EKG Rhythms

Advanced Cardiac Life Support (ACLS) is an essential course designed for healthcare professionals who provide advanced cardiac care to patients in various settings, including in-facility and prehospital environments. This course has been created by experienced providers, board-certified physicians, and veteran ACLS instructors, making it a trusted resource for those who want to enhance their knowledge and skills.

This resource provides a comprehensive approach to reviewing the core EKG rhythms of ACLS practice, covering topics such as pathophysiology, defining criteria and EKG features, clinical manifestations, common etiologies, and EKG presentation for the 15 core rhythms. Whether you’re a seasoned healthcare professional or just starting your career in the field, this resource can help you stay up-to-date with the latest practices and guidelines in advanced cardiac care.

• Ventricular Fibrillation (VFib) is a cardiac arrest condition that occurs when there is a chaotic and asynchronous ventricular depolarization and repolarization pattern in the heart. This condition is caused by areas of normal myocardium alternating with regions of ischemic, injured, or infarcted tissue in the ventricles. This pattern leads to the ventricles’ inability to contract as a unit, which stops cardiac output and causes the heart to quiver and fail to pump blood effectively.

• Rate: VFib’s electrical deflections are rapid and highly disorganized, making the rate uncountable. Baseline undulations occur between 150-500 per minute.
• QRS Complex: No recognizable QRS complex. Regular negative-positive-negative patterns cannot be observed.
• Rhythm: Indeterminate. Electrical waveforms vary in size and shape, portraying a highly disorganized pattern of sharp deflections, and no regular rhythmic patterns can be recognized upon analysis. 
• Amplitude: Subjectively characterizes the condition as fine (2-5mm), medium or moderate (5-10mm), coarse (10-15mm) or very coarse (>15mm), and is measured from peak to trough.

• When VFib occurs, the pulse disappears, but if rapid ventricular tachycardia (VTach) is present, the pulse may disappear before VFib onset. Pulseless VTach rapidly progresses into VFib, which is then considered cardiac arrest.
• Unresponsiveness and physical collapse
• Agonal gasps or apnea may occur in VFib patients due to the brain’s attempt to restore oxygen supply.
• Sudden death.

• Acute coronary syndrome is a common cause of VFib, leading to ischemic areas of myocardial tissue.
• Untreated VTach, both stable and unstable.
• Premature ventricular complexes (PVCs) with the R-on-T phenomenon.
• Introduction of drugs, electrolytes, or acid-base abnormalities that prolong the relative refractory period.
• QT prolongation, either primary or secondary.
• Electrocution or hypoxia can cause VFib, due to the interruption of the normal electrical activity in the heart.

Figure 1. Ventricular Fibrillation. Presented at no pulse, or a rate of zero beats per minute. The EKG rhythm shows high-amplitude waveforms with a disorganized pattern of sharp deflections that vary in size, shape, and rhythm, indicating chaotic electrical activity in the ventricles.

• Cardiac conduction impulses typically occur in an organized pattern to facilitate coordinated myocardial contraction. However, in some cases, this pattern of electrical activity fails to produce effective ventricular contraction, leading to a condition that was previously known as electromechanical dissociation. In such cases, there is insufficient ventricular filling during diastole, which can result in ineffective contractions and a lack of cardiac output. This condition requires prompt recognition and management to prevent serious complications.

• Rate: Can be presented as fast (>100 beats per minute) or slow (<60 beats per minute).
• QRS Complex: Complex can be narrow (<0.12 seconds) or wide (>0.12 seconds).
• Rhythm: Electrical activity is organized, but it is less organized than normal sinus rhythm.

• Physical collapse and unresponsiveness are common symptoms.
• Agonal respiration or apnea.
• Palpation may not detect any pulse.
• Systolic blood pressure may remain low.

Utilize the H’s and T’s Mnemonic to Identify Common Underlying Causes:

In the medical field, understanding the underlying causes of a patient’s condition is crucial to provide effective treatment. One helpful tool for this is the H’s and T’s mnemonic. This acronym helps medical professionals remember the common etiologies that may lead to a patient’s condition. The following are the possible underlying causes:

• Hypovolemia (low blood volume)
• Hypoxia (low oxygen levels)
• Hydrogen ion (acidosis)
• Hypo-/hyperkalemia (low or high levels of potassium)
• Hypothermia (low body temperature)
• Tension pneumothorax (collapsed lung)
• Tamponade, cardiac (fluid buildup around the heart)
• Toxins (e.g., drug overdose or ingestion)
• Thrombosis, pulmonary (blood clot in the lungs)
• Thrombosis, coronary (acute coronary syndrome)

Additionally, it’s essential to note that a narrow QRS and a fast heart rate are typically caused by non-cardiac factors. In contrast, a wide QRS and a slow heart rate are usually related to a cardiac etiology. By understanding the H’s and T’s mnemonic and recognizing these patterns, medical professionals can identify potential underlying causes quickly and develop a treatment plan tailored to each patient’s specific needs.

Pulseless electrical activity (PEA) may manifest as any rhythm that features organized electrical activity but lacks a detectable pulse. This can include a sinus rhythm on the EKG monitor, such as sinus bradycardia or sinus tachycardia, where no pulse is palpable. In such instances, the rhythm can be classified as PEA.

• Asystole, the absence of electrical activity in the heart, can have both primary and secondary causes. In primary asystole, the heart’s electrical system fails to generate a ventricular depolarization, which can result from ischemia or degeneration (i.e., sclerosis) of the sinoatrial (SA) or atrioventricular (AV) node conducting systems. Primary asystole can be life-threatening and requires immediate intervention.
• On the other hand, secondary asystole occurs due to factors outside of the heart’s electrical conduction system, resulting in a failure to generate any electrical depolarization. Some common causes of secondary asystole include hypovolemia (low blood volume), hypoxia (low oxygen levels), hyperkalemia (high levels of potassium), drug toxicity, and tension pneumothorax (collapsed lung). Treatment of secondary asystole involves addressing the underlying cause to restore the heart’s normal electrical activity.

• Rate: No ventricular activity.
• QRS Complex: No recognizable QRS complex is observed.
• Rhythm: No ventricular activity.
• PR Interval: Determination of PR interval is not possible. In some cases, a P-wave may be present, but the absence of the R wave is necessary to be an asystolic rhythm.

• Physical collapse and unresponsiveness. 
• Early agonal breathing or apnea.
• No detectable pulse or blood pressure.
• Eventual fatality.

• End of life (death)
• Insufficient blood supply to the heart (cardiac ischemia)
• Respiratory failure or low oxygen levels (acute hypoxia)
• Exposure to high voltage electrical shock (e.g., electrocution, lightning strike)
• In some cases, a transient period of stunned cardiac activity may occur following defibrillation before normal rhythm is restored.

Asystole is a cardiac condition characterized by the absence of any discernible electrical activity in the heart, resulting in the absence of a palpable pulse. Before the onset of asystole, QRS-like complexes may be observed, which represent minimal electrical activity, often in the form of ventricular escape beats. These QRS-like complexes are then followed by a prolonged period of complete electrical inactivity, which can now be identified as asystole. Once asystole is established, the patient will become unresponsive and pulseless, necessitating prompt intervention to restore normal cardiac function.

• The sinoatrial (SA) node is responsible for initiating electrical impulses that control the heart’s rhythm. In some cases, the SA node may generate impulses at a slow rate, which can be considered a physiological response. However, in other instances, a slow rate of impulse generation may be a physical sign of an underlying condition, such as sinus tachycardia.

Characterized by a regular rhythm of P-waves followed by QRS complexes at a rate of <60 beats per minute. However, this rhythm is often a normal, physiological variant rather than an abnormality.

• Rate: Generally <60 beats per minute. When symptomatic, the rate is typically less than 50 beats per minute.
• QRS Complex: Narrow, with a duration of <0.12 seconds (often <0.11 seconds) in the absence of an intraventricular conduction defect.
• Rhythm: Regular sinus rhythm.
• PR Interval: Regular interval, ranging from 0.12 to 0.20 seconds.
• P-waves: Waves are normal in both size and shape. Each P-wave is followed by a QRS complex, and each QRS complex is preceded by a P-wave.

• At rest, individuals with this condition are typically asymptomatic.
• However, with increased activity and sinus node dysfunction, a constant slow rate can result in symptoms such as easy fatigue, shortness of breath, dizziness or lightheadedness, syncope, hypotension, diaphoresis, pulmonary congestion, and frank pulmonary edema.
• In addition, the EKG can also show acute ST-segment or T-wave deviation or ventricular arrhythmias independently. Proper evaluation and diagnosis of these EKG findings are essential for identifying the underlying cause and developing an appropriate treatment plan.

• Well-conditioned individuals can often experience this phenomenon.
• A vasovagal event, such as vomiting, Valsalva maneuver, rectal stimuli, or inadvertent pressure on the carotid sinus (shaver’s syncope), can cause this condition.
• Acute coronary syndromes that hinder circulation to the SA node (right coronary artery), most commonly inferior acute myocardial infarctions (AMIs), can also lead to this condition.
• Adverse drug effects, such as beta-blockers, calcium channel blockers, digoxin, or quinidine.

Figure 2. Sinus Bradycardia is shown in the EKG strip at a rate of approximately 50 beats per minute. The presentation displays a normal sinus rhythm but at an abnormally lower rate than the usual, resulting in a slower production of deflections. It is essential to identify such abnormalities in heart rate as they may indicate underlying conditions that require medical attention. Proper evaluation and diagnosis of the EKG findings is necessary for developing an appropriate treatment plan to manage sinus bradycardia.

• When it comes to arrhythmias or pathologic conditions, the physical response is more significant than the actual occurrence. This is due to the normal formation and conduction of impulses within the body.

• Rate: Heart rate exceeds 100 beats per minute.
• QRS Complex: May appear regular or wide in case of any underlying abnormality. Every QRS complex is accompanied by a P-wave.
• Rhythm: Regular sinus rhythm.
• PR Interval: Typically less than 0.20 seconds in duration.

• Generally nonspecific, meaning that they can be present in various other conditions as well. 
• Symptoms may or may not be present and their presence is usually due to the underlying cause of tachycardia such as fever, hypovolemia, or other similar conditions. Therefore, the presence of symptoms cannot be solely used for the diagnosis of tachycardia and a proper evaluation is required to identify the root cause.

• May occur due to a variety of factors, including normal exercise, adrenergic stimulation, pain, or anxiety. 
• Can also be associated with various clinical conditions such as hypoxemia, fever, hypovolemia, hyperthyroidism, and anemia.
• A thorough evaluation of the patient’s medical history and physical examination can help in the accurate diagnosis of tachycardia.

Figure 3. The EKG strip shows the presentation of Sinus Tachycardia with a heart rate of around 140 beats per minute. The EKG displays a normal sinus rhythm; however, the rate of the rhythm is significantly faster than usual, leading to a rapid production of deflections. It is crucial to identify such abnormal heart rates, as they may indicate underlying conditions that require prompt medical attention. Therefore, a thorough evaluation of EKG rhythms and findings is essential for proper diagnosis and treatment.

• Atrial impulses travel faster than the sinoatrial (SA) node impulses, causing multiple chaotic, random pathways through the atria.

• Atrial fibrillation is characterized by an irregularly irregular rhythm with variations in both interval and amplitude from R-wave to R-wave. This can also be observed in multifocal atrial tachycardia (MAT).
• Rate: Ventricular response to atrial undulations can range widely from 300 to 400 per minute and may be normal or slow if atrioventricular (AV) nodal conduction is abnormal (e.g., sick sinus syndrome). 
• QRS Complex: Remains less than 0.12 seconds unless distorted by fibrillation, flutter waves, or conduction defects through the ventricles.
• Rhythm: Irregularly irregular. 
• PR Interval: Interval cannot be measured. 
• P-waves: Chaotic atrial fibrillatory waves are the only p-waves observed. 

• The signs and symptoms are closely linked to the ventricular response rate to atrial fibrillation waves.
• Atrial fibrillation with a rapid ventricular response can lead to dyspnea on exertion, shortness of breath, and sometimes acute pulmonary edema.
• Loss of the “atrial kick” can cause a decrease in cardiac output and coronary perfusion.
• Irregular rhythm is commonly perceived as “palpitations.”
• Atrial fibrillation and atrial flutter are sometimes asymptomatic.

• Conditions that may lead to atrial fibrillation may include acute coronary syndromes, coronary artery disease, or congestive heart failure.
• Mitral or tricuspid valve disease.
• Hypoxia, acute pulmonary embolism.
• May be drug-induced, from medications including digoxin, quinidine, beta-agonists, theophylline.
• Associated with clinical conditions such as sepsis, hypertension, and hyperthyroidism.

Figure 4. The EKG strip shows the presentation of Atrial Fibrillation with a heart rate of around 90 beats per minute. One of the key indicators of atrial fibrillation is the absence of P-waves, as well as the presence of coarse fibrillatory waves. This often makes it difficult to identify atrial activity. The QRS complexes are irregularly irregular with varying R-R intervals, which can further complicate the diagnosis and management of the condition. This irregularity is due to the chaotic and disorganized electrical signals that originate from multiple foci within the atria, leading to an irregular ventricular response. Effective treatment strategies may include medication, cardioversion, or ablation therapy, depending on the underlying cause of the condition.

• Atrial flutter is caused by atrial impulses that travel in a circular course around the atria, setting up flutter waves due to their faster rate than sinoatrial (SA) node impulses.

• Rate: Atrial rate ranges from 220-350 beats per minute. The ventricular response is determined by the degree of AV node block or the conduction of atrial impulses. When AV nodal conduction is limited, the ventricular response is often greater than 150-180 beats per minute.
• QRS Complex: In the absence of fibrillation, flutter waves, or conduction defects in the ventricles, the QRS complex remains less than 0.12 seconds.
• Rhythm: The rhythm of the ventricles is often regular, and the ratio is set to the atrial rhythm, such as 2:1 or 4:1.
• PR Interval: Interval cannot be measured.
• P-waves: No true P-waves can be observed.

• Signs and symptoms are dependent on the ventricular response rate to atrial fibrillation waves. Atrial fibrillation with a rapid ventricular response may result in dyspnea on exertion, shortness of breath, and even acute pulmonary edema.
• Absence of “atrial kick” may lead to a decrease in cardiac output and reduced coronary perfusion.
• An irregular rhythm is often observed as palpitations.
• Atrial fibrillation and atrial flutter may also be asymptomatic.

• Acute coronary syndromes, coronary artery disease, or heart failure can contribute to the development of this condition.
• An unhealthy or diseased mitral or tricuspid valve can cause or worsen symptoms.
• Low oxygen levels (hypoxia), acute pulmonary embolism, and other respiratory conditions.
• Certain medications like digoxin, quinidine, beta-agonists, and theophylline.
• Medical conditions such as sepsis, hypertension, and hyperthyroidism.

Figure 5. The EKG strip shows the presentation of Atrial Flutter with a heart rate of approximately 75 beats per minute. Observe the presence of flutter waves in a classic sawtooth pattern. 

• The re-entry phenomenon in the heart occurs when impulses are repeatedly cycled in the atrioventricular (AV) node, caused by an abnormal rhythm circuit that allows a wave of depolarization to travel in a circular pattern. In most cases, the depolarization travels forward through the abnormal pathway and then loops back through the “normal” conduction tissues. Accessory-mediated supraventricular tachycardia (SVT) can include AV nodal reentrant tachycardia or AV reentry tachycardia.

• Characterized by a regular and narrow-complex tachycardia with a sudden onset and cessation, and no visible P-waves. Some medical professionals require the abrupt onset and cessation to be captured on a monitor strip for a diagnosis of reentry supraventricular tachycardia (SVT) to be made.
• Rate: At rest, the heart rate exceeds the upper limit of sinus tachycardia (>220 beats per minute) and is rarely less than 150 beats per minute, with rates up to 250 beats per minute often observed.
• QRS Complex: Normal and narrow.
• Rhythm: Regular.
• P-waves: Rarely seen due to the rapid rate which causes them to be obscured by the preceding T-waves. The low atrial origin of the arrhythmia makes detection of P-waves challenging.

• Patient experiences palpitations at the onset of symptoms, leading to anxiety and discomfort.
• Low exercise tolerance is observed along with very high heart rates.
• Unstable tachycardia may result in additional symptoms.

• A considerable number of individuals with SVT experience an accessory conduction pathway.
• Certain factors such as caffeine, hypoxia, cigarettes, stress, anxiety, sleep deprivation, and various medications may trigger SVT re-entry in healthy individuals.
• The incidence of SVT rises in patients with coronary artery disease, chronic obstructive pulmonary disease, and congestive heart failure who have other health issues.

Figure 6. Accessory-Mediated Supraventricular Tachycardia is observed above at a rate of around 180 beats per minute. It is noteworthy that spontaneous reentry SVT can sometimes manifest in sinus rhythm.

• The re-entry phenomenon and rapid repetitive depolarizations may occur due to the slowed impulse conduction around areas of ventricular injury, infarct, or ischemia. Such areas of injury can also act as sources of ectopic impulses, which are also known as irritable foci, and lead to the impulse taking a circular course.

• QRS complex morphology is consistent in all beats. Presence of three or more consecutive premature ventricular contractions (PVCs) indicates ventricular tachycardia (VT). Non-sustained VT lasts less than 30 seconds, while sustained VT lasts longer.
• Rate: Ventricular rate is more than 100 beats per minute and typically ranges from 120 to 250 beats per minute.
• QRS Complex: Wide and irregular PVC-like complexes with a duration of 0.12 seconds and a large T-wave of opposite polarity from the QRS.
• Rhythm: Regular ventricular rhythm.
• PR Interval: Nonexistent due to AV dissociation.
• P-waves: Infrequent but may be seen. Wide complex tachycardias of ventricular origin, such as VT, are distinguished from supraventricular tachycardias with aberrant conduction by the presence of AV dissociation.

• The development of symptoms of decreased cardiac output, such as orthostasis, hypotension, syncope, and signs of inadequate perfusion, is typical.
• Despite the widespread belief that sustained VTach always produces symptoms, monomorphic VTach can be asymptomatic.
• If left untreated, sustained VTach can deteriorate to unstable VTach and often to VFib.

• A sudden lack of oxygen to the heart causing areas of ventricular irritability and resulting in premature ventricular contractions (PVCs).
• Reduced ejection fraction due to ongoing systolic heart failure.
• Occurrence of PVCs during the relative refractory period of the cardiac cycle, known as the R-on-T phenomenon.
• Prolonged QT interval induced by drugs such as tricyclic antidepressants, procainamide, sotalol, amiodarone, ibutilide, dofetilide, some antipsychotics, digoxin, certain long-acting antihistamines, and certain antibiotics.

Figure 7. Monomorphic Ventricular Tachycardia, observed at a rate of around 210 beats per minute. Notably, the QRS complexes are wide and accompanied by T-waves that have an opposite polarity. 

• When areas of the ventricle experience injury, infarction, or ischemia, the conduction of electrical impulses can slow down. This can cause the impulses to travel in a circular pattern, leading to a phenomenon known as re-entry, which can result in rapid and repetitive depolarizations. Additionally, these areas of injury can serve as sources for ectopic impulses, also known as irritable foci.

• Inconsistency in QRS complex morphology is a defining characteristic of this condition.
• Rate: Ventricular rate exceeds 100 beats per minute, often ranging from 120-250 beats per minute.
• QRS Complex: Wide and bizarre, resembling PVCs with a duration of 0.12 seconds, and a large T-wave of opposite polarity to QRS.
• Rhythm: Ventricular rhythm is regular or irregular, with no atrial activity present.
• PR Interval: Nonexistent due to AV dissociation.
• P-waves: Infrequent but present; the presence of AV dissociation is a defining feature of wide-complex tachycardias originating in the ventricles compared to those originating from supraventricular tachycardias with aberrant conduction.

• Development of symptoms related to decreased cardiac output such as orthostasis, hypotension, syncope, and inadequate perfusion is typical.
• Untreated and sustained Ventricular Tachycardia (VTach) can progress to unstable VTach and eventually to Ventricular Fibrillation (VFib).

• Acute ischemic events may cause areas of ventricular irritability leading to premature ventricular contractions (PVCs).
• PVCs can occur during the relative refractory period of the cardiac cycle, known as the R-on-T phenomenon.
• Certain medications, including tricyclic antidepressants, procainamide, sotalol, amiodarone, ibutilide, dofetilide, some antipsychotics, digoxin, some long-acting antihistamines, and certain antibiotics, may cause a prolonged QT interval and trigger PVCs.
• Inherited long QT interval syndromes. 

Polymorphic ventricular tachycardia presents similarly to monomorphic ventricular tachycardia, except the QRS complexes show varying morphologies. This can cause the rhythm to appear irregular and erratic, which can lead to hemodynamic instability and sudden cardiac arrest.

• Torsades de Pointes is a type of polymorphic ventricular tachycardia that displays a unique subtype.
• During a baseline EKG, the QT interval is unusually prolonged, leading to a higher relative refractory period of the cardiac cycle.
• This prolongation of the QT interval increases the probability of a PVC occurring on the T-wave, leading to the induction of VTach via the R-on-T phenomenon.

• The QRS complexes in this type of ventricular tachycardia exhibit a characteristic spindle-node pattern, with a regular increase and decrease in amplitude that forms a spindle. This spindle is followed by complexes with opposite deflection that create a node at the start of the next spindle.
• Rate: The atrial rate is indeterminate, while the ventricular rate varies between 150 and 250 complexes per minute. 
• QRS Complex: Exhibits the typical spindle-node pattern that is characteristic of this type of tachycardia.
• Rhythm: Ventricular rhythm is irregular.
• PR Interval: Nonexistent.
• P-waves: Nonexistent. 

• The potential for rapid progression to pulseless VTach or VFib is a concerning feature.
• Manifestations of decreased cardiac output, including orthostasis, hypotension, syncope, and signs of inadequate perfusion, are typical in this condition.

• Occurs most often in patients with prolonged QT intervals, where the QT interval is abnormally long during a baseline EKG.
• Drug-induced prolonged QT interval is a major contributing factor, with medications such as tricyclic antidepressants, procainamide, sotalol, amiodarone, ibutilide, dofetilide, some antipsychotics, digoxin, some long-acting antihistamines, and certain antibiotics being potential culprits.
• Inherited forms of long QT syndrome or acute ischemic events can result in electrolyte and metabolic alterations, which can also lead to Torsades de Pointes.

In Torsades de Pointes, the QRS complex displays a characteristic spindle-node pattern. It starts with a negative initial deflection and increasing amplitude, followed by a node, and then a positive initial deflection with spindling in amplitude. This pattern repeats continuously until the rhythm deteriorates to VTach or VFib.

• A partial AV block occurs when there is a delay in the impulse conduction at the atrioventricular (AV) node for a fixed interval. This delay can be a result of a primary conduction abnormality or a secondary problem.

• Rate: Can occur with normal sinus mechanisms (60-100 beats per minute), sinus bradycardia (less than 60 beats per minute), or sinus tachycardia (more than 100 beats per minute).
• QRS Complex: Narrow. In the absence of intraventricular conduction defect, QRS complex is less than 0.12 seconds.
• Rhythm: Regular sinus.
• PR Interval: Fixed and prolonged, measuring more than 0.20 seconds.
• P-waves: Normal size and shape. Every P-wave precedes a QRS complex, and a QRS complex follows every P-wave.

• Classically asymptomatic.

• Drug therapy, such as AV nodal blockers including beta-blockers, nondihydropyridine calcium channel blockers, and digoxin.
• Stimulation of the parasympathetic nervous system, such as from the vasovagal reflex.
• Acute coronary syndromes, which can affect the circulation to the sinoatrial (SA) node, with inferior acute myocardial infarctions (AMIs) being the most common.

Figure 8. This EKG is displaying First-Degree AV Block, with a regular sinus rhythm and a rate of around 70 beats per minute. The PR intervals are noticeably prolonged but remain fixed, indicating no interruption in the conduction of electrical impulses from the atria to the ventricles. Typically, this condition is asymptomatic, and the rhythm is often incidental, found during a routine EKG. 

• AV block typically involves the AV node, which receives its blood supply from branches of the right coronary artery. As the condition progresses, there is a gradual slowing of impulse conduction at the AV node, resulting in a prolonged PR interval. If the conduction delay becomes severe enough, a sinus impulse may be completely blocked and fail to produce a QRS complex.

• electrical conduction. Nevertheless, both rates are generally within normal limits.
• QRS Complex: Typically narrow and last less than 0.12 seconds, but occasional QRS complexes may be absent.
• Rhythm: Atrial complexes follow a regular rhythm, while ventricular complexes follow an irregular rhythm due to the absence of some beats, resulting in a pattern of regular P-waves with irregular QRS complexes.
• PR Interval: The interval progressively lengthens with each cycle until a P-wave fails to produce a QRS complex, leading to a dropped beat.
• P-waves: The size and shape of P-waves are usually normal. However, some P-waves do not result in a QRS complex, causing a skipped beat.

• Frequently occurs as a result of underlying sinus bradycardia, which leads to a drop in electrical conduction. 
• While typically asymptomatic, some patients may present with chest pain, shortness of breath, or decreased consciousness. 
• Hypotension, shock, pulmonary congestion, congestive heart failure, and angina may also accompany the condition.

• Medications that block the AV node, such as beta-blockers, nondihydropyridine calcium channel blockers, and digoxin.
• Conditions that stimulate the parasympathetic nervous system, such as the vasovagal reflex.
• Acute coronary syndrome that affects the right coronary artery, which can lead to inferior myocardial infarctions and damage to the AV node.

Figure 9. This EKG is displaying Second-Degree AV Block Type I, with a heart rate of approximately 50 beats per minute. The PR interval gradually lengthens with each beat until one P-wave is not followed by a QRS complex. This type of block occurs when the conduction of an impulse through the AV node is interrupted, leading to the absence of the QRS complex.

• Impulse conduction is normal through the AV node, but the block occurs below the AV node, most often at the bundle of His or bundle branches. Therefore, there is no prior PR prolongation or first-degree block.

• Rate: Atrial rate usually falls between 60-100 beats per minute, while ventricular rate is slower due to blocked impulses, and can fluctuate.
• QRS Complex: Narrow QRS complex (less than 0.12 seconds) indicates high block relative to AV node, whereas a wide QRS complex (0.12 seconds or more) suggests low block relative to AV node.
• Rhythm: Atrial rhythm is regular, but ventricular rhythm is irregular, except in cases where there is consistent 2:1 or 3:1 block.
• PR Interval: The PR interval remains constant, without any progressive prolongation, as is characteristic of Type I second-degree AV block Mobitz.
• P-waves: P waves are typical in size and shape, but some P waves may not be conducted, and therefore not followed by a QRS complex. This distinguishes Type II second-degree AV block Mobitz from Type I.

• Will typically occur secondary to sinus bradycardia.
• May present as chest pain, shortness of breath, and decreased level of consciousness.
• Hypotension, shock, pulmonary congestion, congestive heart failure, and acute myocardial infarction (AMI) are often reported.

• Pathologies involving the His-Purkinje system, including infranodal block, bundle branch block, and myocardial ischemia or infarction affecting the distal conduction system. Pathologies can result in the intermittent failure of impulses to propagate through the conduction system, leading to dropped beats and second-degree AV block type II.

Figure 10. This EKG is displaying Second-Degree AV Block Type II, with a rate of around 60 beats per minute. Observe the consistent PR-QRS intervals until two beats are dropped, with QRS complexes that are marginally normal, indicating a high nodal block.

• Complete heart block refers to the absence of conduction of electrical impulses between the atria and ventricles, either in an antegrade or retrograde direction, which can result from injury or damage to the cardiac conduction system in various anatomic locations, such as the AV node, the bundle of His, or the bundle branches.

• Rate: This refers to the rates of the atria and ventricles in a third-degree AV block, where there is complete dissociation between the two. The atrial rate remains normal (60-100 beats per minute) while the ventricular rate is slower and dependent on escape beats. The ventricular escape rate can be either slower or faster than the atrial rate, resulting in either a third-degree AV block or AV dissociation, respectively. The ventricular rates for these conditions are roughly 20-40 and 40-55 beats per minute.
• QRS Complex: Can be narrow (<0.12 seconds) or wide (>0.12 seconds), depending on the site of the block relative to the AV node.
• Rhythm: Both the atrial and ventricular rhythms are regular but dissociated, meaning they are not synchronized.
• PR Interval: No observable relationship between the P-waves and R-waves, as they are completely dissociated.
• P-waves: Typical in size and shape, but they are not associated with the QRS complexes.

• Sinus bradycardia is a common underlying cause.
• Symptoms may include chest pain, shortness of breath, and decreased level of consciousness.
• Associated with hypotension, shock, pulmonary congestion, congestive heart failure, and acute myocardial infarction (AMI).

• The acute coronary syndrome affects branches of the left coronary artery.
• Commonly involves the left anterior descending (LAD) artery.
• Affects branches supplying the interventricular septum, including the bundle branches.

Figure 11. This EKG is displaying Third-Degree AV Block, at a rate of around 40 beats per minute. Observe regular P-waves at a rate of 50-55 beats per minute and regular ventricular escape beats at a rate of 35-40 beats per minute; however, there is no apparent correlation between the P-waves and the escape beats.