Cardiac Arrhythmias Done by: Islamova Sh. Group: 646 P. Checked by: Seyitkaliev

Triggered activity, reentry arrhythmias, accelerated automaticity
4. Classification of arrhythmia and

their description
5. Management of arrhythmias
6. Classification of antiarrhythmic drugs based on drug action
7. Used references

membrane Potential

Na+
m
Na+
Na+
Na+
Na+
Na+
h
K+
ca++
K+
K+
K+
ca++
ca++
(Plateau Phase)
K+
K+
K+
Na+
K+
Depolarization
Repolarization

cardiac arrhythmia.
● Arrhythmias may cause sudden death, syncope, heart

failure, dizziness, palpitations or no symptoms at all.
● There are two main types of arrhythmia:
bradycardia: the heart rate is slow (< 60 b.p.m).
tachycardia: the heart rate is fast (> 100 b.p.m).

of abnormally slow automaticity while bradycardia due to AV block

is caused by abnormal conduction within the AV node or the distal AV conduction system.

Mechanisms generating tachycardias include:
- Accelerated automaticity.
- Triggered activity
- Re-entry (or circus movements)

depolarization or changing the threshold potential.
Abnormal automaticity can occur

in virtually all cardiac tissues and may initiate arrhythmias.
Such changes are thought to produce sinus tachycardia, escape rhythms and accelerated AV nodal (junctional) rhythms.

potential at the end of the action potential. These oscillations,

which are called 'after depolarizations', may reach threshold potential and produce an arrhythmia.
The abnormal oscillations can be exaggerated by pacing, catecholamines, electrolyte disturbances, and some medications.
Examples as atrial tachycardias produced by digoxin toxicity and the initiation of ventricular arrhythmia in the long QT syndrome.

'ring' of cardiac tissue surrounds an inexcitable core (e.g. in

a region of scarred myocardium). Tachycardia is initiated if an ectopic beat finds one limb refractory (α) resulting in unidirectional block and the other limb excitable. Provided conduction through the excitable limb (β) is slow enough, the other limb (α) will have recovered and will allow retrograde activation to complete the re-entry loop. If the time to conduct around the ring is longer than the recovery times (refractory periods) of the tissue within the ring, circus movement will be maintained, producing a run of tachycardia.
The majority of regular paroxysmal tachycardias are produced by this mechanism.

– increased rate
c. bradycardia – decreased rate
d. fibrillation – disorganized contractile activity

2. Sites

involved:
a. ventricular
b. atrial
c. sinus
d. AV node
e. Supraventricular (atrial myocardium or AV node)

varies with breathing.
This is usually a benign condition

atrioventricular junction.

Conduction is via the His-Purkinje system; therefore the

QRS shape during tachycardia is usually similar to that seen in the same patient during baseline rhythm.

100-160/min
Symptoms may occur with rapid heart rates including; weakness,

fatigue, dizziness, or palpitations.
Sinus tachycardia is often temporary, occurring under stresses from exercise, strong emotions, fever, dehydration, thyrotoxicosis, anemia and heart failure.
If necessary, beta-blockers may be used to slow the sinus rate, e.g. in hyperthyroidism

condition in which an atrial pacemaker site above the ventricles

sends out an electrical signal early. The ventricles are usually able to respond to this signal, but the result is an irregular heart rhythm.
PACs are common and may occur as the result of stimulants such as coffee, tea, alcohol, cigarettes, or medications.
Treatment is rarely necessary.

It usually begins and ends rapidly, occurring in repeated periods.

This condition can cause symptoms such as weakness, fatigue, dizziness, fainting, or palpitations if the heart rate becomes too fast.
In AVNRT, there are two functionally and anatomically different pathways within the AV node: one is characterized by a short effective refractory period and slow conduction, and the other has a longer effective refractory period and conducts faster.
In sinus rhythm, the atrial impulse that depolarizes the ventricles usually conducts through the fast pathway.
If the atrial impulse (e.g. an atrial premature beat) occurs early when the fast pathway is still refractory, the slow pathway takes over in propagating the atrial impulse to the ventricles. It then travels back through the fast pathway which has already recovered its excitability, thus initiating the most common 'slow-fast', or typical, AVNRT.

QRS complexes, usually at a rate of 140-240 per minute.

Sometimes the QRS complexes will show typical bundle branch block. P waves are either not visible or are seen immediately before or after the QRS complex because of simultaneous atrial and ventricular activation.

comprising the AV node, the His bundle, the ventricle and

an abnormal connection from the ventricle back to the atrium. This abnormal connection is called an accessory pathway or bypass tract.
Bypass tracts result from incomplete separation of the atria and the ventricles during fetal development.
Atrial activation occurs after ventricular activation and the P wave is usually clearly seen between the QRS and T complexes

emergency cardioversion.
If the patient is haemodynamically stable, vagal manoeuvres,

including right carotid massage, Valsalva manoeuvre and facial immersion in cold water can be successfully employed.
If not successful, intravenous adenosine (up to 0.25 mg/kg) , verapamil 5-10 mg i.v. over 5-10 minutes, i.v. diltiazem, or beta-blockers should be tried.
Long-term management
It includes ablation of an accessory pathway. Also, verapamil, diltiazem & β-blockers; are effective in 60-80% of patients.

tissue connects the atria and ventricles and can electrically bypass

the normal pathways of conduction; a re-entry circuit can develop causing paroxysms of tachycardia.
►ECG shows:
- Short PR interval
- Delta wave on the upstroke of the QRS complex
►Drug treatment includes flecainamide, amiodarone or disopyramide.
►Digoxin and verapamil are contraindicated.
►Transvenous catheter radiofrequency ablation is the treatment of choice.

signals come from the atria at a fast but even

rate, often causing the ventricles to contract faster and increase the heart rate.
When the signals from the atria are coming at a faster rate than the ventricles can respond to, the ECG pattern develops a signature "sawtooth" pattern, showing two or more flutter waves between each QRS complex.

is electrical cardioversion.
Patients who have been in atrial flutter

more than 1-2 days should be treated in a similar manner to patients with atrial fibrillation and anticoagulated for 4 weeks prior to cardioversion.
Recurrent paroxysms may be prevented by class Ic and class III agents
The treatment of choice for patients with recurrent atrial flutter is radiofrequency catheter ablation

signals come from the atria at a very fast and

erratic rate. The ventricles contract in an irregular manner because of the erratic signals coming from the atria.
The ECG shows normal but irregular QRS complexes, fine oscillations of the baseline (so-called fibrillation or f waves) and no P waves.
Common causes include CAD, valvular heart disease, hypertension, hyperthyroidism and others. In some patients no cause can be found 'lone' atrial fibrillation.

due to an acute precipitating event such as alcohol toxicity,

chest infection or hyperthyroidism, the provoking cause should be treated.
Strategies for the acute management of AF are ventricular rate control or cardioversion (± anticoagulation).
Ventricular rate control is achieved by drugs which block the AV node
Cardioversion is achieved electrically by DC shock or medically either by IV infusion of an anti-arrhythmic drug such as a class Ic or a class III agent
The choice depends upon:
How well the arrhythmia is tolerated (is cardioversion urgent?)
Whether anticoagulation is required before considering elective cardioversion
Whether spontaneous cardioversion is likely (previous history? reversible cause?).

anticoagulated with warfarin for 4 weeks before cardioversion.
Anticoagulants are

used to minimize the risk of thromboembolism associated with cardioversion unless atrial fibrillation is of less than 1-2 days' duration.
Transoesophageal echocardiography is being used to document the presence or absence of atrial thrombus as a guide to the necessity for long-term anticoagulation.

fibrillation include two strategies:
Rhythm control: antiarrhythmic drugs plus DC cardioversion

plus warfarin
Rate control: AV nodal slowing agents plus warfarin
Recurrent paroxysms may be prevented by oral medication; class Ic agents are employed in patients with no significant heart disease and class III agents are preferred in patients with structural heart disease.
Rate control is usually achieved by a combination of digoxin beta-blockers or calcium channel blockers (diltiazem or verapamil).
Anticoagulation (target INR 2.0-3.0) This is indicated in patients with atrial fibrillation and one of the following major or two of the moderate risk factors:
Major risk factors: Prosthetic heart valve, Rheumatic mitral valve disease, Prior history of CVA/TIA, Age > 75 years, Hypertension, Coronary artery disease with poor LV function
Moderate risk factors: Age 65-75 years, Coronary artery disease but normal LV function, Diabetes mellitus.

ventricular tachyarrhythmias (Sustained ventricular tachycardia and ventricular fibrillation)
torsades de

pointes
normal heart ventricular tachycardia
non-sustained ventricular tachycardia
ventricular premature beats

signal is sent from the ventricles at a very fast

but often regular rate.
The ECG shows a rapid ventricular rhythm with broad (often 0.14 s or more), abnormal QRS complexes. AV dissociation may result in visible P waves
Treatment: in haemodynamically compromised patients, emergency DC cardioversion may be required. If the blood pressure and cardiac output are well maintained, intravenous therapy with class I drugs or amiodarone is usually used. First-line drug treatment consists of lidocaine (50-100 mg i.v. over 5 minutes) followed by a lidocaine infusion (2-4 mg i.v. per minute). DC cardioversion is necessary if medical therapy is unsuccessful.

signals are sent from the ventricles at a very fast

and erratic rate. As a result, the ventricles are unable to fill with blood and pump.
This rhythm is life-threatening because there is no pulse and complete loss of consciousness.
The ECG shows shapeless, rapid oscillations and there is no hint of organized complexes
A person in VF requires prompt defibrillation to restore the normal rhythm and function of the heart. It may cause sudden cardiac death. Basic and advanced cardiac life support is needed
Survivors of these ventricular tachyarrhythmias are, in the absence of an identifiable reversible cause (e.g. acute myocardial infarction, severe metabolic disturbance), at high risk of sudden death. Implantable cardioverter-defibrillators (ICDs) are first-line therapy in the management of these patients

atheletic training.
Rate as low as 50 at rest and 40

during sleep.
Common causes of sinus bradycardia include:
Extrinsic causes ;Hypothermia, hypothyroidism, cholestatic jaundice and raised intracranial pressure. Drug therapy with beta-blockers, digitalis and other antiarrhythmic drugs.
Intrinsic causes; Acute ischaemia and infarction of the sinus node (as a complication of acute myocardial infarction). Chronic degenerative changes such as fibrosis of the atrium and sinus node (sick sinus syndrome).

out electrical signals either too slowly or too fast. There

may be alternation between too-fast and too-slow rates.
This condition may cause symptoms if the rate becomes too slow or too fast for the body to tolerate.
Chronic symptomatic sick sinus syndrome requires permanent pacing (AAI), with additional antiarrhythmic drugs (or ablation therapy) to manage any tachycardia element.
Thromboembolism is common in tachy-brady syndrome and patients should be anticoagulated unless there is a contraindication.

and unlikely to progress.
ECG shows prolonged PR interval.
May be associated

with acute rheumatic fever, diphtheria, myocardial infarction or drugs as digoxin

phenomenon):
Gradually increasing P-R intervals culminating in an omission.
When isolated, usually

physiological and due to increased vagal tone and abolished by exercise and atropine.
Mobitz type II
The P wave is sporadically not conducted. Occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation.
Pacing is usually indicated in Mobitz II block, whereas patients with Wenckebach AV block are usually monitored.

groups due to idiopathic bundle branch fibrosis.
Other causes include coronary

heart disease, calcification from aortic valve, sarcoidosis or congenital.
ECG shows bradycardia, P wave continue, unrelated to regular slow idioventricular rhythm.
Treatment is permanent pacing.

therapy “ablation”.

channel blockers.

Pacemaker potential
Class III:
K + channel blockers

Class IV:
Ca ++

channel blockers

Class II:
Beta blockers

Classification of Anti-Arrhythmic Drugs