Of the cardiology questions in the Part II exam, a large proportion consists of ECG interpretation exercises. The following is a list of such questions. As you can se, they were virtually unknown prior to 2005. These days, it seems the college is trending towards more "data interpretation" style questions,which are easier to mark. With this, ECG and ABG questions proliferate.

Here is a list of all ECG questions in recent history (whatever the value of that might be).

ECG Interpretation in the CICM Part 2 SAQs

Question 30.1 from the first paper of 2019 (right heart failure) Question 30.2 from the first paper of 2019 (Long QT, due to TCA overdose) Question 23.1 from the second paper of 2018 (right ventricular STEMI with CHB) Question 15.1 from the second paper of 2017 (trifascicular block) Question 15.2  from the second paper of 2017 (hyperkalemia) Question 15.3 from the second paper of 2017 (WPW) Question 25.1 from the second paper of 2016 (hypokalemia) Question 25.2 from the second paper of 2016 (HOCM) Question 25.3 from the second paper of 2016 (complete heart block) Question 26.1 from the first paper of 2016 (WPW in AF) Question 26.2 from the first paper of 2016 (atrioventricular lead reversal) Question 26.3 from the first paper of 2016 ( RV hypertrophy ) Question 14.1 from the second paper of 2015 (WPW) Question 14.2 from the second paper of 2015 (inferior STEMI) Question 14.3 from the second paper of 2015 (2:1 atrial flutter with left axis deviation) Question 30.1 from the first paper of 2015 (SVT) Question 30.2 from the first paper of 2015 (hyperkalemia) Question 30.3 from the first paper of 2015 (2nd degree heart block, Mobitz type I) Question 6.1 from the second paper of 2014 (Wellens sign) Question 6.2 from the second paper of 2014 (pericarditis) Question 6.3 from the second paper of 2014 (hyperkalaemia) Question 18.1 from the first paper of 2014 (LV aneurysm) Question 18.2 from the first paper of 2014 (Brugada syndrome) Question 18.3 from the first paper of 2014 (multifocal atrial tachycardia) Question 18.1 from the first paper of 2013 (trifascicular block) Question 18.2 from the first paper of 2013 (hyperkalaemia) Question 18.3 from the first paper of 2013 (severe hypothermia) Question 30.1 from the second paper of 2012 (pericardial effusion - electrical alternans) Question 30.3 from the second paper of 2012 (Right bundle branch block with STEMI) Question 30.4 from the second paper of 2012 (complete heart block) Question 23.1 from the first paper of 2012 (hyperkalaemia) Question 23.2 from the first paper of 2012 (trifascicular block) Question 6.1 from the second paper of 2011 (Right bundle branch block + left posterior fascicular block) Question 6.2 from the second paper of 2011 (digoxin toxicity) Question 6.3 from the second paper of 2011 (SVT) Question 6.4 from the second paper of 2011 (RCA  territory STEMI) Question 26.1 from the first paper of 2011 (pericardial effusion) Question 26.3 from the first paper of 2011 (a fucking normal ECG) Question 10.2 from the second paper of 2009 (LV aneurysm) Question 3.1 from the first paper of 2009 (WPW) Question 15.3 from the second paper of 2008 (Right bundle branch block with STEMI) Question 26.2 from the first paper of 2008 (Right bundle branch block + left posterior fascicular block) Question 26.3 from the first paper of 2008 (RCA  territory STEMI) Question 15 from the second paper of 2005 (right ventricular strain) Question 30 from the first paper of 2005 (flutter with trifascicular block)

There really is no satisfactory way to short-cram in preparation for such questions. One might be tempted to make the facetious remark that people at this level of training would be confident in ECG interpretation, and that no further preparation would be required for the true ICU fellow in the final stages of their training. One might even say that good solid basic knowledge is the key to success in this ECG interpretation section. Of course, this would be complete bullshit. The College seem to have a database of perhaps twenty or thirty ECGs. The cynical trainee will focus on becoming familiar with this selection. If a repeat question comes up, the cynic will be rewarded for counting on the lazyness of  question writers. If the ECG is brand-new, the cynic will not be disadvantaged any more than anybody else.

In the spirit of cheating and cynicism, the following is a list of ECG abnormalities which have appeared prominently in the previous papers. Many of these abnormalities are covered in other chapters (also listed below) but many are not, and so thay have all been lumped together in this page.

Right ventricular hypetrophy

This is an ECG of RV hypetrophy stolen from LITFL.

Edward Burns gives the following electrocardiographic features:

Hyperkalemia

Huge tented T waves seem to hold some sort of fascination for the examiners. In the SAQs, the vehicle for such ECG changes is usually a story about a recent crush injury (as a means of suggesting rhabdomyolysis to the candidates). Previous appeances of hyperkalemia include Question 15.2  from the second paper of 2017,  Question 30.2 from the first paper of 2015 ,  Question 6.3 from the second paper of 2014, Question 18.2 from the first paper of 2013, and Question 23.1 from the first paper of 2012.

Characteristic features (if on were called upon to describe them) include the following:

• Broad QRS complexes
• Peaked T waves
• No typical bundle branch block pattern
• Left axis deviation
• Long PR interval (if P waves are even visible)
• Absent P waves (merged with QRS)
• Absent T-waves (merged with QRS)
• Ultimately, a "sine wave" ECG.

The  "Retrospective review of the frequency of ECG changes in hyperkalemia" by Montague et al (2008) somewhat devalues these questions. Among a case series of ninety hyperkalemic patients, the ECG was neither sensitive at detecting hyperkalemia, nor able to predict hyperkalemic complications.

Trifascicular block

This has come up several times, including Question 15.1 from the second paper of 2017,  Question 18.1 from the first paper of 2013, Question 23.2 from the first paper of 2012 and Question 30 from the first paper of 2005. Basically, the trainee needs to recognise RBBB with left axis deviation and a prolonged PR interval.

The specific features are:

• Right bundle branch block:
  • broad QRS
  • Inverted T waves in anterior leads
  • Sloping S waves in lateral leads
• Axis deviation (because RBBB should have a normal axis)
  • Left axis deviation: suggestive of an anterior fascicle block
    • Positive Lead I
    • Negative lead II and aVF
  • Right axis deviation: suggestive of a posterior fascicle block
    • Negative Lead I
    • Positive lead III and aVF
• A prolonged PR interval (the "third fascicle" is also broken)

Occasionally (eg. in Question 15.1 from the second paper of 2017) the college asks as to how this conduction abnormality is relevant. For instance, in the aforementioned question the pretext for the ECG is a history of syncope and fractured neck of femur. How could this have happened, one might ask. Well; these people classically progress to complete heart block. It does not require a great stretch of the imagination to conceive of this as a possible outcome given that pretty much all of the conduction system is diseased. One is practically running on just one fascicle. Once that breaks, no conduction down the bundle of His will make its way into the LV, giving rise to a complete heart block (albeit with a potentially well-functioning AV node). The solution, predictably, is a permanent pacemaker. 

LV aneurysm

Question 10.2 from the second paper of 2009 presented the candidates with a scenario where a patient  with obvious St segment elevation is comfrotably pain-free. This is an LV aneurysm.

Another similar question (except not pain free) is Question 18.1 from the first paper of 2014, where the patient seems to have had an MI about a week ago. In both cases, the characteristic feature is persisting ST elevation after an MI. Rosenberg et al described this back in 1949. A more modern blog entry by Dr Smith discusses LV aneurysm complicated by RBBB.

Multifocal atrial tachycardia

MAT has appeared in Question 18.3 from the first paper of 2014. It is also known as "Chaotic Atrial Rhythm".  It enjoys a thorous exploration in John Kastor's 1990 article for NEJM.   Lipson and Naimy offer more detail in Circulation (1970). A nice short-form summary of paediatric MAT is also offered by Bradley et al (2006).

The cardinal features are irregularity and a plethora of different P-wave morphologies.

You need to have

• Tachycardia (HR >100)
• Irregular rate
• Variability in P wave morphology

The same findings with a normal heart rate does not qualify for MAT, because it's not tachycardia; you have to call that a "wandering atrial pacemaker".

The CICM question also asked for associated diseases.  In adults, MAT is almost uniformly associated with COPD. Not only are the atria stretched by pulmonary hypertension, but the proarrhythmic bronchodilators also make for an irritable myocardium.  In the paediatric population the differentials are more broad, including bronchiolitis, croup, bronchomalacia, etc.

Supraventricular tachycardia

Question 6.3 from the second paper of 2011 presented only SVT. Question 30.1 from the first paper of 2015 wanted the candidates to discriminate between VT and SVT with aberrancy. The latter being more interesting. The LITFL page on distinguishing VT from SVT with aberrancy is an excellent and highly detailed resource for this issue.

In brief:

Is this VT or SVT with Aberrant Conduction? How do I know?

Supraventricular tachycardia Historical features Young age Previous SVTs terminated with adenosine ECG changes Same RBBB or LBBB pattern as the patient's normal ECG WPW on pre-tachycardia ECG Responds to vagal manoeuvres

Ventricular tachycardia Historical features Old age Ischaemic heart disease, MI HOCM, long QT, Brugada ECG changes No typical RBBB or LBBB morphology Bizarre axis deviation Very broad complexes (>160ms) AV dissociation (P rate is different to QRS rate) Capture beats — occasional normal QRS complexes Fusion beats — a normal and a wide QRS superimposed on top of one another Concordance:         all the chest lead QRSs point in the same direction Brugada’s sign –  From onset of QRS complex to nadir of S-wave is > 100ms Josephson’s sign – Notching near the nadir of the S-wave Left ear of RSR complex is higher than right

Wellens Sign

Question 6.1 from the second paper of 2014 pulled out "Wellens Sign", which is the ECG sign of proximal LAD occlusion. The sign is characterised by deep symmetrical T-wave inversion in V2, V3 and V4.

Professor Hein JJ Wellens co-authored a publication on this topic (Zwaan et al, 2000) but I am pretty sure the sign was already named after him before this paper.

Pericarditis

Question 6.2 from the second paper of 2014 demonstrated pericarditis. The question presented us wth a young man who was experiencing atypical chest pain.

There are only two characteristic features of pericarditis woth remembering:

• Diffuse "non-territorial" ST segment elevation
• PR interval depression.

Benign early repolarisation is a valid differential for this appearance, and is offered in the college model answer.

Pericardial effusion and electrical alternans

Again, this is one of those rapid pattern recognition exercises. One you have seen it, you will never forget. Question 26.1 from the first paper of 2011 shows us a straightforward case, and Question 30.1 from the second paper of 2012 puts it in the context of AF to make things difficult.

In ideal conditions, electrical alternans should look like this:

The phenomenon is caused by the heart swinging back and forth inside a pericardial cavity which has become distended to the size of a small aquarium. The swinging between beats changes the position of the conductive tissues relative to the stationary chest leads, and results in different (and regularly alternating) QRS morphologies.

Severe hypothermia

This was seen in Question 18.3 from the first paper of 2013, an ECG of an elderly woman found collapsed in the bathroom.

Specific findings associated with hypothermia are discussed in a good article by Mattu et al (2002). They include:

• J (Osborn) waves (the uptick of the ST segment which immedately follows the QRS complex, best seen in leads V4 and V5 in the ECG above)
• Prolongation of all intervals PR, QRS and QT
• Atrial and ventricular arrhythmias

Hypothermia may also

• ST depression or elevation
• hypothermia can produce ECG signs that simulate those of acute myocardial ischemia or myocardial infarction.

Brugada Syndrome

Question 18.2 from the first paper of 2014 was the only appearance of Brugada Syndrome. This autosomal dominal "channelopathy" is among the most easily recognisable ECG abnormalities, alongiside STEMI and hyperkalemia. The problem lies in a dodgy sodium channel;

The characteristic ECg findings mentioned in the college answer are "coved" ST segments in leads V1 and V2, with a degree of ST elevation. "Coved" is a weird term to use for this, as the standard definition of "cove" is "a small indentation or recess in the shoreline of a sea, lake, or river". Essentially, the QRS complex finishes high, and the ST-segment slopes diagonally to form an inverted T-wave.

The criteria for the diagnosis of Brugada syndrome as well as  are explored to a fascinating depth by Edward Burns in his article for LITFL. Additionally, there is an excellent 2012 update on this syndrome, co-authored by one of the Brugada brothers. However, the time-poor exam candidate will lose interest in large blocks of text. Point-form summaries ensue:

Population:

• 10 times more common in males
• Ages 20-40

Clinical criteria:

• Characteristic ECG changes
• Also, one of the following:
  • documented polymorphic VT or VF
  • Family history of sudden cardiac death before the age of 45
  • Characteristic ECG changes in family members
  • Syncope
  • Induceable VT
  • Nocturnal agonal respiration

Clinical situations which can worsen this condition:

• Ischaemia
• Hyperthermia or hypothermia
• Hypokalemia
• Cardioversion
• Vagal overactivity (thus, arrests happen at night)
• Drugs:
  • Class 1 antiarrhythmics
  • Beta blockers and calcium channel blockers
  • Alpha-agonists
  • Nitrates
  • Cocaine and alcohol
  • Cholinergic agonists, eg. the "stigmine" drugs

Management of Brugada syndrome:

• Quinidine (though it is a Class 1 agent)
• AICD
• Catheter ablation

Right ventricular hypetrophy and RV  strain pattern

This came up in Question 30.1 from the first paper of 2019

Criteria for RV hypertrophy:

• Right axis deviation
• Dominant R wave in V1
• Dominant S wave in V5-V6
• Normal QRS duration (i.e. not a right bundle branch block)

The characteristic features of RV strain are:

• ST depression / T wave inversion in the anterior leads, V1 - V2
• ST depression / T wave inversion in the inferior and right-facing limb leads ( II, III and aVF)

Long QT interval

This came up in Question 30.2 from the first paper of 2019

TheQT is prolonged (it is about 512 msec in its uncorrected state, or 585 corrected for heart rate).

Differentials, according to Harrigan & Chan (2009), include:

Non-drug-related causes

• Hypokalemia
• Hypocalcemia
• Hypomagnesemia
• Hypothermia
• Thiamine deficiency
• Cardiac ischaemia

Drugs (also see www.qtdrugs.org)

• Cardiac agents
  • Anti-arrhythmics (Type Ia, Ic, and III)
  • Calcium channel-blockers (some) (e.g. bepridil, isradipine, nicardipine)
• Anti-psychotic agents
  • Phenothiazines (some) (e.g. thioridazine, mesoridazine)
  • Butyrophenones (e.g. haloperidol, droperidol)
• Anti-depressants (some) (e.g. tricyclics, fluoxetine, sertraline, venlaflaxine)
• Anti-infective agents
• Fluoroquinolones (some) (e.g. sparfloxacin, gatifloxacin, moxifloxicin)
• Macrolides (some) (e.g. erythromycin, clarithromycin)
• Miscellaneous (pentamidine, amantadine, tetracyclines, foscarnet, quinine, chloroquine)
• Neurologic agents
  • Carbamazepine, fosphenytoin, sumatriptan, zolmitriptan, naratriptan
• Organophosphates
• Gastrointestinal agents (e.g. cisapride, ipecac, octreotide, dolasetron)
• Other (e.g. cocaine, diphenhydramine, methadone, tacrolimus, tamoxifen, probucol, tizanidine, salmeterol)