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ECGs: Life in the fast lane
Terms in this set (9)
10 Causes of T wave inversion in V 1-3
Right bundle branch block
Right ventricular hypertrophy
Raised intracranial pressure
Normal paediatric ECG
Persistent juvenile T wave pattern
Left ventricular hypertrophy - TWI V5-6, I and aVL.
What does this ecg show.
The de Winter ECG pattern is an anterior STEMI equivalent that presents without obvious ST segment elevation.
Key diagnostic features include ST depression and peaked T waves in the precordial leads.
The de Winter pattern is seen in ~2% of acute LAD occlusions and is under-recognised by clinicians.
Unfamiliarity with this high-risk ECG pattern may lead to under-treatment (e.g. failure of cath lab activation), with attendant negative effects on morbidity and mortality.
Some authors have proposed that the de Winter pattern should be considered a "STEMI equivalent", and that patients with chest pain and this ECG pattern should receive emergent reperfusion therapy with PCI or thrombolysis.
Tall, prominent, symmetric T waves in the precordial leads
Upsloping ST segment depression >1mm at the
J-point in the precordial leads
Absence of ST elevation in the precordial leads
ST segment elevation (0.5mm-1mm) in aVR
"Normal" STEMI morphology may precede or follow the deWinter pattern
What are the causes of T wave inversion and long QT.
1. Raised ICP - SAH or large haemorrhagic stroke.
2. Myocardial ischaemia
Name 8 ECG changes of hypokalaemia.
At what potassium level do ECG changes occur.
Changes appear when K+ < 2.7 mmol/l
Increased amplitude and width of the P wave
Prolongation of the PR interval
T wave flattening and inversion
Prominent U waves (best seen in the precordial leads)
Apparent long QT interval due to fusion of the T and U waves (= long QU interval)
With worsening hypokalaemia:
Frequent supraventricular and ventricular ectopics
Supraventricular tachyarrhythmias: AF, atrial flutter, atrial tachycardia
Potential to develop life-threatening ventricular arrhythmias, e.g. VT, VF and Torsades de Pointes
What does this ECG show.
What are your differentials.
What features on ECG suggest VT (rather than SVT with aberrancy)
This ECG shows a regular broad complex tachycardia with an RSR' pattern in V1.
The differential diagnosis could include:
SVT with aberrant conduction — either due to RBBB or WPW.
On closer inspection, the ECG demonstrates some classic features of ventricular tachycardia:
Northwest axis — QRS is positive in aVR, negative in I and aVF.
The taller left rabbit ear sign — There is an atypical RBBB pattern in V1, where the left "rabbit ear" is taller than the right.
Negative QRS complex (R/S ratio < 1) in V6.
These findings indicate VT rather than SVT with aberrancy.
Other factors that increase the likelihood of VT in patients presenting with regular broad complex tachycardia include:
Age > 35 (positive predictive value of 85%).
Structural heart disease — e.g. IHD, CCF, cardiomyopathy.
Family history of sudden cardiac death or arrhythmogenic conditions such as HOCM, Brugada syndrome or ARVC that are associated with episodes of VT.
In any patient with a broad complex rhythm, also consider the possibility of toxic / metabolic conditions such as hyperkalaemia or sodium-channel blockade.
What are the differentials for a narrow complex tachycardia.
What is the diagnosis of this ECG.
When you see a regular narrow complex tachycardia at 150 bpm, you should think of four main diagnoses:
1. Atrial flutter with 2:1 block (especially in elderly, IHD, CCF)
2. AV-nodal reentry tachycardia ("SVT")
3. Orthodromic AV reentry tachycardia in WPW
4. Sinus tachycardia —
should see P waves but may be hidden in the T waves (e.g. with concurrent 1st degree AV block). There should also be some HR variability compared to the other 3 rhythms.
The patient's young age and presence of retrograde P waves (pseudo R' waves) suggest a paroxysmal reentry tachycardia involving the AV node — either AVNRT ("SVT") or orthodromic AVRT.
The next step is a therapeutic trial of vagal maneouvres and/or adenosine.
What does this ECG show.
Runs of tachycardia are interspersed with long sinus pauses (up to 6 seconds).
The sinus rate is extremely slow, varying from 40 bpm down to around 10 bpm in places.
Sinus beats are followed by paroxysms of junctional tachycardia at around 140 bpm.
This is a good example of sick sinus syndrome leading to the tachycardia-bradycardia syndrome.
The flurries of junctional tachycardia are a compensatory phenomenon attempting to maintain cardiac output in the face of critically low sinus node rates.
The syncope likely occurred due to a long sinus pause with temporary loss of cardiac output.
This patient needs a pacemaker!
What is the dose of verapamil in SVT.
Initial dose: 5 to 10 mg (0.1 mg/kg) given as an IV bolus over at least 2 minutes.
Repeat dose: 10 mg (0.15 mg/kg) 30 minutes after the first dose if the initial response is not adequate.
An optimal interval for subsequent doses has not been determined and must be individualized for each patient.
Initial dose: 2.5 to 5 mg
If no response in 15 to 30 minutes and no side effects seen: 5 to 10 mg every 15 to 30 minutes to a maximum total dose of 20 mg
Alternative ACLS dosing regimen:
Initial dose: 5 mg
If no response in 15 minutes and no side effects seen: 5 mg every 15 minutes up to a total dose of 30 mg
What does this ECG show.
SVT: (Fast-Slow AVNRT)
Narrow complex tachycardia ~ 135 bpm.
Retrograde P waves following each QRS complex — upright in aVR and V1; inverted in II, III and aVL.
After treatment these retrograde P waves disappear.
Remember there are three sub-types of SVT:
1. No visible P waves? -> Slow-Fast (80-90%)
2. P waves visible after the QRS complexes? -> Fast-Slow (10%)
3. P waves visible before the QRS complexes? -> Slow-Slow (1-5%)
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