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ECG Interpretation Flashcards

1
Q

What are the leads in a 12 lead ECG?

A

Recordings are made using 10 recording leads attached to electrodes:

  • 4 limb leads with electrodes on the R Arm, L Arm, L Leg and R Leg
  • 6 precordial leads across the chest V1, V2, V3, V4, V5 and V6

Using these, graphs of the electrical activity of the heart are recorded in 12
different views:
- The limb leads are used to create standard bipolar leads I, II, III
- The ‘augmented’ unipolar leads aVR, aVL and aVF
- The precordial
leads record the chest leads V1, V2, V3, V4, V5 and V6

Giving the full ‘12 lead’
ECG

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2
Q

What territories (and arteries) do each leads correspond to?

A

Lateral:

  • I + aVL + V5 + V6
  • L circumflex or diagonal of LAD

Inferior:

  • II + III + aVF
  • RCA and/or L circumflex

Anterior/septal:

  • V1-V4 (V1-2 more septal, V3-4 more anterior)
  • LAD

(aVR is a bit of a forgotten lead but does have come useful clinical applications… somewhere)

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3
Q

How is a standard ECG recorded?

A

Standard recording speed is 25 mm/sec. = one small square (1 mm) on standard ECG paper record equals 40 milliseconds (0.04 secs.)
- If you want visualise an tachyarrhythmia better, you can slow down the speed of the ECG to stretch out the morphology

The voltage
calibration is 10 mm/mV

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4
Q

What do positive and negative complexes indicate on ECG?

A
  • +ve = a peak = depolarisation travels towards a positive electrode
  • -ve = a trough = depolarisation travels away from a positive electrode
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5
Q

What are P waves?

A

Sequential depolarisation of right and left atria

  • R before L but both summate to form P wave
  • 1st 1/3rd = R, middle 2/3rd = both, 3/3rd = L

Vector is from the SAN to AVN

Should be <120ms or 3 small squares

Should be:

  • Upright in leads I, and II and inverted in aVR
  • Monophasic in most leads (e.g. II)
  • Biphasic in V1 - as L and R waveforms move in opposite directions - +ve deflection then -ve deflection

Abnormalities most easily seen:

  • Inferior leads (e.g. II) - As P waves are most prominent
  • V1 - as biphasic and can split out looking at L and R atrial pathology
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6
Q

What are some common abnormalities of P waves and the underlying pathology?

A

P mitrale:

  • Bifid/notched P waves in lead II
  • Seen with L atrial hypertrophy
  • Classically due to mitral stenosis

P pulmonale:

  • Peaked/tall P waves in lead II
  • Seen with R atrial hypertrophy
  • Classically due to pulmonary HTN e.g. cor pulmonale from chronic resp. disease

P wave inversion:

  • In inferior leads/II
  • A non-sinus origin of P wave
  • When PR interval <120ms = AV junction origin (e.g. accelerated junctional rhythm)
  • When PR interval >120ms = origin within atria (e.g. ectopic atrial rhythm)

Variable P wave morphology:
- e.g. >3 different P wave morphology = multifocal atrial tachycardia (rare)

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7
Q

What is the PR segment?

A

Flat/isoelectric segment between end of P and beginning of QRS

Electrical conduction from AVN-Bundle of His-Bundle branches- Purkinje fibres and enter ventricles

PR segment changes in pathology are measured against the baseline formed by the T-P segment (the isoelectric period where no electrical activity is occurring)

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8
Q

What are some common abnormalities of the PR segment and the underlying pathology?

A

Pericarditis:

  • Widespread PR segment depression + saddle shaped/concave ST elevation
    • reciprocal PR elevation and ST depression in aVR and V1

Atrial ischaemia/infarction:

  • PR segment depression or elevation (reciprocal) in patients with MI indicates concomitant atrial ischaemia or infarction
  • Associated with complications + poor outcomes
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9
Q

What is the PR interval?

A

Reflects condition through the AV node

Normal time = 120-200ms or 3-5 small squares

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10
Q

What are some common abnormalities of prolonged PR interval (>5 small squares) and the underlying pathology?

A

First degree heart block/AV block

Second degree heart block - Mobitz type 1 (Wenckebach phenomenon)

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11
Q

What are the features of first degree heart block including its causes and management?

A

Prolonged PR >200ms (5+ small squares)
- Delayed condition through the AV node

Sinus rhythm or sinus bradycardia = common

Aetiologies:

  • Increased vagal tone i.e. from athletic training
  • Inferior MI
  • Mitral valve surgery
  • Myocarditis
  • Electrolyte abnormalities e.g. hyperkalaemia
  • AV nodal blocking drugs e.g. betablockers, CaBs, digoxin, amiodarone

Management:

  • Does not cause haemodynamic instability
  • No specific treatment is required
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12
Q

What are the features of second degree heart block/Mobitz type 1 (Wenckebach phenomenon) including its causes and management?

A

PR interval is prolonged and elongates with each successive beat until a QRS is dropped/there is a non-conducted P wave and the cycle repeats

  • With a shorter PR interval that gradually increases again
  • May present in P:QRS ratios of 3:2, 4:3 or 5:4
  • R-R interval remains constant amongst the clusters despite prolongation of PR

Aetiologies:

  • Usually due to reversible conduction block at AV node
  • Beta-blockers, CaBs, Digoxin, amiodarone
  • Inferior MI, myocarditis, cardiac surgery

Management:

  • Minimal haemodynamic instability
  • Low risk of progression to 3rd degree heart block
  • If asymptomatic - does not require treatment
  • If symptomatic - usually respond to atropine
  • Permanent pacing rarely needed
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13
Q

What are some common abnormalities of shortened PR interval and the underlying pathology?

A

Preexcitation syndromes
- Wolff-Parkinson-White (WPW) = most notable

AV nodal (junctional) rhythm

  • Narrow complex, regular rhythms arising from AVN instead of SAN
  • Absent or inverted P waves + short PR = retrograde P waves
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14
Q

What are the features of Wolff-Parkinson-White syndrome including its causes?

A

Due to the presence of a congenital accessory pathway (Bundle of Kent) connecting atria and ventricles which can (mostly) conduct in both directions

  • This pathway conducts faster = shortened PR <120ms/3 small squares
  • Also serves as an anatomical re-entry circuit = paroxysmal supraventricular tachycardia (SVT, specifically atrioventricular re-entry tachycardia = AVRT) (2x subtypes)
  • Can also occur alongside AF and atrial flutter - which because of the pathway can lead to VT or VF as conduction bypasses AV node

ECG:

  • Short PR <120ms
  • Broad QRS >110ms
  • Delta wave = slurred upstroke to the QRS (will also be reciprocal in relevant leads)
  • Features may become more obvious with increased vagal tone e.g. during Valsalva manoeuvres or with AV blockade
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15
Q

How do you manage the complications of WPW?

A

AVRT:

  • Depending on subtype and stability of patient, may respond to vagal manoeuvres +/- adenosine or CaBs OR amiodarone
  • If haemodyamically unstable, urgent synchronised DC cardioversion is required

Atrial fibrillation and flutter:

  • AV nodal blocking drugs - adenosine, CaBs, beta-blockers - may INCREASE CONDUCTION VIA ACCESSORY PATHWAY AND RESULT IN INCREASE IN VENTRICULAR RATE AND DEGENERATION TO VT OR VF SO AVOID
  • Synchronised DC cardioversion is the therapy of choice
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16
Q

What is a Q wave?

A

Any negative deflection that precedes an R wave
- Represent normal L->R depolarisation of intraventricular septum

Leads:

  • Small = normal in most leads
  • Deeper (>2mm) may be a normal variant in III and aVR
  • Normally not seen in right sided leads V1-3
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17
Q

What are the features of pathological Q waves? What do they indicate?

A 
Features:
- > 40 ms (1 mm) wide
- > 2 mm deep
- > 25% of depth of QRS complex
- Seen in leads V1-3
Usually indicate a current or prior MI

May also indicate:

  • Hypertrophic CM
  • Rotation of the heart
  • Lead placement error e.g. upper limbs placed on lower

Absence of Q waves in V5-6 is also abnormal:
- Most commonly due to LBBB

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18
Q

What are QRS complexes?

A

Represent the depolarisation of both ventricles
- Normally 70-100ms

Width: determines origin -

  • Narrow - <100ms (2.5 small squares) = supraventricular in origin
  • Broad - >100ms = either ventricular in origin, or due to aberrant conduction of supraventricular complexes
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19
Q

What are some examples of conditions with narrow QRS complexes and their features?

A

Arise from 3x main places:

1) SAN = normal conduction, P wave present

2) Atria = abnormal P wave/flutter wave/fibrillatory wave
- Condition = atrial flutter (saw tooth pattern)
- ECG = always rate of 150, regular, narrow complex tachycardia

3) AV node/junction = either no P wave, or abnormal P wave with a PR interval <120ms
- Condition = junctional tachycardia

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20
Q

What are some examples of conditions with broad QRS complexes?

A

QRS >100ms = abnormal
QRS >120ms = required for the Dx of BBB or ventricular rhythm

Other causes of aberrant condition leading to broad complexes:

  • BBB
  • Hyperkalaemia
  • Na-channel blockade e.g. tricyclic poisoning
  • Pre-excitation syndromes e.g. WPW
  • Ventricular pacing
  • Hypothermia
  • Intermittent aberrancy
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21
Q

What are bundle branch blocks? (BBBs)

A

Arise from a defect in the bundle branches which themselves are divisions of the Bundle of His

  • Right bundle contains one fascicle
  • Left bundle subdivides into two fascicles (left anterior and left posterior; the left then bifurcates itself)
  • Ultimately the fibres terminate in Purkinje fibres which innervate individual myocytes allowing for rapid/coordinated contraction

The defects may arise from:

  • Ischemic heart disease
  • HTN
  • MI
  • Hyperkalaemia
  • Digoxin toxicity
  • Rheumatic heart disease
  • Cardiomyopathy
  • Degenerative disease of the conduction system
  • Congenital heart disease e.g. ASD
    etc.

This changes the pathways involved in depolarisation:

  • Impulse may move through muscle fibres in a way that slows electrical movement and changes the direction of the impulses
  • Ventricles do not synchronise, their depolarisation is prolonged and CO may drop
22
Q

What are the features of RBBB?

A

Activation in RV is delayed as depolarisation has to spread across the septum from the left ventricle
- Early part of QRS unchanged as LV is intact

Delayed RV depolarisation produces:

  • A second R wave (R’) in V1-3 (= ‘M’ shaped QRS)
  • A wide, slurred S wave in the lateral leads 1, aVL, V5+6
  • A broad QRS >120ms

These 3 features are needed for diagnosis
- If QRS <120ms = incomplete RBBB

Associated features:
- ST depression + T wave inversion in V1-3

23
Q

What are the features of LBBB?

A

Normally the septum is activated from L->R, producing small Q waves in lateral leads
- LBBB reverses the spread of depolarisation as impulse travels first to the RV from the RBB then to the LV via the septum

This sequence of activation produces:

  • R waves in lateral leads (I, aVL, V5+6) that are either ‘M’ shaped, notched (little bump on downslope), monophasic (single peak) or an RS complex (absence of Q wave + R peak + S trough)
  • Deep S waves in V1-3, especially in V1; possibly as part of an rS complex (small R wave, deep S wave)
  • Prolonged R wave peak time >60ms in V5+6
  • Absence of Q waves in I, V5+6
  • A broad QRS >120ms

These features are needed for diagnosis

Associated features:

  • Appropriate discordance = ST segments and T waves always go in the opposite direction to the main vector of the QRS complex
  • Poor R wave progression in chest leads
  • Left axis deviation
24
Q

What are some mnemonics/memory aids for distinguishing between LBBB and RBBB?

A

‘WiLLiaM MaRRoW’

WiLLiaM = in LBBB there is a ‘W’ in lead V1 and an ‘M’ in V6

MaRRoW = in RBBB there is an ‘M’ in lead V1 and a ‘W’ in V6

Though this is pretty basic and if you take these as the only indications of BBB then you will miss them

Alternatively, a quick hack is:
- If you see a broad QRS, hold the ECG sheet in front of you and turn it 90 degrees clockwise - if the QRS complex in V1 is pointing to the right = RBBB or to the left = LBBB

25
How do you manage bundle branch blocks?
New LBBB in the context of chest pain is traditionally considered as part of the criteria for thrombolysis so you need to be mindful that MI might be the underlying cause and treat appropriately If caused by an underlying, correctable abnormality e.g. drug toxicity, then manage appropriately If it is the consequence of a more permanent injury e.g. post MI and is contributing to a symptomatic bradycardia for example then may need pacing but otherwise no specific treatment is given In otherwise asymptomatic patients BBBs do not need treatment
26
What are some examples of conditions with high voltage QRS morphology?
Often taken to infer the presence of LVH - But can be normal in fit/slim individuals <40yrs - There exist multiple 'voltage criteria' for LVH e.g. Sokolov-Lyon criteria - Must be accompanied by non-voltage criteria to Dx LVH
27
What is electrical alternans? What causes it?
When QRS complexes alternate in height Most important cause is massive pericardial effusion - Occurs due to the heart swinging back and forth in a large fluid filled pericardium - will change the height of the QRS
28
What is second degree AV block/Mobitz II (Hay block) including its causes and management?
Intermittent, non-conducted P waves WITHOUT progressive prolongation of the PR interval - PR interval for conducted beats remains constant - RR interval surrounding the dropped beat is an exact multiple of the preceding RR interval i.e. double the preceding RR interval for a single dropped beat, treble for two dropped beats, etc - In 75% of cases, the conduction block is distal to the bundle of His, so produces broad QRS complexes - May have no pattern or may be a fixed relationship between P waves and QRS e.g. ration of 2:1 or 3:1 block Aetiology: - More likely due to a more permanent, structural change compared to Mobitz I - Infarction (esp. anterior MI), fibrosis, necrosis, rheumatic fever, cardiac surgery - Patients typically often have pre-existing LBBB and so this Mobitz II arises when the last remaining fascicle fails to conduct Management: - Greater risk of haemodynamic compromise, severe bradycardia and progression to 3rd degree heart block - Sudden cardiac death through asystole c. 35% per year - Permanent pacemaker required
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How does a ventricular tachycardia present? Broad QRS complexes with no visible P waves THIS IS A HUGE QUESTION: https://litfl.com/vt-versus-svt-ecg-library/ Also stuff on 3rd degree heart block: https://litfl.com/vt-versus-svt-ecg-library/ Brugada: https://litfl.com/brugada-syndrome-ecg-library/ Axis deviation: - Look at the ECG app you have, has a quick how to interpret at a glance CAlcultating heart rate To calculate heart rate from an ECG you can count the number of large squares in an R-R interval then divide 300 by this number. Therefore 300/3 = 100 bpm - Alternatively, a capped bic biro = 6 seconds, therefore count the number of QRS complexes under the biro*10 Axis deviation Premature ventricualr complexes Accelerated Idioventricular Rhythm (AIVR) Agonal rhythm Sinus arrest vs sinus block
ST segment: - Normally isoelectric point representing the interval between ventricular depolarisation and repolarisation T wave: - Repolarisation of the ventricles QT interval: - Time between the start of ventricular depolarisation and repolarisation
33
What are the ECG signs of L atrial enlargement?
II - P mitrale V1 - MAYBE BUY PREMIUM AND PUT IN PICS FOR THIS DECK... first find all the pics you'd want to include then but and upload; including pics in derm decks, ENT, ophthalmology, CXR interpretation etc... just start collating images first E.g. https://litfl.com/wp-content/uploads/2018/08/P-wave-morphology-LAE-Wagner-2007.png
34
What are the ECG signs of R atrial enlargement?
M
35
How do you diagnose STEMI in the context of new LBBB?
If chest pain + ST elevation + new LBBB should always suspect STEMI but Dx based on this simplified look at an ECG alone is problematic Modified Sgarbossa criteria: based on presence of 'concordance' and 'disproportionate/excessive disconcordance' Concordance: - Abnormal - ST matching the same vector as the greatest vector in the QRS - Rule 1: ≥ 1 lead with ≥1 mm of concordant ST elevation - Rule 2: ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression - e.g. in LBBB, there is always an upright R wave in the lateral leads, so if ST elevation is present - a lateral STEMI can be diagnosed if there is- just one lead with ≥ 1 mm of concordant STE - e.g. in LBBB, V1-V3 will always have a predominant S-wave, therefore any STD (if present) in V1-3 is always concordant and ≥ 1 mm of STD in just one of these leads is diagnostic of posterior STEMI Discordance: - In LBBB without MI, the baseline ST segments and T waves tend to be shifted in a discordant direction (“appropriate discordance”) - This can mask or mimic acute myocardial infarction e.g. in LBBB, in leads V1-V3, the QRS is always predominantly negative (deep S-wave), the normal state is ST Elevation in these right precordial leads. So how can you diagnose anterior STEMI in LBBB? Only if that STE is out of proportion Disproportionate discordance: - Rule 3: ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally excessive discordant STE, as defined by ≥ 25% of the depth of the preceding S-wave (as opposed to the less sensitive 5mm discordance originally proposed) https: //litfl.com/sgarbossa-criteria-ecg-library/ https: //epmonthly.com/article/stemi-in-the-presence-of-lbbb/
36
What are reciprocal changes?
Important in the diagnosis of STEMI Also identifies a patient with an increased likelihood of cardiovascular complication (heart block, malignant ventricular dysrhythmia, cardiogenic shock) and poor outcome (significant left ventricular dysfunction, death) Defined as ST-segment depression occurring on an ECG which also has ST-segment elevation in at least 2 contiguous (looking at one anatomic area of the heart or in sequence e.g. V2+V3) leads - Septal - facing V1+V2; reciprocal 'V7-9' - Anterior - facing V3+V4; reciprocal none - Lateral - facing I, aVL, V5+6; reciprocal II, III, aVF - Inferior - facing II, III, aVF; reciprocal I, aVL - Posterior - facing 'V7-9'; reciprocal V1+V2 Concept of reciprocal change cannot be used in patients who have the following patterns : left bundle-branch block, right bundle-branch block, right ventricular paced rhythm from an implanted pacemaker, and left ventricular hypertrophy (via voltage criteria) with strain https://www.youtube.com/watch?v=jZM0GDhFhHI&ab_channel=TheResuscitationist
37
How do you interpret the cardiac axis on an ECG?
Normal axis: - QRS between -30 and +90 Deviation: - LAD = QRS < -30 - RAD = QRS > +90 - Extreme AD = QRS between -90 and 180 Quadrant method: - Lead 1 and aVF - Examine each lead and determine if it is positive (R>S), isoelectric (R=S) and negative (R
38
What is the three lead analysis method for axis interpretation?
We add lead II to the analysis of I and aVF: - +ve in I = same direction as I - +ve in II = same direction as II - if both +ve = normal axis, between -30 and +90 Physiological vs pathological LAD: - Physiological = 0 to -30 (equiphasic lead II) - Pathological = -30 to -90 (negative lead II) Can be helpful to use your left hand to denote the quadrants and the +ve/-ve direction, hold your left hand: - Vertical = lead I (then) - at 30 degrees = lead II (then) - Horizontal - lead aVF - The direction the palm faces = +ve (and so back of the hand = -ve) and wherever the area is that is overlapped by all three positions = your axis SEE DIAGRAMS FOR MORE HELP
39
What causes RAD?
- RVH - Acute RV strain e.g. pulmonary strain - Lateral STEMI - Chronic lung disease e.g. COPD - Hyperkalaemia - Na-channel blockade - WPW
40
What causes LAD?
- LVH - LBBB - Inferior MI - Ventricular pacing/ectopy - WPW
41
What causes extreme AD?
- Ventricular rhythms e.g. VT, ventricular ectopy - Hyperkalaemia - Severe RVH
42
What is the QTc?
<11.5sq = <460ms Prolongation = potentially worrisome Can lead to Troussardes de pointes - looks like the AM album cover
43
What is a quick way to work out axis deviation?
Look at leads 1-3 Normal = 1, 2, 3 = +ve LAD = RAD =
44
When do you defibrillate?
No pulse + - VF or pulseless VT - If not VF and they're not in a shockable rhythm and - BLS
45
What are the general principles of managing arrhythmias?
Are they unwell? - Chest pain, syncope, SOB, sweaty, BP <90, oliguric etc. - If well, sometimes just observing and getting advice is enough If unwell, what's the heart rate? give 'A' drugs - Slow - atropine, adrenaline - Fast - adenosine (narrow complex), amiodarone (broad complex), atenolol (or any BB) If the drugs don't work/if they are peri-arrest: - Electrical treatment - percussion pacing, external pacing, transvenous pacing (depending on facilities) - Or defibrillation
46
What is a V4R lead?
Can be used as a view of the R ventricle as standard ECG not very specific for it
47
What are dynamic ECG changes?
ECG changes e.g. ischaemia, arrhythmia that come on with Sx and go when Sx go Heart monitor or repeat traces (up to every 10-15 minutes) will clarify the picture
48
How do posterior MIs present on ECG?
ST depression in anterior leads that is persistent is a strong indication Can be confirmed with a posterior ECG
49
How do you assess a narrow complex tachycardia?
Carotid sinus massage : - press on sinus gently and massage in small circles for c.30s Valsalva: - Hold nose and blow Others: - Blow a 50ml syringe - Hold a cube of ice in mouth - Dunk face in cold water All of these will increase vagal tone and hopefully affect the heart - slow or stop the arrhythmia
50
How do you interpret ECGs in people who are paced?
QRS complexes are broad in pacing because the pacing wires are placed at the bottom of the R ventricle - depolarises first then spreads to the L through the septum
51
What are the features of third degree heart block?
Aka complete heart block or AV dissociation P waves and QRS complexes unrelated but both are regular Ventricular rate = c. 30 BPM Patient may experience syncope with exertion as ventricular rate cannot cope with increased work

Finals - Cardiology (14 decks)

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