ECG

Question 1

Method for going through an ECG

Answer 1

• Rate
• Rhythm
• Axis
• P waves
• PR interval
• Q and RS
• QT interval
• ST interval
• T waves

Question 2

How to calculate the Rate

Answer 2

Either 300/Number of big squares within R-R int

Count the number of complexes x 6
(a rhyth strip is 10secs)

Question 3

What are you looking for with the rhythm?

Answer 3

1. Whether it’s irregular → An ectopic/arrhythmia
2. Or whether it’s irregularly-irregular → Atrial fibrillation

Question 4

What is the normal QRS axis distribution, and why do we look at the axis?

Answer 4

Normal axis distribution is between avL (-30) to aVF (90)

We look to rule out LAD and RAD to determine there is correct electrical spread within the heart.

Question 5

What do you look at to determine normal axis spread on ECG

Answer 5

1. Lead I and aVF are + deflected

* Lead II will also be extremely +

Question 6

What would cause suspicion of LAD on ECG and how do you confirm it?

Answer 6

1. Lead I + and aVF is -

This tells you your axis is between -90 to 0 somewhere. But it could still be between -30 and 0.

2. check Lead II, if this is also negative, this confirms LAD

Summary:

Lead I and avL +
Lead II and aVF -

Question 7

What would indicate RAD on ECG

Answer 7

1. Lead I - and aVF +

Question 8

What do you need to be thinking about with P waves?

Answer 8

• Are P waves present? (SA node activation)
• If so, are they followed by a QRS complex (sinus rhythm)
• Duration?
  
  • Should be <3 little squares <0.12s
  • Increaseed duration could indicate atrial hypertrophy
• Shape?
  
  • Sawtooth = AF
  • Fibrillation waves
  • Flat line = no atrial activity at all

Question 9

What do the little and big squares on ECG represent?

Answer 9

Each small square is 1 mm in length and represents 0.04 seconds.

Each larger square is 5 mm in length and represents 0.2 seconds.

Question 10

What is normal for P waves on leads II, aVF and V1?

Answer 10

Lead II and aVF positive

V1 Biphasic

Question 11

How long should the P-R interval be? What does anything larger then this suggest?

Answer 11

<0.2s (one big square)

this suggests atrioventricular (AV) block

Question 12

What are the different types of AV block and can you describe them?

Answer 12

First Degree HB: PR interval >0.2s

Second Degree HB

• Mobitz Type I: The PR interval gets progressively longer until a QRS comlexes ‘drops off’
• Mobitz Type II: The PR interval is fixed but there is dropped beats

Third Degree HB/”complete Heart Block”: The P waves and QRS complexes are completely unrelated.

Question 13

Whats Second degree HB, mobitz type 1 also called?

Answer 13

Wenckebach

Question 14

Where is the Heart block occuring in relation to each type?

Answer 14

• First Degree: between SA node to AV node
• Second Degree
  
  • Mobitz T1: AV node
  • Mobitz T2: After AV node in bundle of His or Purkinje fibres
• Third Degree: anywhere from AV node down causing a complete blockage

Question 15

What could a shortened PR interval indicate?

Answer 15

Simply, the P-wave is originating from somewhere closer to the AV node so the conduction takes less time (the SA node is not in a fixed place and some people’s atria are smaller than others!)

The atrial impulse is getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. This is an accessory pathway and can be associated with a delta wave

Question 16

What is a broad QRS defined as and what does it indicated pathologically?

Answer 16

QRS >0.12s (3ss)

It means the electrical activity is moving through the myocardium instead of the purkinje fibres.

This could indicate a ventricular ectopic

BBB

Hyperkalaemia

Sodium-channel blockade

Question 17

What are the main sodium channel blockers to look out for and what can they cause?

Answer 17

They can cause seizures and ventricular arrhythmias

• Tricyclic antidepressants (= most common)
• Antiarrhythmics (quinidine, procainamide)
• Local anaesthetics (bupivacaine, ropivacaine)
• Antimalarials (chloroquine, hydroxychloroquine)
• Dextropropoxyphene
• Propranolol
• Carbamazepine
• Quinine

Question 18

What is a delta wave, and what else do you need to made the diagnosis of the pathology in question?

Answer 18

A sign that the ventricles are being activated earlier than normal from a point distant to the AV node. The early activation then spreads slowly across the myocardium causing the slurred upstroke of the QRS complex.

To diagnose WPW you need delta waves + tachyarrhythmias

Question 19

What does a pathological Q wave indicate, what lead would you find it in?

Answer 19

A large Q wave, indicates a prior MI

Question 20

Where should you have dominant S waves?

rS

Answer 20

aVR and V₁

Question 21

If you see R> s in leads aVR and V₁ what does that indicate?

Answer 21

In aVR : tricyclic OD

In V_{1 :} Posterior MI? RBBB?

Question 22

What should you see in regards to the QRS complex in leads V₁ to V₄?

Answer 22

Progression of the R wave upwards

Question 23

How to distiguish Left Ventricular Hypertrophy on ECG?

Answer 23

V₂ + V₅ = >7 small squares

Question 24

Where would you see on ECG to indicate an inferior stemi?

Where would you see reciprocal change?

Answer 24

ST elevation in the inferior leads: II, III and aVF

progression of the Q in II, III and aVF

Reciprocal changes in I and aVL

Question 25

Up to 40% of patients with an _____ STEMI will have a concomitant **right ventricular infarction.** **What is the significance of this?**

Answer 25

Up to 40% of patients with an **inferior** STEMI will have a concomitant right ventricular infarction. These patients may develop **severe hypotension** in response to nitrates as they are **heavily dependent on preload.** Be catious of GTN spray here.

Question 26

What vessels are involved in an inferior STEMI or NSTEMI. How would this produce a difference on ECG?

Answer 26

* 80% Right Coronary Artery (RCA) * ST ele. in III \> II * 18% Left circumflex Artery (LCx) * ST ele. in III \< II

Question 27

What would cause suspicion of a Posterior STEMI (20% of MI's)

Answer 27

As the posterior myocardium is not directly visualised by the standard 12-lead ECG, r**eciprocal changes of STEMI are sought in the anteroseptal leads V1-3.** Posterior MI is suggested by the following changes in **V1-3:** * Horizontal ST depression of anteroseptal leads (reciprocal effect) * Tall, broad R waves (\>30ms) * Upright T waves * Dominant R wave (R/S ratio \> 1) in V2 Posterior infarction is confirmed by the presence of ST elevation and Q waves **in the posterior leads (V7-9).**

Question 28

Where would you see ST elevation for anterior/septal/lateral STEMI

Answer 28

* ST segment elevation with Q wave formation in the **precordial leads (V1-6) ± the high lateral leads (I and aVL).** * Reciprocal ST depression in the inferior leads (mainly III and aVF). Septal Leads: V1 - V2 Anterior Leads: V3 - V4 Lateral Leads: V5 - V6, I and aVL

Question 29

What is the issue with NSTEMI's on ECG

Answer 29

ST depression indicating an NSTEmI doesn't correlate to specific leads like STEMI's do

Question 30

Anterior STEMI results from occlusion of the....

Answer 30

Left anterior descending (LAD) Has the worst prognosis mainly due to a larger infarct size?