This a very cool project. How to make an ultrasound simulator on the cheap for use in training scenarios. We’ve already featured the first Australian implentation of this project (The Australian EDUS2 Project) in the 63rd LITFL Review. In yet another great video from SAEM2012, Paul Kulyk and Paul Olszynski the originators of this project tell the world what it’s all about:

Check out the EDUS2 website, where you can access the code, videos and design plans for free — all you need is to provide the hardware.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

aka Pulmonary Puzzle 015

Post coauthor: Chris Nickson

A 40 year old man had been in ICU for nearly 2 weeks and was slow to wean off the ventilator due to ARDS (acute respiratory distress syndrome). A percutaneous dilational tracheostomy (PDT) was performed. Following the procedure he developed a requirement for increased respiratory support.

He was sufficiently stable for a CT chest to be performed. Representative images are shown below:

Click to enlarge

Click to enlarge

Questions

Q1. Describe the CT findings

Answer and interpretation

Q2. What are the important possible causes of the key finding on the CT Chest?

Answer and interpretation

Q3. What clinical findings may be present?

Answer and interpretation

Q4. What are the management priorities?

Answer and interpretation

Q5. How would you treat a tension pneumomediastinum?

Answer and interpretation

Q6. Should chest x-rays be performed after performing percutaneous dilational tracheostomy (PDT)?

Answer and interpretation

References and links

Lifeinthefastlane.com

• Pulmonary Puzzle 003 — Roast duck and juniper beer

Textbooks and journal articles

• Frova G, Sorbello M. Iatrogenic tracheobronchial ruptures: the debate continues. Minerva Anestesiol. 2011 Dec;77(12):1130-3. Epub 2011 Jun 13. PubMed PMID: 21666570. [Fulltext]
• Kumar VM, Grant CA, Hughes MW, Clarke E, Hill E, Jones TM, Dempsey GA. Role of routine chest radiography after percutaneous dilatational tracheostomy. Br J Anaesth. 2008 May;100(5):663-6. Epub 2008 Mar 27. PubMed PMID: 18369239. [Fulltext]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

aka Cardiovascular Curveball 013

A junior colleague asks if he can discuss a case with you.

His patient is a 23 year-old man who presents with 2 hours of rapid regular palpitations associated with ‘not feeling quite right’. These symptoms came on while he was running on a treadmill at his local gym. He has no significant past medical history. Apart from a tachycardia, examination is unremarkable and he is hemodynamically stable.

This is his ECG:

Click to enlarge

Questions

Q1. Describe the ECG.

Answer and interpretation

Your colleague says he thinks it is an SVT with aberrant conduction because the patient is young, haemodynamically stable and has no history of heart disease.

Q2. What is your response?

Answer and interpretation

Your colleague suggests, citing the 2010 ILCOR guidelines, that adenosine could be administered and if the patient reverts then the diagnosis of SVT with aberrancy will be confirmed.

Q3. What is your response to this suggestion?

Answer and interpretation

Q4. How can VT and SVT be reliably distinguished?

Answer and interpretation

Q5. How would you treat this patient?

Answer and interpretation

Q6. What was the diagnosis in the above ECG?

Answer and interpretation

References

• Cummins RO, Hazinski MF. The quest for a terminator. Ann Emerg Med. 2006 Mar;47(3):227-9. Epub 2006 Jan 25. PMID: 16492487.
• Deakin CD, Morrison LJ, Morley PT, Callaway CW, Kerber RE, Kronick SL, Lavonas EJ, Link MS, Neumar RW, Otto CW, Parr M, Shuster M, Sunde K, Peberdy MA, Tang W, Hoek TL, Böttiger BW, Drajer S, Lim SH, Nolan JP; Advanced Life Support Chapter Collaborators. Part 8: Advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science with Treatment Recommendations. Resuscitation. 2010 Oct;81 Suppl 1:e93-e174. PMID: 20956032.
• Hina K, Kusachi S, Takaishi A, Yamasaki S, Sakuragi S, Murakami T, Kita T. Effects of adenosine triphosphate on wide QRS tachycardia. Analysis in 18 patients. Jpn Heart J. 1996 Jul;37(4):463-70. PMID: 8890760.
• Jane-Wit D, Batsford W, Malm B. Ischemic etiology for adenosine-sensitive fascicular tachycardia. J Electrocardiol. 2011 Mar-Apr;44(2):217-21. Epub 2010 Sep 15. PMID: 20832812.
• Lenk M, Celiker A, Alehan D, Koçak G, Ozme S. Role of adenosine in the diagnosis and treatment of tachyarrhythmias in pediatric patients. Acta Paediatr Jpn. 1997 Oct;39(5):570-7. PMID: 9363655.
• Marill KA, Greenberg GM, Kay D, Nelson BK. Analysis of the treatment of spontaneous sustained stable ventricular tachycardia. Acad Emerg Med. 1997 Dec;4(12):1122-8. PMID: 9408427.
• Marill KA, deSouza IS, Nishijima DK, Senecal EL, Setnik GS, Stair TO, Ruskin JN, Ellinor PT. Amiodarone or procainamide for the termination of sustained stable ventricular tachycardia: an historical multicenter comparison. Acad Emerg Med. 2010 Mar;17(3):297-306. PMID: 20370763.
• Mattu, A. The Pinnacle: ECG cases that would make an electrophysiologist blush. Presentation at the 2011 ACEP Scientific Assembly. [pdf of slideshow]
• Neumar RW, Otto CW, Link MS, Kronick SL, Shuster M, Callaway CW, Kudenchuk PJ, Ornato JP, McNally B, Silvers SM, Passman RS, White RD, Hess EP, Tang W, Davis D, Sinz E, Morrison LJ. Part 8: adult advanced cardiovascular life support: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010 Nov 2;122(18 Suppl 3):S729-67. Review. Erratum in: Circulation. 2011 Feb 15;123(6):e236. PMID: 20956224. [Free Fulltext]
• Tomlinson DR, Cherian P, Betts TR, Bashir Y. Intravenous amiodarone for the pharmacological termination of haemodynamically-tolerated sustained ventricular tachycardia: is bolus dose amiodarone an appropriate first-line treatment? Emerg Med J. 2008 Jan;25(1):15-8. PMID: 18156531.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

• The ST segment is the flat, isoelectric section of the ECG between the end of the S wave (the J point) and the beginning of the T wave.
• It represents the interval between ventricular depolarisation and repolarisation.
• The most important cause of ST segment abnormality (elevation or depression) is myocardial ischaemia / infarction.

Causes of ST segment elevation

• Acute myocardial infarction
• Coronary vasospasm (Printzmetal’s angina)
• Pericarditis
• Benign early repolarisation
• Left bundle branch block
• Left ventricular hypertrophy
• Ventricular aneurysm
• Brugada syndrome
• Ventricular paced rhythm
• Raised intracranial pressure

Morphology of the Elevated ST segment

Myocardial infarction

Acute STEMI may produce ST elevation with either concave, convex or obliquely straight morphology.

ST segment morphology in other conditions

Pericarditis	BER	LBBB	LV aneurysm	Brugada

Patterns of ST elevation

Acute ST elevation myocardial infarction (STEMI)

Causes ST segment elevation and Q-wave formation in contiguous leads, either:

• Septal (V1-2)
• Anterior (V3-4)
• Lateral (I + aVL, V5-6)
• Inferior (II, III, aVF)
• Right ventricular (V1, V4R)
• Posterior (V7-9)

There is usually reciprocal ST depression in the electrically opposite leads.

Follow the links above to find out more about the different STEMI patterns.

Anterolateral STEMI

Coronary Vasospasm (Prinzmetal’s angina)

This causes a pattern of ST elevation that is very similar to acute STEMI — i.e. localised ST elevation with reciprocal ST depression occurring during episodes of chest pain. However, unlike acute STEMI the ECG changes are transient, reversible with vasodilators and not usually associated with myocardial necrosis. They may be impossible to differentiate on the ECG.

Prinzmetal's angina

Pericarditis

Pericarditis causes widespread concave ST segment elevation with PR segment depression in multiple leads — typically I, II, III, aVF, aVL and V2-6. There is reciprocal ST depression and PR elevation in leads aVR and V1.

Click here to find out more about pericarditis. 

• Concave “saddleback” ST elevation in leads I, II, aVL, V4-6 with depressed PR segments.
• There is reciprocal ST depression and PR elevation in aVR.

Benign Early Repolarisation

Causes mild ST elevation with tall T-waves mainly in the precordial leads. Is a normal variant commonly seen in young, healthy patients. There is often notching of the J-point — the “fish-hook” pattern.

Click here to find out more about benign early repolarisation.

Benign Early Repolarisation

• There is slight concave ST elevation in the precordial and inferior leads with notching of the J-point (the “fish-hook” pattern)

Left Bundle Branch Block

In left bundle branch block, the ST segments and T waves show “appropriate discordance” — i.e. they are directed opposite to the main vector of the QRS complex. This produces ST elevation with upright T waves in leads with a negative QRS complex (dominant S wave), while producing ST depression and T wave inversion in leads with a positive QRS complex (dominant R wave).

Click here to find out more about left bundle branch block.

Left Bundle Branch Block

• Note the ST elevation in leads with deep S waves — most apparent in V1-3.
• Also note the ST depression in leads with tall R waves — most apparent in I and aVL.

Left Ventricular Hypertrophy

LVH causes a similar pattern of repolarisation abnormalities as LBBB, with ST elevation in the leads with deep S-waves (usually V1-3) and ST depression/T-wave inversion in the leads with tall R waves (I, aVL, V5-6).

Click here to find out more about LVH. 

Left Ventricular Hypertrophy

• Severe LVH with extremely deep S waves in V1-3 producing associated ST elevation (not due to myocardial ischaemia).
• Also note the ST depression and T-wave inversion in the lateral leads I, aVL and V6 .

Ventricular Aneurysm

This is an ECG pattern of residual ST elevation and deep Q waves seen in patients with previous myocardial infarction. It associated with extensive myocardial damage and paradoxical movement of the left ventricular wall during systole.

Click here to find out more about ventricular aneurysm.

Ventricular Aneurysm

• There is ST elevation with deep Q waves and inverted T waves in V1-3.
• This pattern suggests the presence of a left ventricular aneurysm due to a prior anteroseptal MI.

Brugada Syndrome

This in an inherited channelopathy (a disease of myocardial sodium channels) that leads to paroxysmal ventricular arrhythmias and sudden cardiac death in young patients. The tell-tale sign on the resting ECG is the “Brugada sign” — ST elevation and partial RBBB in V1-2 with a “coved” morphology.

Click here to read more about Brugada syndrome. 

Brugada syndrome

• There is ST elevation and partial RBBB in V1-2 with a coved morphology — the “Brugada sign”.

Ventricular Paced Rhythm

Ventricular pacing (with a pacing wire in the right ventricle) causes ST segment abnormalities identical to that seen in LBBB. There is appropriate discordance, with the ST segment and T wave directed opposite to the main vector of the QRS complex.

Click here to read more about paced rhythms. 

Sequential atrial and ventricular pacing

Raised intracranial pressure

Raised ICP (e.g. due to intracranial haemorrhage, traumatic brain injury) may cause ST elevation or depression that simulates myocardial ischaemia or pericarditis. More commonly, raised ICP is associated with widespread, deep T-wave inversions (“cerebral T waves”).

Click here to find out more about the ECG changes seen with raised intracranial pressure. 

ST elevation due to traumatic brain injury

• Widespread ST elevation with concave (pericarditis-like) morphology in a patient with severe traumatic brain injury.

Less common causes of ST segment elevation

• Pulmonary embolism and acute cor pulmonale (usually in lead III)
• Acute aortic dissection (classically causes inferior STEMI due to RCA dissection)
• J-waves (hypothermia, hypercalcaemia)
• Hyperkalaemia
• Sodium-channel blocking drugs (secondary to QRS widening)
• Following electrical cardioversion
• Cardiac tumour
• Mitral valvuloplasty
• Pancreatitis / gallbladder disease
• Myocarditis
• Septic shock
• Anaphylaxis

Transient ST elevation after DC cardioversion from VF

J waves in hypothermia simulating ST elevation

Causes of ST depression

• Myocardial ischaemia / NSTEMI
• Reciprocal change in STEMI
• Posterior MI
• Digoxin effect
• Hypokalaemia
• Supraventricular tachycardia
• Right bundle branch block
• Right ventricular hypertrophy
• Left bundle branch block (see above)
• Left ventricular hypertrophy (see above)
• Ventricular paced rhythm (see above)

 Morphology of ST depression

• ST depression can be either upsloping, downsloping, or horizontal.
• Horizontal or downsloping ST depression > 1 mm at the J-point is relatively specific for myocardial ischaemia.
• Upsloping ST depression is non-specific for myocardial ischaemia.
• Reciprocal change has a morphology that resembles “upside down” ST elevation.
• ST depression in posterior MI occurs in V1-3 and is associated with dominant R waves and upright T waves.

ST depression: upsloping (A), downsloping (B), horizontal (C)

ST segment morphology in myocardial ischaemia

Reciprocal change

ST elevation in III	Reciprocal change in aVL

ST segment morphology in posterior MI

Patterns of ST depression

Myocardial Ischaemia

ST depression due to subendocardial ischaemia may be present in a variable number of leads and with variable morphology. It is often most prominent in the left precordial leads V4-6. Widespread ST depression with ST elevation in aVR is seen in left main coronary artery occlusion.

NB. ST depression localised to the inferior or high lateral leads is more likely to represent reciprocal change than subendocardial ischaemia. The corresponding ST elevation may be subtle and difficult to see, but should be sought. This concept is discussed further here.

Widespread subendocardial ischaemia due to LMCA occlusion

Reciprocal Change

ST elevation during acute STEMI is associated with simultaneous ST depression in the electrically opposite leads:

• Inferior STEMI produces reciprocal ST depression in aVL (± lead I).
• Lateral or anterolateral STEMI produces reciprocal ST depression in III and aVF (± lead II).
• Reciprocal ST depression in V1-3 occurs with posterior infarction (see below).

Reciprocal ST depression in aVL with inferior STEMI

Reciprocal ST depression in III and aVF with high lateral STEMI

Posterior Myocardial Infarction

Acute posterior STEMI causes ST depression in the anterior leads V1-3, along with dominant R waves (“Q-wave equivalent”) and upright T waves. There is ST elevation in the posterior leads V7-9.

Click here to read more about posterior MI. 

Posterior MI

Digoxin Effect

Treatment with digoxin causes downsloping ST depression with a “sagging”  morphology, reminiscent of Salvador Dali’s moustache.

Click here to read more about digoxin effect.

Hypokalaemia

Hypokalaemia causes widespread downsloping ST depression with T-wave flattening/inversion, prominent U waves and a prolonged QU interval.

Click here to read more about hypokalaemia. 

Hypokalaemia

Right ventricular hypertrophy

RVH causes ST depression and T-wave inversion in the right precordial leads V1-3.

Click here to read more about right ventricular hypertrophy. 

Right ventricular hypertrophy

Right Bundle Branch Block

RBBB may produce a similar pattern of repolarisation abnormalities to RVH, with ST depression and T wave inversion in V1-3.

Click here to read more about right bundle branch block. 

Right bundle branch block

Supraventricular tachycardia

Supraventricular tachycardia (e.g. AVNRT) typically causes widespread horizontal ST depression, most prominent in the left precordial leads (V4-6). This rate-related ST depression does not necessarily indicate the presence of myocardial ischaemia provided that it resolves with treatment.

AV-nodal re-entry tachycardia

Further Reading

• ECG BASICS – Waves, Intervals, Segments and Clinical Interpretation
• ECG CLINICAL CASES – Your favourite ECG’s placed in clinical context with a challenging Q&A approach
• ECG and Cardiology Eponymous Syndromes – Cheats guide to eponymous emancipation
• ECG Reference Sites on the WEB – the best of the rest

Author Credits

References

• Chan TC, Brady WJ, Harrigan RA, Ornato JP, Rosen P. ECG in Emergency Medicine and Acute Care. Elsevier Mosby 2005.
• Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002 Apr 20;324(7343):963-6. Review. PubMed PMID: 11964344; PubMed Central PMCID: PMC1122906. Full text.
• Phibbs BP. Advanced ECG: Boards and Beyond (second edition). Elsevier 2006.
• Smith SW. T/QRS ratio best distinguishes ventricular aneurysm from anterior myocardial infarction. Am J Emerg Med. 2005 May;23(3):279-87. PubMed PMID: 15915398.
• Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

If you haven’t checked out LITFL’s ECG Library recently, I suggest you get on over and have a look around… It is turning into something truly awesome!

There is still the odd nut or bolt missing, but whether you’re after the ECG Basics, an A-Z collection of ECG diagnoses, or trying to visualise how to localise a myocardial infarction you’ll find something marvelous. And we haven’t even mentioned the eponymous syndromes or the ‘test yourself’ clinical cases yet!

Dr Ed Burns has been slaving away on this project for some time now, largely behind the scenes, and the ECG Library’s escalating awesomeness is in large part down to him. We’ve also been fortunate to welcome aboard another ECG geek in Dr John Larkin, so you can expect exponential elevations in ecgstasy on LITFL from now on!

Another great addition to the library is the ECG Academy page collecting together Dr Nick Tullo’s brilliant videos. Ever wanted private tuition from a cardiac electrophysiologist? Well, now you can… Here’s a taster of one his great ‘chalktalk’ sessions:

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

Meanwhile the LITFL team is going to ever increasing extremes to ensure that the future of the ECG Library is in good hands— we’ve got prospective contributors reading ECGs within a day of being born!

Training for future ECG Library contributors starts early!

ECG Clinical Interpretation: A to Z by diagnosis

A

• Atrial flutter
• Atrial fibrillation
• Arrhythmogenic right ventricular dysplasia (AVRD)
• AV block: 1st degree
• AV block: 2nd degree, Mobitz I (Wenckebach)
• AV block: 2nd degree, Mobitz II
• AV block: 2nd degree, “fixed ratio blocks” (2:1, 3:1)
• AV block: 2nd degree, “high grade AV block”
• AV block: 3rd degree (complete heart block)
• AVNRT

B

• Benign Early Repolarisation
• Beta-blocker toxicity
• Bidirectional ventricular tachycardia
• Bifascicular block
• Biventricular enlargement
• Biatrial enlargement
• Brugada syndrome

C

• Calcium channel blocker toxicity
• Carbamazepine cardiotoxicity
• Cardiomyopathy
• Chronic obstructive pulmonary disease (COPD)

D

• Dextrocardia
• Digoxin effect
• Digoxin toxicity
• Dilated cardiomyopathy

E

• Ectopic atrial tachycardia
• Electrical alternans
• Emphysema
• Escape rhythms, junctional
• Escape rhythms, ventricular

F

• Fusion beats

H

• High take-off
• Hypercalcaemia
• Hyperkalaemia
• Hypocalcaemia
• Hypokalaemia
• Hypomagnesaemia
• Hypothermia
• Hyperthyroidism
• Hypertrophic Obstructive Cardiomyopathy (HCM)
• Hypothyroidism

I

• Interventricular Conduction Delay
• Intracranial haemorrhage
• Intrinsicoid deflection

J

• J-point elevation
• Junctional premature beat

L

• Lead reversals: Limb Lead Reversals (overview)
• Lead reversal: Left arm/right arm
• Left atrial enlargement
• Left anterior fascicular block
• Left axis deviation
• Left bundle branch block
• Left posterior fascicular block
• Left ventricular aneurysm
• Left ventricular hypertrophy
• LMCA Obstruction (Dominant aVR)
• Lown-Ganong-Levine syndrome
• Low QRS Voltage

M

• Movement artefact
• Multifocal atrial tachycardia
• Myocardial ischemia
• Myocarditis

P

• Pacemaker rhythms
• Pacemaker-mediated tachycardia
• Paediatric ECG
• Pericardial tamponade
• Pericarditis
• Persistent ST elevation (LV aneurysm morphology)
• Polymorphic ventricular tachycardia
• Poor R wave progression (PRWP)
• Preexcitation
• Premature beats, atrial
• Premature beats, junctional
• Premature beats, ventricular
• Pulmonary disease, chronic
• Pulmonary embolism

Q

• Quetiapine toxicity

R

• Raised intracranial pressure
• Right atrial enlargement
• Right axis deviation
• Right bundle branch block
• Right ventricular hypertrophy
• Right ventricular outflow tract (RVOT) tachycardia
• Right ventricular strain
• R-wave peak time

S

• Sgarbossa criteria (diagnosing AMI in LBBB)
• Shivering artefact
• Short QT syndrome
• Sinus rhythm
• Sinus arrhythmia
• Sinus bradycardia
• Sinus node dysfunction (Sick sinus syndrome)
• Sinus node exit block
• Sinus node reentrant tachycardia (AVNRT)
• Sinus tachycardia
• Sodium channel blocker overdose
• ST elevation in aVR (LMCA/3VD)
• STEMI, anterior
• STEMI, high lateral
• STEMI, inferior
• STEMI, lateral
• STEMI (old)
• STEMI, posterior
• STEMI, right ventricular
• Subarachnoid haemorrhage

T

• Tako Tsubo Cardiomyopathy
• Torsades de Pointes
• Tremor artifact
• Tricyclic overdose (sodium-channel blocker toxicity)
• Triple vessel disease
• Trifascicular block

V

• Ventricular fibrillation
• Ventricular flutter
• Ventricular premature beat
• Ventricular tachycardia
• Ventricular tachycardia: Right Ventricular Outflow Tract (RVOT) tachyardia
• VT versus SVT with aberrancy

W

• Wellens Syndrome
• Wolff-Parkinson White Syndrome

References

• ECG CLINICAL CASES — Your favourite ECG’s placed in clinical context with a challenging Q&A approach
• ECG IMAGE Database — Searchable database of LITFL ECG’s
• ECG and Cardiology Eponymous Syndromes — Cheats guide to eponymous emancipation
• The Art of infarct localisation
• ECG Exam Template — a framework for the FACEM part 2 exam.
• ECG Reference Sites on the WEB — the best of the rest

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Ever wondered what the ultrasound boys do in the ‘sonocave‘?

…tonsillar ultrasound of course!

The guys from UltrasoundVillage provide insight into the procedure of tonsillar ultrasound.

Rationale

Clinically differentiating peritonsillar abscess (quinsy)  from uncomplicated tonsillitits can be difficult. Traditional teaching dictates the uvula should be displaced away from the side of a quinsy, and that a quinsy tends to obliterate the palatoglossal fold.

In reality we find clinical assessment is relatively unreliable…

Tonsillar Ultrasound Technique

• Chose either a sterilised endocavity transducer or a hockey stick transducer for this procedure.
• Cover it with an unused condom.
• Explain the procedure to the patient, reassuring them it is not as bad as it looks!

• Spray the oropharynx with a local anaesthetic ENT spray. Now introduce the transducer carefully with the imaging plane transversely oriented.
• Gently push the transducer against the enlarged tonsil watching for any flow within the area of interest. Add colour Doppler. Record images measuring the size of any collection in both the transverse and longitudinal planes.
• Noting the depth from mucosal surface to collection, and from mucosal surface to carotid gives the proceduralist a sense of relative depths.

Uncomplicated Tonsillitis - Left Tonsillar fossa

Peritonsillar Abscess - Right Tonsillar fossa

Differentiation between solid enlarged tonsil and peritonsillar abscess is made by close observation of the heterogenous predominantly hypoechoic material within the tonsillar area.

• If an abscess has formed subtle movement of the probe will cause the pus to flow within the collection.
• If the tonsillar enlargement remains solid, no such flow occurs.

The addition of colour Doppler also assists. There is no flow within an abscess, whereas an inflamed enlarged but solid tonsil tends to be hyperaemic. In the first case note the vascular flow within the solid tonsil.
In the second case the flash of blue within the image is artefact, not hyperaemia

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

aka ECG Exigency 014

A 67-year old male is brought to hospital by ambulance following an episode of syncope at home. He had just finished eating lunch at home when he developed severe crushing retrosternal chest pain radiating to his left arm, profuse sweating and vomiting. Shortly after the onset of the pain he lost consciousness and awoke to find himself on the floor. En route in the ambulance he has several brief runs of non-sustained VT associated with dizziness and an impalpable radial pulse.

On arrival to ED, his observations are: BP 80/50, HR 130 regular, SaO2 91% on 15L, RR 30. He looks unwell, grey, sweaty and dyspnoeic. Chest exam reveals bilateral basal crepitations extending to the midzones. Heart sounds are normal with no murmurs. This is his ECG…

Click on image to enlarge

Q1. Describe the ECG

Answer and interpretation

 Q2. What is the significance of the ECG changes?

Answer and interpretation

 Q3. What is the electrophysiological basis for the ECG changes?

Answer and interpretation

 Q4. What is the predictive value of these ECG changes?

Answer and interpretation

Click here for a more in-depth look at the relevant literature

Click here for some more ECG examples

Q5. What are the implications of this ECG pattern for the treatment of acute coronary syndromes?

Answer and interpretation

Q6. Can you guess what happened next?

Reveal answer

Acknowledgements

A big thank-you to Perth Emergency Physician Dr Michelle Johnston (@Eleytherius) for providing me with this great case!

Further Reading

The learning material above is reproduced from our Life in the Fastlane ECG library. You can view the original ECG library page here. Also, check out these other recent additions to our ECG library.

• Right ventricular infarction
• Posterior infarction
• Inferior STEMI
• Lateral STEMI
• Pericarditis
• Benign Early Repolarisation

Related Blog Posts

• Dr Smith presents several excellent ECG cases involving ST elevation in aVR
• The great Amal Mattu discusses lead aVR for EMRAP-TV
• “Another Widow Maker” – LITFL’s Peter Allely on LMCA occlusion

References

• Aygul N, Ozdemir K, Tokac M, Aygul MU, Duzenli MA, Abaci A et al. Value of lead aVR in predicting acute occlusion of proximal left anterior descending coronary artery and in-hospital outcome in ST-elevation myocardial infarction: an electrocardiographic predictor of poor prognosis. J Electrocardiol. 2008 Jul-Aug;41(4):335-41 [abstract].
• Barrabes JA, Figueras J, Moure C, Cortadellas J, Soler-Soler J. Prognostic value of lead aVR in patients with a first non-ST-segment ele- vation acute myocardial infarction. Circulation 2003; 108: 814 – 819 [full text].
• Chan TC, Brady WJ, Harrigan RA, Ornato JP and Rosen PR. ECG in Emergency Medicine and Acute Care. Elsevier 2005.
• Engelen DJ, Gorgels AP, Cheriex EC, De Muinck ED, Ophuis AJ, Dassen WR et al. Value of the electrocardiogram in localizing the occlusion site in the left anterior descending coronary artery in acute anterior myocardial infarction. J Am Coll Cardiol. 1999 Aug;34(2):389-95 [full text].
• Eskola MJ, Nikus KC, Holmvang L, et al. Value of the 12-lead electrocardiogram to define the level of obstruction in acute anterior wall myocardial infarction: Correlation to coronary angiography and clinical outcome in the DANAMI-2 trial. Int J Cardiol 2009;131:378–383 [abstract].
• Gorgels AP, Engelen DJ, Wellens HJ. Lead aVR, a mostly ignored but very valuable lead in clinical electrocardiography. J Am Coll Cardiol. 2001 Nov 1;38(5):1355-6 [full text].
• Gorgels AP, Vos MA, Mulleneers R, de Zwaan C, Bär FW, Wellens HJ. Value of the electrocardiogram in diagnosing the number of severely narrowed coronary arteries in rest angina pectoris. Am J Cardiol. 1993 Nov 1;72(14):999-1003 [abstract].
• Gul EE, Nikus KC. An unusual presentation of left anterior descending artery occlusion: significance of lead aVR and T-wave direction. J Electrocardiol. 2011 Jan-Feb;44(1):27-30 [full text].
• Hennings JR, Fesmire FM. A new electrocardiographic criteria for emergent reperfusion therapy. Am J Emerg Med. 2011 Jun 22. Epub ahead of print [abstract].
• Jong G, Ma T, Chou P, et al. Reciprocal changes in 12-lead electrocardiography can predict left main coronary artery lesion in patients with acute myocardial infarction. In Heart J 2006;47:13-20 [full text].
• Kireyev D, Arkhipov MV, Zador ST, Paris JA, Boden WE. Clinical utility of aVR-The neglected electrocardiographic lead. Ann Noninvasive Electrocardiol. 2010 Apr;15(2):175-80 [abstract].
• Kosuge M, Ebina T, Hibi K, Endo M, Komura N, Hashiba K et al. ST-segment elevation resolution in lead aVR: a strong predictor of adverse outcomes in patients with non-ST-segment elevation acute coronary syndrome. Circ J. 2008 Jul;72(7):1047-53 [full text].
• Kosuge M, Ebina T, Hibi K, Morita S, Endo M, Maejima N, et al. An early and simple predictor of severe left main and/or three-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Am J Cardiol. 2011 Feb 15;107(4):495-500 [abstract].
• Kosuge M, Kimura K, Ishikawa T, Ebina T, Shimizu T, Hibi K, et al. Predictors of left main or three-vessel disease in patients who have acute coronary syndromes with non-ST-segment elevation. Am J Cardiol 2005; 95: 1366 – 1369 [abstract].
• Kosuge M, Kimura K, Ishikawa T, Ebina T, Hibi K, Tsukahara K, et al. Combined prognostic utility of ST segment in lead aVR and troponin T on admission in non-ST-segment elevation acute coronary syndromes. Am J Cardiol 2006; 97: 334 – 339 [abstract].
• Kosuge M, Ebina T, Hibi K, Morita S, Komura N, Hashiba K et al. Early, accurate, non-invasive predictors of left main or 3-vessel disease in patients with non-ST-segment elevation acute coronary syndrome. Circ J. 2009 Jun;73(6):1105-10 [full text].
• Kühl JT, Berg RM. Utility of lead aVR for identifying the culprit lesion in acute myocardial infarction. Ann Noninvasive Electrocardiol. 2009 Jul;14(3):219-25 [abstract].
• Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiol. 2008 Nov-Dec;41(6):626-9 [abstract].
• Ozmen N, Yiginer O, Uz O, Kardesoglu E, Aparci M, Isilak Z et al. ST elevation in the lead aVR during exercise treadmill testing may indicate left main coronary artery disease. Kardiol Pol. 2010 Oct;68(10):1107-11 [abstract].
• Pickard AS, Becker RC, Schumock GT, Frye CB. Clopidogrel-associated bleeding and related complications in patients undergoing coronary artery bypass grafting. Pharmacotherapy. 2008 Mar;28(3):376-92 [abstract].
• Rostoff P, Piwowarska W, Konduracka E, Libionka A, Bobrowska- Juszczuk M, Stopyra K, et al. Value of lead aVR in the detection of significant left main coronary artery stenosis in acute coronary syndrome. Kardiol Pol 2005;62:128-37 [abstract].
• Uthamalingam S, Zheng H, Leavitt M, Pomerantsev E, Ahmado I, Gurm GS, Gewirtz H. Exercise-induced ST-segment elevation in ECG lead aVR is a useful indicator of significant left main or ostial LAD coronary artery stenosis. JACC Cardiovasc Imaging. 2011 Feb;4(2):176-86 [abstract].
• de Winter RJ, Verouden NJW, Wellens HJJ, Wilde AAM. A new sign of proximal LAD occlusion. N Engl J Med 2008;359:2071-3 [full text].
• Wiviott SD, Braunwald E, McCabe CH, Montalescot G, Ruzyllo W, Gottlieb S, et al. TRITON-TIMI 38 Investigators. Prasugrel versus clopidogrel in patients with acute coronary syndromes. N Engl J Med. 2007 Nov 15;357(20):2001-15 [abstract].
• Williamson K, Mattu A, Plautz CU, Binder A, Brady WJ. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006 Nov;24(7):864-74 [pdf].
• Wong CK, Gao W, Stewart RA, French JK, Aylward PE, White HD; for the HERO-2 Investigators. The prognostic meaning of the full spectrum of aVR ST-segment changes in acute myocardial infarction. Eur Heart J. 2011 Aug 19 [abstract].
• Yamaji H, Iwasaki K, Kusachi S, Murakami T, Hirami R, Hamamoto H, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol. 2001 Nov 1;38(5):1348-54 [full text].

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

A reader (Christopher Watford) recently contacted the LITFL team with a query regarding a Visual Aid Question (VAQ) from the first sitting of the 2007 examination. So the team set about investigating the validity of the query using the power of social media…

For me, this scenario has been fascinating for a number of reasons

• I have observed first hand the power of social media in medical education. The LITFL team were be able to readily and rapidly access a large number of eminent emergency physicians, cardiologists and electrophysiologists and receive timely and accurate responses.
• This fellowship examination case involves an ECG that has been seen by countless examiners, examinees and registrars in training…yet it has taken 4 years before one astute reader has posted a comment that led us to review, interrogate and question the appropriateness of the scenario ECG
• Is there fear and trepidation surrounding public comment? The fact is that I am sure others have made a similar observation when reviewing this question yet failed to alert us of the issues. Was this lack of feedback associated with emergency physicians being too time-poor, too indecisive or too catatonically apathetic to comment?
• Finally I wonder if the abnormality was actually picked up by the candidates and examiners during the examination marking process but deemed too insignificant to warrant comment in the official examiners report…?

Anyway… Enough hyperbole —here is the VAQ question replicated in full from the first sitting of the fellowship written examinations form 2007 — can you spot the issue?

Scenario

A 49 year old woman presents to your emergency department with central chest pain. His observations are:

Question

a.	Describe and interpret her ECG	(50%)
b.	Outline your disposition considerations	(50%)

Official ACEM Response

ACEM Answer and Interpretation

The pertinent observer

An astute reader writes...

The Cardiologist

The right honorable Dr Wes MD

The Electrophysiologist

The EP Fellow Mark Perrin MD

The Reversal

Tor...can we see what it really looks like?

The KISS principle

Chris Nickson...give us lowly ER docs some take home basics!

References:

• Unrecognised limb lead misplacement Christopher Watford
• Limb Lead reversal Mark Perrin
• Incorrect electrode cable connection during electrocardiographic recording  Velislav N. Batchvarov  Europace (2007) 9, 1081–1090  [doi:10.1093/europace/eum198]

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Here’s another volume from LITFL’s ever growing ECG Library — all you need to know about the ECG diagnosis of right ventricular infarction.

Check out the rest of the entries in our ECG A to Z by diagnosis.

Clinical Significance

• Right ventricular infarction complicates up to 40% of inferior STEMIs. Isolated RV infarction is extremely uncommon.
• Patients with RV infarction are very preload sensitive (due to poor RV contractility) and can develop severe hypotension in response to nitrates or other preload-reducing agents.
• Hypotension in right ventricular infarction is treated with fluid loading, and nitrates are contraindicated.

The ECG changes of RV infarction are subtle and easily missed!

How to spot right ventricular infarction

The first step to spotting RV infarction is to suspect it… in all patients with inferior STEMI!

In patients presenting with inferior STEMI, right ventricular infarction is suggested by the presence of:

• ST elevation in V1 — the only standard ECG lead that looks directly at the right ventricle.
• ST elevation in lead III > lead II — because lead III is more “rightward facing” than lead II and hence more sensitive to the injury current produced by the right ventricle.

Other useful tips for spotting right ventricular MI (as described by Amal Mattu and William Brady in ECGs for the Emergency Physician):

• If the magnitude of ST elevation in V1 exceeds the magnitude of ST elevation in V2.
• If the ST segment in V1 is isoelectric and the ST segment in V2 is markedly depressed.
• NB. The combination of ST elevation in V1 and ST depression in V2 is highly specific for right ventricular MI.

Right ventricular infarction is confirmed by the presence of ST elevation in the right-sided leads (V3R-V6R).

Right-sided leads

There are several different approaches to recording a right-sided ECG:

• A complete set of right-sided leads is obtained by placing leads V1-6 in a mirror-image position on the right side of the chest (see diagram, below).
• It may be simpler to leave V1 and V2 in their usual positions and just transfer leads V3-6 to the right side of the chest (i.e. V3R to V6R).
• The most useful lead is V4R, which is obtained by placing the V4 electrode in the 5th right intercostal space in the midclavicular line. ST elevation in V4R has a sensitivity of 88%, specificity of 78% and diagnostic accuracy of 83% in the diagnosis of RV MI.

Reproduced from Morris and Brady, 2002. Click image for link to original reference.

NB. ST elevation in the right-sided leads is a transient phenomenon, lasting less than 10 hours in 50% of patients with RV infarction.

Example ECGs

Inferior STEMI. Right ventricular infarction is suggested by:

• ST elevation in V1
• ST elevation in lead III > lead II

Repeat ECG of the same patient with V4R electrode position:

• There is ST elevation in V4R consistent with RV infarction

Another example of right ventricular MI:

• There is an inferior STEMI with ST elevation in lead III > lead II.
• There is subtle ST elevation in V1 with ST depression in V2.
• There is ST elevation in V4R.

This ECG shows a full set of right-sided leads (V3R-V6R), with V1 and V2 in their original positions. RV infarction is diagnosed based on the following findings:

• There is an inferior STEMI with ST elevation in lead III > lead II.
• V1 is isoelectric while V2 is significantly depressed.
• There is ST elevation throughout the right-sided leads V3R-V6R.

Related Topics

• Posterior infarction

Further Reading

• ECG BASICS – Waves, Intervals, Segments and Clinical Interpretation
• ECG CLINICAL CASES – Your favourite ECG’s placed in clinical context with a challenging Q&A approach
• ECG and Cardiology Eponymous Syndromes – Cheats guide to eponymous emancipation
• ECG Reference Sites on the WEB – the best of the rest

References

• Mattu A, Brady W. ECGs for the Emergency Physician 1, BMJ Books 2003.
• Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
• Morris F, Brady WJ. ABC of clinical electrocardiography: Acute myocardial infarction-Part I. BMJ. 2002; 324: 831-4. [full text]
• Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002; 324: 963-6. [full text]
• Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog

Part of the LITFL site development includes upgrading, updating or just simply writing simple striaghtforward reviews of day-t0-day clinical cases. As such we are working our way through the ECG library (mainly for our own benefit) and thought it would be cool to share some of these musings

Clinical Significance

• Posterior infarction accompanies 15-20% of STEMIs, usually occurring in the context of an inferior or lateral infarction.
• Isolated posterior MI is less common (3-11% of infarcts).
• Posterior extension of an inferior or lateral infarct implies a much larger area of myocardial damage, with an increased risk of left ventricular dysfunction and death.
• Isolated posterior infarction is an indication for emergent coronary reperfusion. However, the lack of obvious ST elevation in this condition means that the diagnosis is often missed.

Be vigilant for evidence of posterior MI in any patient with an inferior or lateral STEMI.

How to spot posterior infarction

As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal changes of STEMI are sought in the anteroseptal leads V1-3.

Posterior MI is suggested by the following changes in V1-3:

• Horizontal ST depression
• Tall, broad R waves (>30ms)
• Upright T waves
• Dominant R wave (R/S ratio > 1) in V2

In patients presenting with ischaemic symptoms, horizontal ST depression in the anteroseptal leads (V1-3) should raise the suspicion of posterior MI.

• Typical appearance of posterior infarction in V2

Posterior infarction is confirmed by the presence of ST elevation and Q waves in the posterior leads (V7-9).

Explanation of the ECG changes in V1-3

The anteroseptal leads are directed from the anterior precordium towards the internal surface of the posterior myocardium. Because posterior electrical activity is recorded from the anterior side of the heart, the typical injury pattern of ST elevation and Q waves becomes inverted:

• ST elevation becomes ST depression
• Q waves become R waves
• Terminal T-wave inversion becomes an upright T wave

The progressive development of pathological R waves in posterior infarction (the “Q wave equivalent”) mirrors the development of Q waves in anteroseptal STEMI.

• This picture illustrates the reciprocal relationship between the ECG changes seen in STEMI and those seen with posterior infarction. The previous image (depicting posterior infarction in V2) has been inverted. See how the ECG now resembles a typical STEMI!

Posterior leads

Leads V7-9 are placed on the posterior chest wall in the following positions (see diagram below):

• V7 – Left posterior axillary line, in the same horizontal plane as V6.
• V8 – Tip of the left scapula, in the same horizontal plane as V6.
• V9 - Left paraspinal region, in the same horizontal plane as V6.

Reproduced from Morris and Brady, 2002. Click image for link to original reference.

The degree of ST elevation seen in V7-9 is typically modest – note that only 0.5 mm of ST elevation is required to make the diagnosis of posterior MI!

Example ECGs

Example 1

Inferolateral STEMI. Posterior extension is suggested by:

• Horizontal ST depression in V1-3
• Tall, broad R waves (> 30ms) in V2-3
• Dominant R wave (R/S ratio > 1) in V2
• Upright T waves in V2-3

The same patient, with posterior leads recorded. Marked ST elevation in V7-9 with Q-wave formation confirms involvement of the posterior wall, making this an inferior-lateral-posterior STEMI (= big territory infarct!).

Example 2

In this ECG, posterior MI is suggested by the presence of:

• ST depression in V2-3
• Tall, broad R waves (> 30ms) in V2-3
• Dominant R wave (R/S ratio > 1) in V2
• Upright terminal portions of the T waves in V2-3

(The ECG changes extend out as far as V4, which may reflect superior-medial misplacement of the V4 electrode from its usual position).

• The same patient, with posterior leads recorded. Posterior infarction is diagnosed based on the presence of ST segment elevation >0.5mm in leads V7-9.
• Note that there is also some inferior STE in leads III and aVF (but no Q wave formation) suggesting early inferior involvement.

Example 3

The ST depression and upright T waves in V2-3 suggest posterior MI. There are no dominant R waves in V1-2, but it is possible that this ECG was taken early in the course of the infarct, prior to pathological R-wave formation. There are also some features suggestive of early inferior infarction, with hyperacute T waves in II, III and aVF.

An ECG of the same patient taken 30 minutes later: there is now some ST elevation developing in V6. With the eye of faith there is perhaps also some early ST elevation in the inferior leads (lead III looks particularly abnormal).

ECG #3. The same patient with posterior leads recorded. Posterior infarction is confirmed by the presence of ST elevation >0.5mm in leads V7-9.

Related Topics

• Right ventricular infarction

Further Reading

• ECG BASICS – Waves, Intervals, Segments and Clinical Interpretation
• ECG CLINICAL CASES – Your favourite ECG’s placed in clinical context with a challenging Q&A approach
• ECG and Cardiology Eponymous Syndromes – Cheats guide to eponymous emancipation
• ECG Reference Sites on the WEB – the best of the rest

References

• Edhouse J, Brady WJ, Morris F. ABC of clinical electrocardiography: Acute myocardial infarction-Part II. BMJ. 2002; 324: 963-6. [full text]
• Mattu A, Brady W. ECGs for the Emergency Physician 2, BMJ Books 2008.
• Morris F, Brady WJ. ABC of clinical electrocardiography: Acute myocardial infarction-Part I. BMJ. 2002; 324: 831-4. [full text]
• Phibbs BP. Advanced ECG: Boards and Beyond (second edition). Elsevier 2006.
• Surawicz B, Knilans T. Chou’s Electrocardiography in Clinical Practice (6th edition), Saunders 2008.
• Van Gorselen EO, Verheugt FW, Meursing BT, Oude Ophuis AJ. Posterior myocardial infarction: the dark side of the moon. Neth Heart J. 2007; 15: 16-21.

Life in the Fast Lane Medical Blog - Emergency Medicine education blog