11 ECG Patterns Worth Knowing

While there are plenty of overtly abnormal ECG patterns that are universally recognized as indicators of impending trouble – there are a number of patterns that, despite looking unfamiliar can be equally significant for the patient.

While it remains important to understand the in’s and out’s of ST changes, bundle branch blocks and AV dissociation; I recommend keeping these 11 patterns in the back of your mind when assessing patients with chest pain or syncope.

Six of these patterns suggest problems with the conduction system of the heart while the remaining five are considered “STEMI equivalents” and should be treated as serious indicators of coronary vascular disease.


 

ELECTRICAL PATTERNS

Prolonged QT interval

The QT interval represents the time it takes for the ventricles to depolarize and then repolarize, ready for the next heart beat. This interval is measured from the start of the QRS complex to the end of the T wave.

In some circumstances, this interval can become abnormally prolonged. This may be due to either a congenital condition or a combination of external factors i.e. toxins, electrolyte imbalance etc. Having an abnormally long QT interval increases the risk of a patient developing life threatening ventricular arrhythmias.

It is important to note that the QT interval changes proportionally to the heart rate (the QT narrows as the HR increases and widens as the HR slows). For this reason the QTc or corrected QT interval is commonly used to determine whether a patients QT is abnormally prolonged. There are many formulae for calculating QTc available, however most ECG machines will provide a QTc value for you.

In general terms, a QTc greater than 450ms is considered prolonged, while a QTc greater than 500ms will increase the risk of developing ventricular arrhythmias.

Patients with abnormally long QT intervals should be assessed for pathological causes of QT prolongation (toxicity, electrolytes etc.). If no cause is found and marked QT prolongation persists post treatment, patients should receive cardiology assessment for congenital causes of the condition.

 

qtprolong

Image reproduced from the Cleveland Clinic @ https://my.clevelandclinic.org/health/articles/long-qt-syndrome

 

Wolff Parkinson White Syndrome

Wolff Parkinson White (WPW) syndrome is a condition characterized by the pre-excitation of the ventricles via an additional electrical pathway known as the bundle of Kent (linking the atria to the ventricles).

Typically electrical currents from the SA node are ‘slowed down’ as they pass through the AV node before moving into the ventricles. In WPW, the electricity can enter the ventricles via the bundle of Kent without being slowed by the resistance of the AV node. This means that part of the ventricles will be stimulated fractionally earlier than the AV node can convey the message to the bundle of HIS.

As with other accessory pathways, electrical impulses may travel back up the bundle of Kent from the ventricles into the atria. This type of circuit allows electrical impulses to rapidly travel in a cycle from the AV node, through the ventricles and back to the AV node via retrograde (backward) conduction through the bundle of Kent. This is known Atrioventricular reciprocating tachycardia (a type of SVT).

Patients with WPW are at an increased risk of AVRT and are also at a slightly higher risk of sudden cardiac death.

Symptomatic patients with WPW should be referred to a cardiologist for further assessment and management (patients may require treatment with medication of ablation).

WPW patients with palpitations or extreme tachycardia should be treated according to their clinical condition and ECG findings. WPW patients with SVT may be responsive to vagal maneuvers or medications but as with all tachyarrhythmia’s, DC cardioversion may be required if the patient is unstable.

ECG characteristics of WPW are:

  • A short PR interval (less than 120 milliseconds)
  • The presence of a delta wave (an early upward slurring of the initial section of the QRS complex signifying early excitation of the ventricles).
  • Patients may also present with AVRT (a type of SVT).

 

WPW

Globally shortened PR interval with delta waves evident in all leads – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes/

 

Brugada Syndrome

Brugada syndrome is characterized by a mutation of the gene responsible for controlling sodium channels within the myocardium. Dysfunction of these channels can lead to abnormal depolarization and potentially the development of lethal tachyarrhythmias.

Brugada was only recently discovered 1992 but has since been linked to a high risk of sudden cardiac death with an estimated 10% annual risk of sudden death.

The one ECG finding characteristic of Brugada syndrome is the presence of the ‘Brugada sign’ – coved (down-sloping) ST elevation of greater than 2mm followed immediately by an inverted T wave in more than one of the following leads (V1, V2 or V3).

Brugada sign may not always be present on a patients ECG and may only be uncovered by particular stimulus i.e. drugs, cardioversion, fever, ischemia or electrolyte imbalances.

Brugada can only be diagnosed when the Brugada sign is present on an ECG and the patient presents with relevant clinical signs i.e. episodes of VT or VF, family history of sudden death under 45, Brugada sign on the ECG of family members, syncope, agonal respirations during sleep etc.

Patients with Brugada sign and relevant clinical history should be referred for urgent cardiology assessment to determine whether their risk of sudden cardiac death necessitates the insertion of an implantable automated cardioverter defibrillator.

 

brugada

Typical ‘Brugada sign’ in V1-3 – ECG reproduced from The Student Physiologist @ https://thephysiologist.org/study-materials/brugada-syndrome/

 

Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy (HCM) is characterized by the abnormal thickening of the myocardial muscles comprising the ventricle walls. Typically HCM involves hypertrophy (thickening) of the left ventricle, however different patterns exist including hypertrophy of the inter-ventricular septum and concentric hypertrophy.

HCM is relatively common and has been attributed to a genetic mutation that affects the regulation of the proteins responsible for building and repairing the myocardium.

HCM is associated with a 1-2% annual risk of sudden cardiac death and is the leading cause of sudden death in young athletes. As the walls of the myocardium thicken, the naturally occurring conduction pathways are interrupted and various accessory pathways may develop which put the patient at a greatly increased risk of conduction abnormalities and lethal arrhythmias.

Patients with HCM may present with chest pain, dyspnea or exertional syncope. If any of these symptoms are present, patients should be urgently referred for cardiology assessment to determine whether an AICD is required. Further testing (including echocardiography) will be required to establish a formal diagnosis, but ECG clues can be the first step in uncovering this condition in young adults.

Wolff-Parkinson White syndrome may be present in up to 30% of patients with HCM due to the development of accessory pathways such as the bundle of Kent.

ECG characteristics of HCM vary depending on the area of the heart affected but can include:

  • Increased QRS voltages (QRS complexes which are much taller than normal) and non-specific ST segment changes in the chest leads (signifying ventricular hypertrophy).
  • Deep narrow Q waves in lateral and inferior leads (signifying asymmetrical septal hypertrophy).
  • P mitrale (M shaped doubled P waves) may signify left atrial hypertrophy, which may follow ventricular enlargement.
  • Giant T wave inversion may be present in the case of apical hypertrophy.
  • Atrial arrhythmias and VT may also be seen in conjunction with HCM.

 

hcm

Increased QRS voltages in the inferior and precordial leads, Dagger like Q waves in the inferolateral leads, Deep T wave inversion in the lateral leads – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/hcm/

 

Second Degree AV Block – Mobitz 2

Mobitz type 2 refers to the intermittent failure of an impulse generated in the atria to conduct through to the ventricles. Where mobitz type 1 indicates a gradual fatigue of the working AV node which leads to regular failure, type 2 indicates a mechanical failure at or below the level of the bundle of HIS. Typically this failure is due to damage or injury to the electrical conduction systems from cellular necrosis, fibrosis or inflammation.

Mobitz type 2 is more clinically significant than mobitz 2 as patients are more likely to present with symptomatic bradycardia and insufficient cardiac output. Mobitz type 2 is also significantly more likely to deteriorate to complete (third degree) heart block. This rhythm is associated with a 35% risk of Asystole and sudden cardiac death each year.

The reason Mobitz 2 is so important to remember is that can be quite subtle on an ECG while still flagging potentially significant complications for the patient. Third-degree block is obviously more significant, however it is much more obvious. First degree and Mobitz 1 can also be subtle, however they pose little risk to the patient if left unmanaged. Mobitz 2 is sneaky and can cause patients problems.

A cardiologist should assess the need for pacemaker insertion in patients with a mobitz 2 ECG and concerning symptoms such as syncope.

Mobitz type 2 ECG’s are characterized by:

  • The intermittent presence of P waves that are not followed by QRS complexes and are not preceded by the gradual lengthening of PR intervals.
  • P waves will maintain a regular rate with an even P-P interval. PR intervals remain constant.
  • Multiple P waves may occur together with absent QRS complexes.

 

mob2

Arrows indicate P waves with no associated QRS complexes – Rhythm strip reproduced from EKG Strip Search @ http://www.ekgstripsearch.com/2nd_2.htm

 

Arrhythmogenic Right Ventricular Dysplasia

Arrhythmogenic right ventricular dysplasia is a congenital heart disease that is characterized by the pathological replacement of myocardial cells in the right ventricle with fatty or fibrous tissue. This tissue is not conductive like myocardial tissue and as such the presence of this tissue obstructs and interferes with the conduction of normal electrical signals within the heart.

ARVD is the second leading cause of sudden cardiac death in young people (following behind HCM). For some patients the first sign that they have this disease will be the development of a ventricular arrhythmia and possible cardiac arrest.

While echocardiography and radiological investigation are the most sensitive investigations for this condition, there are some important ECG findings that we should be mindful of in patients with symptoms of palpitations, syncope or exertional collapse.

Patients diagnosed with ARVD who are deemed high risk may be treated with medication to prevent arrhythmias or have an AICD inserted. As such, any patient suspected to have findings suggestive of ARVD should receive cardiology assessment.

ECG characteristics that suggest ARVD include:

  • The presence of an epsilon wave (a small positive inflection buried in the end of the QRS complex)
  • T wave inversion and QRS widening in the anterior leads (v1-3)
  • Episodes of ventricular tachycardia with a left bundle branch block appearance.

 

arvc

Epsilon waves present in all QRS complexes, T wave inversion V1-5 (also in inferior leads) – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/basics/arrhythmogenic-right-ventricular-cardiomyopathy/


 

ISCHEMIC PATTERNS (STEMI equivalents)

Through the use of universal ‘STEMI’ criteria, we are hoping to identify patients in the acute phase of a myocardial infarction who will benefit from the timely delivery of therapy (like PCI or TPA) to restore coronary blood flow and potentially circumvent permanent heart damage.

In New South Wales the diagnostic criteria from a STEMI is “persistent ST segment elevation greater than or equal to 1mm in two or more contiguous limb leads or ST segment elevation greater than or equal to 2mm in two contiguous chest leads or presumed new LBBB pattern” (NSW Chest pain pathway, 2011). While this definition fits (for the most part) with different guidelines around the world, there are some important exceptions to the rule.

The following patterns are commonly referred to as ‘STEMI equivalents’. While these ECG’s don’t fit the traditional mold of an acute infarct, the patient outcomes and treatment requirements are in line with more recognizable patterns of ST elevation. If any of these patterns are identified in a patient with ongoing chest pain or hemodynamic compromise urgent cardiology review should be arranged.

Wellens Syndrome

This pattern is very specific for a critical stenosis of the proximal segment of the LAD coronary artery. While this pattern is not necessarily a ‘STEMI equivalent’, it should be taken very seriously as these patients are at significant risk of imminent anterior infarct without appropriate and timely treatment.

These patients should be monitored closely and reviewed by a cardiologist. Care should be taken to differentiate Wellens from an anterior STEMI pattern (STEMI = more than 2mm ST elevation, poor R wave progression, unrelieved pain, higher troponin levels).

Wellens ECG’s are characterized by:

  • Slight ST elevation (0 – 1mm) in the anterior leads (may extend through all chest leads) – combined with – inverted or biphasic T waves in the anterior leads (may extend through all chest leads).

 

wellens

ST elevation with associated T wave inversion V1-4 – ECG reproduced from RebelEM @ http://rebelem.com/r-e-b-e-l-ecg-week-wellens-syndrome-stemi/

 

De Winters T waves

De Winters T waves are predictive of an acute occlusion of the proximal left anterior descending (LAD) coronary artery. This pattern has been seen in 2% of patients with acute LAD occlusion in the literature. Because the pattern is unfamiliar to many clinicians, De Winters T waves may be associated with an increased risk of under treatment. This pattern should be treated as being equivalent to an anterior STEMI.

ECG characteristics of De Winters T waves include:

  • Tall (often very prominent) T waves in the precordial leads
  • More than 1mm of ST depression in the precordial leads
  • Very slight (0.5-1mm) ST elevation in lead aVR.

 

T waves associated with De Winters are often referred to as being ‘hyper acute’. Symmetrical hyper acute T waves in the absence of hyperkalemia should be considered as an indicator of myocardial ischemia.

dewint

ST depression with very tall T waves V2-6 – ECG reproduced from Dr Smiths ECG Blog @ https://hqmeded-ecg.blogspot.com.au/2014/04/chest-pain.html

 

Sgarbossa Criteria

While the new onset of a left bundle branch block is always considered pathological, this pattern is no longer routinely associated with a STEMI. Instead, different formulas have been developed to help us determine when acute myocardial ischemia is present in the patient with a concurrent LBBB (this includes patients with permanent pacemakers who typically exhibit LBBB morphology on their ECGs). One such formula is the Sgarbossa criteria.

In patients with LBBB, there is typically some element of ST segment discordance, meaning the ST segment will be shifted in the opposite direction to the QRS complex. If the majority of the QRS complex is below the isoelectric line (negative) then you can expect the ST segment to be elevated above the isoelectric line (positive). This also means that ST segments will be negative when QRS complexes are positive.

Sgarbossa criteria focuses on patients with alterations to this rule of ‘normal discordance’. There are three main variations to this pattern and each of these variations is associated with a numerical score. If the patient has a cumulative score of greater than (or equal to) three, their ECG is 90% specific for diagnosing myocardial ischemia.

The three variations considered in Sgarbossa criteria are included below with their respective numerical score:

  • Concordant ST elevation > 1mm (Positive ST segment in a lead with a positive QRS complex) = 5 points
  • Concordant ST depression > 1mm (Negative ST segment in a lead with a negative QRS complex i.e. V1-3) = 3 points
  • Excessively discordant ST elevation > 5mm (very positive ST segment in a lead with a negative QRS complex) = 2 points

 

sgarb

Original Sgarbossa criteria reproduced from https://www.aliem.com/2013/12/modified-sgarbossa-criteria-ready-primetime/ referenced as “Cai, Mehta, Sgarbossa et al, 2013”.

 

In order to improve the sensitivity of the original Sgarbossa criteria the Smith-Modified Sgarbossa criteria was developed. These modified criteria essentially replace the third variant (excessively discordant ST elevation > 5mm) to the following:

  • 1 lead anywhere with > 1mm ST elevation and proportionally excessive discordant ST elevation as defined by > 25% of the depth of the preceding S wave.

This modification is useful as the un-quantified inclusion of discordant ST elevation as a diagnostic feature did not account well for patients with high voltage ECG’s.

sgarb2

Image reproduced from Wikem @ https://wikem.org/wiki/Sgarbossa%27s_criteria

 

Left Main Coronary Artery Occlusion

Occlusion or critical stenosis of the left main coronary artery is commonly associated with an ECG pattern that does not fit the routinely accepted definitions of a STEMI. Nevertheless, this condition necessitates immediate treatment and potential revascularization just the same as a more commonly recognized STEMI.

This pattern is caused by a widespread myocardial perfusion deficit (as would be the case if flow through the left main was restricted). This pattern can also be seen in other conditions causing diffuse ischemia of the myocardium such as severe triple vessel disease, proximal LAD occlusion or any other condition causing global tissue hypoxia i.e. post cardiac arrest.

ECG characteristics of this pattern include:

  • ST elevation > 1mm in aVR
  • ST elevation in aVR > V1
  • Widespread ST depression in the inferolateral leads (II, III, aVF, V4-6).

 

lmca

ST Elevation in aVR with diffuse ST depression in the inferolateral leads – ECG reproduced from Johnson Francis (Cardiophile MD) @ https://cardiophile.org/ecg-in-left-main-coronary-artery-stenosis/

 

Posterior STEMI

A standard 12 lead ECG doesn’t look at the posterior wall of the heart. For this reason any injury to the posterior wall can only be identified on a standard ECG through the presence of reciprocal changes. When considering an infarct causing ST elevation in the posterior territory of the heart, the opposite territory that will reciprocate these changes is the anterior surface of the heart.

Posterior STEMI is most commonly associated with either inferior or lateral STEMI as the same vessels (right coronary & circumflex) supply the posterior wall. Posterior STEMI without inferior or lateral ST elevation is possible but less common. If posterior STEMI changes are present in the context of an inferior or lateral infarct, the area of ischemic myocardium is considerably larger and may be associated with worse patient outcomes.

If ECG changes are seen on a standard 12 lead ECG that suggest a posterior infarct, it may be helpful to perform a posterior ECG by moving V4-6 further around the patients chest to look more directly at the posterior wall of the heart.

ECG characteristics of a posterior STEMI include:

  • Horizontal ST depression with upright T waves and tall broad R waves V1-3 (supported by >1mm ST elevation in the posterior leads V7-9).

 

posterior

Horizontal ST depression can be seen with upright T waves in the anterior leads (V1-3) – Associated with inferolateral ST elevation – ECG reproduced from life in the fast lane @ https://lifeinthefastlane.com/ecg-library/pmi/


 

Reference

Cai Q, Mehta N, Sgarbossa E, et al. The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time? Am Heart J. 2013;166(3):409-413.

 

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