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ECGs + arrhythmias Flashcards

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1
Q

What does one small square represent?

A

0.04s

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2
Q

What does one large square represent?

A

0.2s

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3
Q

How many large squares is 1 second?

A

5

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4
Q

What are the lateral leads?

A

I, aVL, V5, V6

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5
Q

What are the inferior leads?

A

II, III, aVF

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6
Q

What are the anterior leads?

A

V2, V3, V4

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7
Q

Which is the septal lead?

A

V1

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8
Q

What vessels correspond to the lateral, anterior and inferior leads?

A
  • Lateral - circumflex artery
  • Anterior - LAD artery
  • Inferior - RCA
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9
Q

What is a structure for assessing ECGs?

A
  1. Name, DOB, clinical context
  2. Rate (60-100bpm)
  3. Rhythm strip (regular or irregular and PQ relationship)
  4. (Axis)
  5. Parameters - PR, QRS, cQTC
  6. Morphology:
    • Broad/narrow
    • BBB?
    • ST
    • T waves
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10
Q

How can you calculate the rate?

A
  • 300/larges squares between R waves
  • QRS complexes in 10 seconds x 6 (useful if irregular rhythm)
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11
Q

What happens in sinus rhythm?

A

The action potential starts in the sinus node

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12
Q

How do you assess rhythm?

A
  1. Assess atrial rhythm:
    - See if sinus rhythm…
    • Is there a +ve P wave in lead II
    • Is there a -ve P wave in aVR
  2. Assess ventricular rhythm
    - Look as QRS…
    • What’s the interval between
    • Is it regular/irregular
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13
Q

What leads do you look at to assess axis? When indicates normal axis?

A
  • I and aVF
  • Both should be positive
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14
Q

What is the normal cardiac axis?

A

-30 - 90 degrees

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15
Q

P wave:
1. What does it represent?
2. What do you check?

A
  1. Atrial depolarisation
  2. Present? Height -> tall in RA enlargement
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16
Q

PR interval:
1. What does it represent?
2. What is the normal duration?
3. What do you check?

A
  1. Atrial depolarisation and contraction
  2. 3-5 small squares
  3. Length -> prolonged = heart block, short = pre-excitation syndrome
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17
Q

Q wave:
1. What do you check?

A
  1. Depth -> >1 small square = abnormal. Can be a sign of a previous MI
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18
Q

QRS:
1. What does it represent?
2. What is the normal duration?
3. What do you check?
4. What is indicated by wide QRS complexes?

A
  1. Ventricular depolarisation
  2. 3 small squares
  3. Width, height -> V hypertrophy
  4. BBB:
    - Look in lead I
    - Think about using indicators in a car
    - If QRS is -ve = LBBB (indicator down to go L)
    - If QRS +ve = RBBB (indicator up to go R)
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19
Q

ST:
1. What does it represent?
2. What do you check for?

A
  1. No electrical activity
  2. Elevation/depression
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20
Q

QT interval:
1. What do you check?

A
  1. Width -> if less than 1/2 R-R = normal
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21
Q

T wave:
1. What does it represent?
2. What do you check?
3. What is a key cause of abnormal T waves?

A
  1. Ventricular repolarisation
  2. Where they are +ve/-ve (normally -ve in V1 and aVR), height -> tall in hyperkalemia
  3. Ischaemia
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22
Q

What are the shockable rhythms?

A
  • VF
  • VT
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23
Q

How can VT be classified?

A
  1. Narrow complex tachycardia = tachycardia with narrow QRS complexes (<0.12s)
  2. Broad complex tachycardia = tachycardia with broad QRS complexes (>0.12s)
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24
Q

What’s the management of VT if life threatening features?

A
  • Synchronised DC cardio version under sedation or GA
  • IV amiodarone if initial shocks are unsuccessful
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25
Q

What features indicate a pt with tachy/bradycardia is unstable?

A
  • Shock
  • LOC
  • Heart muscle ischaemia (chest pain)
  • Shock/severe HF
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26
Q

Give 4 differentials for narrow complex tachycardia?

A
  • Sinus tachycardia
  • SVT
  • AF
  • Atrial flutter
27
Q

What can cause sinus tachycardia?What is the management?

A
  • ST occurs in response to an underlying cause e.g. sepsis, pain
  • Manage underlying cause
28
Q

What are the common causes AF?

A

SMITH:
- Sepsis
- Mitral valve pathology
- Ischaemic heart disease
- Thyrotoxicosis
- Hypertension

29
Q

What happens in AF?

A
  • Disorganised electrical activity in the atria -> uncoordinated, rapid, irregular atrial contraction
  • Chaotic electrical activity passes through to the ventricles -> irregular ventricular contraction
30
Q

What are the effects of AF?

A
  • Irregularly irregular ventricular contractions
  • Tachycardia
  • HF due to impaired filling of the ventricle
  • Increased risk of stroke
31
Q

Appearance of AF on ECG?

A
  • Absent P waves
  • Narrow QRS complexes
  • Irregularly irregular QRS complexes
32
Q

What causes atrial flutter?

A
  • An extra electrical pathway in either atrium -> re-entrant rhythm
  • The signal goes round and round the atrium without interruption -> atrial rate = 300bpm
  • The signal does not enter the ventricles every lap which results in two atrial contractions for every one ventricular contraction -> ventricular rate = 150bpm
33
Q

What is the management of atrial flutter?

A
  • Anticoagulation based on CHA2DS-VASC
  • Radio-frequency ablation of re-entrant rhythm can be permanent solution
34
Q

Appearance of atrial flutter on ECG? What is the atrial rate?

A
  • Regular QRS complexes
  • Sawtooth pattern (2 p wave per 1 QRS)
  • Rate 300bpm
35
Q

What is the management of atrial flutter?

A
  • Anticoagulation based on CHA2DS-VASc
  • Radio-frequency ablation can be permanent solution
36
Q

What is SVT?

A

Supra ventricular tachycardia

37
Q

Appearance of SVT on ECG?

A
  • Regular QRS complexes
  • QRS followed by T wave then QRS etc.
38
Q

What’s the most common type of SVT? What does this entail?

A
  • Atrioventricular re-entrant tachycardia (aka Wolf-Parkinson White)
  • Accessory pathway meaning electrical signals re-enter AV node -> increased ventricular contractions
39
Q

How can you spot an accessory pathway on ECG (e.g. in WPW)

A
  • Slurred upstroke in QRS
  • Also called delta wave
  • Will also be a short PR
40
Q

Stepwise management of SVT in stable patients?

A
  1. Valsalva manoeuvre (blow hard into a syringe)
  2. Carotid sinus massage
  3. Adenosine
41
Q

How does adenosine work? How is it given? What do you need to warn patients about?

A
  • Interrupts the AV node/accessory pathways and resets sinus rhythm
  • Given as a rapid IV bolus
  • Causes brief asystole which can be scary for patients
42
Q

Management of SVT in unstable patients?

A

Synchronised cardio version with a defib +/- amiodarone if they need help establishing sinus rhythm

43
Q

Give 4 differentials for broad complex tachycardia

A
  • Ventricular fibrillation
  • Polymorphic VT (aka torsades de pointes)
  • AF with BBB
  • SVT with BBB
44
Q

What causes tornadoes de pointes?

A
  • Prolonged QT
  • Waiting a long time for repolarisation can result in spontaneous depolarisation in some muscle cells
  • These abnormal depolarisations are called afterdepolarisations
  • They can spread throughout the ventricles and cause a contraction before repolarisation
  • When this leads to recurrent contractions it is called torsades de pointes
45
Q

What causes prolonged QT?

A
  • Long QT syndrome (inherited condition)
  • Meds - antipsychotics, citalopram, flecanide, amiodarone, macrolide abx
  • Electrolyte imbalances - hypokalaemia, hypomagnesaemia, hypocalcaemia
46
Q

What can tornadoes de pointes lead to?

A

Will either terminate spontaneously and revert to sinus rhythm or progress to ventricular tachycardia. Ventricular tachycardia can lead to cardiac arrest

47
Q

What’s the management of prolonged QT?

A
  • Stop meds affecting QT
  • Correct electrolyte disturbances
  • Beta blockers (not sotalol)
  • Pacemakers/implantable cardioverter defibrillator
48
Q

What’s the management of torsades de pointes?

A
  • Correct underlying cause (of prolonged QT)
  • Magnesium infusion (even if normal serum Mg)
  • Defibrillation in VT occurs
49
Q

What are ventricular ectopics?

A

Premature ventricular beats caused by random electrical discharges outside the atria

50
Q

How do ventricular ectopics appear on ECG?

A

Isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG

51
Q

What is bigeminy?

A

Refers to when every other beat is a ventricular ectopic

52
Q

Give 3 broad causes of bradycardia?

A
  • Meds (BB)
  • Heart block
  • Sick sinus syndrome
53
Q

What happens in heart block?

A

Impaired electrical conduction between atria and ventricles

54
Q

What happens in 1st degrees heart block? How does this look on ECG? Presentation and management?

A
  • Delayed conduction through AV node
  • PR >0.2s (5 small squares/1 big square)
  • P followed by QRS
  • Commonly asymptomatic and no treatment required
55
Q

What happens in 2nd degree heart block?

A

Some atrial impulses do not make it through AV node

56
Q

What are two types of 2nd degree heart block? Include the management?

A
  • Mobitz 1: progressive prolongation of PR until a dropped beat occurs. Rx = usually no tx required
  • Mobitz 2: PR constant but P wave often not followed by QRS. Rx = usually need pacing
57
Q

How does 3rd degree heart block look on ECG? What is it also called? What is the management?

A
  • No observable relationship between P and QRS
  • Aka complete heart blood
  • PPM (permanent pacemaker)
58
Q

What is sick sinus syndrome?

A

Encompasses conditions that cause SAN dysfunction

59
Q

What often causes sick sinus syndrome?

A

Idiopathic degenerative fibrosis of the SAN

60
Q

What is asystole?

A

The absence of electrical activity in the heart (resulting in cardiac arrest)

61
Q

What increases the risk of asystole?

A
  • Mobitz type 2
  • Third-degree HB (complete heart block)
  • Previous asystole
  • Ventricular pauses longer than 3 seconds
62
Q

Bradycardia: What is the management of unstable patients and those at risk of asystole?

A
  • IV atropine (first line)
  • Inotropes (isoprenaline/adrenaline)
  • Temporary cardiac pacing
  • Permanent pacemaker
63
Q

What are options for temporary cardiac pacing?

A
  • Transcutaneous pacing - using pads on the pts chest
  • Transvenous pacing - using a catheter through the venous system and simulating the heart directly

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