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The “3 SIMPLE Rules”: an easy and accurate tool for recognizing VT

17 Dic
Following the discussion on ectopy and aberrancy (view Ectopy or aberrancy? Google Ecg+ community comments on a clinical case.)  Ken Grauer, EKG master and author of many EKG books, gave us the permission to share his “3 SIMPLE Rules” to recognize VT in a simple ad accurate way.
 
  • Rule #1 Is there extreme axis deviation during WCT

Extreme axis deviation is easy to recognize. The QRS complex will be entirely negative in either lead I or lead aVF. The presence of extreme axis deviation during a WCT rhythm is virtually diagnostic of VT.
  • Rule #2 Is lead V6 all (or almost all) negative?

IF ever the QRS in lead V6 is either all negative (or almost all negative)  then VT is highly likely.
  • Rule #3 Is the QRS during WCT “ugly”?

The “uglier” the QRS the more likely the rhythm is. VT originates from a ventricular focus outside of the conduction system. As a result VT is more likely to be wider and far less organized (therefore “uglier”) in its conduction pattern
 
The “3 simple rules” is an extract from ACLS 2013 Arrhythmias  where you can find the complete explanation and much more on arrhythmias.
Visit Ken Grauer Amazon page to find out more and discover all the amzing EKG books he wrote. They are accurate and reliable for use in many emergency situation.
I’ll include Ken’s reply in the main script of the post cause it contains some very important adjuncts and expalnations. At the end of the replay you’ll find the link to download the full text of the section regarding the WCT topic. You’ll also appreciate the perfect Ken’s italian. I’m amazed….
Molto grazie Mario per la pubblicazione del mio consiglio su le tre semplici regole per diagnosticare VT! I’ll make a few brief additions to what Mario wrote. RULE #1 – Remember that slight or even moderate axis deviation is of no help. The QRS complex must be ALL negative in either lead I or in lead aVF. If it is – then the rhythm is almost always VT. RULE #2 – Again, moderate negativity in lead V6 is common and means nothing. But if the QRS complex in lead V6 is either all negative or shows no more than a tiny r wave – then VT is likely. This is because such marked negativity in lead V6 implies that the impulse is moving away from the apex – and that almost always means VT. RULE #3 – Supraventricular rhythms with either preexisting bundle branch block or aberrant conduction typically resemble some form of conduction defect (ie, either RBBB, LBBB or RBBB with LAHB and/or LPHB). However, if the QRS complex is amorphous (ie, very “ugly” and formless) – then it is much more likely to be originating from the ventricles. Occasionally, patients may have unusual forms of IVCD – so this rule is not 100% accurate – but it is a helpful supportive point in the differential diagnosis. For those wanting more complete description of the 3 Rules (and other pointers in assessing wide tachycardias) – feel free to download these Sections from my ACLS-2013-ePub – GO TO – https://www.dropbox.com/s/8bc9h5cumo7e4vy/8.0%2C9.0%2C10.0-%20ACLS-2013-e-PUB-WCT-Criteria-%2810-13.11-2014%29-LOCK.pdf?dl=0 – Detailed description of the 3 Simple Rules begins in Section 08.17. Spero che questo vi aiuta.”
Ken Grauer
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Ectopy or aberrancy? Google Ecg+ community comments on a clinical case.

16 Dic
 75 yrs old female, confused, chest pain and hypotensive. Below ypu can see the 12 leads EKG pre and post cardioversion

TVCardioversion

EK post cardio

The question about ectopy and aberrancy, even if of minor influence on theraphy that was based on clinical presentation, was interestingly debated in ECG+ community.

Prof. Ken Grauer and other members of community gave the solution on why the above 12 leads EKG was, with good approximation, referrable to a VT and not to a SVT conducted with aberrancy.

Those are the EKG criteria they individuated:

  1. Extreme axis “northwest axis”: (neg in lead I, positive in lead aVR);
  2. Lead V1 is amorphous
  3. Lead V6 is almost all negative
  4. No diphasic RS complexes in any of the precordial leads
  5. Monophasic R-wave in lead V1(taller left “rabbit-ear”)
  6. Diphasic QR complexes in leads V2 and V3.
  7. Monophasic QS complexes in leads V4, V5, and V6.
  8. Josephson’s sign (notching on the nadir of S wave)

Those criteria, even if present in this case, are universally valid.

If you want to discover more on this topic MEDEST already posted on this topic in a previous post

There you can find alle the references on EKG criteria for differential diagnosis between ectopy and aberrancy in wide comples tachycardia.

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Do You…..Torsade?

13 Mag

 

26 yrs old female with PM/ICD implanted for conenital Long QT Syndrome referring one syncopal episode before our arrival.
3 more consecutive episodes occurred during the observation.
Torsade

EKG records during syncopal episodes (click to enlarge)

The 12 Leads EKG is also shown.
Torsade 12 Leads

12 leads EKG of the case (click to enlarge)

The symptoms (and the EKG findings ) stopped after Amio 150 mg. The patients was asyntomatic until the arrival in ED.
If the ryhthm during syncopal episodes is pretty clear, the 12 L EKG analysys is really intriguing.
The PM is in VVI mode, but it looks like the atrial sensing is not working and so the ventricle is contracting at his own pace resulting in a rate of 45 bpm. At this rate, as shown on the 12 leads EKG, the QTc is 552 ms (normal value <460 ms in women). This increases the probability of torsade.
It looks like even the ICD is not working properly cause of the absence of shock despite the duratio of Torsade.
In conclusion, malfunctioning PM inducing bradycardia and Torsade. (Very)Suspected malfunctioning ICD.
Amio is not the appropriate therapy (but still an option) in this case.
Magnesium 2 mg is the first choice therapy for Torsade. Lido and isopreterenolo are other reasonable options.
To learn more:
Further readings:

MEDEST you tube

 

 

 

ST↑ in aVR: un’alterazione di tutto rispetto

16 Apr

homer_the_scream

Qualche mese fa MEDEST ha pubblicato un post in merito ad un caso clinico in cui un ECG con alterazione del tratto ST in aVR era stato trascurato per un atteggiamento di diffusa sufficienza con cui molti clinici guardano alle alterazioni presenti in questa derivazione.

Approfittiamo di questo ECG, registrato ieri a domicilio in un paziente di con dolore toracico, per puntualizzare alcuni concetti fondamentali riguardo alle alterazioni del tratto ST in aVR:

STE aVR_c

Click to enlarge/Clicca per ingrandire

  • L’elevazione del tratto in ST↑ ≥1 mm in aVR, nel contesto di diffuse alterazioni ischemiche (ST↓), è un segno ischemico molto grave, patognomonico per occlusione del tronco comune (LMCA), della discendente anteriore (LAD) o di malattia dei tre vasi (3VD)
  • I pazienti con ST↑ ≥1 mm in aVR e clinica tipica devono essere sottoposti PTCA in urgenza
  • L’assenza di ST↑ in aVR esclude con molta accuratezza la probabilità di occlusione del tronco comune
  • I criteri sopra esposti non sono applicabili in caso di TPSV o in assenza di segni clinici di ischemia
  • ST ↑ in aVR+ST↑ in aVL indicano occlusione del tronco comune (LMCA)
  • ST ↑ in aVR+ST↑ in V1 indicano occlusione del tronco comune (LMCA) o della discendente anteriore (LAD)
    • ST ↑ in aVR >ST↑ in V1 fa sospettare l’occlusione del tronco comune (LMCA) piuttosto che quello della discendente anteriore (LAD)
  • ST↑ in aVR ≥ 1mm è associato con un aumento fino a 6 volte della mortalità
  • ST↑ in aVR ≥ 1.5mm è associato ad una mortalità che può andare dal 25% al 70%

In conclusione aVR merita più considerazione, perchè il rilievo di ST↑ in questa derivazione indica lesioni a carico di vasi motlo critici per la circolazione coronarica e la prognosi di questi pazienti è altamente sfavorevole.

MEDEST you tube

 

 

 

References:

  1. aVR the forgotten lead
  2. ST Elevation in aVR – LMCA occlusion?
  3. aVR The Neglected Lead
  4. Williamson K, Mattu A, Plautz CU, et al. Electrocardiographic applications of lead aVR. Am J Emerg Med. 2006 Nov;24(7):864-74
  5. Rokos IC, French WJ, Mattu A, et al. Appropriate cardiac cath lab activation: optimizing the electrocardiogram interpretation and clinical decision making for acute ST-elevation myocardial infarction. Am Heart J. 2010 Dec; 160(6):995-1003
  6. Nikus KC, Eskola MJ. Electrocardiogram patterns in acute left main coronary artery occlusion. J Electrocardiology. 2008 Nov-Dec;41(6):626-9
  7. Kosuge M, Ebina T, Hibi K, et at. 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
  8. Nikus K, Pahlm O, Wagner G, et al. Electrocardiographic classification of acute coronary syndromes: a review by a committee of the International Society for Holter and Non-Invasive Electrocardiology. 2010 Mar-Apr;43(2):93, 97-98
 

 

Dolore epigastrico in diabetica

28 Mag

Download English transcript

ECG pediatrico in emergenza

11 Gen

Chi non ha mai avuto dubbi sull’interpretazione dell’ECG pediatrico?

Frequenza, ritmo, morfologia sono completamente diversi da quello dell’adulto, ed alcuni aspetti a prima vista molto “pericolosi” sono in realtà assolutamente normali nel bambino.

In questo breve video-podcast Amal Mattu rivede alcuni concetti base dell’ECG pediatrico.

Non un compendio completo di elettrocardiografia pediatrica ma alcuni utlissimi concetti che possono migliorare la pratica quotidiana.

ECG seriati e cambiamenti dinamici del tratto ST

7 Gen

Uomo di 67 anni riferisce dolore toraico tipico, risolto al momento del primo contatto medico.

Durante il trasporto verso l’ospedale di zona (non PTCA) lamenta recrudescenza dei sintomi.

Vengono registrati ECG seriati che dimostrano cambiamenti dinamici in senso ischemico del tratto ST in sede anteriore.

(Clicca sulle immagini per ingrandirle)

ECG1ECG2ECG3

Immediatemente dirottato verso il vicino centro di emodinamica dove viene sottoposto a PTCA che dimostra occlusione critica con placca instabile dell’IVA.

Il tempo tra il primo contatto medico e la PTCA è di 35 min.

Gli ECG seriati ed il monitoraggio del trend del tratto ST devono essere ritenuti una manovra standard nella gestione del dolore toracico in medicina d’urgenza preospedaliera.

Dizziness and amyloidosis in prehospital.

4 Gen

68 years old male referring dizziness and lighthead. Denies chest pain.

Pale cold sweating is laying on bed. Chest and abdominal examination are negative. Cardiac examination reveals arrithmiyc tones and free pauses. No smoking no diabetes.

His past history is positive for cardiac amyloidos  (proteinuria Bence Jones k)  triple A surgically corrected many years ago. Hypertension and AFib farmacologiccally cardioverted 1 year ago.  He is in treatment with Propafenone 150×4, Ramipril and Warfarin. No smoking no diabetes.

This morning ha did a routine control ECG and echo. All the parameters where fine. The documentation is not with him right now so is not possible a proper confrontation with the actual findings.

Vital signs:

BP is 70/50, satO2 room air 98%.

The 12 leads EKG is shown below

12 der

and a longer monitor recording….

strip

Which are the EKG findings?

When the patient is invited to stand refers presyncopal signs and tends to faint. BP drops and the skin become pale and sweaty

Which is the racommended management?

Blood exams are normal except TnI tha is slightly elevated (0,23) and the INR is 3

Which is your diagnosis?

Episodio presincopale in Amiloidosi cardiaca

3 Gen

Uomo di 68 anni riferisce da alcune ore sensazione presincopale, senso di testa vuota, sudorazione algida.

E’ pallido e sudato. Giace disteso sul letto con le gambe sollevate. Torace ed addome negativi, obiettività neurologica nei limiti.

La sua storia patologica parla di un’amiloidosi AL (prevalentemente cardica, con proteinuria di BJ cat. K, funzione renale conservata), di un pregresso intervento per endoprotesi su AAA. E’ Iperteso in trattamento con ramipril. Un anno fa ha avuto un episodio di FA persistente cardiovertita farmacologicamente. Da allora assume Rytmonorm 150×4 e Coumadin. Non fuma, non è diabetico.

Questa matitna aveva effettuato un ECG ed un Ecocardiogramma di controllo che lui riferisce come nella norma ma di cui non esibisce la documentazione.

La PA attuale è 70/50, satO2 in aria 98%.

Questo è l’ECG a 12 derivazioni.

12 der

e questa una stirp più lunga per una migliore definizione del ritmo

strip

Qual’è la diagnosi elettrocardiografica?

Il paziente appena invitato a mettersi seduto lamenta senso di svenimento, diventa pallido e compare sudorazione algida. I sintomi regrediscono in clinostatismo.

Cosa fareste a questo punto?

Il profilo ematochimico in DEA è nella norma (emocromo, elettroliti, creatinina, funz epatica, pancreatica e glicemia) a parte un lieve movimento degli enzimi cardiaci (TnI 0,23) e 3 di INR.

Qual’è la vostra ipotesi diagnostica?

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