Killer ECG Patterns Flashcards
25-year-old with exertional dizziness.
Voltage criteria for left ventricular hypertrophy (LVH) — S wave in V1 + R wave in V5 > 35mm (note there are many different ways of measuring voltage criteria for LVH)
Deep, narrow Q waves in lateral leads I, aVL, V5-6
Dx: Hypertrophic Cardiomyopathy (HCM)
Patients with an ECG suggestive of HCM who are symptomatic require immed
17-year-old noticed “high” heart rate on Apple watch.
On first glance this ECG may appear to represent left ventricular hypertrophy, as we see large voltage QRS complexes and ST/T wave abnormalities in lateral leads.
However, on closer inspection, other abnormalities are present:
Very short PR interval (< 120ms)
Broad QRS complexes with a slurred upstroke to the QRS complexes – the delta wave
Dx: Wolff-Parkinson-White Syndrome (WPW)
Identification of a short PR interval and a delta wave on the ECG only confirms the presence of a WPW pattern. The diagnosis of WPW syndrome is made when there is a history or subsequent development of an arrhythmia.
The preferred long-term approach for patients with an accessory pathway is ablation. In the acute setting, knowledge of the presence of an accessory pathway is critical as some standard therapies for tachyarrhythmias may cause clinical deterioration in patients with WPW.
75-year old with atypical chest pain.
Sinus tachycardia ~120 bpm
Low QRS voltages
Electrical alternans (= alternating tall and short QRS complexes)
Dx: The combination of low QRS voltages and electrical alternans is highly suggestive of massive pericardial effusion. The addition of sinus tachycardia is concerning for pericardial tamponade.
This patient needs an immediate bedside echo to confirm the presence of
30-year old with palpitations.
Right axis deviation
Dominant R wave in V1
Widespread T-wave inversion in inferior (II, III, aVF) and precordial leads (V1-6)
Localised subtle widening of QRS complexes in V1-3
A small blip following each QRS complex, best seen in V1 and the inferior leads — this is known as an Epsilon wave
Dx:
Right axis deviation and a dominant R wave in V1 are signs of Right Ventricular Hypertrophy (RVH)
Concurrent T-wave inversion in inferior and right precordial (V1-3) reflect a Right Ventricular Strain pattern, and are another sign of RVH
These findings, along with localised QRS widening in V1-3 and the presence of Epsilon waves, are highly suggestive of Arrhythmogenic Right Ventricular Dysplasia (ARVD)
Echocardiography is the first-line investigation, and may demonstrate a
60-year old with shortness of breath.
Severe bradycardia (HR ~ 30 bpm)
Flattening, broadening and near-disappearance of P waves (still barely visible in V1-3)
Prolongation of the PR interval
Broad QRS complexes (~120 ms)
Symmetrically peaked T waves in V2-5
Dx: Severe hyperkalaemia
This patient presented to ED with pulmonary oedema after missing several dialysis sessions. Shortly after this ECG was taken, her HR dropped to < 10 bpm with no palpable pulse requiring a brief period of CPR. ROSC was rapidly achieved following empirical administration of IV calcium gluconate. Bedside VBG taken on arrival later revealed a K+ of 7.9.
30-year old with drowsiness.
Sinus tachycardia ~110 bpm — P waves are visible in V2
Borderline 1st degree AV block
Broad QRS complexes (120 ms, or 3 small squares)
Dominant R’ wave in lead aVR
Dx: The combination of broad QRS complexes and a dominant R’ wave in aVR is strongly suggestive of poisoning with a sodium-channel blocking agent. The most commonly encountered examples include:
Tricyclic antidepressants (TCAs)
Propranolol
Carbamazepine
Type IA and IC antiarrhythmics (quinidine, procainamide, flecainide)
Local anaesthetics
Cocaine
These agents can cause seizures and cardiotoxicity (hypotension, broad-complex tachycardia) in overdose.
TCAs also cause tachycardia due to their anticholinergic effects, whilst propranolol can cause bradycardia due to beta-blocking effects.
Other mimics that can cause this ECG pattern include hyperkalaemia and Brugada Syndrome. Always consider these differentials and correlate with the clinical context.
25-year old with collapse, apparently alcohol intoxicated.
Widespread, giant T wave inversions
Grossly prolonged QT interval (~ 600ms)
Dx: This ECG pattern is characteristic of **raised intracranial pressure ** and is classically seen in the context of massive intracranial haemorrhage, particularly:
Spontaneous subarachnoid haemorrhage
Haemorrhagic stroke / intraparenchymal haemorrhage
Similar ECG patterns have also been reported in patients with raised ICP due to:
Large-territory ischaemic stroke causing cerebral oedema (e.g. MCA occlusion)
Traumatic brain injury
The main differential diagnosis for widespread “giant” T-wave inversion such as this is apical hypertrophic cardiomyopathy (HCM). Although myocardial ischaemia and electrolyte abnormalities can cause widespread T-wave inversion and QT prolongation, neither condition would cause the gigantic “cerebral T waves” seen here.
40-year old with syncope.
At first glance, this ECG may appear normal with no evidence of arrhythmia or AV block to explain the syncopal episode. However, on closer inspection there are some localised abnormalities in the right precordial leads V1 and V2:
RBBB-like pattern with secondary R’ wave following the QRS complex
ST elevation at the J point > 2mm with a “coved” morphology — the ST segment slopes diagonally downwards from the J point, with a slight upward convexity best appreciated in V2
Associated T wave inversion
Dx: In a patient presenting with syncope, this ECG pattern is diagnostic of Brugada Syndrome.
Brugada syndrome is:
An arrhythmogenic sodium channelopathy caused by a mutation in the cardiac sodium gene — this can be inherited or spontaneous
Most common in South East Asian males, with presentation around age 40
Associated with increased risk of paroxysmal ventricular arrhythmias (polymorphic VT, VF) and sudden cardiac death
Patients present with:
Sudden cardiac death
Symptomatic ventricular arrhythmias (paroxysmal syncope, seizure-like events, nocturnal agonal respirations)
Asymptomatic – after family screening or incidental finding on ECG recording
The only effective treatment is insertion of an implantable cardioverter-defibrillator (ICD).
Diagnosis of Brugada syndrome requires both:
**Diagnostic (Type 1) ECG pattern **– either spontaneously, or during pharmacological challenge with class I antiarrhythmics
At least one clinical criterion
Clinical Criteria:
1. Positive family history: Sudden cardiac death in family member aged < 45; type 1 ECG pattern in family member
2. Arrhythmia-related symptoms: Cardiac syncope; seizure-like events; nocturnal agonal respirations
3. Documented ventricular arrhythmias: Polymorphic ventricular tachycardia (PVT); ventricular fibrillation (VF)
Diagnostic difficulties arise when faced with patients that do not meet the above criteria, for example:
Idiopathic type 1 ECG
Type 2 or 3 ECG pattern
