Sunday, 13 November 2016

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.

Supraventricular Tachycardia (SVT)

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm arising from improper electrical activity in upper part of the heart. There are four main types: atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff-Parkinson-White syndrome. Symptoms may include palpitations, feeling faint, sweating, shortness of breath, or chest pain.

They start from either the atria or atrioventricular node. They are generally due to one of two mechanisms: re-entry or increased automaticity. The other type of fast heart rhythm are ventricular arrhythmias—rapid rhythms that start within the ventricle. Diagnosis is typically by electrocardiogram (ECG), holter monitor, or event monitor. Blood tests may be done to rule out specific underlying causes such as hyperthyroidism or electrolyte abnormalities.

Specific treatments depend on the type of SVT. They can include medications, medical procedures, or surgery. Vagal maneuvers or a procedure known as catheter ablation may be effective in certain types.

Atrial Trigeminy

Atrial trigeminy in which there are two atrial premature contractions (APC's) for every normal sinus complex.

Atrial Bigeminy

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. Atrial Bigeminy is a harmless, benign rhythm, and does not normally require treatment.  

Atrial Flutter

Atrial flutter is an abnormal heart rhythm that occurs in the atria of the heart. When it first occurs, it is usually associated with a fast heart rate or tachycardia (beats over 100 per minute), and falls into the category of supra-ventricular tachycardias. While this rhythm occurs most often in individuals with cardiovascular disease (e.g. hypertension, coronary artery disease, and cardiomyopathy) and diabetes mellitus, it may occur spontaneously in people with otherwise normal hearts. It is typically not a stable rhythm, and frequently degenerates into atrial fibrillation (AF). However, it does rarely persist for months to years.

Atrial flutter was first identified as an independent medical condition in 1920 by the British physician Sir Thomas Lewis (1881–1945) and colleagues.

There are two types of atrial flutter, the common type I and rarer type II.  Most individuals with atrial flutter will manifest only one of these. Rarely someone may manifest both types; however, they can only manifest one type at a time.

Type I

Type I atrial flutter, also known as common atrial flutter or typical atrial flutter, has an atrial rate of 240 to 340 beats/minute. However, this rate may be slowed by antiarrhythmic agents.
  • Counterclockwise atrial flutter (known as cephalad-directed atrial flutter) is more commonly seen. The flutter waves in this rhythm are inverted in ECG leads II, III, and aVF.
  • The re-entry loop cycles in the opposite direction in clockwise atrial flutter, thus the flutter waves are upright in II, III, and aVF.

Type II
Type II flutter follows a significantly different re-entry pathway to type I flutter, and is typically faster, usually 340-440 beats/minute. Left atrial flutter is common after incomplete left atrial ablation procedures.

Modified Lead Placement for Atrial Flutter:

A Lewis Lead (also called the S5 lead) is a modified ECG lead used to detect atrial flutter waves when atrial flutter is suspected clinically, based on signs and symptoms, but is not definitely demonstrated on the standard 12 lead ECG. In order to create the Lewis Lead, the right arm electrode is moved to the manubrium adjacent to the sternum. Then the left arm electrode is moved to the right, fifth intercostal space adjacent to the sternum. The left leg electrode is placed on the right lower costal margin. The Lewis Lead is then read as Lead I on the ECG and, since in most patients it will be roughly perpendicular to the wave of ventricular depolarization, atrial flutter waves may be more apparent.

Atrial Fibrillation (AF)

Atrial fibrillation (AF or A-fib) is an abnormal heart rhythm characterized by rapid and irregular beating. Often it starts as brief periods of abnormal beating which become longer and possibly constant over time. Most episodes have no symptoms. Occasionally there may be heart palpitations, fainting, lightheadedness, shortness of breath, or chest pain. The disease is associated with an increased risk of heart failure, dementia, and stroke. It is a type of supraventricular tachycardia (SVT).

Atrial fibrillation is diagnosed on an electrocardiogram (ECG). Characteristic findings are the absence of P waves, with disorganized electrical activity in their place, and irregular R-R intervals due to irregular conduction of impulses to the ventricles. At very fast heart rates atrial fibrillation may look more regular, which may make it more difficult to separate from SVT or ventricular tachycardia.

QRS complexes should be narrow, signifying that they are initiated by normal conduction of atrial electrical activity through the intraventricular conduction system. Wide QRS complexes are worrisome for ventricular tachycardia, although, in cases where there is a disease of the conduction system, wide complexes may be present in A-Fib with rapid ventricular response.

If paroxysmal AF is suspected but an ECG during an GP visit shows only a regular rhythm, AF episodes may be detected and documented with the use of ambulatory Holster monitoring.

Sinus Arrest

Sinoatrial arrest (also known as sinus arrest or sinus pause) is a medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat. It is defined as lasting from 2.0 seconds to several minutes. Since the heart contains multiple pacemakers, this interruption of the cardiac cycle generally lasts only a few seconds before another part of the heart, such as the atrio-ventricular junction or the ventricles, begins pacing and restores the heart action. This condition can be detected on an electrocardiogram (ECG) as a brief period of irregular length with no electrical activity before either the sinoatrial node resumes normal pacing, or another pacemaker begins pacing. If a pacemaker other than the sinoatrial node is pacing the heart, this condition is known as an escape rhythm. If no other pacemaker begins pacing during an episode of sinus arrest it becomes a cardiac arrest. This condition is sometimes confused with sinoatrial block, a condition in which the pacing impulse is generated, but fails to conduct through the myocardium. Differential diagnosis of the two conditions is possible by examining the exact length of the interruption of cardiac activity. If the next available pacemaker takes over, it is in the following order:

1. Atrial escape (rate 60–80): originates within atria, not sinus node (normal P morphology is lost).
2. Junctional escape (rate 40–60): originates near the AV node; a normal P wave is not seen, may occasionally see a retrograde P wave.
3. Ventricular escape (rate 20–40): originates in ventricular conduction system; no P wave, wide, abnormal QRS.
Treatment includes stop medications that suppress the sinus node (beta blocker, Calcium channel blocker, digitalis); may need pacing.

Sinus Exit Block

Sinus Exit Block does looks very much the same as Sinus Arrest with one important distinction. With SA Block the R-R interval measurement is within plus or minus 2 small boxes.

Second degree type I sinoatrial exit block (Wenckebach) demonstrates progressive shortening of the R-R or P-P intervals until a P wave is blocked in the SA node (which would not appear on the ECG). A "sinus pause" ensues afterward which would be shorter than two of the preceding R-R intervals.

Second degree type II sinoatrial exit block occurs when there are consistent R-R and P-P intervals, then a P wave is blocked in the SA node (not seen on the ECG). The subsequent "sinus pause" is an exact interval of the preceding R-R intervals (usually two times).

Third degree sinoatrial exit block occurs when no SA nodal action potentials are able to leave the SA node. No P waves are seen on the ECG. When a junctional escape ensues and the rhythm may be confused with a junctional rhythm. If there is no junctional escape rhythm that is present, a long pause can occur resulting in asystole and cardiac arrest.

Sinus Arrhythmia

One of the most common arrhythmias is a sinus arrhythmia. It involves cyclic changes in the heart rate during breathing. It is very common in children and often found in young adults. Patients with sinus arrhythmia do not experience any cardiovascular symptoms.

The sinus node rate can change with inspiration/expiration, especially in younger people. The heart rate speeds up with inspiration (since it inhibits your vagal nerve) and decreases with expiration (stimulates your vagal nerve).

Sinus Tachycardia

Sinus tachycardia (also colloquially known as sinus tach or sinus tachy) is a sinus rhythm with an elevated rate of impulses, defined as a rate greater than 100 beats/min (bpm) in an average adult. The normal resting heart rate in the average adult ranges from 60–100 beats/min. Note that the normal heart rate varies with age, with infants having normal heart rate of 110–150 bpm, in contrast to the elderly, who have slower normal.

ECG characteristics:

  • Rate: Greater than or equal to 100.
  • Rhythm: Regular.
  • P waves: Upright, consistent, and normal in morphology (if no atrial disease)
  • P–R interval: Between 0.12–0.20 seconds and shortens with increasing heart rate
  • QRS complex: Less than 0.12 seconds, consistent, and normal in morphology.

Sinus Bradycardia

Sinus bradycardia is a sinus rhythm with a rate that is lower than normal. In humans, bradycardia is generally defined to be a rate of under 60 beats per minute.

ECG characteristics:
  • Rate: Less than 60 beats per minute.
  • Rhythm: Regular.
  • P waves: Upright, consistent, and normal in morphology and duration.
  • P-R Interval: Between 0.12 and 0.20 seconds in duration.
  • QRS Complex: Less than 0.12 seconds in width, and consistent in morphology.

Normal Sinus Rhythm

A sinus rhythm is any cardiac rhythm where depolarisation of the cardiac muscle begins at the sinus node. It is characterised by the presence of correctly oriented P waves on the electrocardiogram (ECG). Sinus rhythm is necessary, but not sufficient, for normal electrical activity within the heart.

The term normal sinus rhythm (NSR) is sometimes used to denote a specific type of sinus rhythm where all other measurements on the ECG also fall within designated normal limits, giving rise to the characteristic appearance of the ECG when the electrical conduction system of the heart is functioning normally. However, other sinus rhythms can be entirely normal in particular patient groups and clinical contexts, so the term is sometimes considered a misnomer and its use is sometimes discouraged.

ECG characteristics of normal sinus rhythm

By convention, the term "normal sinus rhythm" is taken to imply that not only are the P waves (reflecting activity of the sinus node itself) normal in morphology, but that all other ECG measurements are also normal. Criteria therefore include:
  1. Normal heart rate (classically 60 to 100 beats per minute for an adult).
  2. Regular rhythm, with less than 0.16 second variation in the shortest and longest durations between successive P waves.
  3. The sinus node should pace the heart – therefore, P waves must be round, all the same shape, and present before every QRS complex in a ratio of 1:1.
  4. Normal P wave axis (+15 to +75 degrees)
  5. Normal PR interval, QRS complex and QT interval.
  6. QRS complex positive in leads I, II, aVF and V3-V6, and negative in lead aVR.