Abnormal electrical conduction or automaticity changes heart rate and rhythm. Arrhythmias vary in severity—from mild, producing no symptoms, and requiring no treatment (such as sinus arrhythmia, in which heart rate increases and decreases with respiration) to catastrophic ventricular fibrillation, which mandates immediate resuscitation. Arrhythmias are generally classified according to their origin (ventricular or supraventricular). Their effect on cardiac output and blood pressure, partially influenced by the site of origin, determines their clinical significance. (See the appendix Types of cardiac arrhythmias.)
Each arrhythmia may have its own specific cause. Common causes include:
· congenital defects
· myocardial ischemia or infarction
· organic heart disease
· drug toxicity
· degeneration or obstruction of conductive tissue
· connective tissue disorders
· electrolyte imbalances
· hypertrophy of heart muscle
· acid-base imbalances
· emotional stress.
Electrocardiogram changes that occur with age include:
· longer PR, QRS, and QT intervals
· lower amplitude of QRS complex
· leftward shift of QRS axis.
Altered automaticity, reentry, or conduction disturbances may cause cardiac arrhythmias. Enhanced automaticity is the result of partial depolarization, which may increase the intrinsic rate of the sinoatrial node or latent pacemakers, or may induce ectopic pacemakers to reach threshold and depolarize.
Ischemia or deformation causes an abnormal circuit to develop within conductive fibers. Although current flow is blocked in one direction within the circuit, the descending impulse can travel in the other direction. By the time the impulse completes the circuit, the previously depolarized tissue within the circuit is no longer refractory to stimulation; therefore, arrhythmias occur.
Conduction disturbances occur when impulses are conducted too quickly or too slowly.
Signs and symptoms
Signs and symptoms of arrhythmias result from reduced cardiac output and altered perfusion to the organs and may include:
· dizziness, syncope, and weakness
· chest pain
· cool, clammy skin
· altered level of consciousness
· reduced urinary output
Diagnostic test results
· Electrocardiography detects arrhythmias as well as ischemia and infarction by showing prolonged or shortened intervals, elevated or depressed T waves, premature contractions, or absence of waves.
· Blood tests reveal electrolyte abnormalities, such as hyperkalemia or hypokalemia and hypermagnesemia or hypomagnesemia, as well as drug toxicities.
· Arterial blood gas analysis reveals acid-base abnormalities, such as acidemia or alkalemia.
· Holter monitoring, event monitoring, and loop recording show the presence of an arrhythmia.
· Exercise testing detects exercise-induced arrhythmias.
· Electrophysiologic testing identifies the mechanism of an arrhythmia and the location of accessory pathways; it also assesses the effectiveness of antiarrhythmic drugs, radiofrequency ablation, and implantable cardioverter-defibrillators (ICDs).
Follow the specific treatment guidelines or protocols for each arrhythmia. Treatment generally focuses on the underlying problem and may include:
· antiarrhythmic medications
· electrolyte correction
· correction of acid-base balance
· radiofrequency ablation
· cardiopulmonary resuscitation.
SITES OF COMMON CARDIAC ARRHYTHMIAS