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Progress test study > ECG > Flashcards

ECG Flashcards

1
Q

Method for going through an ECG

A
  • Rate
  • Rhythm
  • Axis
  • P waves
  • PR interval
  • Q and RS
  • QT interval
  • ST interval
  • T waves
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2
Q

How to calculate the Rate

A

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

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

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3
Q

What are you looking for with the rhythm?

A
  1. Whether it’s irregular → An ectopic/arrhythmia
  2. Or whether it’s irregularly-irregular → Atrial fibrillation
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4
Q

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

A

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.

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5
Q

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

A
  1. Lead I and aVF are + deflected

* Lead II will also be extremely +

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6
Q

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

A
  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.

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

Summary:

Lead I and avL +
Lead II and aVF -

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7
Q

What would indicate RAD on ECG

A
  1. Lead I - and aVF +
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8
Q

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

A
  • 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
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9
Q

What do the little and big squares on ECG represent?

A

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.

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10
Q

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

A

Lead II and aVF positive

V1 Biphasic

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11
Q

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

A

<0.2s (one big square)

this suggests atrioventricular (AV) block

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12
Q

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

A

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.

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13
Q

Whats Second degree HB, mobitz type 1 also called?

A

Wenckebach

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14
Q

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

A
  • 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
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15
Q

What could a shortened PR interval indicate?

A

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

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16
Q

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

A

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

17
Q

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

A

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
18
Q

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

A

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

19
Q

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

A

A large Q wave, indicates a prior MI

20
Q

Where should you have dominant S waves?

rS

A

aVR and V1

21
Q

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

A

In aVR : tricyclic OD

In V1 : Posterior MI? RBBB?

22
Q

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

A

Progression of the R wave upwards

23
Q

How to distiguish Left Ventricular Hypertrophy on ECG?

A

V2 + V5 = >7 small squares

24
Q

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

Where would you see reciprocal change?

A

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

25
Q

Up to 40% of patients with an _____ STEMI will have a concomitant right ventricular infarction.

What is the significance of this?

A

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.

26
Q

What vessels are involved in an inferior STEMI or NSTEMI.

How would this produce a difference on ECG?

A
  • 80% Right Coronary Artery (RCA)
    • ST ele. in III > II
  • 18% Left circumflex Artery (LCx)
    • ST ele. in III < II
27
Q

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

A

As the posterior myocardium is not directly visualised by the standard 12-lead ECG, reciprocal 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).

28
Q

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

A
  • 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

29
Q

What is the issue with NSTEMI’s on ECG

A

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

30
Q

Anterior STEMI results from occlusion of the….

A

Left anterior descending (LAD)

Has the worst prognosis mainly due to a larger infarct size?

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