Cardiac arrhythmia
A cardiac arrhythmia, also called cardiac dysrhythmia, is a disturbance in the regular rhythm of the heartbeat.
Several forms of cardiac arrhythmia are life-threatening and a medical emergency.
Frequency too high/low
Some arrhythmias may be too fast. These are known as tachycardia (more than 100 beats/min), and, if short in duration, are usually not life threatening. People perceive tachycardia as "heart palpitations". They may be brought on by stress or substances including caffeine, alcohol or various drugs, and often resolve when the stress or consumption of the causative substance is ended or reduced. Slow rhythms, known as bradycardia (less than 60 beats/min), too, are usually not life threatening.
Either arrhythmia may require medical treatment, however, if persistent or if they appear related to other symptoms, such as chest pain, shortness of breath, dizziness, or weakness.
Fibrillation
A more serious variety of arrhythmia is known as fibrillation. Fibrillation occurs when the heart muscle begins a quivering motion instead of a normal, healthy pumping rhythm. In the upper chambers of the heart, known as the atria, fibrillation is the result of a serious health problem that needs medical attention, but may not be an emergency.
The most serious arrhythmia is one that occurs in the lower chambers, or ventricles. When a heart goes into ventricular fibrillation, effective pumping of the blood stops. The individual goes into cardiac arrest, and will not survive unless cardiopulmonary resuscitation (CPR) and defibrillation are provided immediately.
CPR can prolong the survival of the heart muscle, but the defibrillator is the intervention which is most likely to restore a more healthy heart rhythm. It does this by applying an electric shock to the heart, after which sometimes the heart will revert to a rhythm that can once again pump blood.
Almost every person goes into ventricular fibrillation in the last few minutes of life as the heart muscle reacts to diminished oxygen, blood flow or trauma or irritants. When death is premature - as, for instance, due to an accident or a heart attack affecting someone otherwise in good health - the intervention of CPR and a defibrillator are appropriate.
Origin of impulse
In normal conditions heartbeat impulses are generated in the sinoatrial node. If the impulse is generated in other parts of the heart it is regarded as a pathological phenomenon.
Diagnosis
The most simple and effective diagnostic test for assessment of heart rhythm is
electrocardiogram (abbreviated ECG or EKG). Holter monitors are 24 hour ECGs.
The mechanism responsible for clinically important arrhythmias can occasionally be further characterized by electrophysiologial studies.
- Mode of initiation
- Automaticity
- Enhanced or abnormal
- Spontaneous onset of tachycardia
- No premature beats leading to the arrhythmia
- Gradual increase in the rate of the arrhythmia over the first 5-10 beats ("warm up")
- EKG appearance of the first tachycardia's beat is identical to the rest
- Reentry
- Initiation is with a premature beat followed by a slight pause
- This is followed by the arrhythmia (corresponding to premature beat, unidirectional block, slow conduction)
- "Warm up" is unusual
- EKG appearance of the first tachycardia beat need not be identical to the rest
- Mode of termination in response to overdrive pacing (pacing the heart at a rate faster than the tachycardia rate). Sometimes the application of electrical pacing from outside the heart itself is useful diagnostically. This is most commonly done by placing an electrode into the cardiac chambers and delivering electrical current across the endocardium
- Automaticity
- Often shows "overdrive suppression"
- The arrhythmia seems to be terminated by pacing only to return after several seconds with a gradual resumption of the pre-pacing rate
This is related to increased activity of the Na+ - K+ pump with Na+ loading. This causes the cell to have a more negative resting membrane potential and takes longer to reach threshold.
- Reentry
- Often terminates in response to overdrive pacing
- Without subsequent arrhythmia resumption
Tachycardia stops because paced impulses have entered circuit in both limbs causing bi-directional block
The precise role of triggered activity as a mechanism on human arrhythmias has not been studied in adequate detail to characterize modes of initiation or response to pacing.
Other means exist to differentiate more clearly among arrhythmias at the time of invasive electrophysiologic study.
SADS
SADS, or sudden arrhythmia death syndrome, is a term used to describe sudden death due to cardiac arrest brought on by an arrhythmic episode. Victims of SADS are typically in adolescence or their early 20s, and were previously not diagnosed with any type of cardiac disease.
The most common causes of SADS are long QT syndrome, Brugada syndrome, and hypertrophic cardiomyopathy.
List of common cardiac arrhythmias
Atrial fibrillation,
Atrial flutter,
Supraventricular tachycardia, and
Sick sinus syndrome
Pulseless Electrical Activity,
Ventricular tachycardia,
Ventricular fibrillation, and
Asystole
First-degree heart block,
Second-degree heart block: Type I a.k.a. Mobitz I or Wenckebach,
Second-degree heart block: Type II a.k.a. Mobitz II, and
Third-degree heart block a.k.a. complete heart block
Anti-arrhythmic therapies
There are many classes of anti-arrhythmic medications and many individual drugs within these classes. They are organized based on their action on the heart muscle cell, the cardiac myocyte.
Class I a Drugs - these drugs moderately block the sodium influx channel and prolong repolarization of the cardiac myocyte. Quinidine, procainamide, and disopyramide.
Class I b Drugs - these drugs have the lowest potency as sodium channel blockers, produce little if any change in action potential duration, and usually shorten repolarization. Lidocaine, phenytoin, tocainide and mexilitene.
Class I c Drugs - these drugs are the most potent sodium channel blocking agents, and have little effect on repolarization. Encainide, flecainide, propafenone, and moricizine.
Class II Drugs - these drugs act indirectly on electrophysiological parameters by blocking beta-adrenergic receptors, commonly known as beta-blockers.
Class III Drugs - these drugs act by mechanisms that are not well understood, possibly by affecting potassium influx. Amiodarone and bretylium.
Class IV Drugs - these drugs act primarily on the AV node, slowing conduction, including the calcium channel blockers.
Miscellaneous Drugs - digoxin, adenosine.
Arrhythmias are also treated electrically. Cardioversion is the application of electrical current across the chest wall to the heart and it is used for treatment of supraventricular or ventricular tachycardia. Defibrillation differs in that it is used for ventricular fibrillation and more electricity is delivered with defibrillation than with cardioversion. In cardioversion, the recipient is usually awake and may be sedated for the procedure. In defibrillation, the recipient has lost consciousness so there is no need for sedation. Electrical treatment of arrhythmia includes cardiac pacing. Pacing is usually done for very slow heartbeats from drug overdose or myocardial infarction.
Referenced By
Brachycardia | Bradycardia | Cardiac arrhythmia/bradycardia | Cardiologist | Cardiology | Electrocardiogram | Electrocardiograph | Electrocardiography | Heart | Heart condition | Heart disease | Ischaemic heart disease | Left atrium | Left ventricle | Medical emergency | Right atrium | Right ventricle | Tachycardia | Ventricle (heart) | Ventricles of the heart
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