Phase 3: end of the rapid repolarisation and the membrane potential returns to (-90mV) resting state.
Phase 4: after when the membrane potential returned to resting state there will be still some extra sodium inside the cells and extra potassium ions outside the cells, sodium-potassium pump is stimulated to transport the potassium in to the cells and sodium out side the cells.
(Figure1) shows the cardiac action potential phases
The cardiac cells have important characteristics which are Automaticity (which is the ability of the cardiac pacemaker cells to produce electrical impulses), Excitability-Irritability (response to the electrical impulses), Conductivity (the ability of cardiac cells to receive the electrical impulses and transmitting them) and Contractility (ability of cardiac cells to contract).
As the heart is able to generate it is own electrical impulses. The conduction system which consists of two areas called nodes that contain conduction cells and special pathways that transmit the impulse transmits signals throughout the (atria) and (ventricles) chambers of the heart to make it beat in a regular coordinated rhythm.
Electrical conduction pathway
The normal heartbeat starts when an electrical impulse is fired from the sinoaterial node (SA node) from the right atrium. The sinus node is controlling the rate and rhythm of the heart and therefore it is the heart’s “pacemaker”. (SA node) which initiate 60 to 100 electrical impulses per minute, impulses transmit down via the muscle of both atria through (intra-arterial conduction pathways) leading to the depolarization of the atrium.
Atrioventricular node (AV node), which can function as a secondary pacemaker if AV node stopped from working, located in the lower right atrium and this transmits the impulses from atria to the bundle of His. This makes 40 to 60 impulses per minute.
Bundle of His, it is located under AV node and transmits electrical impulses to it is branches.
Bundle branches (BB) , the lower part of the His bundle and separated in to right bundle branch which goes in to the right ventricle and left bundle branch which goes in to left ventricle. The BB transmits electrical impulses to the Purkinje’s fibers.
Purkinje’s fibers connected to the muscular walls of ventricles and transmit electrical impulses to the cells of the ventricular muscle.
Ventricular muscle, receives electrical impulses from Purkinje’s fibers and contracts.
Purkinje’s fibers, bundle branches and ventricular muscle can generate 20 to 40 impulses per minute.
(figer2) electrical conduction pathway of heart (figer3) electrical impulses per time (msec)
Arrhythmias
Arrhythmia is a disorder of the heart’s electrical system where changes in the regular heart beat occurs. When the pathway of the conduction is damaged or blocked which leads the heart beats slowly (bradycardia) or excess pathways exist which may lead the heart beat too quickly (tachycardia). In both cases the heart’s rhythm changes and this affect the heart’s ability to pump blood around the body. These abnormal heartbeats are referred as arrhythmia. Arrhythmia can occur in the atria or in the ventricles. Arrhythmia may occur at any age, and are most often a nuisance rather than a serious problem and many will remain as undiagnosed.
Arrhythmia can be defined in terms where it happens or their effect on the cardiac arrhythmias for example the disturbance of rhythm arises from above AV node called (superventricular arrhythmia) and the disturbances which arise from AV junction or with in AV node it self called (ventricular arrhythmia).
Arrhythmia can occur as a result of heart diseases (cardiomyopathies) for example when heart tissue is damaged as a result of (heart attack), stress, caffeine, tobacco, alcohol, diet pills, and cough and cold medicines. The main symptoms are palpitations, dizziness fainting or collapsing breathlessness and chest pain.
Diagnostic tests of arrhythmia
Electrocardiogram (ECG) electrocardiogram is a recording of the electrical activity of the heart by placing Electrode stickers on the chest and then connected to a recording machine. Electrical signals which produce a pattern on graph paper in the ECG. By analyzing the pattern of these waves the arrhythmia can be monitored.
Holter Monitor
A Holter monitor shows changes in the cardiac rhythm over with in 24-hour of the course and this way used when it is not possible detected during a resting or exercise ECG
Cardiac Event Monitor
This type of recording device is used for several days or weeks when arrhythmia is infrequent. The device then records up to 70 seconds of ECG readings.
Bradycardia
This defined as when the heart rate is less than 60 beats per minute (bpm) and in the situations when the heart rate is lower than accepted the bradycardia could be exist. And bradycardia includes: sinus bradycardia (SA): when there is a diseases in SA node and this causes SA node to produce electrical impulses and fires at low rate this causes lower in the heart rate. Adrinoventricular (AV) node (heart block): in which caused by failure of AV node to conduct and transmit the electrical impulses to ventricles or a proportion of the electrical impulses can not reach the ventricles or complete heart block.
When the pacemaker function of the SA node stops or fails and the heart rate decreased the AV node start to initiate electrical impulses as secondary pacemaker and maintains the heart rate between 30 to 40 bpm this called (junctional rhythm) and if this fails the bundle of His start initiating and firing and maintain ventricular escape rhythm between 20 to 30 bpm. Acute episodies of bradycardia can cause loss of consciousness and chronic one cause fatigue and lethalness.
Tachycardia
This is defined as the heart rate greater than 100 bpm and this includes Superventricular arrhythmia which arises from the atria which can be divided to:
Sinus tachycardia (AT): this occurs when the SA node initiates electrical impulses at high and rapid rate; this is during hard working such as excises and in response of some other drugs such (atropine, nicotine, thyroxine, salbutamol, and aminophyllin). Sinus node re-entry tachardya: this occurs when some SA node firing impulses rapidly and this causes circle of electrical impulses with in localized myocardial tissues. Atrial flutter: this is due to re entry of the circuit with in right atrium and causes the rapid atrial rhythm to about 300bpm; this causes rises in blood pressure as result of the atrial contraction disturbance. Atrial tachycardia: it may arise any where from the atria, this may occur during the structural heart diseases and the contraction rate of the atria is between 150 to 200bpm. AV junction: this is caused by the presence of a re-entry circuit within AV node or from the pathway of most junctions. The atrial rate is between 120 to 260rpm. Wolff-Parkinson white syndrome: which is a specific superventricular tachycardia where an accessory pathway conducts electrical activity from atria to the ventricles directly and produces the circuit around this pathway and AV node. This causes serious fatality conditions. Atrial fibrillation (AF): this is the most common Superventricular tachardia, which is characterized by irregular rapid atrial rate (between 300 to 600rpm). This occurs to chaotic conduction of electrical impulses with in the atria. There is uncoordinated multiple re-entry impulses which cause loss of atrial systolic action and this cause irregular response from ventricular.
Anti-Arrhythmic drugs
There are large variety drugs used for the arrhythmia and classified according to the Vaughan-Williams system in to four classes according to their site of actions:
Class I: this group consists in the drugs which act on the transport of the sodium ions across the cell membrane during the initiation of the impulses and the cellular activation, this reduce the action potential (AP) in the (phase 0). This class is further subdivided in to (IA, IB and IC) according their duration action on the action potential. (IA) drugs including ( Quinidine, Procainamide and Disopyramide) increase the duration of the AP. (IB) drugs including (Lignocaine, Phenytoin) are shorten the AP duration and (IC) drugs including (Flecainide, Encainide) unchanged the AP duration.
Class II: they effect on the sympathetic nervous system of the heart, even they do not effect on the AP of the most cardial cells but they reduce the depolarization (phase4) of the pacemaker cells. Drugs are including (Propranone and Atenolol)
Class III: they prolong the duration of the AP and increases the length of the refractorary period, but has no any effect on the (phase1). Drugs are including (Amiodarone, Sotalol, Dofetilide and Bretylium)
Class IV: these drugs are act as antagonist of the transport of the calcium across the cell membrane in which followed by transporting of sodium ions in to the cells. Drugs are including (Verapamil and Diltiazem).
According to the action site of the drugs on the heart cells, drugs are classified to:
AV node: these drugs which act on the AV node site are Verapamil, Diltizatiuon, Adenosine, Digoxin and Beta blockers.
Ventricles: which act on the ventricles are Lignocaine, Mexiletine and Tocainide.
Tria, ventricles and accessory AV pathways: Quinidine, Disopyramide, Amiodarone Flecainide, Procainamide and Propafenone.
Mexiletine: this drug can be given by mouth or paraenterally with therapeutic and toxic effects. The drug given intravenously with a dose 100-250 mg for 5-10 minutes followed by 250mg over one hour and then 250mg for two hours. The infusion dose can be followed 0.5-1000 mg per minute. By mouth initial dose 400 mg (may be increased to 600 mg after myocardial infarction if opioid analgesics also given), followed after 2 hours by 200–250 mg 3–4 times daily.
Side effects nausea, vomiting, constipation, diarrhoea, taste disturbance, dry mouth.
Tocainide: the intravenous dosage given 750mg over 15 minute and maximum daily dosage is 1200 mg. has side effects including light headness, tremor, confusion and convulsions.
Lignocaine: By intravenous injection, 100 mg over a few minutes (50 mg in lighter patients or those whose circulation is severely impaired), followed immediately by infusion of 4 mg/minute for 30 minutes, 2 mg/minute for 2 hours, then 1 mg/minute. Side effects including dizziness, paraesthesia, or drowsiness confusion, respiratory depression and convulsions, hypotension and bradycardia may occur.
Disopyramide: By mouth 300–800 mg daily in divided doses
By slow intravenous injection, 2 mg/kg over at least 5 minutes to a maximum of 150 mg, then 200 mg every 8 hours for 24 hours or 400 micrograms/kg/hour, by intravenous infusion maximum 300 mg in first hour and 800 mg daily.
Side effects: effects include dry mouth, blurred vision, urinary retention, and very rarely angle-closure glaucoma, gastro-intestinal irritation.
Procainamide: By slow intravenous injection, 50 mg/minute, 100 mg .By intravenous infusion, 500–600 mg over 25–30 minutes with ECG monitoring, followed by maintenance at rate of 2–6 mg/minute, then if necessary oral anti-arrhythmic treatment starting 3–4 hours after infusion. Side effects: nausea, vomiting, pro-arrhythmic effects, dyspnoea and visual disturbances.
Flecainide: By mouth for ventricular arrhythmias, initially 100 mg twice daily (maximum 400 mg), reduced after 3–5 days if possible. For Supraventricular arrhythmias, 50 mg twice daily, increased if required to maximum 300 mg daily.
By slow intravenous injection, 2 mg/kg over 10–30 minutes maximum 150 mg. Side effects are including: nausea, vomiting, pro-arrhythmic effects, and dyspnoea and visual disturbances.
Amiodaron: By mouth, 200 mg 3 times daily for one week then reduced to 200 mg twice daily for one more r week and usually 200 mg daily or the minimum required to control the arrhythmia. By intravenous infusion via central venous catheter, initially 5 mg/kg over 20–120 minutes with ECG monitoring, following infusion given if necessary according to response up to maximum 1.2 g in 24 hours. Side effects are including nausea, vomiting, taste disturbances and raised serum transaminases.
Adinosine: By rapid intravenous injection into central or large peripheral vein 3 mg over 2 seconds with cardiac monitoring; if necessary followed by 6 mg after 1–2 minutes, and then by 12 mg after a further 1–2 minutes. With side effects including transient facial flush, chest pain, dyspnoea, bronchospasm, choking sensation, nausea, and light-headedness.
Verapamil: used for supraventricular arrhythmias By mouth 40–120 mg 3 times daily and By slow intravenous injection over 2 minutes and further 5 mg after 5–10 minutes for supraventricular arrhythmias in paroxysmal tachyarrhythmias when required. Side effects are including: constipation, less commonly nausea, vomiting, flushing, headache, dizziness, fatigue, ankle oedema.
Sotalol: By mouth initially 80 mg daily in 1–2 divided doses increased gradually at intervals of 2–3 days to usual dose of 160–320 mg daily in 2 divided doses. Higher doses of 480–640 mg daily for life-threatening conditions of ventricular arrhythmias.
By intravenous injection over 10 minutes, acute arrhythmias 20–120 mg. side effects arrhythmogenic effect.
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References:
- Cardiac arrhythmias, practical notes on interpretation and treatment, sixth edition, David. H Benet.
- Introduction to basic cardiac Dysrhythimas, second edition, Sandra Atwood, Cheryl Stanton. Jenny Storey.
- Basic Dyrhythmias, Third edition, Robert J. Huszar.
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last accessed 12/03/2008
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last accessed 13/03/2008
