ECG cases 2.0 Flashcards
A 61-year-old lady is brought in by ambulance with palpitations and dizziness. GCS 15. HR 190, BP 75/50.
What does the ECG show?
What are the causes of conduction delay? What cause it is here and why?
Management?
Irregularly irregular broad complex tachycardia, rate ~190 bpm
Right axis deviation
AF
Conduction delay may be due to aberrancy (right bundle branch block) or pre-excitation.
Accessory pathway in this case
-Extremely rapid ventricular rates – up to 300 bpm in some places. This is too rapid to be conducted via the AV node
-Beat-to-beat variation in QRS morphology
DC cardioversion
What does this show?
left lateral Accessory pathway
Sinus rhythm, rate 90 bpm
Normal P wave axis, persistent right axis deviation
PR interval is relatively short at ~120ms, and there are broad QRS complexes with a slurred upstroke to the QRS complex – the delta wave
Dominant R wave in V1 – this is associated with a left-sided AP and is sometimes termed a Type A Wolff-Parkinson-White (WPW) pattern
Negative delta wave in aVL simulates the Q waves of lateral infarction – this is known as the “pseudo-infarction pattern”
Management of a pre-excitation AF? If Unstable? Stable? Long term? What do you avoid and why?
Shocked -> DC cardioversion
Stable - procainamide
Ablation
Avoid AV nodal blocking drugs (e.g. adenosine, calcium channel blockers, beta blockers)
[Most APs have a shorter refractory period than the AV node, hence the ventricular rate can be more rapid if AV conduction occurs preferentially via the AP
Normally, anterograde conduction occurs via both the AP and AV node, and these wavefronts fuse in the ventricles. Conduction through the AV node is actually a brake on AP conduction, ceasing its propagation path in the ventricle -> VT/VF]
procainamide mechanism
Na channel blocker - class I antiarrhythmic that targets the AP
Prolongs action potential duration in atrial and ventricular myocardium
No AV nodal blocking effect
Effective in both reversion, and in slowing ventricular rate
Safe in children
What are the 2 types of tachyarrhythmia in WPW
Atrial fibrillation or flutter. Due to direct conduction from atria to ventricles via an AP, bypassing the AV node (as in our patient above)
Atrioventricular re-entry tachycardia (AVRT). As the name suggests, this is due to formation of a re-entry circuit involving the AP and AV node
In AF when would you suspect an accessory pathway?
extremely rapid ventricular rates
beat-to-beat variation in QRS
ecg of wpw shows?
PR interval < 120ms
Delta wave: slurring slow rise of initial portion of the QRS
QRS prolongation > 110ms
Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major component of the QRS complex)
Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction)
Why do you get the delta wave in WPW?
impulses bypassing the AV node via an AP
WPW
Sinus rhythm with a very short PR interval (< 120 ms)
Broad QRS complexes with a slurred upstroke to the QRS complex — the delta wave
Dominant R wave in V1 suggests a left-sided AP, and is sometimes referred to as “Type A” WPW
Tall R waves and inverted T waves in V1-3 mimicking right ventricular hypertrophy (RVH) — these changes are due to WPW and do not indicate underlying RVH
Negative delta wave in aVL simulating the Q waves of lateral infarction — this is referred to as the “pseudo-infarction” pattern
left-sided AP (type A WPW),
with dominant R wave in V1 and right precordial T-wave inversions simulating RVH.
Right-sided WPW
Sinus rhythm with very short PR interval (< 120 ms)
Broad QRS complexes with a slurred upstroke to the QRS complexes — the delta wave
Dominant S wave in V1 indicates a right-sided AP — sometimes referred to as “Type B” WPW
Tall R waves and inverted T waves in the inferior leads and V4-6 mimic the appearance of left ventricular hypertrophy (LVH) — again, this is due to WPW and does not indicate underlying LVH
right-sided AP (Type B WPW):
Dominant S wave in V1
Negative delta waves in leads III and aVF simulate the Q waves of prior inferior MI (= pseudo-infarction pattern)
Pt is conscious when the machine alarms? How did you come about your diagnosis?
Artefact
Yellow: Abrupt onset without ‘R-on-T’ phenomenon - Polymorphic VT is usually initiated by a premature ventricular complex (PVC) or premature atrial complex (PAC) that ‘lands’ on the preceding T wave
Blue: Apparent ventricular rate approaching 600 bpm = Too fast for VT
Red: QRS complexes ‘marching’ through at 60 bpm (every 5 squares)
16-year-old female with intentional polypharmacy overdose. HR 72 reg, BP 100/62, GCS 15
Describe ECG ?
Rx?
Sinus rhythm, rate 72 bpm
1st degree AV block (PR interval ~210ms)
Northwest axis
Dominant R’ wave in aVR reflects terminal right axis deviation of the QRS
There is marked intraventricular conduction delay (IVCD) with QRS duration ~160ms
Absolute QT interval is 460ms
Bicarbonate
In overdose which drugs cause Na channel blockade? ECG? Rx?
Class 1 antiarrhythmics - Eg flecainide
TCAs - eg amitriptyline
Carbamazepine
Propranolol
Sodium bicarbonate + hyperventillation
In overdose which drugs cause K efflux blockade?
ECG?
Rx?
Antipsychotics
TCAs
Class 1 / 3 antiarrhythmics
Optomise K/Mg/Ca
Ca chanel blocker overdose ecg? rx?
1st degree heart block
Bradycardia
Calcium, high dose euglycaemic insulin, inotropes
Bblockers in OD cause what ecg? rx?
1/2/3 block
High dose euglycaemic insulin
Inotropes
Pacing
A 47-year-old woman presents with four hours of right shoulder pain and diaphoresis. HR 70 reg, BP 177/87, SpO2 95 RA.
Reading states inferior ischemia. Is it?
No - limb lead reversal
A uniformly positive P-QRS-T complex in aVR, or uniformally negative complex in lead I, should always prompt us to consider and check lead misplacement, especially when the QRS complex is otherwise normal.
This ECG - P wave axis is abnormal – upright in aVR, negative in II
Q waves and T-wave inversion in leads I, II, III, aVF
A 65-year-old woman presents with one hour of central chest pain following three days of exertional dyspnoea and lethargy. BP 79/51, HR 105 reg, SpO2 93 RA
What does the ECG show?
Causes?
RBBB
Widespread ST depression
STE in aVR
-> diffuse subendocardial ischaemia due to oxygen supply-demand mismatch.
Causes
1. Hypotension or hypoxia
2. LMCA/LAD stenosis/insufficiency
3. Severe triple vessel disease
4. ROSC post cardiac arrest
[In the absence of ST elevation in other leads, acute coronary occlusion is rarely the cause of this pattern. It is usually the unmasking of coronary disease but not an occlusion]
A 57-year-old man is referred in by his GP following two weeks of episodic left axillary pain. HR 73, BP 134/64, SpO2 97 RA. Pain-free ECG (top) followed by ECG when pain starts
What does they show?
Top - T-wave inversion in V2-4, without significant ST segment changes
Bottom - There is “pseudonormalisation” of previously inverted T-waves in V2-4
ST segment elevation is seen in V2-3
= Wellens syndrome
[differentials for right precordial T-wave inversion in patients with symptoms of ACS are:
1. Ischaemia (including Wellens Syndrome)
2. Posterior myocardial infarction
3. Right ventricular strain (including pulmonary embolism)
4. Hypertrophic cardiomyopathy (especially apical type)]
What is wellens syndrome? What does it suggest?
biphasic or deeply inverted T waves in V2-3, plus a history of recent chest pain that is not resolved.
highly specific for critical stenosis of the left anterior descending artery (LAD)
[75% will have a pattern of deeply inverted T waves in leads V2-3 (type B)
25% will demonstrate a biphasic T wave with negative terminal portion (type A). These type A changes can be subtle and are more often overlooked.]
[The pattern is usually present in the pain free state — it may be obscured during episodes of ischaemic chest pain, when there is “pseudonormalisation” of T waves in V2-3]
A 60-years-old male was brought to Emergency department after loss of consciousness
Left main coronary occlusion
1) Widespread horizontal ST depressions, most prominent in leads I, II and V4-6’
2) ST elevation in aVR ≥ 1mm, 3) ST elevation in aVR ≥ V1
