signal on an EKG/ECG (MacKinnon & Haque, 2025).

Cardiac cells that are resting have a negative polarization. Sodium ions are outside of the cell, and potassium ions are inside the cell. Both ions carry a positive charge; however, sodium ions have a stronger charge than potassium. Thus, the inside ion state of the cell is electrically weaker than the outside, so it is negative. The polarized state is a "ready state." When the cell is ready to accept an electrical impulse, a large amount of potassium leaks out. This leak causes a discharge of electricity, and the cell becomes positively charged. This discharge is called depolarization. The electrical wave created at this pacemaker site travels from cell to cell along the electrically sensitive conduction pathways and from there throughout the heart. Now, cell recovery begins. Sodium and potassium ions are shifted back to their original place by the sodium-potassium pump. This process is called repolarization (Grider et al., 2023).

Electrical impulses result from a brief but extremely rapid flow of positively charged ions (sodium) back and forth across the cell membrane.

The cardiac action potential illustrates the changes in the membrane potential of a cardiac cell during depolarization and repolarization.

Five electrochemical phases are recognized, starting with Phase "0". Yes, that is correct, zero through four, totaling five phases. Just go with it. The minds of clinical scientists are a mystery to the rest of us (Demyanets, 2024).

Phase 0

Rapid depolarization ends the cell's relaxation state. Thus, presumably, the "0" designation indicates coming to a readiness for the beginning of cell contraction. The electrical activity that mirrors physiological contraction is also known when considering the atrial portion of the heart as a "P" wave. Depolarization of the ventricular heart is a QRS complex (Wei et al., 2023).

• This phase is also called "upstroke," "overshoot," or "spike."
• Begins when a cell receives an impulse.
• Sodium moves quickly into the cell through the fast sodium channels.
• Potassium then leaves the cell.
• Calcium moves slowly into the cell through calcium channels.
• This movement produces about +20 microvolts of positive electrical power.
• The cell depolarizes, and the process of cardiac contraction begins.

Phase 1

Early repolarization, e.g., "partial" repolarization of the cell membrane due to sodium ion passage, creating an electrical current (Wei et al., 2023).

• The rapid flow of sodium into the cell is stopped as the fast sodium channels close.
• Potassium begins to reenter the cell, and sodium begins to leave.
• This movement is about zero mV and is therefore neutrally charged, neither positively nor negatively charged.
• This action is the absolute refractory period.

Phase 2

Plateau phase (slow repolarization, part of the absolute refractory period). Calcium shift causes a stasis or "holding" of the electrical charge (Wei et al., 2023).

• Slow repolarization continues.
• Calcium continues to flow into the cell through slow calcium channels.

Phase 3

Final repolarization of the cell occurs as calcium and sodium movement is shut down. Leaving the cell at a baseline charge and eager to go (Wei et al., 2023).

• Rapidly, the cell completes repolarization.
• Calcium channels close.
• Potassium rapidly flows out of the cell.
• Active transport via the potassium-sodium pump begins restoring potassium to the inside of the cell and sodium to the outside of the cell.
• The cell is now in the negative state due to the outflow of potassium.
• Gradually, the cell becomes extremely sensitive to external stimuli until its original sensitivity has been restored, called the relative refractory period.

Phase 4

Return to the resting stage, at the resting potential of -89 millivolts. Do not be fooled. Holding a negative charge means the outflow or net efflux from the cell is a positive charge (Wei et al., 2023).

• Corresponds to diastole.
• Calcium and sodium remain outside the cell.
• Potassium remains inside the cell.
• During this phase, the heart is "polarized" and getting ready for discharge.
• Once another stimulus occurs, the cell will reactivate.

Image 5: Cardiac Cycle

Automaticity

The heart can initiate an electrical impulse. The heart can begin and maintain rhythmic activity without the aid of the nervous system. A heart removed from the body can beat on its own for a limited period. The highest degree of automaticity is found in the pacemaker cells of the sinus node. The atria, AV Node, bundle of His, bundle branches, Purkinje fibers, and the ventricular myocardium have less automaticity (Nora Eccles Harrison Cardiovascular Research & Training Institute, n.d.).

Excitability

The heart can respond to an electrical impulse. A cardiac cell will respond to an electrical stimulus with an abrupt change in its electrical potential. Each cardiac cell that receives an electrical impulse will change its ionic composition and its respective polarity. Once an electrical potential begins in a cardiac cell, it will continue until the entire cell is polarized (Nora Eccles Harrison Cardiovascular Research & Training Institute, n.d.).

Conductivity

The heart can conduct an electrical impulse. All areas of the heart appear to depolarize simultaneously because a cardiac cell transfers an impulse to a neighboring cell very rapidly (Nora Eccles Harrison Cardiovascular Research & Training Institute, n.d.).

Contractility is the ability of the heart to respond by contracting.

The heart is all about electricity.

The normal cardiac impulse arises in the specialized pacemaker cells of the SA node, located about 1 millimeter (mm) beneath the right atrial epicardium at its junction with the superior vena cava. The impulse then spreads over the atrial myocardium to the left atrium via Bachmann's bundle and the AV node region via the anterior, middle, and posterior internodal tracts connecting the sinus and AV nodes. These represent the usual routes of spread but are not specialized tracts analogous to the Purkinje system. When the impulse reaches both atria, they depolarize electrically, producing a P wave on the EKG/ECG, and then contract mechanically, producing the wave of the atrial pressure pulse and propelling blood forward into the ventricles.

Conduction slows when the impulse reaches the AV node, allowing sufficient time for blood to flow from the atria into the ventricles. After the impulse emerges from the AV node, conduction resumes rapidly through the bundle of His to the right and left bundle branches. It terminates in the Purkinje fibers in the ventricular muscle.

Stimulation of the myocardium causes progressive contraction of the myocardial cells. Therefore, wave deflections correspond to the cardiac cycle's mechanical events, including contraction and relaxation of the cardiac chambers. Repolarization is only electrical, and during that, the heart is at rest.

Three major waves of electric signals appear on the EKG/ECG. Each one shows a different part of the heartbeat (Bhattacharyya & Munshi, 2020).

• The first wave is called the P wave. It records the electrical activity of the atria.
• The second and largest wave, the QRS wave, records the electrical activity of the ventricles.
• The third wave is the T wave. It records the heart's return to the resting state.

Image 6 : Cardiac Electric Cycle

Image 7: EKG/ECG and Cardiac Cycle

Voltage, or the strength of the heart's electrical impulses, is represented on the vertical Y-axis. Each microvolt of positive electrical current raises the stylus 1 centimeter (cm) or one large square. The waveform baseline or bioelectric line is electrically neutral, usually without any deflections, e.g., a flat line (Sattar & Chhabra, 2023).

P Wave

A P wave on an EKG/ECG represents atrial depolarization. This wave represents one electrical activity associated with an impulse from the SA node and the electrical spread (conduction) through the atria. The SA node is, physiologically, located in the right atrium, so the right atrium begins constriction or depolarization. This depolarization represents the first half of the P wave. As depolarization spreads to the left atrium, we observe that process in the second half of the P wave (Douedi & Douedi, 2023). The total duration of the P wave should be, in general, three small squares, with 2.5 small squares of height.

In leads I and II, which we will get to soon, P waves should always be positive or above the baseline, while in lead aVR, again, looking ahead, in a normal sinus rhythm, it 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).

PR Interval

PR Interval represents the time from the start of atrial depolarization, 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 might indicate a first-degree AV block presence, while short intervals accompany disorders of AV acceleration, such as Wolf-Parkinson-White (WPW) syndrome (Hacking, 2025).

QRS Complex

QRS represents ventricular depolarization (phase 0 of the action potential) until the end of ventricular depolarization (Lome, n.d.a).

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 or ventricular rhythms. Each component of the complex, the Q, R, and S waves, carries unique significance.

The duration of the entire QRS is under 120 milliseconds or three small squares. An extended QRS might indicate the presence of a bundle branch block 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.

Q Wave

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 (Burns, E. & Buttner, 2024b).

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, one small box. Abnormal Q waves are a strong indication of the presence of an old myocardial infarction.

R Wave

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.).

S Wave

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

ST Segment

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 milliseconds, 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 bundle branch block, Prinzmetal angina, blunt trauma to the heart, Brugada syndrome, and even subarachnoid hemorrhage.

T Wave

The T wave is the process of ventricular repolarization (ACLS Medical Training, n.d.). It 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.

QT Interval

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 milliseconds 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 Pointe, ventricular tachycardia (VT), or ventricular fibrillation (VF).

U Wave

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 is often present when they are seen (School of Health Sciences, n.d.).

J Wave

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).

Epsilon Wave

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

Image 8: Cardiac Cycle Components

Utilize a systematic approach.

• Is it a regular rhythm?
• Are there P waves?
• What is the QRS width?
• Does each QRS have a P wave in front?
• What is the heart rate?

Image 9: Normal Sinus Rhythm

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

Methods for calculating the heart rate:

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

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 10: EKG/ECG Boxes

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

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.
• 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 or irregular?
• To determine if the atrial rate is regular or irregular, measure the distance between two consecutive P-P intervals. Use a point from one P wave to the same point on the next P wave. Then compare this with another P-P interval. If the atrial rate is regular, the P-P interval will measure the same.
• Determine if the ventricular rate is regular or irregular, and measure the distance between two consecutive R-R intervals. Use a point from one R wave to the same point on the next R wave. Then compare this with another R-R interval. If the ventricular rate is regular, the R-R interval will measure the same.
• Is the rhythm regular? Irregular? 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 .10 seconds or less, it is considered narrow and is presumed to be supraventricular in origin.
• If the QRS complex is greater than .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 the T Wave

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

Image 11 : EKG/ECG Examples

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 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, escape pacemakers exist.

Escape pacemakers are cells that will initiate a heartbeat should the faster normal pace fail to descend along the standard conduction pathway. Escape cells exist in the AV junction and the ventricles (Burns & Buttner, 2024c).

The AV junction is the AV node and the non-branching 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.

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.

Table 4: Case Study One

Your colleague slaps this 12-lead down in front of you, saying, "What do you make of this? It does not look right somehow, yet our artificial intelligence that reads the EKGs/ECGs keeps spitting it out as 'abnormal, beyond system parameters'." The client is a 68-year-old male who was brought in after collapsing on a golf course. Lab panels indicate mildly decreased sodium and potassium levels, with other results within reference ranges. Vital signs: Blood pressure 142/94 millimeters of mercury (mmHg), pulse - 48, respiratory rate - 20, O2 saturation - 97%. The client is alert and grumpy.

Image 12 : Case Study 1 EKG/ECG

Here is what you see: This is a bradycardia (heart rate of 45 bpm). It is regular. QRS complexes are narrow. No regular P waves are present, yet no flutter or fibrillating atrial waves are visible.

Disclaimer: There are two possibilities present. I prefer the first and only noticed the second while reviewing sources. Discerning between what is evidentiary and alternate actualities is why health care is considered an art, as well as a science. Let us see what you think.

1. Sinus arrest is observed, accompanied by a junctional escape rhythm in which the retrograde P wave is concealed within the QRS complex, indicating simultaneous excitation of both the atria and ventricles.

2. There is exceptionally fine atrial fibrillation (which is usually only seen in long-lasting atrial fibrillation that has been present for many years). Since the rhythm is regular, it could then not be a bradyarrhythmia in atrial fibrillation, but a junctional escape rhythm in atrial fibrillation and 3rd degree AV block.

Clinical decision = Allow me to be direct, in medical cardiology, as well as other branches of health provision, if the client is not actively expiring, then there is time for consults. The client needs a consultation. If he remains stable, what is recommended is a Holter monitor at home and on the golf course; if unstable, sequential 12-leads would allow comparative views of cardiac activity with workup for a pacemaker. The colleague was right to ask the opinion of someone else, especially if they are not sure of the rhythm or need to double-check what AI was reading. While a Holter monitor will be beneficial, the client should also be referred to cardiology, as the blood pressure was elevated and the pulse was low.

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

This ventricular pacemaker occurs when an electrical impulse is delayed, blocked, or both in one or more portions of the conduction system. In contrast, the impulse is conducted normally through the rest of the conduction system. The results are a delayed impulse entering cardiac cells in which the normally conducted impulse has depolarized. If they have repolarized sufficiently, the delayed impulse will again depolarize the cardiac cells prematurely, thus producing unwanted ectopic beats and rhythms.

Let us get this clear and out of the way. The industry standard in healthcare is the 12-lead EKG/ECG. That is not what is used for monitoring a client. For ongoing client care, including pre-admission work by emergency responders, a standard three-lead configuration of foam-backed sticky electrodes is used.

Image 14: Einthoven's Triangle

Lead I:

• The positive electrode is placed just below the left clavicle.
• The negative electrode is placed just below the right clavicle.
• The neutral or grounding electrode is placed on or close to the left leg (typically placed on the left side, below the left pectoral).
• Provides information about the left lateral wall of the chest.

Lead II:

• The positive electrode is placed near the left leg (typically placed below the left pectoral muscle).
• The negative electrode is just below the right clavicle.
• The neutral or grounding electrode is just below the right clavicle.
• 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:

• The positive electrode is at the left pectoral muscle (instead of the traditional left leg).
• The negative electrode is just below the left clavicle.
• The neutral or ground electrode is placed just below the right clavicle.
• Provides information about the inferior wall of the heart.

Image 15: Standard Limb Leads

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. Known as augmented limb leads, unipolar limb leads, or just unipolar leads, they 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 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 nor 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 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 are 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.

Image 16: Augmented EKG/ECG Leads

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, are the horizontal plane, unipolar leads.

Lead V1:

• It is placed in the fourth intercostal space just to the right of the sternum.
• 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:

• It is placed in the fourth intercostal space just to the left of the sternum.
• Anterior view.
• Provides a good view of electrical activity in the right ventricle.
• QRS is mostly negative.

Lead V3:

• Placed exactly halfway between the positions of lead V2 and V4.
• View of the heart's sternocostal surface.

Lead V4:

• It is placed in the fifth intercostal space at the mid-clavicular line.
• Septal view and left ventricle.
• QRS is mostly positive.

Lead V5:

• It is placed at the same horizontal level as V4 on the anterior axillary line.
• Lateral view of the septum and left ventricle.
• QRS is mostly positive.

Lead V6:

• It is placed at the same horizontal level as V4 and V5 on the mid-axillary line.
• Lateral view of the septum and left ventricle.
• QRS is mostly positive.

Image 17: Precordial Chest Leads

MCL, or modified chest leads, are different placements of electrodes used to focus on premature beats, bundle branch blocks, or supraventricular rhythms. It is sometimes difficult to discern whether a fast rhythm is supraventricular tachycardia (SVT) or ventricular tachycardia (VT); a modified lead may come into play (Francis, 2016).

MCL1:

• It is a variation of V1, where the negative electrode is situated below the left clavicle, close to the left shoulder. Positive electrode in the fourth intercostal space to the right of the sternum and ground just below the right clavicle.
• Useful in assessing the anterior wall of the left ventricle and conduction through the ventricles.
• QRS appears mostly as negative deflections.
• This lead is useful in assessing the width of the QRS complex to differentiate SVT from VT.

MCL6:

• This variation is a deviation of chest lead V6.
• The negative electrode is placed just below the left clavicle. The positive electrode is placed in the fifth intercostal space at the left midaxillary line (like lead V6) while the ground is placed below the right shoulder.
• This lead may be used as an alternative to MCL1 for the same purposes and views of the low lateral wall of the left ventricle while monitoring ventricular conduction changes.

An EKG/ECG strip displays a single lead reading from client monitors, while a 12-lead sheet provides diagnostic information from twelve different perspectives. Abnormalities unnoticed in one lead may be visible in another.

Quick trick. However, different manufacturers of EKG/ECG machines produce various-looking EKG/ECG sheets; a standard print format is employed.

Knowing this allows you always to recognize which lead you are looking at on any given EKG/ECG sheet.

The term "aberrant" originated in the emerging field of cardiology a century ago. Over time, it has experienced varying levels of usage due to differing definitions (Well Wisp, 2025). Periodically, the term has been revived and then fallen out of favor, reflecting ongoing debate within the discipline. In this context, we adopt a broad definition: any presentation that appears abnormal or noteworthy (Sissons, 2024). While this definition may prompt discussion and divergent opinions, the fluctuating use of the declarative term "aberrancy" reflects its contested place in medical terminology.

What we as health professionals always want to see is a healthy sinus rhythm. When normal heartbeats are triggered by the SA node in the upper right atrium of the heart, what is produced is a regular rhythm of 60 to 100 bpm. This normal sinus rhythm adjusts to the body's needs, increasing or decreasing with activity or rest (Goldberger et al., 2013).

Image 18 : Normal Sinus Rhythm, Lead II and V1

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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.

Just as a reminder, a normal SA-produced P wave will show right atrial depolarization followed rapidly by left atrial depolarization. A distinctive high-to-low, top-to-bottom, atrial polarization 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 19 : Sinus Bradycardia, Lead II and V1

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 heart monitor is considered diagnostic of sinus bradycardia.

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Too fast of 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 (Henning & Krawiec, 2023).

Image 20: Sinus Tachycardia, Lead II and V1

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.

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.

Tachycardia means fast. Supraventricular means the origin of the impulses is from above the cardiac ventricles. These high and fast aberrant rhythms tend to be clustered together due to their shared diagnostics.

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

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

A brief overview of the cardiac conduction system: The SA node, located in the right atrium, is the main pacemaker, generating electrical impulses at a rate of 60–100 bpm. These impulses travel to both atria through the internodal pathways, causing coordinated atrial contractions that move blood into the ventricles. The signal then proceeds to the AV node, situated between the atria and ventricles, and continues down the bundle of His to the right and left ventricles. From the bundle of His, the impulse spreads to the Purkinje fibers within the ventricular myocardium, resulting in ventricular contraction and blood ejection throughout the body.

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.

Table 8: Junctional Tachycardia

Image 21: Junctional Tachycardia
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
(Scanlon, 2025a)

The P wave immediately before the Q can be seen on lead II. This negative P wave inflection is common for all junctional rhythms as the depolarization pacing point originates within the AV node, as the depolarization wave must travel upwards into the atria simultaneously, or the closest thing to concurrent, as the aberrant firing wave heads to the His bundle and ventricles (Scanlon, 2025a).

Atrial fibrillation (AFib or AF) 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.

Image 23: AFib

Complications of AFib can be serious.

• Blood clots – Due to ineffective pumping, blood can churn and pool in the atria, allowing thrombus, embolus, 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 an elevated 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.

Table 10: Atrial Fibrillation

Image 24: AFib EKG
Heart Rate	Rhythm	P Wave	PR Interval	QRS
Atrial rate usually > 400	Irregular	No identifiable P waves	None	Narrow < 0.12
(Scanlon, 2025b)

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, three diverse types of AFib.

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!"

The distinctive saw-tooth pattern of the atrial flutter waves is characteristic of multiple P waves successfully constricting the atria, yet only penetrating 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 will typically run 252-320 bpm. In comparison, ventricular rates will range around 120-160 bpm, with the most common ventricular rate in atrial flutter being 150 bpm, due to a phenomenon known as 2:1 AV block.

Table 11: Atrial Flutter

Image 25: Atrial Flutter
Heart Rate	Rhythm	P Wave	PR Interval	QRS
The atrial rate is usually 250-320, and the ventricular rate 120-160	Regular	Saw-tooth P waves	Varies	Narrow < 0.12
(Prutkin, 2024)

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 26: Atrial Flutter with Variable Conduction

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.