LITFL

Question 1

What look for to determine right ventricular infarction/RCA occlusion

Answer 1

This is an elevation greater than 3 and 2 and ST elevation V1 or V2, greater than aVR

Question 2

Irregularly irregular rhythm, left bundle branch morphology, rate 86-300

Answer 2

These findings indicate atrial fibrillation in the context of Wolff-Parkinson-White syndrome

Question 3

Tx for afib RVR with WPW

Answer 3

DC Cardioversion 200J with fentanyl or ketamine sedation that doesn’t affect BP too much

Question 4

When you see the combination of…

Bradycardia
Blocks — e.g. AV block, bundle branch blocks
Bizarre QRS complexes

Answer 4

hyperkalaemia!

Question 5

Severe Hyperkalemia EKG findings?

Answer 5

bradycardia, flattening and loss of P waves, QRS broadening and T wave abnormalities

Question 6

Features consistent with sodium-channel blockade:

Answer 6

Interventricular conduction delay — QRS > 100 ms in lead II
Right axis deviation of the terminal QRS:
Terminal R wave > 3 mm in aVR
R/S ratio > 0.7 in aVR
Patients with tricyclic overdose will also usually demonstrate sinus tachycardia secondary to muscarinic (M1) receptor blockade.

Question 7

Severe hypokalemia findings

Answer 7

The combination of…

Widespread ST depression / T wave inversion
Prominent U waves
Long QU interval (> 500 ms)

Question 8

Wellens Wave vs Hypokalemia

Answer 8

The main differentiating factor
Wellens: – biphasic T waves go UP then DOWN.
Hypokalaemia: – T waves go DOWN then UP.

Question 9

Right ventricular strain pattern

Answer 9

T wave inversions in the right precordial leads V1-4 plus the inferior leads (especially the rightward-facing lead III)

Question 10

ECG findings associated with PE other than sinus tach and S1Q3T3

Answer 10

T wave inversions in V1-V4 and III,
New right axis deviation
New right bundle branch block
New dominant R wave in V1
Non-specific ST segment changes

Question 11

Sign of proximal Left main occlusion?

Answer 11

AVR elevation and diffuse depression. Can also be seen in SVT

Question 12

The ECG classic features of hypothermia:

Answer 12

Bradycardia
Osborn waves (J waves) = notching at the J point seen in V2-6
Long QT interval (~ 600 ms)
Shivering artifact

Question 13

Pericaridal effusion ECG findings

Answer 13

The triad of tachycardia, low QRS voltages and electrical alternans

Question 14

Giant T-wave inversions in multiple leads, most prominent in V2-6
Marked QT prolongation > 600 ms. What does that mean?

Answer 14

Elevated ICP likely from ICH

Question 15

differential for widespread T wave inversions?

Answer 15

hypokalemia, Wellens, elevated ICP

Question 16

differential for wide complex regular tachycardia

Answer 16

VT and SVT with aberrancy from afib or Wpw

Question 17

classic features of ventricular tachycardia:

Answer 17

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.

Question 18

When you see a regular narrow complex tachycardia at 150 bpm, you should think of four main diagnoses:

Answer 18

Atrial flutter with 2:1 block (especially in elderly, IHD, CCF)

AV-nodal reentry tachycardia (“SVT”)

Orthodromic AV reentry tachycardia in WPW

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.

Question 19

What are DeWinter’s waves?

Answer 19

ST depression with rocket-shaped T waves in the precordial leads V1-6

It is becoming increasingly recognised as an anterior STEMI equivalent

Question 20

Describe sick sinus syndrome with tachy brady

Answer 20

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.

The flurries of junctional tachycardia are a compensatory phenomenon attempting to maintain cardiac output in the face of critically low sinus node rates.

Question 21

features of chronic pulmonary disease:

Answer 21

Rightward QRS axis (+90 degrees).
Peaked P waves in the inferior leads > 2.5 mm (P pulmonale).
Rightward P-wave axis (inverted in aVL).
“Clockwise rotation” of the heart with a delayed R/S transition point (transitional lead = V5).
Absent R waves in the right precordial leads (SV1-SV2-SV3 pattern).
Low voltages in the left-sided leads (I, aVL, V5-6).

Question 22

Why does torsades almost never happen in antipsychotic overdose?

Answer 22

However, tachycardia (which is almost ubiquitous in significant poisoning with quetiapine, olanzapine or clozapine) is actually protective against TdP.

Question 23

Severe hyperkalemia

Answer 23

Bizarre complexes
QRS prolongation
Peaked T waves
Sine wave appearance

Question 24

severe digoxin toxicity features

Answer 24

Atrial tachycardia
Frequent ventricular ectopic beats
High-grade AV block
Alternating LBBB and RBBB morphology,

Question 25

What does salvador dali downsloping st depression ad t waves mean?

Answer 25

therapeutic doses of digoxin; not predictive of toxicity

Question 26

classic features of acute pericarditis:

Answer 26

Widespread concave ST elevation with PR depression — most notable in I, II, III, aVF, V5-6. PR elevation in the inverted leads aVR and V1. Downward sloping of the TP segment = “Spodick’s sign”. No reciprocal changes of STEMI. ST segment / T wave ratio > 0.25 (favours pericarditis over BER)

Question 27

multifocal atrial tachycardia (MAT)

Answer 27

Irregular narrow-complex tachycardia (> 100 bpm) Multifocal atrial activity (3 or more distinct P wave morphologies) No evidence of flutter / AF

Question 28

n a patient presenting with a regular broad-complex tachycardia and no evidence of atrial activity, the main diagnostic considerations are:

Answer 28

Ventricular tachycardia. SVT with aberrant conduction due to bundle branch block. SVT with aberrant conduction due to WPW.

Question 29

Why is it important to differentiate between SVT WPW/aberrancy and VT?

Answer 29

VTs usually respond well to AV-nodal blocking drugs, whereas patients with VT may suffer precipitous haemodynamic deterioration if erroneously administered an AV-nodal blocking agent.

Question 30

There are some additional features suggest of right ventricular infarction:

Answer 30

STE in lead III > lead II. | Deep ST depression in V2 with an isoelectric ST segment in V1.

Question 31

differnece between ventricular escape from AIVR and VT?

Answer 31

just rate ventricular escape less than 50, AIVR between 50-110, VT over 110

Question 32

LAE

Answer 32

deep, wide terminal portion of the P wave in V1

Question 33

right atrial enlargement

Answer 33

P waves in II ~ 2.5mm in height).

Question 34

SVT with LBBB vs RVOT

Answer 34

RVOT is a relatively common form of right ventricular VT, occurring in two main groups: Patients with structurally normal hearts (= 70% of idiopathic VT). Patients with arrhythmogenic right ventricular cardiomyopathy. Difference is LBBB is usually leftward axis. RVOT is normal axis

Question 35

2 causes of pacemaker tachycardia

Answer 35

Sensor Induced Tachycardia (SIT): Modern pacemakers are programmed to allow increased heart rates in response to physiological stimuli such as exercise, tachypnoea, hypercapnia or acidaemia. Sensors may “misfire” in the presence of distracting stimuli such as vibrations, loud noises, fever, limb movement, hyperventilation or electrocautery (e.g. during surgery). or Pacemaker Mediated Tachycardia (PMT): This is a re-entrant rhythm involving the pacemaker circuit.

Question 36

normal on the paediatric ECG:

Answer 36

Rightward QRS axis > +90° Dominant R wave in V1 RSR’ pattern in V1 T wave inversions in V1-3 (“juvenile T-wave pattern”) Slightly peaked P waves

Question 37

Differences in mgmt of afib vs flutter

Answer 37

mostly similar with rate control and anticoagulation but flutter is harder to rate control but easier to cardiovert with less energy (50 J) and easier to ablate

Question 38

“regularised AF”

Answer 38

due to digoxin toxicity: The underlying rhythm is AF, which is being treated with digoxin. There is complete heart block, prevent atrial impulses from reaching the ventricles. There is an accelerated junctional rhythm maintaining cardiac output.

Question 39

Prognostic Value of the ECG in TCA toxicity

Answer 39

In patients with TCA overdose, the degree of QRS prolongation correlates with the degree of clinical toxicity: QRS width > 100 ms is predictive of seizures. QRS width > 160 ms is predictive of cardiotoxicity (e.g. broad-complex dysrhythmias, hypotension).