EKG Interpretation Cheat Sheet & Heart Arrhythmias Guide

You will read rhythm strips on every floor, and the strip often tells you the patient is in trouble before the patient does. The EKG records the heart's electrical activity as waveforms through electrodes on the skin. An arrhythmia (dysrhythmia) is a disturbance in that rhythm caused by altered conduction of the electrical impulses that drive atrial and ventricular contraction and, with it, cardiac output.

Interpreting EKG

Reading a strip is a learned skill: know the normal conduction pathway, know the machine, and know what each arrhythmia looks like. Work the same way every time (rate, rhythm, P wave, PR interval, QRS) and the squiggly lines start making sense.

Sinus Tachycardia

Heart rate above 100 bpm originating from the sinus node.

• Rate: 100 to 180 bpm
• P wave precedes each QRS
• PR interval normal
• QRS normal
• Conduction normal, rhythm regular

Causes include exercise, anxiety, fever, drugs, anemia, heart failure, hypovolemia, and shock. Often asymptomatic. Treat the underlying cause. Carotid sinus pressure (carotid massage) or a beta-blocker may slow the rate.

Sinus Bradycardia

Heart rate below 60 bpm originating from the sinus node.

• Rate: less than 60 bpm
• P wave precedes each QRS
• PR interval normal
• QRS normal
• Conduction normal, rhythm regular

Causes include drugs, vagal stimulation, hypoendocrine states, hypothermia, or sinus node involvement in MI. Can be normal in athletes (good stroke volume). Often asymptomatic, but watch for syncope, fatigue, and dizziness. Treat the underlying cause and give an anticholinergic such as atropine sulfate as prescribed.

Premature Atrial Contraction

Ectopic beats from the atria, not a sustained rhythm. Cells fire before the normal beat is due, felt by the patient as palpitations.

• Premature, abnormal-looking P waves that differ in configuration from normal P waves
• QRS follows the P wave except in very early or blocked PACs
• P wave often buried in the preceding T wave

Causes include coronary or valvular disease, atrial ischemia, coronary artery atherosclerosis, heart failure, COPD, electrolyte imbalance, and hypoxia. Usually no treatment needed; procainamide or quinidine (antidysrhythmics) and carotid sinus massage may be used.

Atrial Flutter

Abnormal rhythm in the atria. Atrial rhythm is regular but the atrial rate runs 250 to 400 bpm with a sawtooth appearance. QRS complexes are uniform in shape but often irregular in rate.

• Atrial rhythm regular
• Atrial rate 250 to 400 bpm
• Sawtooth P wave configuration
• QRS uniform in shape, irregular in rate

Causes include heart failure, tricuspid or mitral valve disease, pulmonary embolism, cor pulmonale, inferior wall MI, carditis, and digoxin toxicity. If the patient is unstable with a ventricular rate above 150 bpm, prepare for immediate cardioversion. If stable, drug therapy may include a calcium channel blocker, beta-blocker, or antiarrhythmic. Anticoagulation may be needed because blood pools in the atria.

Atrial Fibrillation

Disorganized, uncoordinated twitching of the atrial muscle from overly rapid atrial impulses.

• Atrial rate: 350 to 600 bpm
• Ventricular rate: 120 to 200 bpm
• P wave not discernible, irregular baseline
• PR interval not measurable
• QRS normal
• Rhythm irregular, usually rapid unless controlled

Causes include atherosclerosis, heart failure, congenital heart disease, COPD, hypothyroidism, and thyrotoxicosis. May be asymptomatic, but watch for palpitations, dyspnea, and pulmonary edema. Goal: give prescribed treatment to slow the ventricular response, reduce atrial irritability, and eliminate the cause.

Premature Junctional Contraction

A PJC fires when a region of the heart becomes more excitable than normal.

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

Causes include MI or ischemia, digoxin toxicity, and excessive caffeine or amphetamine use. Correct the underlying cause and discontinue digoxin if appropriate.

Atrioventricular Blocks

AV blocks are conduction defects in the AV junction that impair conduction of atrial impulses to the ventricles. Three types: first, second, and third degree.

First Degree AV Block

• Rate usually 60 to 100 bpm
• PR interval prolonged, usually 0.20 seconds
• QRS usually normal
• Rhythm regular

Usually asymptomatic. Causes include inferior wall MI or ischemia, hyperkalemia, hypokalemia, digoxin toxicity, calcium channel blockers, amiodarone, and antidysrhythmics. Correct the underlying cause. Give atropine if the PR interval exceeds 0.26 seconds or symptomatic bradycardia develops.

Second Degree AV Block, Mobitz I (Wenckebach)

• Atrial rhythm regular
• Ventricular rhythm irregular
• Atrial rate exceeds ventricular rate
• PR interval lengthens slightly with each cycle until a QRS drops (dropped beat)
• PR interval shorter after the dropped beat

Manifestations: vertigo, weakness, irregular pulse. Causes include inferior wall MI, cardiac surgery, acute rheumatic fever, and vagal stimulation. Correct the cause; atropine or a temporary pacemaker for symptomatic bradycardia; discontinue digoxin if appropriate.

Second Degree AV Block, Mobitz II

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

Manifestations same as Mobitz I. Causes include severe coronary artery disease, anterior wall MI, acute myocarditis, and digoxin toxicity. Treat with atropine, epinephrine, and dopamine for symptomatic bradycardia; discontinue digoxin if appropriate; install a pacemaker.

Third Degree AV Block (Complete Heart Block)

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

Manifestations: hypotension, angina, heart failure. Causes include congenital abnormalities, rheumatic fever, hypoxia, MI, Lev's disease, Lenegre's disease, and digoxin toxicity. Treat bradycardia with atropine, epinephrine, and dopamine; consider a pacemaker.

Premature Ventricular Contractions (PVC)

Premature ventricular beats from increased automaticity of ventricular cells. Usually not harmful, but concerning if more than 6 occur in 1 minute, if they come in pairs or triplets, if they are multifocal, or if they land on or near a T wave.

• Atrial rhythm regular
• Ventricular rhythm irregular
• QRS premature, usually followed by a full compensatory pause
• QRS wide and distorted, usually greater than 0.14 seconds
• Premature QRS complexes occurring singly, in pairs, or in threes

Often asymptomatic, but watch for palpitations, weakness, and lightheadedness. Assess the cause and treat as indicated. Treat if the patient has underlying disease, because PVCs can precipitate ventricular tachycardia or fibrillation. Assess for life-threatening PVCs and give antiarrhythmic medication as prescribed.

Ventricular Tachycardia

VT is 3 or more consecutive PVCs. It is a medical emergency: cardiac output falls because decreased diastolic filling (preload) cannot sustain it.

• Rate 100 to 250 bpm
• P wave blurred into the QRS with no association to it
• PR interval absent
• QRS wide and bizarre; T wave in the opposite direction
• Rhythm usually regular
• May start and stop suddenly

Manifestations: lightheadedness, weakness, dyspnea, unconsciousness. Causes include MI, aneurysm, CAD, rheumatic heart disease, mitral valve prolapse, hypokalemia, hyperkalemia, pulmonary embolism, and anxiety.

Pulseless Ventricular Tachycardia

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

Ventricular Tachycardia with Pulse

If hemodynamically stable, follow ACLS protocol for amiodarone; if ineffective, perform synchronized cardioversion.

Ventricular Fibrillation

Rapid, ineffective quivering of the ventricles that is rapidly fatal.

• Rapid, uncoordinated, ineffective contractions
• Rhythm chaotic
• QRS wide and irregular
• P wave not seen
• PR interval not seen

Most often caused by myocardial ischemia or infarction. May follow untreated VT, electrolyte imbalances, digoxin or quinidine toxicity, or hypothermia. Manifestations: loss of consciousness, pulselessness, loss of blood pressure, cessation of respirations, possible seizures, and sudden death.

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

Atrial Tachycardia

A fast, regular atrial rhythm from an ectopic focus above the AV node, faster than sinus tachycardia and with abnormal P waves.

• Atrial rate 100 to 250 bpm, regular
• A single, consistent P wave shape that differs from the normal sinus P wave (often inverted or unusual because of the ectopic origin)
• An isoelectric segment usually visible between P waves
• QRS normal unless conduction is aberrant

Causes include catecholamine excess, digoxin toxicity, cardiomyopathy, and chronic lung disease. Treat the underlying cause; vagal maneuvers, beta-blockers, or calcium channel blockers may control the rate, and persistent focal cases may be referred for ablation.

Supraventricular Tachycardia (SVT)

A regular, narrow-complex tachycardia originating at or above the AV node, typically from a reentry circuit. It often starts and stops abruptly.

• Rate usually 150 to 220 bpm, regular
• QRS narrow (less than 0.12 seconds) unless a bundle branch block coexists
• P waves often hidden in the QRS or T wave and hard to identify
• Rhythm very regular

Manifestations include palpitations, lightheadedness, dyspnea, and chest discomfort. If the patient is unstable, prepare for synchronized cardioversion. If stable, try vagal maneuvers first, then adenosine; a beta-blocker or calcium channel blocker may follow.

Torsade de Pointes

A polymorphic ventricular tachycardia tied to a prolonged QT interval, with QRS complexes that twist around the baseline (the amplitude and polarity shift from beat to beat). It can be rapidly fatal or degenerate into ventricular fibrillation.

• Ventricular rate roughly 150 to 250 bpm
• QRS amplitude and axis twist around the isoelectric line, the defining feature
• Preceded by a prolonged QT interval, often with a short-long-short R-R sequence at onset

Causes include congenital long QT syndrome, hypokalemia, hypomagnesemia, hypocalcemia, and QT-prolonging drugs (certain antiarrhythmics, antipsychotics, and antibiotics). Give IV magnesium sulfate, correct electrolytes, stop the offending drug, and defibrillate if the patient is pulseless.

ST Segment Depression

ST depression is an EKG finding rather than a rhythm: the ST segment sits abnormally below the baseline and often signals myocardial ischemia.

• Measured as the vertical distance between the J point and the baseline (the PR segment)
• Horizontal or downsloping depression of at least 0.5 mm in two or more contiguous leads suggests ischemia
• Depression of 1 mm or more is more specific and carries a worse prognosis; 2 mm or more in three or more leads suggests a high probability of NSTEMI

Other causes include digoxin effect, hypokalemia, and ventricular hypertrophy with strain. Correlate with symptoms, serial EKGs, and cardiac markers, and escalate promptly when ischemia is suspected.