EKG Interpretation & Heart Arrhythmias Cheat Sheet

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EKG Interpretation and Heart Arrhythmias Guide for Nurses
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Use this EKG interpretation cheat sheet that summarizes all heart arrhythmias in an easy-to-understand fashion. 

One of the most useful and commonly used diagnostic tools is electrocardiography (EKG) which measures the heart’s electrical activity as waveforms. An EKG uses electrodes attached to the skin to detect electric current moving through the heart. These signals are transmitted to produce a record of cardiac activity. Arrhythmia or dysrhythmia are disturbances in the normal cardiac rhythm of the heart which occurs as a result of alterations within the conduction of electrical impulses. These impulses stimulate and coordinate atrial and ventricular myocardial contractions that provide cardiac output.

Interpreting EKG

Ever wonder how nurses and doctors be able to read ECG papers at ease? How they differentiate atrial tachycardia from atrial fibrillation or on how to even know what atrial fibrillation or tachycardia is?

EKG interpretation takes some serious skill, a keen eye and a good theoretical foundations on the different arrhythmias and the concepts around heart’s conduction and about the EKG machine itself. It takes time to develop a skill in interpreting EKGs, but once you get the hang of it, you’ll be able to interpret any squiggly line in the EKG paper.

Sinus Tachycardia

Sinus tachycardia is a heart rate greater than 100 beats per minute that originated from the sinus node.

  • Rate: 100 to 180 beats per minute
  • P Waves precede each QRS complex
  • PR interval is normal
  • QRS complex is normal
  • Conduction is normal
  • Rhythm is regular

Causes of sinus tachycardia may include exercise, anxiety, fever, drugs, anemia, heart failure, hypovolemia and shock. Sinus tachycardia is often asymptomatic. Management however is directed at the treatment of the primary cause. Carotid sinus pressure (carotid massage) or a beta blocker may be used to reduce heart rate.

Sinus Bradycardia

Sinus bradycardia is a heart rate less than 60 beats per minute and originates from the sinus node (as the term “sinus” refers to sinoatrial node). It has the following characteristics

  • Rate is less than 60 beats per minute
  • P Waves precede each QRS complex
  • PR interval is normal
  • QRS complex is normal
  • Conduction is normal
  • Rhythm is regular

Causes may include drugs, vagal stimulation, hypoendocrine states, hypothermia, or sinus node involvement in MI. This arrhythmia may be normal in athletes as they have quality stroke volume. It is often asymptomatic but manifestations may include: syncope, fatigue, dizziness. Management includes treating the underlying cause and administering anticholinergic drugs like atropine sulfate as prescribed.

Premature Atrial Contraction

Premature Atrial Contraction are ectopic beats that originates from the atria and they are not rhythms. Cells in the heart starts to fire or go off before the normal heartbeat is supposed to occur. These are called heart palpitations and has the following characteristics:

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  • Premature and abnormal-looking P waves that differ in configuration from normal P waves
  • QRS complex after P waves except in very early or blocked PACs
  • P waves often buried in the preceding T wave or identified in the preceding T wave.

Causes includes coronary or valvular heart diseases, atrial ischemia, coronary artery atherosclerosis, heart failure, COPD, electrolyte imbalance and hypoxia. Usually there is no treatment needed but may include procainamide and quinidine administration (antidysrhythmic drugs) and carotid sinus massage.

Atrial Flutter

Atrial flutter is an abnormal rhythm that occurs in the atria of the heart. Atrial flutter has an atrial rhythm that is regular but has an atrial rate of 250 to 400 beats/minute. It has sawtooth appearance. QRS complexes are uniform in shape but often irregular in rate.

  • Normal atrial rhythm
  • Abnormal atrial rate: 250 to 400 beats/minute
  • Sawtooth P wave configuration
  • QRS complexes uniform in shape but irregular in rate

Causes includes heart failure, tricuspid valve or mitral valve diseases, pulmonary embolism, cor pulmonale, inferior wall MI, carditis and digoxin toxicity.

Management if the patient is unstable with ventricular rate of greater than 150 bpm, prepare for immediate cardioversion. If patient is stable, drug therapy may include calcium channel blocker, beta-adrenergic blockers, or antiarhythmics. Anticoagulation may be necessary as there would be pooling of blood in the atria.

Atrial Fibrillation

Atrial fibrillation is disorganized and uncoordinated twitching of atrial musculature caused by overly rapid production of atrial impulses. This arrhythmia has the following characteristics:

  • Atrial Rate: 350 to 600 bpm
  • Ventricular Rate: 120 to 200 bpm
  • P wave is not discernible with an irregular baseline
  • PR interval is not measurable
  • QRS complex is normal
  • Rhythm is irregular and usually rapid unless controlled.

Causes includes atherosclerosis, heart failure, congenital heart disease, chronic obstructive pulmonary disease, hypothyroidism and thyrotoxicosis. Atrial fibrillation may be asymptomatic but clinical manifestation may include palpitations, dyspnea, and pulmonary edema. Nursing goal is towards administration of prescribed treatment to decrease ventricular response, decrease atrial irritability and eliminate the cause.

Premature Junctional Contraction

Premature Junctional Contraction (PJC) occurs when some regions of the heart becomes excitable than normal. It has the following characteristics.

  • PR interval less than 0.12 seconds if P wave precedes QRS complex
  • QRS complex configuration and duration is normal
  • P wave is inverted
  • Atrial and ventricular rhythms irregular

Causes of PJC may include myocardial infarction or ischemia, digoxin toxicity, excessive caffeine or amphetamine use. Management includes correction of underlying cause, discontinuation of digoxin if appropriate.

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Atrioventricular Blocks

AV blocks are conduction defects within the AV junction that impairs conduction of atrial impulses to ventricular pathways. The three types are first degree, second degree and third degree.

First Degree AV Block

  • Rate is usually 60 to 100 bpm
  • PR intervals are prolonged for usually 0.20 seconds
  • QRS complex is usually normal
  • Rhythm is regular

First degree AV block is asymptomatic and may be caused by inferior wall MI or ischemia, hyperkalemia, hypokalemia, digoxin toxicity, calcium channel blockers, amiodarone and use of antidysrhythmics. Management includes correction of underlying cause. Administer atropine if PR interval exceeds 0.26 second or symptomatic bradycardia develops.

Second Degree AV Block Mobitz I (Wenckebach)

  • Atrial rhythm is regular
  • Ventricular rhythm is irregular
  • Atrial rate exceeds ventricular rate
  • PR interval progressively  but only slightly, longer with each cycle until QRS complex disappears (dropped beat)
  • PR Interval shorter after dropped beat.

Clinical manifestations include vertigo, weakness, and an irregular pulse. This may be caused by Inferior wall MI, cardiac surgery, acute rheumatic fever, vagal stimulation. Treatment includes correction of underlying cause, atropine or temporary pacemaker for symptomatic bradycardia and discontinuation of digoxin if appropriate.

Second Degree AV Block Mobitz II

  • Atrial rhythm is regular
  • Ventricular rhythm maybe regular or irregular depending on the degree of block
  • P-P interval constant
  • QRS complex periodically absent or disappears

Clinical manifestations same as Mobitz I. Causes includes: severe coronary artery diseases, anterior wall MI, acute myocarditis and digoxin toxicity. Treatment includes: atropine, epinephrine, and dopamine for symptomatic bradycardia. Discontinuation of digoxin if appropriate. Installation of pacemaker.

Third Degree AV Block (Complete Heart Block)

  • Atrial rhythm regular
  • Ventricular rhythm regular and rate slower than atrial rate
  • No relation between P waves and QRS complexes
  • NO constant PR interval
  • QRS interval normal or wide and bizarre

Manifestations include: hypotension, angina and heart failure. This may be caused by congenital abnormalities, rheumatic fever, hypoxia, MI, LEv’s disease, Lenegre’s disease and digoxin toxicity. Management includes atropine, epinephrine, and dopamine for bradycardia. Installation of pacemaker may also be considered.

Premature Ventricular Contractions (PVC)

Early or premature ventricular contractions are caused by increased automaticity of ventricular muscle cells. PVCs usually are not considered harmful but are of concern if more than six occur in 1 minute, if they occur in pairs or triplets if they are multifocal or if they occur or near a T wave.

  • Atrial rhythm is regular
  • Ventricular rhythm is irregular
  • QRS complex premature, usually followed by a complete compensatory pause
  • QRS complex is also wide and distorted, usually >0.14 second.
  • Premature QRS complexes occurring singly, in pairs, or in threes

Clinical manifestations includes palpitations, weakness, lightheadedness but it is most of the time asymptomatic. Management includes assessment of the cause and treat as indicated. Treatment is indicated if the client has underlying disease because PVCs may precipitate ventricular tachycardia or fibrillation. Assess for life threatening PVCs. Administer antiarrhythmic medication as prescribed.

Ventricular Tachycardia

Ventricular tachycardia (VT) is three or more consecutive PVCs. it is considered a medical emergency because cardiac output (CO) cannot be maintained because of decreased diastolic filling (preload).

  • Rate is 100 to 250 beats per minute
  • P wave is blurred in the QRS complex but the QRS complex has no associate with P wave.
  • PR Interval is not present
  • QRS complex is wide and bizarre; T wave is in the opposite direction
  • Rhythm is usually regular
  • May start and stop suddenly

Clinical manifestations of VT includes lightheadedness, weakness, dyspnea and unconsciousness. Causes includes MI, aneurysm, CAD, rheumatic heart diseases, mitral valve prolapse, hypokalemia, hyperkalemia, and pulmonary embolism. Anxiety may also caused VT.

Pulseless Ventricular Tachycardia

Management for Pulseless VT: Initiate cardiopulmonary resuscitation; follow ACLS protocol for defibrillation, ET intubation and administration of epinephrine or vasopressin.

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Ventricular Tachycardia with Pulse

Management with Pulse VT: If hemodynamically stable, follow ACLS protocol for administration of amiodarone, if ineffective, initiate synchronized cardioversion.

Ventricular Fibrillation

Ventricular fibrillation is rapid, ineffective quivering of ventricles that may be rapidly fatal.

  • Rate is rapid and uncoordinated, with ineffective contractions
  • Rhythm is chaotic
  • QRS complexes wide and irregular
  • P wave is not seen
  • PR interval is not seen

Causes of ventricular fibrillation is most commonly myocardia ischemia or infarction. It ma result from untreated ventricular tachycardia, electrolyte imbalances, digoxin or quinide toxicity, or hypothermia. Clinical manifestations may include loss of consciousness, pulselessness, loss of blood pressure, cessation of respirations, possible seizures and sudden death.

Start CPR is pulseless. Follow ACLS protocol for defibrillation, ET intubation and administration of epinephrine or vasopressin.

Other Arrhythmias

Atrial Tachycardia

2nd Degree AV Block Type 1, Mobitz I

Torsade de Pointes

Pulseless Ventricular Tachycardia

Supraventricular Tachycardia

ST Depression

EKG Interpretation Cheat Sheets

Download the printable cheat sheet for EKG interpretation below. To download, simply click on the images and save.

ArrythmiasDescriptionCausesTreatment
Sinus Arrhythmia
  • Irregular atrial and ventricular rhythms.
  • Normal P wave preceding each QRS complex.
  • Normal variation of normal sinus rhythm in athletes, children, and the elderly.
  • Can be seen in digoxin toxicity and inferior wall MI.
  • Atropine if rate decreases below 40 bpm.
Sinus Tachycardia
  • Atrial and ventricular rhythms are regular.
  • Rate > 100 bpm.
  • Normal P wave preceding each QRS complex.
  • Normal physiologic response to fever, exercise, anxiety, dehydration, or pain.
  • May accompany shock, left-sided heart failure, cardiac tamponade, hyperthyroidism, and anemia.
  • Atropine, epinephrine, quinidine, caffeine, nicotine, and alcohol use.
  • Correction of underlying cause.
  • Beta-adrenergic blockers or calcium channel blockers for symptomatic patients.
Sinus Bradycardia
  • Regular atrial and ventricular rhythms.
  • Rate < 60 bpm.
  • Normal P wave preceding each QRS complex.
  • Normal in a well-conditioned heart (e.g., athletes).
  • Increased intracranial pressure; increased vagal tone due to straining during defecation, vomiting, intubation, mechanical ventilation.
  • Follow ACLS protocol for administration of atropine for symptoms of low cardiac output, dizziness, weakness, altered LOC, or low blood pressure.
  • Pacemaker
Sinoatrial (SA) arrest or block
  • Atrial and ventricular rhythms normal except for missing complex.
  • Normal P wave preceding each QRS complex.
  • Pause not equal to multiple of the previous rhythm.
  • Infection
  • Coronary artery disease, degenerative heart disease, acute inferior wall MI.
  • Vagal stimulation, Valsalva’s maneuver, carotid sinus massage.
  • Treat symptoms with atropine I.V.
  • Temporary pacemaker or permanent pacemaker if considered for repeated episodes.
Wandering atrial pacemaker
  • Atrial and ventricular rhythms vary slightly.
  • Irregular PR interval.
  • P waves irregular with changing configurations indicating that they aren’t all from SA node or single atrial focus; may appear after the QRS complex.
  • QRS complexes uniform in shape but irregular in rhythm.
  • Rheumatic carditis due to inflammation involving the SA node.
  • Digoxin toxicity
  • Sick sinus syndrome
  • No treatment if patient is asymptomatic
  • Treatment of underlying cause if patient is symptomatic.
Premature atrial contraction (PAC)
  • Premature, abnormal-looking P waves that differ in configuration from normal P waves.
  • QRS complexes after P waves except in very early or blocked PACs.
  • P wave often buried in the preceding T wave or identified in the preceding T wave.
  • May prelude supraventricular tachycardia.
  • Stimulants, hyperthyroidism, COPD, infection and other heart diseases.
  • Usually no treatment is needed.
  • Treatment of underlying cause if patient is symptomatic.
  • Carotid sinus massage.
Paroxysmal Supraventricular Tachycardia
  • Atrial and ventricular rhythms are regular.
  • Heart rate > 160 bpm; rarely exceeds 250 bpm.
  • P waves regular but aberrant; difficult to differentiate from preceding T wave.
  • P wave preceding each QRS complex.
  • Sudden onset and termination of arrhythmia
  • When a normal P wave is present, it’s called paroxysmal atrial tachycardia; when a normal P wave isn’t present, it’s called paroxysmal junctional tachycardia.
  • Physical exertion, emotion, stimulants, rheumatic heart diseases.
  • Intrinsic abnormality of AV conduction system.
  • Digoxin toxicity.
  • Use of caffeine, marijuana, or central nervous system stimulants.
  • If patient is unstable prepare for immediate cardioversion.
  • If patient is stable, vagal stimulation, or Valsalva’s maneuver, carotid sinus massage.
  • Adenosine by rapid I.V. bolus injection to rapidly convert arrhythmia.
  • If patient has normal ejection fraction, consider calcium channel blockers, beta-adrenergic blocks or amiodarone.
  • If patient has an ejection fraction less than 40%, consider amiodarone.
Atrial flutter
  • Atrial rhythm regular, rate, 250 to 400 bpm
  • Ventricular rate variable, depending on degree of AV block
  • Saw-tooth shape P wave configuration.
  • QRS complexes uniform in shape but often irregular in rate.
  • Heart failure, tricuspid or mitral valve disease, pulmonary embolism, cor pulmonale, inferior wall MI, carditis.
  • Digoxin toxicity.
  • If patient is unstable with ventricular rate > 150bpm, prepare for immediate cardioversion.
  • If patient is stable, drug therapy may include calcium channel blockers, beta-adrenergic blocks, or antiarrhythmics.
  • Anticoagulation therapy may be necessary.
Atrial Fibrillation
  • Atrial rhythm grossly irregular rate > 300 to 600 bpm.
  • Ventricular rhythm grossly irregular, rate 160 to 180 bpm.
  • PR interval indiscernible.
  • No P waves, or P waves that appear as erratic, irregular base-line fibrillatory waves
  • Heart failure, COPD, thyrotoxicosis, constrictive pericarditis, ischemic heart disease, sepsis, pulmonary embolus, rheumatic heart disease, hypertension, mitral stenosis, atrial irritation, complication of coronary bypass or valve replacement surgery
  • If patient is unstable with ventricular rate > 150bpm, prepare for immediate cardioversion.
  • If stable, drug therapy may include calcium channel blockers, beta-adrenergic blockers, digoxin, procainamide, quinidine, ibutilide, or amiodarone.
  • Anticoagulation therapy to prevent emboli.
  • Dual chamber atrial pacing, implantable atrial pacemaker, or surgical maze procedure may also be used.
Junctional Rhythm
  • Atrial and ventricular rhythms are regular.
  • Atrial rate 40 to 60 bpm.
  • Ventricular rate usually 40 to 60 bpm.
  • P waves preceding, hidden within (absent), or after QRS complex; usually inverted if visible.
  • PR interval (when present) < 0.12 second
  • QRS complex configuration and duration normal, except in aberrant conduction.
  • Inferior wall MI, or ischemia, hypoxia, vagal stimulation, sick sinus syndrome.
  • Acute rheumatic fever.
  • Valve surgery
  • Digoxin toxicity
  • Correction of underlying cause.
  • Atropine for symptomatic slow rate
  • Pacemaker insertion if patient is refractory to drugs
  • Discontinuation of digoxin if appropriate.
Premature Junctional Conjunctions
  • Atrial and ventricular rhythms are irregular.
  • P waves inverted; may precede be hidden within, or follow QRS complex.
  • QRS complex configuration and duration normal.
  • MI or ischemia
  • Digoxin toxicity and excessive caffeine or amphetamine use
  • Correction of underlying cause.
  • Discontinuation of digoxin if appropriate.
First-degree AV block
  • Atrial and ventricular rhythms regular
  • PR interval > 0.20 second.
  • P wave preceding each QRS complex.
  • QRS complex normal.
  • Inferior wall MI or ischemia or infarction, hypothyroidism, hypokalemia, hyperkalemia.
  • Digoxin toxicity.
  • Use of quinidine, procainamide, beta-adrenergic blockers, calcium
  • Correction of the underlying cause.
  • Possibly atropine if PR interval exceeds 0.26 second or symptomatic bradycardia develops.
  • Cautious use of digoxin, calcium channel blockers, and beta-adrenergic blockers.
Second-degree AV block Mobitz I (Wenckebach)
  • Atrial rhythm regular.
  • Ventricular rhythm irregular.
  • Atrial rate exceeds ventricular rate.
  • PR interval progressively, but only slightly, longer with each cycle until QRS complex disappears.
  • PR interval shorter after dropped beat.
  • Severe coronary artery disease, anterior wall MI, acute myocarditis.
  • Digoxin toxicity
  • Atropine, epinephrine, and dopamine for symptomatic bradycardia.
  • Temporary or permanent pacemaker for symptomatic bradycardia.
  • Discontinuation of digoxin if appropriate.
Third-degree AV block (complex heart block)
  • Atrial rhythm regular.
  • Ventricular rhythm regular and rate slower than atrial rate.
  • No relation between P waves and QRS complexes.
  • No constant PR interval.
  • QRS interval normal (nodal pacemaker) or wide and bizarre (ventricular pacemaker).
  • Inferior or anterior wall MI, congenital abnormality, rheumatic fever.
  • Atropine, epinephrine, and dopamine for symptomatic bradycardia.
  • Temporary or permanent pacemaker for symptomatic bradycardia.
Premature ventricular contraction (PVC)
  • Atrial rhythm regular
  • Ventricular rhythm irregular
  • QRS complex premature, usually followed by a complete compensatory pause
  • QRS complex wide and distorted, usually >0.14 second.
  • Premature QRS complexes occurring singly, in pairs, or in threes; alternating with normal beats; focus from one or more sites.
  • Ominous when clustered, multifocal, with R wave on T pattern.
  • Heart failure; old or acute myocardial ischemia, infarction, or contusion.
  • Myocardial irritation by ventricular catheters such as a pacemaker.
  • Hypercapnia, hypokalemia, hypocalcemia.
  • Drug toxicity by cardiac glycosides, aminophylline, tricyclic antidepressants, beta-adrenergic.
  • Caffeine, tobacco, or alcohol use.
  • Psychological stress, anxiety, pain
  • If warranted, procainamide, lidocaine, or amiodarone I.V.
  • Treatment of underlying cause.
  • Discontinuation of drug causing toxicity.
  • Potassium chloride IV if PVC induced by hypokalemia.
  • Magnesium sulfate IV if PVC induced by hypomagnesaemia.
Ventricular Tachycardia
  • Ventricular rate 140 to 220 bpm, regular or irregular.
  • QRS complexes wide, bizarre, and independent of P waves
  • P waves no discernible
  • May start and stop suddenly
  • Myocardial ischemia, infarction, or aneurysm
  • Coronary artery disease
  • Rheumatic heart disease
  • Mitral valve prolapse, heart failure, cardiomyopathy
  • Ventricular catheters.
  • Hypokalemia, Hypercalcemia.
  • Pulmonary embolism.
  • Digoxin, procainamide, epinephrine, quinidine toxicity, anxiety.
  • If pulseless: initiate CPR; follow ACLS protocol for defibrillation.
  • If with pulse: If hemodynamically stable, follow ACLS protocol for administration of amiodarone; if ineffective initiate synchronized cardioversion.
Ventricular Fibrillation
  • Ventricular rhythm and rate are rapid and chaotic.
  • QRS complexes wide and irregular, no visible P waves
  • Myocardial ischemia or infarction, R-on-T phenomenon, untreated ventricular tachycardia,
  • Hypokalemia, hyperkalemia, Hypercalcemia, alkalosis, electric shock, hypothermia.
  • Digoxin, epinephrine, or quinidine toxicity.
  • If pulseless: start CPR, follow ACLS protocol for defibrillation, ET intubation, and administration f epinephrine or vasopressin, lidocaine, or amiodarone; ineffective consider magnesium sulfate.
Asystole
  • No atrial or ventricular rate or rhythm.
  • No discernible P waves, QRS complexes, or T waves
  • Myocardial ischemia or infarction, aortic valve disease, heart failure, hypoxemia, hypokalemia, severe acidosis, electric shock, ventricular arrhythmias, AV block, pulmonary embolism, heart rupture, cardiac tamponade, hyperkalemia, electromechanical dissociation.
  • Cocaine overdose.
  • Start CPR.
Matt Vera is a registered nurse with a bachelor of science in nursing since 2009 and is currently working as a full-time writer and editor for Nurseslabs. During his time as a student, he knows how frustrating it is to cram on difficult nursing topics and finding help online is near to impossible. His situation drove his passion for helping student nurses through the creation of content and lectures that is easy to digest. Knowing how valuable nurses are in delivering quality healthcare but limited in number, he wants to educate and inspire students in nursing. As a nurse educator since 2010, his goal in Nurseslabs is to simplify the learning process, breakdown complicated topics, help motivate learners, and look for unique ways of assisting students in mastering core nursing concepts effectively.

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