EKG: A Quick Reference Guide

Common EKG types, their causes and diagnoses

A brief explanation of several of the more common EKG waveforms which may be encountered during a cardiac emergency response. This reference guide is by no means complete and is merely intended as a refresher resource. Interpreting an EKG waveform should be performed by certified medical professionals only.

Ventricular Fibrillation EKG

Characteristics:

Ventricular fibrillation exhibits a chaotic rhythm and unmeasurable rate. QRS complexes are non-identifiable as are T and P-waves. The P-R interval is not measurable.

Rhythm	Chaotic
Rate	Unmeasurable
QRS	Absent
P wave	Absent
P-R interval	Not measurable
Additional Info	–

What Causes Ventricular Fibrillation?

Ventricular fibrillation, also called V-fib, occurs when the contraction of the ventricles, normally well coordinated, is disrupted. This occurs when electrical impulses arise from multiple foci within the ventricles causing a chaotic pattern to arise and effectively causing the heart to cease pumping blood ^[1]. Instead of the ventricles fully contracting to expel blood, V-fib causes the heart to quiver, meaning cardiac output will be non-existent and death will occur rapidly unless life support is put in place.

Other Factors to Consider:        

V-fib is a serious condition that will cause death within a matter of minutes unless properly and promptly treated ^[2]. It is the leading cause of cardiac arrest occurring outside of a hospital setting. V-fib can occur from a number of conditions including MI (Myocardial Infarction), electric shock, severe hypothermia, anti-arrhythmic drugs, and hypoxia among other conditions ^[3]. Defibrillation is the most effective form of treatment for V-fib ^[4]. Some drugs may be administered as well.

Ventricular Tachycardia

Characteristics:

Ventricular rhythm is usually regular with an increased rate of 100-125 bpm. The P-wave is absent. The QRS is bizarre and wide appearing. The P-R interval is non-measurable.

Rhythm	Regular
Rate	100-125 bpm
QRS	Bizarre appearing; Wide
P wave	Absent
P-R interval	Non-Measurable
Additional Info	–

What Causes Ventricular Tachycardia?

Ventricular tachycardia, abbreviated V-tach, is a broad class of arrhythmia consisting of several different types. All forms originate in the lower chambers of the heart. It occurs when 3 or more premature ventricular contractions (PVCs) are present and the rate is over 100 beats per minute ^[5]. The arrhythmia usually occurs due to heart disease, most typically from myocarditis, but also from heart attack, cardiomyopathy, myocardial ischemia etc. It can also occur in younger patients without a history of heart disease and may be difficult to establish cause in such cases^[6]. V-tach’s various forms and overall unpredictability make it a significant arrhythmia from a clinical perspective.

As previously mentioned ventricular tachycardia may occur in several varieties, with the most common being monomorphic (originating from a single focus) in nature among a handful of other varieties (see Ventricular Tachycardia Monomorphic)^[7]. The condition may occur in short bursts lasting only briefly and causing brief symptoms or none at all. V-tach may also be long lasting in nature and is more serious in this form, requiring immediate treatment to prevent death and serious injury^[8].

Other Factors to Consider:        

Those exhibiting V-tach very typically show signs of a weak or essentially absent pulse^[9]. Hypotension will lead to a decreased level of consciousness and, subsequently, will most likely result in a decreased level of responsiveness to outside stimuli^[10]. Similarly, V-tach may also be caused by changes in blood pressure, lack of oxygen, anti-arrhythmic drugs, or changes in pH^[11]. Symptoms may include a weak pulse as mentioned, syncope, palpitations, light-headedness, chest pain, and anxiety^[12]. Tachypnea may also accompany V-tach. Treatment is similar to that of V-Fib in cases in which no pulse is detectable^[13].

Ventricular Tachycardia Monomorphic

Characteristics:

Ventricular tachycardia monomorphic displays a regular rhythm with an increased rate, typically between 100 and 250 beats per minute. The QRS is wider than normal and bizarre looking, although it is uniform in appearance. P-waves are absent. P-R interval is non-measurable.

Rhythm	Regular
Rate	Fast (100-250 bpm)
QRS	Wide; Bizarre looking; Uniform in appearance
P wave	None
P-R interval	Non-measurable
Additional Info	–

What Causes Ventricular Tachycardia Monomorphic?

Ventricular tachycardia monomorphic (V-tach monomorphic) as opposed to polymorphic V-tach as well as other forms of the arrhythmia such as Torsades de pointes, originates from a single focus located within the ventricle, either left or right^[14]. As such, all QRS complexes will appear identical, owing to the fact that they are originating from the same place^[15]. This form of V-tach is especially life threatening when it is sustained which is the most common form of ventricular tachycardia in general.

Other Factors to Consider:        

V-tach monomorphic is likely to impair cardiac output^[16]. Treatment will thus depend on whether the patient is stable or unstable and is often similar in nature to that of other forms of V-tach^[17]. If unstable, treatment will often be in the form of immediate cardioversion. Some patients may only exhibit minor or slight symptoms at first but should still be intervened upon in some form. Due to impaired cardiac output, those exhibiting V-tach very typically show signs of a weak or essentially absent pulse^[18]. Hypotension most often leads to a decreased level of consciousness and the likely outcome of a subsequent significant decrease in the level of responsiveness to outside stimuli^[19]. Angina, shortness of breath, and heart failure may also accompany this arrhythmia as well as other forms of V-tach^[20].

Ventricular Tachycardia Polymorphic

Characteristics:

Polymorphic V-tach exhibits an irregular or regular rhythm with an increased rate. The QRS is usually widened but of different morphology. The P-wave is absent and the P-R interval is not able to be measured.

                   

Rhythm	Regular or irregular
Rate	Fast 100-300 bpm
QRS	Normal or widened
P wave	Absent
P-R interval	Non-Measurable
Additional Info	–

What Causes Ventricular Tachycardia Polymorphic?

Polymorphic V-tach is one of several forms of V-tach. This particular form of V-tach is caused by multiple foci from different points of origin within the ventricles^[21]. This, in turn, causes the resulting QRS complexes to vary in amplitude, duration, and axis and thus vary in their overall morphology continuously^[22].

Polymorphic V-tach can occur in brief, even asymptomatic episodes. It can also happen in recurrent, more severe episodes lasting for a longer duration and causing syncope or worse. As such, polymorphic V-tach is a serious condition that can lead to sudden cardiac death and should, therefore, be treated immediately and with care, although the stability of the patient will typically determine treatment^[23].

Other Factors to Consider:        

Prior heart disease, as well as medication, can cause polymorphic V-tach ^[24]. Symptoms and treatment of the arrhythmia are usually similar in nature to other forms of V-tach. Some patients, as previously mentioned, may only exhibit minor or slight symptoms initially but should still be intervened upon to some degree. Due to impaired cardiac output, those exhibiting V-tach very typically show signs of a weak or essentially absent pulse^[25]. Hypotension most often leads to a decreased level of consciousness and the likely outcome of a subsequent significant decrease in the level of responsiveness to outside stimuli^[26]. Initially, electrolyte imbalances and ischemia are sought to be corrected after which synchronized cardioversion is typically employed^[27].

Ventricular Tachycardia Torsade de Pointes

Characteristics:                    

Rhythm	Typically irregular
Rate	Increased; 150-250 bpm
QRS	Varies; Appears to twist around baseline
P wave	Absent
P-R interval	Non-Measurable
Additional Info	–

What Causes Torsade de Pointes?

Torsade de pointes or TdP is a particular type of polymorphic V-tach frequently occurring in the setting of QT interval prolongation^[28]. It is characterized by changes in QRS amplitude (morphology will change from beat to beat) and the QRS will appear to twist around the baseline or isoelectric axis on an EKG read although this twisting characteristic may not always be present^[29]. The arrhythmia is typically not long lasting but rather occurs in brief episodes. However, it re-occurs frequently and is associated with an unstable blood pressure^[30]. It may change into ventricular tachycardia or ventricular fibrillation.

Other Factors to Consider:        

The treatment of Torsades will generally vary from that of more typical variations of V-tach^[31]. The cause may be due to drug therapy and is often treated with mechanical override atrial pacing^[32]. Intravenous magnesium is the typical drug used to treat TdP. Symptoms are similar to those of other forms of V-tach including palpitations, dizziness, and syncope. Sudden cardiac death can occur.

Wandering Atrial Pacemaker

Characteristics:

Wandering atrial pacemaker (WAP) is often characterized by an irregular rhythm and normal rate. QRS is normal. WAP must exhibit at least three differently shaped P-waves.The P-R interval may be affected but not necessarily.

Rhythm	Possibly irregular
Rate	Normal
QRS	Normal
P wave	Shape and size vary with every beat
Additional Info	–

What Causes Wandering Atrial Pacemaker?

In wandering atrial pacemaker arrhythmia the electrical impulses that cause the atrium to contract are wandering or moving from the SA node (the proper site of electrical generation of impulses) to other atrial sites or to the AV junction^[33]. These changes in impulse origination affect P-wave morphology and thus the appearance of P-waves will typically vary from beat to beat. WAP must exhibit at least three differently shaped P-waves. Athletes with well-trained hearts are may demonstrate the arrhythmia, as well as young children. The condition will commonly come and go and thus can be hard to definitively diagnose and many patients do not even realize they have the disorder^[34].

Other Factors to Consider:        

WAP is most common in older adults and younger children as well as athletes. The arrhythmia may be caused by factors such as increased digoxin toxicity, increased vagal tone, or certain forms of heart disease like rheumatic carditis^[35]. Typically no treatment is necessary for the arrhythmia and, as stated previously, some patients are not even aware that anything is out of the norm with their hearts or take note when it comes on episodically.

Wolff-Parkinson-White Syndrome

Characteristics:

Wolf-Parkinson-White syndrome is characterized by a regular rhythm and normal rate. The QRS is typically wide and distorted at the beginning. P-wave is normal and P-R interval is shortened.

       

Rhythm	Regular
Rate	Normal
QRS	Typically wide
P wave	Normal
P-R interval	Shortened
Additional Info	Short PR interval distorts QRS complex

What Causes Wolff-Parkinson-White Syndrome?

Wolf-Parkinson-White syndrome (WPW for short) occurs when an accessory or alternative heart conduction pathway develops apart from and bypasses travel through the AV junction (the AV junction being the pathway typically responsible for conduction of the electrical signal from the upper atrium to the lower ventricles in a normal functioning heart).These bypass routes of conduction, called bypass tracts, can conduct signals both away from and toward the ventricles (retrograde and anterograde, respectively) and are formed during cardiac development^[36]. As such, WPW is classified a congenital defect and occurs most frequently in children and those aged 20-35^[37]. It is considered a rare disorder and is associated with a slight chance of cardiac death^[38].

Other Factors to Consider:        

Symptoms may be as mild as chest discomfort or palpitations and as severe as syncope. The syncope is due to poor cerebral circulation from an increased ventricular rate or from tachyarrhythmia. Symptoms may arise any time between childhood to middle age. Electrical cardioversion as well as antiarrhythmic drugs may be used as treatment.

1. ^[1]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
2. ^[2]Burns, Edward MD. “Ventricular Fibrillation.” Lifeinthefastlane.com. Web. 15 June 2016.↩
3. ^[3]Burns, Edward MD. “Ventricular Fibrillation.” Lifeinthefastlane.com. Web. 15 June 2016.↩
4. ^[4]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
5. ^[5]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
6. ^[6]Compton, Steven J, MD. “Ventricular Tachycardia.” Medscape.com. Dec 31, 2015. Web. 22 June 2016↩
7. ^[7]Burns, Edward MD. “Ventricular Tachycardia.” Lifeinthefastlane.com. Dec 31, 2015. Web. 22 June 2016↩
8. ^[8]Burns, Edward MD. “Ventricular Tachycardia.” Lifeinthefastlane.com. Dec 31, 2015. Web. 22 June 2016↩
9. ^[9]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
10. ^[10]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
11. ^[11]“Ventricular Tachycardia.” Webmd.com. 22 June 2016.↩
12. ^[12]Compton, Steven J, MD. “Ventricular Tachycardia.” Medscape.com. Dec 31, 2015. Web. 22 June 2016↩
13. ^[13]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
14. ^[14]Burns, Edward MD. “Ventricular Tachycardia.” Lifeinthefastlane.com. Dec 31, 2015. Web. 23 June 2016↩
15. ^[15]Burns, Edward MD. “Ventricular Tachycardia.” Lifeinthefastlane.com. Dec 31, 2015. Web. 23 June 2016↩
16. ^[16]Burns, Edward MD. “Ventricular Tachycardia.” Lifeinthefastlane.com. Dec 31, 2015. Web. 23 June 2016↩
17. ^[17]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
18. ^[18]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
19. ^[19]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
20. ^[20]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
21. ^[21]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
22. ^[22]Burns, Edward MD. “Premature Junctional Complex (PJC).” Lifeinthefastlane.com. Dec 31, 2015. Web. 31 March 2016↩
23. ^[23]Burns, Edward MD. “Premature Junctional Complex (PJC).” Lifeinthefastlane.com. Dec 31, 2015. Web. 31 March 2016↩
24. ^[24]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
25. ^[25]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
26. ^[26]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
27. ^[27]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
28. ^[28]Burns, Edward MD. “Polymorphic VT & Torsades de Pointes (TdP).” Lifeinthefastlane.com. Dec 31, 2015. Web. 31 March 2016↩
29. ^[29]Jatin, Dave MD. “Torsade de Pointes.” Medscape.com. Nov 15, 2015. Web. 28 June 2016↩
30. ^[30]Jatin, Dave MD. “Torsade de Pointes.” Medscape.com. Nov 15, 2015. Web. 28 June 2016↩
31. ^[31]Jatin, Dave MD. “Torsade de Pointes.” Medscape.com. Nov 15, 2015. Web. 28 June 2016↩
32. ^[32]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
33. ^[33]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
34. ^[34]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
35. ^[35]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
36. ^[36]Burns, Edward MD. “Wolff-Parkinson-White Syndrome.” Lifeinthefastlane.com. Dec 31, 2015. Web. 31 March 2016↩
37. ^[37]ECG Interpretation Made Incredibly Easy! (5th Edition). Ambler: Lippincott, Williams & Wilkins, 2011. Pdf.]↩
38. ^[38]Burns, Edward MD. “Wolff-Parkinson-White Syndrome.” Lifeinthefastlane.com. Dec 31, 2015. Web. 31 March 2016↩