Pericarditis

Acute pericarditis is a type of pericarditis (inflammation of the sac surrounding the heart, the pericardium) usually lasting less than 6 weeks. It is by far the most common condition affecting the pericardium.

Typical ECG changes in acute pericarditis includes:

• stage 1 - diffuse, positive, ST elevations with reciprocal ST depression in aVR and V1. Elevation of PR segment in aVR and depression of PR in other leads especially left heart V5, V6 leads indicates atrial injury.
• stage 2 - normalization of ST and PR deviations
• stage 3 - diffuse T wave inversions (may not be present in all patients)
• stage 4 - ECG becomes normal OR T waves may be indefinitely inverted

The two most common clinical conditions where ECG findings may mimic pericarditis are acute myocardial infarction (AMI) and generalized early repolarization.

Parasystole

Parasystole is a kind of arrhythmia caused by the presence and function of a secondary pacemaker in the heart, which works in parallel with the SA node. Parasystolic pacemakers are protected from depolarization by the SA node by some kind of entrance block. This block can be complete or incomplete.
Parasystolic pacemakers can exist in both the atrium or the ventricle. Atrial parasystolia are characterized by narrow QRS complexes.

There are two forms of ventricular parasystole, fixed parasystole and modulated parasystole. Fixed ventricular parasystole occurs when an ectopic pacemaker is protected by entrance block, and thus its activity is completely independent from the sinus pacemaker activity. Hence, the ectopic pacemaker is expected to fire at a fixed rate. Therefore, on ECG, the coupling intervals of the manifest ectopic beats will wander through the basic cycle of the sinus rhythm. Accordingly, the traditional electrocardiographic criteria used to recognize the fixed form of parasystole are:

• the presence of variable coupling intervals of the manifest ectopic beats;
• inter-ectopic intervals that are simple multiples of a common denominator;
• fusion beats.

P Wave Asystole

Another form of Asystole you may encounter is called P wave asystole or Ventricular Asystole. The features are the same as traditional Asystole, but with one exception, there will be P waves present in the ECG tracing. The patient is clinically dead. The patient will not survive with just atrial depolarization and will require CPR.

Asystole

Asystole, also known as flatline, is a condition in which there is no electrical activity from the heart and thus no blood flow. 

It leads to cardiac arrest. 

Survival rates in a cardiac arrest patient with asystole are much lower than in a patient with a defibrillable rhythm; asystole is not a "shockable" rhythm in and of itself.

ECG example of asystole

ECG rhythm strip example of asystole

Ventricular Standstill

Ventricular standstill is the absence of any ventricular activity for more than a few seconds. There may be atrial activity as evidenced by P waves in which case complete heart block is blocking all impulses from reaching the ventricles and the backup or subsidiary pacemaker has failed, or there may be an absence of atrial and ventricular activity.

Agonal Rhythm

An agonal heart rhythm is a variant of asystole with a heart rate is less than 20 bpm, without P waves and with wide, bizarre QRS complexes seen on the electrocardiogram. Clinically, an agonal rhythm is regarded as asystole and should be treated equivalently, with cardiopulmonary resuscitation. As in asystole, the prognosis for a patient presenting with this rhythm is very poor.

ECG strip shows Agonal rhythm

ECG strip shows Agonal rhythm

12-Lead ECG shows Agonal rhythm

3rd Degree AV Block

Third-degree atrioventricular block (AV block), also known as complete heart block, is a medical condition in which the impulse generated in the sinoatrial node (SA node) in the atrium of the heart does not propagate to the ventricles.

Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles. This is known as an escape rhythm. Since this accessory pacemaker also activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG).

• The P waves with a regular P-to-P interval (in other words, a sinus rhythm) represent the first rhythm.
• The QRS complexes with a regular R-to-R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is lack of any apparent relationship between P waves and QRS complexes.

Patients with third-degree AV block typically experience severe bradycardia (an abnormally low measured heart rate), hypotension, and at times, hemodynamic instability.

Second Degree AV Block Mobitz Type 2

Type 2 Second-degree AV block, also known as "Mobitz II," is almost always a disease of the distal conduction system (His-Purkinje System).

Mobitz II heart block is characterized on a surface ECG by intermittently nonconducted P waves not preceded by PR prolongation and not followed by PR shortening. There is usually a fixed number of non-conducted P waves for every successfully conducted QRS complex, and this ratio is often specified in describing Mobitz II blocks. For example, Mobitz II block in which there are two P waves for every one QRS complex may be referred to as "2:1 Mobitz II block".

The medical significance of this type of AV block is that it may progress rapidly to complete heart block, in which no escape rhythm may emerge. In this case, the person may experience a Stokes-Adams attack, cardiac arrest, or sudden cardiac death. The definitive treatment for this form of AV Block is an implanted pacemaker.

The impairment is usually below the AV node. Although the terms infranodal block or infrahisian block are often applied to this disorder, they refer to the anatomic location of the block, whereas Mobitz II refers to an electrocardiographic pattern.

Second Degree AV Block Mobitz Type I (wenckebach)

Type 1 Second-degree AV block, also known as Mobitz I or Wenckebach periodicity, is almost always a disease of the AV node.

Mobitz I heart block is characterized by progressive prolongation of the PR interval on the electrocardiogram (ECG) on consecutive beats followed by a blocked P wave (i.e., a 'dropped' QRS complex). After the dropped QRS complex, the PR interval resets and the cycle repeats.

One of the baseline assumptions when determining if an individual has Mobitz I heart block is that the atrial rhythm has to be regular. If the atrial rhythm is not regular, there could be alternative explanations as to why certain P waves do not conduct to the ventricles.
This is almost always a benign condition for which no specific treatment is needed. In symptomatic cases, intravenous atropine may transiently improve conduction.

First Degree AV Bock

First-degree atrioventricular block (AV block), or PR prolongation, is a disease of the electrical conduction system of the heart in which the PR interval is lengthened beyond 0.20 seconds.

In first-degree AV block, the impulse conducting from atria to ventricles through the atrioventricular node (AV node) is delayed and travels slower than normal.

Ventricular Hexageminy

Hexageminy — every sixth beat is a PVC.

Ventricular Pentageminy

Pentageminy — every fifth beat is a PVC.

Ventricular Quadrigeminy

Quadrigeminy — every fourth beat is a PVC.

Ventricular Trigeminy

The ECG trace above shows ventricular trigeminy; the ventricular ectopic beats (2nd, 5th, 8th, and 11th) are separated by two sinus beats.

Ventricular Bigeminy

Bigeminy or bigemini is a heart rhythm problem in which there is a continuous alternation of long and short heart beats. Most often this is due to ectopic beats occurring so frequently that there is one after each sinus beat. The two beats are figuratively two twins (hence bi- + gemini). The ectopic beat is typically a premature ventricular contraction (PVC). For example, in ventricular bigeminy, a sinus beat is shortly followed by a PVC, a pause, another normal beat, and then another PVC. In atrial bigeminy, the other "twin" is a premature atrial contraction (PAC).

After any PVC there is a pause that can lead to the development of bigeminy. A PVC wavefront often encounters a refractory AV node that does not conduct the wavefront retrograde. Thus the atrium is not depolarized and the sinus node is not reset. Since the sinus p wave to PVC interval is less than the normal P-P interval, the interval between the PVC and the next p wave is prolonged to equal the normal time elapsed during two P-P intervals. This is called a "compensatory" pause. The pause after the PVC leads to a longer recovery time which is associated with a higher likelihood of myocardium being in different stages of re-polarization. This then allows for re-entrant circuits and sets up the ventricle for another PVC after the next sinus beat. The constant interval between the sinus beat and PVC suggests a reentrant etiology rather than spontaneous automaticity of the ventricle.

Atrial premature complexes (APCs) do not have a compensatory pause since they reset the sinus node but atrial or supraventricular bigeminy can occur. If the APCs are very premature, the wave front can encounter a refractory AV node and not be conducted. This can be mistaken for sinus bradycardia if the APC is buried in the t wave since the APC will reset the SA node and lead to a long P-P interval.

Ventricular Triplets (salvo)

The appearance of 3 consecutive PVCs is called as ventricular triplet, ventricular salvo or non-sustained ventricular tachycardia, (if the duration is self terminating within 30 seconds).  

Ventricular Couplets

The above is an example of a ventricular couplet or two consecutive PVCs.

Multifocal PVCs

Multifocal PVCs all look different from each other on the same ECG. They occur at different intervals, at various times in the QRS cycle, with different coupling intervals. Multiformed PVCs usually have the same coupling intervals (because they originate in the same ectopic site but their conduction through the ventricles differ. Multiformed PVCs are common in digitalis intoxication.

Premature Ventricular Contraction (PVC)

A premature ventricular contraction (PVC) — also known as a premature ventricular complex, ventricular premature contraction (or complex or complexes) (VPC), ventricular premature beat (VPB), or ventricular extrasystole (VES) — is a relatively common event where the heartbeat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node, the normal heartbeat initiator. The electrical events of the heart detected by the electrocardiogram (ECG) allow a PVC to be easily distinguished from a normal heart beat. Although a PVC can be a sign of decreased oxygenation to the heart muscle, often PVCs are benign and may even be found in otherwise healthy hearts.

A PVC may be perceived as a "skipped beat" or felt as palpitations in the chest. In a normal heartbeat, the ventricles contract after the atria have helped to fill them by contracting; in this way the ventricles can pump a maximized amount of blood both to the lungs and to the rest of the body. In a PVC, the ventricles contract first and before the atria have optimally filled the ventricles with blood, which means that circulation is inefficient. However, single beat PVC abnormal heart rhythms do not usually pose a danger and can be asymptomatic in healthy individuals. A PVC is a type of ectopic beat.

Ventricular Fibrillation (VF)

Ventricular fibrillation (V-fib or VF) is when the heart quivers instead of pumps due to disorganized electrical activity in the ventricles. It results in cardiac arrest with loss of consciousness and no pulse. This is followed by irreversible death in the absence of treatment. Ventricular fibrillation is found initially in about 10% of people in cardiac arrest.

Ventricular fibrillation can occur due to coronary heart disease, valvular heart disease, cardiomyopathy, Brugada syndrome, long QT syndrome, or intracranial haemorrhage. Diagnosis is by an electrocardiogram (ECG) showing irregular unformed QRS complexes without any clear P waves. An important differential diagnosis is torsade's de pointes.

Treatment is with cardiopulmonary resuscitation (CPR) and defibrillation. Biphasic defibrillation may be better than monophasic.

Ventricular Tachycardia (VT)

Ventricular tachycardia (V-tach or VT) is a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart. Although a few seconds may not result in problems, longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillation. Ventricular tachycardia is found initially in about 7% of people in cardiac arrest.

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems, or a heart attack. Diagnosis is by an electrocardiogram (ECG) showing a rate of greater than 120 bpm and at least three wide QRS complexes in a row. It is classified as non-sustained versus sustained based on whether or not it lasts less than or more than 30 seconds. The term "ventricular tachycardias" refers to the group of irregular heartbeats that includes ventricular tachycardia, ventricular fibrillation, and torsades de pointes.

Ventricular Flutter

Ventricular flutter: is an arrhythmia, specifically a tachycardia affecting the ventricles with a rate of more than 250-350 beats per minute. 

The ECG shows a sinusoidal waveform with no clear definition of the QRS and T waves. It is a critically unstable arrhythmia that can lead to death. It has been proposed as a possible transition stage between ventricular tachycardia and fibrillation.

Ventricular flutter example

Ventricular flutter rhythm strip example

Ventricular flutter 12-lead example

Polymorphic Ventricular Tachycardia (PVT)

Polymorphic ventricular tachycardia (PVT) is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complexes varying in amplitude, axis and duration. The commonest cause of PVT is myocardial ischaemia.

Accelerated Idioventricular Rhythm (AIVR)

Accelerated idioventricular rhythm is ventricular rhythm with a rate of between 40 and 120 beats per minute. Idioventricular means “relating to or affecting the cardiac ventricle alone“ and refers to any ectopic ventricular arrythmia. Accelerated idioventricular arrhythmias are distinguished from ventricular rhythms with rates less than 40 (ventricular escape) and those faster than 120 (ventricular tachycardia). Though some other references limit to between 60 and 100 beats per minute. It is also referred to as AIVR and "slow ventricular tachycardia."

It can be present at birth. However, it is more commonly associated with reperfusion after myocardial injury.

Idioventricular Rhythm

Normally, the pacemaker of the heart that is responsible for triggering each heart beat (ventricular contraction) is the SA (Sino Atrial) node. However, if the ventricle does not receive triggering signals at a rate high enough from either the SA node or the AV (Atrioventricular) node, the ventricular myocardium itself becomes the pacemaker (escape rhythm). This is called Idioventricular Rhythm. Ventricular signals are transmitted cell-to-cell between cardiomyocytes and not by the conduction system, creating wide sometimes bizarre QRS complexes (> 0.12 sec). The rate is usually 20-40 bpm.

If the rate is >40 bpm, it is called accelerated idioventricular rhythm. The rate of 20-40 is the "intrinsic automaticity" of the ventricular myocardium. It can be regarded as a "backup plan" or "redundancy" built into the body.

Premature Junctional Complex (PJC)

The 5th beat on the rhythm strip above shows a PJC complex

Premature junctional contractions (PJCs), also called atrioventricular junctional premature complexes or junctional extrasystole, are premature cardiac electrical impulses originating from the atrioventricular node of the heart or "junction." This area is not the normal but only a secondary source of cardiac electrical impulse formation. These premature beats can be found occasionally in healthy people and more commonly in some pathologic conditions, typically in the case of drug cardiotoxicity, electrolyte imbalance, mitral valve surgery, and cold water immersion. If more than two such beats are seen, then the condition is termed junctional rhythm. On the surface ECG, premature junctional contractions will appear as a normally shaped ventricular complex or QRS complex, not preceded by any atrial complex or P wave or preceded by an abnormal P wave with a shorter distance or interval between the P wave and the QRS. Rarely, the abnormal P wave can follow the QRS.

Junctional Tachycardia

Junctional tachycardia is a form of supraventricular tachycardia characterized by involvement of the AV node. It can be contrasted to atrial tachycardia. It is a tachycardia associated with the generation of impulses in a focus in the region of the atrioventricular node due to an AV disassociation. In general, the AV junction's intrinsic rate is 40-60 bpm so junctional tachycardia implies a rate >60 bpm.

On an ECG, Junctional Tachycardia exhibits the following classic criteria:

• P Waves: The P Wave may be inverted in leads II, III and aVF or not visible
• Narrow QRS complexes (which is consistent with non-ventricular rhythms)

It can coexist with other superventricular tachycardias due to the disassociation between the SA node and the AV node. Junctional Tachycardia can appear similar to atrioventricular nodal reentrant tachycardia (AVNRT). One form is junctional ectopic tachycardia.

Accelerated Junctional Rhythm

Accelerated junctional rhythm occurs when the AV junction fires impulses at above 60 bpm. Rhythm will be very regular. The QRS complex is narrow (0.10 sec or less).

Junctional Escape Rhythm/Complex

A junctional escape beat is a delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the sinoatrial node falls below the rate of the atrioventricular node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. It is a protective mechanism for the heart, to compensate for the SA node no longer handling the pacemaker activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so.

A junctional escape complex is a normal response that may result from excessive vagal tone on the SA node (e.g. digoxin toxicity), a pathological slowing of the SA discharge, or a complete AV block. Junctional rhythms (if a bradycardia) can cause decreased cardiac output. Therefore, the person may exhibit signs and symptoms similar to other bradycardia such as lightheadedness, dizziness, hypotension, and syncope. This rhythm can usually be tolerated if the rate is above 50 bpm.

ECG Characteristics:

• Rate: 40-60 bpm
• Rhythm: Irregular in single junctional escape complex; regular in junctional escape rhythm.
• P waves: Depends on the site of the ectopic focus. They will be inverted, and may appear before or after the QRS complex, or they may be absent, hidden by the QRS.
• PR interval: If the P wave occurs before the QRS complex, the interval will be less than 0.12 seconds.
• QRS Complex: Usually normal in duration and morphology, less than 0.12 seconds.

Junctional Rhythms

Junctional rhythm describes an abnormal heart rhythm resulting from impulses coming from a locus of tissue in the area of the atrioventricular node, the "junction" between atria and ventricles.
Under normal conditions, the heart's sinoatrial node determines the rate by which the organ beats - in other words, it is the heart's "pacemaker." The electrical activity of sinus rhythm originates in the sinoatrial node and depolarizes the atria. Current then passes from the atria through the bundle of His, from which it travels along Purkinje fibers to reach and depolarize the ventricles. This sinus rhythm is important because it ensures that the heart's atria reliably contract before the ventricles.
In junctional rhythm, however, the sinoatrial node does not control the heart's rhythm - this can happen in the case of a block in conduction somewhere along the pathway described above. When this happens, the heart's atrioventricular node takes over as the pacemaker. In the case of a junctional rhythm, the atria will actually still contract before the ventricles; however, this does not happen by the normal pathway of activation and instead is due to a backwards or retrograde conduction (conduction comes from the AV node into and through the atria).
Junctional rhythm can be diagnosed by looking at an ECG: it usually presents without a P wave or with an inverted P wave. Retrograde P waves refers to the depolarization from the AV node back towards the SA node.

Premature Atrial Contraction (PAC)

Premature atrial contractions (PACs), also known as atrial premature complexes (APC) or atrial premature beats (APB), are a common cardiac dysrhythmia characterized by premature heartbeats originating in the atria. While the sinoatrial node typically regulates the heartbeat during normal sinus rhythm, PACs occur when another region of the atria depolarizes before the sinoatrial node and thus triggers a premature heartbeat. The exact cause of PACs is unclear; while several predisposing conditions exist, PACs commonly occur in healthy young and elderly people without heart disease, and by themselves are not considered an abnormal finding. PACs found in healthy young are more likely to lead to other heart conditions or even death. Elderly people that get PACs usually don't need any further attention besides follow ups due to unclear evidence. PACs are often completely asymptomatic and may be noted only with Holter monitoring, but occasionally they can be perceived as a skipped beat or a jolt in the chest. In most cases, no treatment other than reassurance is needed for PACs, although medications such as beta blockers can reduce the frequency of symptomatic PACs.

On an electrocardiogram (ECG), PACs are characterized by an abnormally shaped P wave. Since the premature beat initiates outside the sinoatrial node, the associated P wave appears different from those seen in normal sinus rhythm. Typically, the atrial impulse propagates normally through the atrioventricular node and into the cardiac ventricles, resulting in a normal, narrow QRS complex. However, if the atrial beat is premature enough, it may reach the atrioventricular node during its refractory period, in which case it will not be conducted to the ventricle and there will be no QRS complex following the P wave.

Multifocal Atrial Pacemaker (MAT)

Multifocal (or multiform) atrial tachycardia (MAT) is an abnormal heart rhythm, specifically a type of supraventricular tachycardia, that is particularly common in older people and is associated with exacerbations of chronic obstructive pulmonary disease (COPD). Normally, the heart rate is controlled by a cluster of cells called the sinoatrial node (SA node). When a number of different clusters of cells outside of the SA node take over control of the heart rate, and the rate exceeds 100 beats per minute, this is called multifocal atrial tachycardia (if the heart rate is ≤100, this is technically not a tachycardia and it is then termed multifocal atrial rhythm).

'Multiform' simply describes the variable P wave shapes and is an observation, 'multifocal' is an inference about the underlying cause. Although these are interchangeable terms, some purists prefer the former nomenclature since it does not presume any underlying mechanism.

The P waves and PR intervals are variable due to a phenomenon called wandering atrial pacemaker (WAP). The electrical impulse is generated at a different focus within the atria of the heart each time. WAP is positive once the heart generates at least three different P wave formations from the same ECG lead. Then, if the heart rate exceeds 100 beats per minute, the phenomenon is called multifocal atrial tachycardia.

Wandering Atrial Pacemaker (WAP)

A wandering atrial pacemaker, (WAP), is an atrial arrhythmia that occurs when the natural cardiac pacemaker site shifts between the sinoatrial node (SA node), the atria, and/or the atrioventricular node (AV node). This shifting of the pacemaker from the SA node to adjacent tissues is identifiable on ECG Lead II by morphological changes in the P-wave; sinus beats have smooth upright P waves, while atrial beats have flattened, notched, or diphasic P-waves. It is often seen in the very young, very old, in athletes and rarely causes symptoms or requires treatment.