How to Identify Cardiac Arrhythmias (With Videos)

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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?

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

So What’s an ECG?

ECG (or sometimes EKG) stands for electrocardiogram which was invented Willem Einthoven wherein during his experimentation, instead of using the usual adhesive leads as we have today, he would immerse each of the patients limb into containers of salt solutions and from there, their ECG was recorded. Willem Einthoven won the 1924 Nobel Prize in Medicine.

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:

  • 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.

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.

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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)

http://www.youtube.com/watch?v=NEGnCKC0Mrk

  • 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.

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.

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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

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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.

6 COMMENTS

  1. Thank you for this great review material!I read all these stuff in the book but the visual/auditory stimulation that these videos provide has helped me master the differences between the various dysrhythmias,thanks a lot!I hope you continue posting helpful articles!

  2. I was diagnosed with unstable angina and suffers from chest pain every now and then even though I take trimitazidine as my maintenance anti anginal drug daily. I still suffer anginal pain. I’m dead afraid I’ll suffer from a heart attack soon. Thank you to this page as it helps answering my queries. So informative.

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