Pathology of Arrhythmia

Broad classification of dysrhythmia

Broadly classifies as: - Atrial (supraventricular) - Junctional (associated with the Av node) - Ventricular (These are the site of abnormality) Can cause tachycardia or bradycardia

Second degree heart block

some conduction make it through - more serious damage to the atrioventricular node - leads to partial Atrioventricular Block, where some but not all of the atrial depolarisation (P wave) will lead to ventricular depol (QRS complex)

Delayed after depolarisation

• Following every AP, some of the Ca2+ entering in phase 2 has to be removed back to ECF • Done via Ca2+/3Na+ exchange • Net influx of + and insignificant depolarisation (normally) • If [Ca2+]i rises (cardiac glycosides, increased HR, high levels of NA or ADR), the after- depolarisations can get increasingly larger • Can become self-perpetuating (triggering AP) • Delayed repolarisation (prolonged QT interval) increases [Ca2+]i • Leads to increased after-depolarisations and can lead to dangerous ventricular dysrhythmias

Circus re entry movement

• The circuits are short in length and so the frequency of impulses generated is high • Either a unidirectional block (as in the diagram) or a transient block - one that allows some impulses but not all through - can generate these circus re-entries

Reminder of basic physiology

The spontaneous electrical discharge of the Sino atrial node is from the combined effects of the: - Funny Sodium channels - L Type slow calcium channels - Decrease in the K+ outflow

Common types of tachyarythymia

- Atrial Fibrilation - SVT Supraventricular tachycardia

1. Heart Block

- Damage (usually ischaemia) to part of the conducting system - usually affect AVN -Atrioventricular Node is the only pathway for electrical conduction between the atria and the ventricles

Dysrhytymia arise from FOUR broad catergories of events.

1. HEART BLOCK 2. ECTOPIC PACEMAKER ACTIVITY 3. DELAYED AFTER REPOL 4. CIRCUS REENTRY

Delayed After depolarisation

-Delayed afterdepolarizations (DADs), on the other hand, begin during phase 4 - after repolarization is completed, but before another action potential would normally occur. - They are due to elevated cytosolic calcium concentrations, as might be seen with digoxin toxicity -The overload of the sarcoplasmic reticulum may cause spontaneous Ca2+ release during repolarization, causing the released Ca2+ to exit the cell through the 3Na+/Ca2+-exchanger which results in a net depolarizing current.

Dysrhythmia can arise from 4 broad categories of events

1. Heart Block 2. Ectopic Pacemaker Activity 3. Delayed after depolarisation 4. Circus Re-entry

What causes the other areas of the heart to develop their own intrinsic rate?

1. If damaged: Ischaemia, CHD, Rheumatic disease, hypertension etc 2. Increased sympathetic activity (stress, exercise etc.) 3. Increased sensitivity to catecholamines (GA, caffeine, hyperthyroidism etc.) 4.Cardiac Glycoside overdose

Second degree block (subtypes)

1. Mobitz type 2 2. 2: 1 or 3: 1 3. Wenckebach

What is the underlying physiology causes of dysrhythmia?

1. Changes in the heart cells. 2. Changes in the conduction of the impulse through the heart 3. COMBINATION: Changes in the heart cells + changes in the conduction of impulses through the cells

Types of heart block

1. FIRST DEGREE: conduction is slowed but makes it through 2. SECOND DEGREE: conduction is partially blocked but some makes it through 3. THIRD DEGREE: conduction is completely blocked (none make it through)

Atrial Fibrillation

AF is the most common type of serious arrhythmia. It involves a very fast and irregular contraction of the atria. In AF, the heart's electrical signals don't begin in the SA node. Instead, they begin in another part of the atria or in the nearby pulmonary veins. The signals don't travel normally. They may spread throughout the atria in a rapid, disorganized way. This causes the walls of the atria to quiver very fast (fibrillate) instead of beating normally. As a result, the atria aren't able to pump blood into the ventricles the way they should.

What can you see on the ECG for first degree heart block?

Abnormally long P-R interval (P-R interval represents the time between the atrial depol and the ventricular depol) Otherwise every atrial depolarisation (P wave) is passed to the ventricles >200ms (normal: 120-200)

What is afterdepolarization?

Afterdepolarizations are abnormal depolarizations of cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electrical conduction system of the heart. Afterdepolarizations may lead to cardiac arrhythmias.

Atrial Flutter

Atrial Flutter Atrial flutter is similar to AF. However, the heart's electrical signals spread through the atria in a fast and regular—instead of irregular—rhythm. Atrial flutter is much less common than AF, but it has similar symptoms and complications.

Bradyarrhytmia

Bradyarrhythmias occur if the heart rate is slower than normal. If the heart rate is too slow, not enough blood reaches the brain. This can cause you to pass out. In adults, a heart rate slower than 60 beats per minute is considered a bradyarrhythmia. Some people normally have slow heart rates, especially people who are very physically fit. For them, a heartbeat slower than 60 beats per minute isn't dangerous and doesn't cause symptoms. But in other people, serious diseases or other conditions may cause bradyarrhythmias.

Cardiac glycoside

Cardiac glycosides[1] are organic compounds containing a glycoside (sugar) that act on the contractile force of the cardiac muscle. Because of their potency in disrupting the function of the heart, most are extremely toxic. These glycosides are found as secondary metabolites in several plants, but also in some insects, such as the milkweed butterflies.

How does cathecolamines cause heart to develop intrinsic rate in other areas?

Catecholamines, acting on b1 receptors, increase the rate of depolarisation -can cause pacemaker activity to arise from cells which are normally quiescent

When does the heart block have a larger serious potential effect on the heart?

Clinically speaking, the blocks tend to have more serious potential the closer they are to the 'end' of the electrical path (the muscles of the heart regulated by the heartbeat), and less serious effects the closer they are to the 'start' (at the SA node), because the potential disruption becomes greater as more of the 'path' is 'blocked' from its 'end' point. Therefore, most of the important heart blocks are AV nodal blocks and infra-Hisian blocks. SA blocks are usually of lesser clinical significance, since in the event of SA block, the AV node contains a secondary pacemaker which would still maintain a heart rate of around 40 - 60 beats per minute, sufficient for consciousness and much of daily life in the majority of individuals

First degree heart block

Conduction is slowed but some makes it through AV node is only slightly affected Conduction is slowed

Ectopic beats

Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fibers or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation (i.e., the sinoatrial node). An ectopic beat can be further classified as either: a premature ventricular contraction, or a premature atrial contraction. Some patients describe this experience as a 'flip' or a 'jolt' in the chest, or a 'heart hiccups', while others report dropped or missed beats.

Early after depolarisation

Early afterdepolarizations Early afterdepolarizations (EADs) occur with abnormal depolarization during phase 2 or phase 3, -increase in the frequency of abortive action potentials before normal repolarization is completed. - Phase 2 may be interrupted due to augmented opening of calcium channels - phase 3 interruptions are due to the opening of sodium channels.

Ectopic beats

Ectopic beat (or cardiac ectopy) is a disturbance of the cardiac rhythm frequently related to the electrical conduction system of the heart, in which beats arise from fibers or group of fibers outside the region in the heart muscle ordinarily responsible for impulse formation (i.e., the sinoatrial node).

Other types of dysrhythmia

Ectopic beats Sustained ventricular arrythymia is MORE serious (VT and AF)

VENTRICULAR ECTOPIC BEAT

Hearrbeat initiated by ventricles instead of SA node 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.[1] 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.[2]

Heart Block

Heart block is a disease or inherited condition that causes a fault within the heart's natural pacemaker due to some kind of obstruction (or "block") in the electrical conduction system of the heart. Despite the severe-sounding name, heart block may often cause no symptoms at all in some cases, or occasional missed heartbeats in other cases (which can cause lightheadedness, syncope (fainting), and palpitations), or may require an artificial pacemaker to be implanted, depending upon exactly where in the heart conduction is being impaired and how significantly it is affected. Heart block has nothing to do with coronary heart disease, which damages the heart's blood vessels and can cause angina (chest pain) or myocardial infarction (heart attack). In severe cases where the hearts ability to control and trigger heartbeats may be completely ineffective or unreliable, heart block can usually be treated by inserting an artificial pacemaker, a medical device that provides correct electrical impulses to trigger heart beats, compensating for the natural pacemaker's unreliability. Therefore, heart block frequently has no effects, or mild and occasional effects, and is not life-threatening in the vast majority of cases, and is usually treatable in more serious cases. The human heart uses electrical signals to maintain and initiate the regular heart beat in a living person; incorrect conduction can lead to mild or serious symptoms depending upon the location of the blockage and how severely conduction is being blocked. Conduction is initiated by the sinoatrial node ("sinus node" or "SA node"), and then travels to the atrioventricular node ("AV node") which also contains a secondary "pacemaker" that acts as a backup for the SA nodes, then to the bundle of His and then via the bundle branches to the point of the apex of the fascicular branches (shown in the diagram on the right). Blockages are therefore classified based on where the blockage occurs - namely the SA node ("Sinoatrial block"), AV node ("AV block" or AVB), and at or below the bundle of His ("Intra-Hisian" or "Infra-Hisian block" respectively). Infra-Hisian blocks may occur at the left or right bundle branches ("bundle branch block") or the fascicles of the left bundle branch ("fascicular block" or "Hemiblock"). SA and AV node blocks are each divided into three degrees, with second degree blocks being divided into two types (written either "type I or II" or "type 1 or 2"). The term "Wenckebach block" is also used for second degree type 1 blocks of either the SA or AV node; in addition second degree blocks type 1 and 2 are also sometimes known as "Mobitz 1" and "Mobitz 2". Clinically speaking, the blocks tend to have more serious potential the closer they are to the 'end' of the electrical path (the muscles of the heart regulated by the heartbeat), and less serious effects the closer they are to the 'start' (at the SA node), because the potential disruption becomes greater as more of the 'path' is 'blocked' from its 'end' point. Therefore, most of the important heart blocks are AV nodal blocks and infra-Hisian blocks. SA blocks are usually of lesser clinical significance, since in the event of SA block, the AV node contains a secondary pacemaker which would still maintain a heart rate of around 40 - 60 beats per minute, sufficient for consciousness and much of daily life in the majority of individuals

ATRIAL ECTOPIC BEAT

Heartbeat start in the atria instead of the sa node 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.

P-R Interval

In electrocardiography, the PR interval is the period, measured in milliseconds, that extends from the beginning of the P wave (the onset of atrial depolarization) until the beginning of the QRS complex (the onset of ventricular depolarization); it is normally between 120 and 200ms in duration

How does ischaemic damage cause heart to develop their intrinsic rate in other areas?

Ischaemic damage can cause cells to become leaky to Na+ (and develop a "funny" current)

What is Arrhythmia?

It describe the conditions where the coordinated eletrical sequence of the heart is disrupted

Arrhythmia/ Dysrhythmia

It is the irregular beating of the heart - Normal beats: 60-100bpm Arrhythmia is branched out to Tachycardia and Bradycardia- >100bpm or <100bpm

Mobitz type 2

Most beats are conducted with a normal P-R Interval BUT occasionally there is an atrial depolarisation without the ventricular depolarisation

Early after depolarisation

Occur towards the end of phase 2 Prolonged QT Triggered by fluctuating increase in Calcium permeability- this can set off self sustaining depolarisation

2. Ectopic pacemakers

Other areas of the heart can develop their intrinsic rate

Paroxysmal Supraventricular Tachycardia PSVT

PSVT is a very fast heart rate that begins and ends suddenly. PSVT occurs because of problems with the electrical connection between the atria and the ventricles. In PSVT, electrical signals that begin in the atria and travel to the ventricles can reenter the atria, causing extra heartbeats. This type of arrhythmia usually isn't dangerous and tends to occur in young people. It can happen during vigorous physical activity. A special type of PSVT is called Wolff-Parkinson-White syndrome.

Premature beat (extra)

Premature (extra) beats are the most common type of arrhythmia. They're harmless most of the time and often don't cause any symptoms. When symptoms do occur, they usually feel like fluttering in the chest or a feeling of a skipped heartbeat. Most of the time, premature beats need no treatment, especially in healthy people. Premature beats that occur in the atria (the heart's upper chambers) are called premature atrial contractions, or PACs. Premature beats that occur in the ventricles (the heart's lower chambers) are called premature ventricular contractions, or PVCs. In most cases, premature beats happen naturally. However, some heart diseases can cause premature beats. They also can happen because of stress, too much exercise, or too much caffeine or nicotine.

Wenckebach

Progressive lengthening of the P-R interval until a P wave fails to produce a QRS complex P-R interval then shortens and normal conduction occurs before the P-R Interval starts to lengthen again

Classification of heart block

SA and AV node blocks are each divided into three degrees, with second degree blocks being divided into two types (written either "type I or II" or "type 1 or 2"). The term "Wenckebach block" is also used for second degree type 1 blocks of either the SA or AV node; in addition second degree blocks type 1 and 2 are also sometimes known as "Mobitz 1" and "Mobitz 2".

Basic Physiology: Inherent rates:

SA node (fastest: pacemaker): 60-100bpm AV: 40-60bpm Bundle of His: 20-40 Purkinje Fibre: 20-40

Supra-ventricular Arrhythmia

Supraventricular arrhythmias are tachycardias (fast heart rates) - start in the atria or atrioventricular (AV) node. -the AV node is a group of cells located between the atria and the ventricles. Types of supraventricular arrhythmias include • atrial fibrillation (AF) • atrial flutter • paroxysmal supraventricular tachycardia (PSVT) • Wolff-Parkinson-White (WPW) syndrome.

Third degree heart block

The AV node is completely blocked and no electrical activity pass from the atria to the ventricles The atria depolarises and beat at their own inherent rate Ventricular beat and depolarise at a rate set by the parking fibres

Main types of arrhythmia

The four main types of arrhythmia are premature (extra) beats, supraventricular (SU-prah-ven-TRIK-yu-lar) arrhythmias, ventricular arrhythmias, and bradyarrhythmias (bray-de-ah-RITH-me-ahs). - Premature beats - Supraventricular arrhythmia - Ventricular arrhythmia - Bradyarrhythmia

VENTRICULAR ARRHYTHMIA

These arrhythmias start in the heart's lower chambers, the ventricles. They can be very dangerous and usually require medical care right away. - Ventricular Tachycardia - Ventricular Fibrilation

3. Circus Reentry Movements CRM

This describe when electrical impulses can re stimulate or re-enter a region of the heart after its refractory period has passed Comes from an unusual direction before the tissue would have been restimulated by the next stimulation from SAN

2:1/ 3: 1

This describes the ratio of the P wave to the QRS complex 2:1 Block has 2 p waves for each QRS 3:1 Block has 3 P waves for each QRS

Ventricular Fibrilation

V-fib occurs if disorganized electrical signals make the ventricles quiver instead of pump normally. Without the ventricles pumping blood to the body, sudden cardiac arrest and death can occur within a few minutes. To prevent death, the condition must be treated right away with an electric shock to the heart called defibrillation (de-fib-rih-LA-shun). V-fib may occur during or after a heart attack or in someone whose heart is already weak because of another condition.

Ventricular Tachycardia

Ventricular tachycardia is a fast, regular beating of the ventricles that may last for only a few seconds or for much longer. A few beats of ventricular tachycardia often don't cause problems. However, episodes that last for more than a few seconds can be dangerous. Ventricular tachycardia can turn into other, more serious arrhythmias, such as v-fib.

What is an arrhythmia? EXTRA

What is an arrhythmia? The rhythm of the heart is normally generated and regulated by pacemaker cells within the sinoatrial (SA) node, which is located within the wall of the right atrium. SA nodal pacemaker activity normally governs the rhythm of the atria and ventricles. Normal rhythm is very regular, with minimal cyclical fluctuation. Furthermore, atrial contraction is always followed by ventricular contraction in the normal heart. When this rhythm becomes irregular, too fast (tachycardia) or too slow (bradycardia), or the frequency of the atrial and ventricular beats are different, this is called an arrhythmia. The term "dysrhythmia" is sometimes used and has a similar meaning.

WPW Syndrome

Wolff Parkinson White WPW syndrome is a condition in which the heart's electrical signals travel along an extra pathway from the atria to the ventricles. This extra pathway disrupts the timing of the heart's electrical signals and can cause the ventricles to beat very fast. This type of arrhythmia can be life threatening.

What is Wolf-Parkinson-White Syndrome ?

a supraventricular arrthymia - occurs when there is additional electrical conduction between the atria and the ventricles - this usually occurs on the left where there is no AV node so there is so delay - depolarisation will reach the ventricles early - PR interval is short QRS has early upstroke - Second part of the QRS is normal as the conduction of the AVN catches up Can cause paroxysmal tachycardia and re-entry circuit