Dysrhythmia	Description	Etiology	Symptoms/Consequences	Treatment
Dysrhythmias of Sinus Node
Sinus dysrhythmia	Phasic shortening, then lengthening of P-P and R-R intervals	Respiratory variation in impulse initiation by SA node	Usually none	Usually none Atropine if rate below 40 beats/min
Sinus tachycardia	P waves present followed by QRS complex Rhythm regular Heart rate 100–150 beats/min	Increased metabolic demands Decreased oxygen delivery Heart failure Shock Hemorrhage Anemia	May produce palpitations Prolonged episodes may lead to decreased cardiac output	Treat underlying cause Occasionally sedatives
Sinus bradycardia	P waves present followed by QRS complex Rhythm regular Heart rate <60 beats/min	Physical fitness Parasympathetic stimulation (sleep) Brain lesions Sinus dysfunction Digitalis excess	Very low rates may cause decreased cardiac output: light-headedness, faintness, chest pain	Atropine if cardiac output is decreased Pacemaker Treat underlying cause if necessary
Atrial Dysrhythmias
Premature atrial beats	Early P wave QRS complex may or may not be normal Rhythm irregular	Stress Ischemia Atrial enlargement Caffeine Nicotine	May produce palpitations Frequent episodes may decrease cardiac output is sign of chamber irritability	Sedation Eliminate nicotine and caffeine May require no other treatment
Atrial tachycardia	P wave present (may merge into previous T wave), QRS complex usually normal; rapid heart rate (usually >150 beats/min)	Sympathetic stimulation Chemical stimuli (caffeine, nicotine) Drug toxicity Fluid-electrolyte imbalance Thoracic surgery	Palpitations Possible anxiety Hypotension	Usually none if short burst (<1 min) Prolonged episodes may require carotid artery pressure, vagal stimulation, verapamil, digitalis, beta blockers, calcium channel blockers
Atrial fibrillation	Rapid, irregular P waves (>350/min) Ventricular rhythm irregularly irregular Ventricular rate varies, may increase to 120–150/min if untreated	Rheumatic heart disease Mitral stenosis Atrial infarction Coronary atherosclerotic heart disease Hypertensive heart disease Thyrotoxicosis	Hypotension Palpitations Pulse deficit Decreased cardiac output if rate is rapid Promotes thrombus formation in atria	Digitalis Cardizem Amiodarone Anticoagulation Cardioversion
Atrial flutter	“Sawtooth” or “picket fence” P waves (220–350 beats/min) Ratio of atrial to ventricular rate constant (3:1, 4:1, etc.)	Heart failure Mitral valve disease Pulmonary embolus	Occasional palpitations Chest pain	Cardioversion Anticoagulation medications if cardioversion unsuccessful
Ventricular Dysrhythmias
Premature ventricular beats (PVBs)	Early, wide, bizarre QRS complex, not associated with a P wave Rhythm irregular	Stress Acidosis Ventricular enlargement Electrolyte imbalance Myocardial infarction Digitalis toxicity Hypoxemia Hypercapnia	Same as for premature atrial beats	Check Mg++, K+ levels MEDICATIONS: Procainamide Disopyramide (Norpace) Lidocaine Mexiletine Sodium bicarbonate Potassium Oxygen Treat heart failure
Ventricular tachycardia	No P wave before QRS complex; QRS complex wide and bizarre; ventricular rate >100, usually 140–240	PVBs striking during vulnerable period Hypoxemia Drug toxicity Electrolyte imbalance Bradycardia	Decreased cardiac output: hypotension, loss of consciousness, respiratory arrest	MEDICATIONS: Lidocaine Procainamide Amiodarone Cardioversion Electrolytes
Ventricular fibrillation	Chaotic electrical activity No recognizable QRS complex	Myocardial infarction Electrocution Freshwater drowning Drug toxicity	No cardiac output Absent pulse or respiration Cardiac arrest	Defibrillation MEDICATIONS: Epinephrine Lidocaine Sodium bicarbonate Bretylium Magnesium sulfate CPR
Pulseless electrical activity (PEA)	Organized ECG rhythm	Electromechanical dissociation Escape rhythms	Pulseless Minimal or no perfusion	CPR Epinephrine Fluid challenge
Ventricular standstill	Can be distinguished from ventricular fibrillation only by ECG P waves may be present No QRS complex “Straight line”	Myocardial infarction Chronic diseases of conducting system	Same as for ventricular fibrillation	CPR Pacemaker Intracardiac epinephrine
Impulse Conduction Deficits
First-degree atrioventricular [AV] block	P-R interval prolonged, >0.20 sec	Rheumatic fever Digitalis toxicity Degenerative changes of coronary atherosclerotic heart disease Infections (e.g., Lyme carditis) Decreased oxygen in AV node	Warns of impaired conduction	Usually none as long as it occurs as an isolated deficit Atropine if P-R interval >0.26 sec or bradycardia
Bundle branch block	Same as normal sinus rhythm (NSR) except QRS complex duration >0.10 sec	Hypoxia Acute myocardial infarction Heart failure Coronary atherosclerotic heart disease Pulmonary embolus Hypertension	Same as first-degree AV block	Usually none unless severe blockage of left posterior division (see text)
Second-degree AV blocks	P waves usually occur regularly at rates consistent with SA node initiation (not all P waves followed by QRS complex; P-R interval may lengthen before nonconducted P wave or may be consistent; QRS complex may be widened)	Acute myocardial infarction Same as first-degree AV block	Serious dysrhythmia that may lead to decreased heart rate and cardiac output, hypotension	May require temporary pacemaker If symptomatic (e.g., hypotension, dizziness), atropine 1 mg
Complete third-degree AV block	Atria and ventricles beat independently P waves have no relation to QRS complex Ventricular rate may be as low as 20–40 beats/min	Digitalis toxicity Infectious disease Coronary artery disease Myocardial infarction	Very low rates may cause decreased cardiac output: light-headedness, fainting, chest pain	Pacemaker isoproterenol to increase heart rate Epinephrine if isoproterenol ineffective

From Phipps, W, Long, B, Woods, N, and Cassmeyer, V (eds): Medical-Surgical Nursing, ed. 5. Mosby, St. Louis, 2007.