EKG, ECG Interpretation

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

The right side of the heart receives deoxygenated blood from the body via the vena cava into the right atria. Blood is ejected from the right atria 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 Atria. Blood is ejected from the left atria 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:

The septum and valves separate the two atria and two ventricles of the heart. Blood is pumped through the chambers, aided by four heart valves. The valves are open and close to let the blood flow in only one direction. The four heart valves are:

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

Our heart supplies or pushes oxygenated blood to the cells throughout the body. 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.

Myocardial muscle cells (mechanical cells) are the myocardium or the body of the heart. These contain contractile filaments that contract 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 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 (Na+), potassium (K+), and calcium (Ca++). 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 ECG (Hill, 2021).

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, the sodium ion has a stronger charge than the potassium. Thus, the inside ion state of the cell electrically is 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 begins cell recovery. Sodium and potassium ions are shifted back to their original place by the sodium-potassium pump. This process is called repolarization.

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

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

Five electrochemical phases are starting with Phase “0”. Yes, that is correct, zero through four, totaling five phases. Just go with it. Clinical scientists' minds have odd quirks (Beck, 2018).

Phase 0.

Rapid Depolarization ends the cell relaxation state. Thus, presumably, the “0” designation indicates coming to a readiness for the beginning of cell contraction. The electrical activity which mirrors physiological contraction is also known when considering the atrial portion of the heart as a “P” wave. Depolarization with the ventricular heart is a QRS complex.

• 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 mV or 20 micro volts of positive electrical power
• 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

• 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 0 mV and is therefore neutrally charged, neither positive nor negative charged
• This action is the absolute refractory period

Phase 2.

Plateau Phase (slow repolarization, part of absolute refractory period). Calcium shift causes a stasis or “holding” of the electrical charge. In the electrical mirror of heart activity, think of this as the “T” interval.

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

Phase 3.

Final Repolarization of the cell as calcium and sodium movement is shut down. Leaving the cell at a baseline charge and raring to go.

• 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
• Cell 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 Resting Stage, at the resting potential of -89 millivolts (mV). Do not be fooled. Holding a negative charge means the outflow or net efflux from the cell is a positive charge (Beck, 2018).

• 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:

Image Source: ECG Cycle vs. Action Potentials, complements of Wikimedia Commons

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, atrioventricular (AV) Node, Bundle of His, bundle branches, Purkinje Fibers, and the ventricular myocardium have less automaticity.

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.

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.

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

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:

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

Methods for calculating the heart rate:

• 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 HR is 300 beats/min, 2 squares →150, 3 squares →100, 4 squares → 75, 5 squares → 60, 6 squares → 50 beats/min.

Image 10:

Image Source: Curtesy Wikimedia Commons

The Six-Second Method: Count the number of complete R waves within 6 seconds and multiply that number by 10. This count is the one-minute heart rate. This method can be used when the rhythm is "regular” or “irregular" (Manu, 2018).

• 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 11:

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

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 beats per minute

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, 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? 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 P-R interval

• If the P-R 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 P-R interval is 0.12 to 0.20 seconds.
• Is the P-R 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 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) FLB's detected?

Image 12:

Image Source: Compliments of Wikimedia Commons

• 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 ventricular tachycardia

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 beats/minute. 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 atrioventricular (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 nonbranching 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 beats/ minute.

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 beats/minute.

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 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:

Lead I:

• Positive electrode is placed just below the left clavicle
• Negative electrode place just below the right clavicle
• Neutral or grounding electrode 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:

• Positive electrode near the left leg (typically placed below the left pectoral muscle)
• Negative electrode just below the right clavicle
• Neutral or grounding electrode 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:

• Positive electrode is at the left pectoral muscle (instead of traditional leg left)
• Negative electrode just below the left clavicle
• Neutral or ground electrode 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, an electrocardiogram can create an augmented theoretical null point in the center of Einthoven’s triangle allowing a view of the absolute potential in each electrode (My.EKG, 2021).

Sound 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 ECG strip. The waves moving toward you, a negative deflection. At the same time, electrical events doing neither will just be minimized or even merge with the baseline (Bernard.Health, 2021).

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 ECG, P, QRS, and T should be negative in this lead.

Lead aVL:

• The augmented unipolar left arm lead 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 Leads

Standard leads, plus augmented leads make up the first six of a 12-lead ECG. Surprise! These first six leads share one important characteristic, they all view the heart from the frontal plane, as though the client 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 client!

Well, we can. Welcome to the six precordial leads

The precordial, or chest leads, view the heart's electrical conduction from the 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 hearts 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:

There are various uncommon, used for special situations, lead patterns out there. Just so you are aware, here are the most common of uncommon heart 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 or ventricular tachycardia; a modified lead may come into play.

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 supraventricular tachycardia (SVT) from ventricular tachycardia (VT).

MCL6:

• This variation is a deviation of chest lead V6.
• The negative electrode is placed just below the left clavicle. 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 the low lateral wall of the left ventricle while monitoring ventricular conduction changes.

An ECG strip is the single lead readout common to client monitors. A 12-lead sheet is the standard of care for diagnostic work, as it shows the same time increment view from how many viewpoints? Correct, twelve different planes of view. What may be hidden in one view may show clearly from another point of view.

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

This trick allows you always to know which lead you are looking at on any given ECG sheet.

We consider normal a regular contracting heartbeat stemming from an electrical stimulus originating from the sinoatrial node (SA) located in the upper right atrium of our heart. An even, regular beat, at a rate of 60 to 100 electrical waves each minute flowing through the heart myocardium's typical depolarization channels, is called a normal sinus rhythm (NSR). A normal heart rate is responsive to bodily demands such as exercise or exertion, speeding or slowing the heart rate to compensate for circulatory body demands (Sauer, 2020).

Image 18:

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Sinus bradycardia is a regular rhythm originating from the SA node that is slower than 60 beats per minute. In sinus bradycardia, the P vector on the 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 (Homoud, 2021)

Image 19:

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 S-A node, vagal stimulation, hypothyroidism, increased intracranial pressure, or pharmacologic agents, such as digoxin and propranolol quinidine, or procainamide.

Hints that slow heart rate should be considered include dizziness, fatigue, syncope. Sinus bradycardia may be asymptomatic.

A 12-lead 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 almost 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 beats per minute with the electrical stimulus arising from the SA node and the presence of evenly paired P with QRS waves qualifies as sinus tachycardia (Felman, 2020).

Image 20:

There are various 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 (beats per minute) in a resting adult, faster than 150 bpm in infants to around six years old.

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, and isoproterenol, nicotine, electrolyte imbalances, fatigue, blood loss, and other situations which places stress on the body.

Have you ever heard that there is a healthy arrhythmia?

Well, this is it. When your cardiac system is vigorous enough that, guided by the vagal nerve, there is a slight slowing in the resting heart rate after a big breath followed by a slight speeding up during exhalation. Now that is a healthy sinus arrhythmia!

Sinus arrhythmia is most common among children and frequent among adults. It is not pathogenic and requires no treatment.

Image 21:

If there is any danger from sinus arrhythmia, it is misdiagnosed as a more serious arrhythmia. The rate is usually 60-100 beats/min but may be transiently faster or slower. Should the rate be problematic, consider a rate-specific treatment. The rhythm itself is not an issue.

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

A sinus pause is not your friendly neighborhood sinus arrhythmia.

Sinus arrest or sinus pause is an indication of a dysfunction in the SA node. This arrest or pause leads to the dropping or pausing of electrical conduction in the normal sense. The electrical depolarization cycle is initiated yet somehow blocked before the impulse can leave the SA node. These missed beats may cause little to significant symptoms yet should never be taken lightly. Whatever mechanism may be blocking a beat here and there could easily manifest into a significant and potentially deadly sinus heart block.

Interestingly our older clients are where sinus arrest is most often seen. This sinus arrest has led to the hypothesis that it is due to accumulative deterioration or damage to the SA node, which may hold, though it is difficult to do a blind study. When found in younger adults or children, sinus arrest can often be directly correlated with a specific cardiac event or a severe electrolyte imbalance. Possible symptoms accompanying sinus arrest include feeling an occasional missed beat, fatigue, dizziness, or angina.

Image 22:

Usually, the rate associated with this is 60-100 beats/min but may be faster or slower.

The rhythm on ECG will be irregular. The SA node initiates an impulse, but that impulse is blocked before leaving the node itself. This block results in an 222absent or dropped PQRST complex.

In sinus arrest, the pause is not a multiple of other P-P intervals. Treatment may include Atropine or a pacemaker if symptomatic.

Sinus exit blocks are when a depolarization wave leaves the SA node yet fails to be conducted to the atria and therefore fails to stimulate the ventricles. Delays of the SA depolarization wave before they can kick start the muscular compression wave of the heartbeat also occur as atrioventricular (AV) blocks. There are three main types. We will get to the three major AV blocks a little later.

Failure of SA node conduction is a crisis. It may lead to the creation of an abnormal P wave and a following normal-looking QRS complex. Or a complete blocking of P wave generation leading to a condition known as sinus arrest, where secondary escape pacemaker cells are called upon to replace the missing SA conduction impulse.

Sinus arrest leads to symptoms such as bradycardia (remember, the firing of escape beats is always slower than the genuine impulse generator), dizziness, syncope, or palpitations.

Image 23:

Sinus Exit Block - Sinoatrial Block
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100	Irregular	P before every QRS	12-20 sec	<10
Image Source: Adapted from Wikimedia Commons

Generally, this rhythm will run around 60-100 beats/min but may be slightly faster or slower. The pattern should show as irregular as the SA node initiates each impulse, yet some impulses are blocked before leaving the node itself. This results in the occasional dropped PQRST complex. Note that the pause in these absences is the same as the distance between two P-P intervals of the underlying rhythm. Each PQRS should be uniform and upright in appearance in leads I, II, and aVL.

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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 are problematic, and clients who report the feeling of skipped heartbeats need to be assessed for premature heartbeats.

Let us start in the atrium, however, outside of the SA node, which is the official timekeeper and pacesetter of our heart. Premature atrial contractions (PACs) come from early depolarization somewhere in the atrium outside of the SA node leading to an interruption or replacement of the SA node-derived beat. Conduction initiation comes from areas of irritation, inflammation, or spots just firing off early for no discernable reason. These early depolarizations take off like wildfire and initiate an untimely contraction that flows through the atrium and then down into the ventricles, creating an early beat with a malformed P wave, though relatively normal QRS complex.

Ask about the client’s clinical history. Of particular interest are any previous cardiac disorders or structural heart disease. Reviewing medication for any proarrhythmic drug use is important and for the presence of stress, fatigue, caffeine, alcohol, tobacco, and such conditions as hypertension or hyperthyroidism. An electrolyte study focusing on sodium or magnesium levels is also handy.

Symptoms of dizziness, syncope, and of course, the perception of a skipped heartbeat may accompany PACs. Be aware that when a PAC occurs, the early triggering of the ventricles will mean a contraction carrying less than a full volume of blood, so the feeling of skipping is an accurate perception by the client.

Keep in mind that premature beats are identified by their site of origin (atrial, junctional, and ventricular). PACs occur when an irritable site within the atria discharges before the next SA node is due to discharge.

Image 24:

PACs with a wide complex are referred to as aberrantly conducted PACs, acknowledging the conduction wave's eccentric route. PACs and other early beats may occur in pairs (couplet), bursts (premature atrial tachycardia) (PAT), or even every other beat (bigeminy).

In the absence of other pathology, the heart rate tends to stay normal, from 60-100 when there are only occasional premature atrial contractions. Be aware that the presence of a sinus tachycardia may serve to promote more frequent PACs, depending on the overall client condition prompting a fast heart rate.

The rhythm will be irregular due to the early PACs. The presence of the early atrial impulse will throw the rhythm into the irregular category.

The P wave of the early beat differs from SA node P waves and is early, premature. The aberrant P waves may be flattened or notched. They may even be lost in the preceding T wave, which is where a 12-lead ECG shines as it allows detection by changing up the vector of observation.

The PR interval, sometimes abbreviated to PRI, may vary from .12- .20 depending on how near the pacemaker site is to the SA node. A longer PRI means the initiation site is higher up in the atrium, e.g., closer to the SA node, while a shorter PRI indicates the pacemaker site is nearer the AV node.

The QRS complex will usually <.10 but may be prolonged.

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.   

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.

Women are twice as likely to experience SVT as men at any age. In general, about 2.25 Americans out of 1000 fit the diagnosis of SVT (Hahn, 2020).

Be aware that SVT symptoms are often misdiagnosed as a panic attack. So, when in doubt, slide on some ECG patches and get to the truth of the matter. An unusual accompanying symptom of SVT is drumroll, please, polyuria.

SVT can be a spontaneous occurrence with no known trigger. More commonly, mechanisms such as too many energy drinks, cocaine, sepsis, dehydration, or increased intracardiac pressures contribute to this arrhythmia. Cardiac structural changes may also prompt an SVT response, such as congestive heart failure, myocardial infarction, pulmonary embolus, or valvular regurgitation or stenosis.

Vagal maneuvers up to and including carotid massage, Valsalva maneuver, even cold immersion have been used as a treatment to break the SVT cycle. Pharmacologic agents that tone down AV node sensitivity and help to end the SVT reentry pattern include adenosine, verapamil, esmolol, and diltiazem (Hahn, 2020).

Supraventricular tachycardias come in two basic types, regular or irregular. SVT is referring to the interval of QRS frequency. The fast, regular rhythms originating in the atrium of the heart are AVNRT, AVRT, and Junctional tachycardia.

Of the regular SVTs, Atrioventricular Nodal Reentrant Tachycardia (AVNRT) is the most common in 60% of cases diagnosed with an SVT. Female clients compose 70% of all AVNRT. Atrioventricular Reentry Tachycardia (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 present in the atrioventricular node (AV node). A slow conduction pathway and a fast one. When two pathways occur, there is a chance of a reciprocating reentry stimulus to occur during cardiac stress. In AVRT, the AV node interplays with an accessory pathway which feeds it an untimely depolarization signal. This interplay establishes a circular trigger keeping one depolarization working its way around and around through the AV node like a hula hoop of cardiac constriction.

Image 25:

Atrioventricular Nodal Reentrant Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
120-250	Regular	Absent hidden by preceding QRS	Hard to see .12-.20	Narrow <.12
Image Source: Adapted from Wikimedia Commons

Atrioventricular Reentry Tachycardias are the second most common of the regular SVT’s 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.

Image 26:

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 .12-.20	Narrow <.12
Image Source: Adapted from Wikimedia Commons

Not to add confusion. However, it does make a difference in which direction the circular conduction pathway rotates. The most common circular track is an antegrade conduction pathway through the AV node is known as Orthodromic. Orthodromic has the following characteristics. RP interval < (less than) the PR interval, or RP interval > (greater than) the PR interval in a slowly conducting accessory pathway. Also, look for retrograde P waves (leads I, II, III, aVF, V1). In a slow pattern, less than 100 bpm, a delta wave might be seen. Yet only with normal sinus rhythm rate, not with tachycardia. The above image is that of the more common Orthodromic AVRT.

Image 27: Electrical Conduction Chain of Events

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

That is, 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 and possesses a different set of characteristics, such as a short RP interval (< 100 msec). A regular, wide QRS complex (≥ 120 msec). Delta waves, the up slurring of the R wave, can be seen at rates equivalent to normal sinus rhythm and tachycardia (Patti, 2020).

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

Image 28:

Antidromic Atrioventricular Reentry Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
150-250	Regular	Retrograde and before QRS	Long	Wide >0.12
Image Source: Adapted from Crimelysis

Antidromic AVRT is about 5% of the cases of AVRT. Notice the delta waves easily visible in V4, V5, V6. The P is crushing into the QR in leads I and II.

A quick word about another antidromic reentry pathway is Wolff-Parkinson-White (WPW) syndrome. WPW is another example of accessory pathway reentry rhythm gone wild. It has little to do with the atrium of the heart, so that we will be discussing it later. Occasionally, well, rarely really, the culprit accessory pathway in WPW acts so that the AV node is the retrograde pathway. These typically present with a wide QRS complex, regular, and extremely rapid tachycardia (Patti, 2020).

Junctional rhythms are protective impulses from the AV node, the junction, whenever the heart’s main rhythm generator, the SA node, fails. For the sake of convenience, fast junctional rhythms are often listed among SVTs. So, we will look at arrhythmias originating with the junction here.

A quick review of the cardiac conduction system: The SA node in the heart’s right atrium is the main cardiac pacemaker, generating an electrical burst 60-100 times per minute. This depolarizing impulse travels to both atria through the internodal pathways, creating a spreading wave of muscle contraction as they pass through the atrial myocardium, heart muscle. Atrial contraction occurs simultaneously and pushes blood into the heart ventricles. The electrical impulse keeps moving along a set conduction pathway down into the AV node, conveniently located between the atria and the ventricles. The AV node sends the impulse through the bundle of His to the right and left cardiac ventricles. To be more specific, the bundle of His sheds the depolarization wave onto the Purkinje fibers that thread through the ventricular myocardium's insides, causing the strong ventricular walls to contract and push blood through the body.

The AV node is able, on need, to serve as an emergency pacemaker should the SA node fail. The inherent rate of the AV node junction on its own is 40-60 bpm, significantly slower than the SA node.

Circumstances may arise when the junction, the AV node, accelerates faster than the primary SA pacemaker. When that happens, junctional tachycardia follows as the heart muscle follows the quickest depolarization cycle present.

Image 29:

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
Image Source: Adapted from Wikimedia Commons

Note the P wave immediately before the Q as seen on lead II. This P wave is common for all junctional rhythms as the depolarization pacing point are in the AV node, and the depolarization wave must travel upwards into the atria simultaneously, or the closest thing to concurrent, as the same aberrant firing wave heads to the His bundle and ventricles (Knapp, 2020).

Junctional Rhythm Types

Rhythms sourced from the AV node are characterized by rate.

• Junctional bradycardia rate is <40 bpm.
• Junctional rhythm runs 40-60 bpm.
• Accelerated junctional rhythm runs from 60-100 bpm.
• Junctional tachycardia > 100 bpm.

Junctional rhythms will have a regular RR interval, and as a signature sign, one of the following P wave variations:

Absent P waves

A sign that the AV node is sending depolarization impulses simultaneously to the atria and ventricles

Inverted P waves

When the AV depolarization reaches the atria before the ventricles

Post QRS P waves

When the AV depolarization reaches the ventricles first

Before we leave the top of the heart, we need to discuss a few fine fast arrhythmias that can lead to a lot of mischief, the atrial tachycardias. This trio of aberrancies is often excluded from the rest of the SVT’s due to their irregular rate and rhythm. They are, nevertheless, supraventricular tachycardias, even though a goodly percentage of cardiologists harumph at that designation. We talked about the fast and irregular among the SVTs, Atrial Fibrillation (AFib), Atrial Flutter, and Multifocal Atrial Tachycardia (MAT).

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 initiating from within the heart atria. Whether from areas of inflammation, irritation, scaring, or from medication or chemical toxicities. Tachycardia, yes. Faster than 100 bpm. The speed may be driven by increased cardiac demand, as in COPD, where some 60% of MAT cases come from or from the changing structure of the cardiac wall in congestive heart failure. Multifocal Atrial Tachycardia is a condition associated with up to 45% mortality (Buxton, 2020) (Tandon, 2020).

Image 30:

Multifocal Atrial Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
QRS rate usually >100	Irregular	More than 3 distinct P waves	Varies	Narrow <0.12
Image Source: Adapted from Wikimedia Commons, Courtesy of Jason E Roediger

In lead, II notice the arrows, which each point out distinctly different P wave morphologies. P-P waves will be largely irregular. Not fibrillation, not flutter, but irregular from the multiplicity of electrical stimulation points.

MAT is not in itself life-threatening. However, the comorbidities frequently associated with it are severe. A rapid irregular pulse may be the only indication of the presence of MAT. Complaints that might cause a client to possess this arrhythmia include increased shortness of breath, chest pain, palpitations, lightheadedness, or feelings of syncope.

Multifocal atrial arrhythmias can lead to some direct complications. These include myocardial infarction from unsteady oxygen supply and demand, pulmonary emboli, or atrial thrombi, especially stroke (Tandon, 2020).

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Atrial Fibrillation (AFib or AF) is considered the most common type of treated cardiac arrhythmia, affecting between 2.7 to 6.1 million Americans (Thomas, 2020).

The rhythmic contraction of the atria counts for around 10% towards the overall output of the heart. When irritation, inflammation, or any other disorganizing factor gets in the way of the orderly metronome of the SA node, the chaotic firing of random atrial depolarization impulses leads to fibrillation, e.g., atrial quivering. AFib is a cardiac output disaster, especially in the elderly or those with comorbid medical conditions, as the billows-like effect from organized contractions can no longer push adequate quantities of blood into the ventricles. Despite this lack of compression, many people are asymptomatic with AFib. Those who do feel sudden fatigue, shortness of breath, dizziness, or chest pain tend to be surprised at how irregular their heart has become (Vaidya, 2018).

Image 31:

Image Source: Compliments of CDC.gov

Complications of AFib can be serious (NHLBI, 2019).

• 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 different 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 high 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 nuisance.

Image 32:

Atrial Fibrillation
Heart Rate	Rhythm	P Wave	PR Interval	QRS
Atrial rate usually >400	Irregular	No identifiable P waves	None	Narrow <0.12
Image Source: Adapted from Wikimedia Commons

The QRS rate of AFib will be all over the scale. Fast, then slower, then well, chaotic. So unpredictable that there are, in some viewpoints, three different types of atrial fibrillation.

Paroxysmal atrial fibrillation

A rhythm that switches back and forth between AFib and NSR

Permanent atrial fibrillation

The atrial fibrillation, which is present all the time and the de facto baseline rhythm

Persistent atrial fibrillation

Runs of fibrillation, when they occur, that tend to last longer than one week or until delivery of a small electric cardioversion shock or medications, reset the heart back to a normal sinus rhythm

In unstable clients, emergent, electrical cardioversion back to an NSR is needed. In clients whose condition allows more time, the consideration of rather to control the rhythm or control the heart rate must be explored. Generally, medication therapies must be individualized, and some surgical options are available. Oh, and anticipate that the client will be put on anticoagulants to minimize the occurrence of clot formation.

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 ventricle 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. While 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 atrioventricular block, which we will cover later.

Image 33:

Atrial Flutter
Heart Rate	Rhythm	P Wave	PR Interval	QRS
The atrial rate usually 250-320 Ventricular rate 120-160	Regular	Sawtooth P waves	Varies	Narrow <0.12
Image Source: Adapted from Wikimedia Commons

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 (Jancin, 2020).

Image 34: V1- Atrial Flutter with variable conduction

Image source: Complements of Wikimedia Commons

Atrial flutter tends to go hand in hand with an atrioventricular block (AV block). AV blocks are depolarization conduction delays, or at times complete barriers, to electrical conduction from the atria to the ventricles. Something as innocuous as increased vagal tone occurring during sleep, exercise, pain, or even stimulation of the carotid sinus. An AV block may also be related to cardiac fibrosis or sclerosis, ischemic heart disease, changes to the myocardial tissue, medications, or elevated plasma potassium (Medzcool, 2020).

The absent or slowed conduction from atria to ventricles, an atrioventricular block, is described by degrees. The seriousness of the conduction problem ranges from one to three. First degree AV block, second degree AV block type I (aka Wenckebach or Mobitz I} or type II (Mobitz II), and third-degree (complete) AV block (Petkar, 2021).

No talk on heart arrhythmias would be complete unless it meandered into this, the where’s Waldo of heart contractions. The Wandering Pacemaker.

A wandering atrial pacemaker is an arrhythmia originating in the atria where the pacemaker cells shift between the SA node, odd source spots within the atria themselves, and the AV node. These shifting, skipping about stimuli sites are generally best seen from lead II by looking for morphologic changes in the P waveform. It is most often seen in the young, the old, 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. Wandering atrial pacemaker is a favorite rhythm for instructors to give interns or learners while saying, “What’s wrong here?” (Rogoff, 2021).

Image 40:

Wandering Atrial Pacemaker
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100	Mostly Regular	From at least three sources	Mostly Regular	Narrow
Image Source: CEUfast.com

At least three different sources of atrial stimulation are present. QRS should be consistent and narrow. If this heart rate were faster, the arrhythmia would be considered multifocal atrial tachycardia.

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Wolff-Parkinson-White (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 supraventricular tachycardia. The accessory pathways (APs) 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 (Calkins, 2021).

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.

Image 41: Delta Wave

Image Source: Delta Wave, compliments of Wikimedia Commons

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 Q’s. There is no inferior MI on this ECG.

For a diagnosis, Wolff-Parkinson-White Syndrome (WPW) must be seen in more than one lead.

Image 42:

Wolff-Parkinson-White
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100 or more	Regular	Slurs into Q	Short when using accessory pathway	>.10
Image Source: Adapted from Wikimedia Commons

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 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 ventricles via orthodoxy conduction pathways.

Delta Wave: Slurring occurs at the beginning of the QRS complex.

Secondary T wave changes: Because ventricular depolarization is abnormal, repolarization will also be abnormal, causing ST and T wave changes 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 Myocardial infarction. These are negative delta waves, not Q waves, and they reflect pre-excitation and not myocardial necrosis.

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Any early, untimely cardiac contraction arising from the ventricles is a premature ventricular complex (PVC). Many, if not most people who have the occasional PVC are completely unaware of them. Those who do perceive them tend to describe the sensation as a skipped beat or pounding heart. Both are accurate descriptions of what is brought about by the hemodynamic changes of sudden, early ventricular contractions.

Image: 43

Premature Ventricular Complexes
Heart Rate	Rhythm	P Wave	PR Interval	QRS
60-100	Regular atrial	Disassociated from the abnormal QRS	None on Abnormal QRS	Wide on abnormal beat >.12
Image Source: Wellcome Collection, Adapted work is licensed under a Creative Commons Attribution 4.0 International License

Rate: Atrial and ventricular rate dependent upon the underlying rhythm.

Rhythm: Irregular due to PVC. If PVC is sandwiched between two normal beats, it is called interpolated, and the overall rhythm will be regular.

P Waves: A P wave is not associated with the PVC.

PRI: None with the PVC because the ectopic beat originates in the ventricles.

QRS: >.12 wide and bizarre. T wave frequently in the opposite direction of the QRS complex. If the QRS is negative, the T wave is usually upright; if the QRS is positive, the T wave is usually inverted.

PVCs may be due to Stress, activity, valvular disease, CAD, MI, caffeine, antihistamines, decongestants. The PVC may produce a weak pulse, and it is the client who should be treated, not the monitor.

Image 44:

Paired PVCs are referred to as couplets. Every other beat, a PVC is referred to as bigeminy PVCs.

Image 45:

Every third beat, a PVC is referred to as trigeminy.

Image 46:

PVCs occurring from more than one ventricular escape source during a sixty-second cycle are called multifocal PVCs.

Image 47:

Image 48:

When considering abnormal ventricular beats, the top considerations are where the source originates and the speed. All contractions of ventricular origin tend to have wide >.12 QRS complexes and a lack of PRI consistency. So, let us talk speed.

Without irritation from comorbid or causation factors, a ventricular escape rhythm rate will be limited to 15-40 bpm.

Three or more ventricular origin beats in a row constitute IVR. Typically, IVR is transient, with a brisk return to a heartbeat of atrial derivation. Syncope, dizziness, and all that accompanies the rapid hemodynamic slowing which accompanies this rhythm.

Rate: Intrinsic rate is 20-40 beats per minute.

Rhythm: Atrial not discernible, ventricular essentially regular.

P waves: Absent.

PRI: None.

QRS: >.12

It may be due to: MI, metabolic imbalances, or severe hypoxia. Treatment includes activation of emergency code, CPR if a client is pulseless. Lidocaine is contraindicated since it may knock out the last available pacemaker.

Image 49:

Accelerated Idioventricular Rhythm
Heart Rate	Rhythm	P Wave	PR Interval	QRS
40-100	Regular	Absent or not related to rhythm	NA	>.12
Image Source: Adapted from Wikimedia Commons, Courtesy of Jason E Roediger

Faster than a ventricular escape rhythm, yet not fast enough to meet the blood pressure dropping ventricular tachycardia criteria. An accelerated idioventricular rhythm might, rarely, be considered a benign or asymptomatic arrhythmia. However, do not get complacent with the lack of symptoms as AIVR is most common during cardiac tissue recovery from a myocardial injury. A time when any additional stress on the heart can tip recovery into adversity.

Rate: Atrial not discernable, ventricular 40-100 beats/minute.

Rhythm: Ventricular rate regular, an atrial rate not discernable.

P waves: Absent.

PR Interval: None.

QRS Complex: > .12

T Wave: NA.

QT Interval: Regular.

It may be due to Heart disease (e.g., acute myocardial infarction, digitalis toxicity, reperfusion of a previously occluded coronary artery), may occur during resuscitation, drugs (e.g., digoxin), dilated cardiomyopathy, and during outpatient procedures (especially during spinal anesthesia).

Ventricular tachycardia (V-Tach, VT) is a regular fast heart rate originating from an area of ventricular irritation. Short bursts of rapid ventricular contractions may not endanger a person. However, the less efficient circulation of blood from prolonged bouts can be life-endangering.

Characteristic findings indicating VT are tachycardia at >100 bpm, wide QRS complexes >.12, and AV dissociation. VT can be monomorphic, originating from one electrical excitation where all QRS complexes look alike. Or polymorphic, where multiple spots of electric stimulation are firing within the ventricles. Polymorphic VT is seen when each QRS shows a different morphology.

Bursts of VT lasting under 30 seconds are referred to as non-sustained V-Tach, while stretches longer than 30 seconds are referred to as sustained V-Tach.

Symptoms of ventricular tachycardia fall along the lines of reduced cardiac output and include hypotension, dizziness, syncope, cardiogenic shock, cardiac arrest.

Image 50:

Ventricular Tachycardia
Heart Rate	Rhythm	P Wave	PR Interval	QRS
100-250	Regular	Absent or not related to rhythm	NA	>.12
Image Source: CEUfast.com

Rate: Ventricular rate 100-250 beats/minute; atrial tends not to be discernible.

Rhythm: Atrial not discernible, ventricular essentially regular.

P Waves: May or may not be present. If present, they have no set relationship to the QRS complexes. P waves may appear between the QRS complexes at a rate different from that of the VT.

P-R Interval: None.

QRS Complex: Wide, >.12 ms (or 3 small ECG squares). Often difficult to differentiate between QRS and T wave. Three or more PVCs in a row at a rate of 100 per minute are referred to as a "run" of VT. There may be a long or a short run. A client may or may not have a pulse. If it is unclear whether a regular, wide QRS tachycardia is VT or Supraventricular Tachycardia, treat the rhythm as VT until proven otherwise.

Note: Ventricular tachycardia can occur in the absence of apparent heart disease.

T Wave: Difficult to separate from QRS.

QT Interval: Should be 390-450 ms. If longer be on alert for Torsades de Pointes.

Other Components: ≥ 3 consecutive wide QRS complexes at a frequency ≥ 100/minute and signs of AV dissociation confirm VT diagnosis. Should the rapid QRS complexes appear identical to the client's NSR QRSs, suspect a supraventricular tachycardia is occurring.

It may be due to: An early or a late complication of a heart attack, or during cardiomyopathy, alveolar heart disease, myocarditis, electrolyte imbalance, or following heart surgery.

Torsades de pointes (TdP) is a type of polymorphic VT signified by a prolonged QT interval. The characteristic that makes TdP distinctive is how the QRS complexes twist around the isoelectric baseline during self-limiting bursts.

Around 50% of clients discovered with intervals of TdP are not symptomatic. However, 10% of those presenting with TdP will experience cardiac death (Cohagan, 2020).

The R on T phenomenon plays a significant role in TdP due to the prolonged QT interval that is associated with it. For example, as a PVC, stomps on the tail of an extended T wave torsades de pointes or polymorphic VT may be triggered. This occurrence magnifies the need for a thorough review of client medications as drug-induced long QT syndrome is, unfortunately, common (Cohagan, 2020).

Image 51:

Torsades de Pointes
Heart Rate	Rhythm	P Wave	PR Interval	QRS
>100	Irregular	Absent or not related to rhythm	NA	>.12
Image Source: Adapted from Wikimedia Commons

Rate: Generally, >100 bpm

Rhythm: Irregular with an oscillating or spindle looking twist around the baseline

P Waves: Absent, yet if by chance you see some, they will not be related to the QRS complexes

P-R Interval: Chaotic

QRS Complex: Each differs from its neighbor. There will be an overall effect of tall QRSs, which shorten then regain height. This complex goes with the spindle or torsade’s effect.

T Wave: In the QRS complexes just before the torsades effect triggers, look for long prominent T waves. Also, keep an eye out for the R on T phenomenon, which can trigger VT or VF.

QT Interval: Prolonged QT intervals may be congenital, or more commonly, an unwanted effect of some prescription and over-the-counter medications.

Other Components: TdP is a significant adverse arrhythmia. However, the great concern when present increases in rate and degenerates into an even deadlier arrhythmia, ventricular fibrillation.

It may be due to: R on T trigger, antiarrhythmics, antipsychotics, antiemetics, antifungals, antimicrobials, basically any pharmaceutical with the adverse effect of prolonging the cardiac QT interval. Also, beware of substances that slow the hepatic metabolism. Slower liver breakdown of complex chemicals can turn a previously tolerated QT-prolonging substance into a landmine trigger, just waiting for an early R wave to activate the torsades effect (Cohagan, 2020).

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Ventricular fibrillation (V-fib or VF) is where the lower heart chambers quiver rather than constrict. Too many electrical polarization signals, arriving much too rapidly, reduce the strong rhythmic myocardial contractions to chaotic spasms. V-fib is a lethal arrhythmia resulting in rapid loss of consciousness, no pulse, and cardiac death in the absence of treatment.

Nearly 70% of cardiac arrest victims experience ventricular fibrillation. Without treatment, clinical death comes within minutes when V-fib is the prominent rhythm. Even when rescue efforts succeed, residual damage from the anoxic brain and neurologic damage requires follow-up and perhaps long-term treatment (Ludhwani, 2020).

V-Fib tends to accompany damage to the structure of the heart. Anything that can irritate or inflame the Purkinje cells of the ventricles has the potential to initiate the fast and multiple stimuli sites leading toward VF. Myocardial infarction, for example, shows V-Fib incidence of from 3 to 12% during the acute phase of myocardial damage. Many common conditions are associated with the chaotic irritability of V-Fib, including electrolyte abnormalities (hypokalemia, hyperkalemia, hypomagnesemia), acidosis, hypothermia, hypoxia, cardiomyopathies, family history of sudden cardiac death, congenital QT abnormalities, and alcohol use (Ludhwani, 2020).

Image 52:

Rate: Rapid and disorganized

Rhythm: Irregular and chaotic

P Waves: Absent but may be recognized among the chaos

P-R Interval: Not measurable

QRS Complex: Composed of fibrillatory waves, wide irregular oscillations of the baseline

T Wave: Not measurable

QT Interval: Not measurable

Other Components: Coarse VF is where most waveforms are 3mm or wider. Fine VF is where most waveforms are less than 3mm

Asystole is synonymous with Ventricular Standstill and death. Asystole is usually associated with prolonged circulatory insufficiency and cardiogenic shock. It could also be drug-related, hypothermia-related, and at times reversible.

Image 53:

Fixed-rate pacemaker

They are used primarily on clients with significant or complete heart blocks. The rate is pre-set to a rate such as 70 bpm, though rate changes can be made using external magnetic control (most commonly).

Demand pacemaker

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

R Triggered Pacemaker

When dealing with heart blocks possessing occasional sinus rhythm, the ventricular synchronized demand-type pacemaker, 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 clients with sinus rhythm and only an occasional heart block, the R wave blocked pacemaker stops firing when it detects a natural R wave produced by the client.

Atrial Triggered Pacemaker

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

Image 55:

Dual Chamber Pacemaker

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

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

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 paced has been depolarized. The term is that the pacemaker has "captured" the chamber being paced. Paced QRS is wide, bizarre, and resembles PVCs.

Image 56:

Sensing refers to the pacemaker's ability to recognize the client’s intrinsic rhythm to determine if it needs to fire. Most pacemakers function in the demand mode and fire when needed.

When a pacemaker fails to send a needed impulse, it is said to have malfunctioned, failed to fire, failed to output. Usually, this means a low battery or that one of the connecting wires anchored in the heart wall is at fault. At times, the type of electrical artifacts that crop up on ECGs can fool the pacemaker to not fire. A no output incident is revealed as the lack of a pacemaker spike where there should be one.

Image 58:

There is no P or QRS after the pacemaker has fired when loss of capture exists, just a spike. This loss of capture usually means a pacemaker needs to be adjusted to detect the heart's need to be paced. A pacing wire may have lost contact with the chamber wall, which can occur when the heart is too damaged to respond.

Under-sensing: 

Under-sensing occurs when the pacemaker fires too soon after an intrinsic beat, and there are pacer spikes where there should not be. These can appear in the T wave, on the QRS, or anywhere on the heart rhythm's tracing. Under-sensing requires adjustment with the wires or battery replacement.