ECG Flashcards

1
Q

what is pathway conduction in heart?

A

conduction starts in SA node then to AV node where slight delay before travelling down bundle of his that then split to right + left bundle branches which lead to purkinje fibers

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2
Q

why is atrial wave smaller than ventricle wave on ECG?

A

atria wave smaller than ventricle wave because atria has less muscle mass so smaller depolarisation

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3
Q

what is P wave?

A

atrial depolarisation

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4
Q

what is QRS complex?

A

ventricular depolarisation (0.12sec) - shows how long excitation takes to spread through ventricles

*remember depolarisation NOT contraction

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5
Q

what is small Q wave?

A

septal depolarisation from left to right

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6
Q

what is T wave?

A

ventricular repolarisation

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7
Q

what is U wave?

A

extra wave that can sometimes be seen at end of T wave (same shape but smaller)
= origin is uncertain, maybe represent repolarisation of papillary muscles (contract to pull chordae tendineae to close mitral/tricuspid valves)

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8
Q

what is PR interval?

A

0.12-0.2 seconds = time taken for electrical impulse to travel from SA node through atria to AV node, down bundle of His and into ventricular muscle

  • measure from start if P wave to start of QRS complex (probs should be called PQ interval but isn’t)
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9
Q

what is ST interval? And what do abnormalities suggest?

A

= ventricular depolarisation and repolarisation
changes due to abnormalities from ischaemia (when ventricles contract)

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10
Q

what can alter QT interval?

A

= ventricles contract in the interval
- can be altered genetically

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11
Q

what size are large squares in ECG?

A

5mm, means 0.2 seconds

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12
Q

how do you calculate the heart rate on ECG?

A

300/number of large squares

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13
Q

what do
a) lead I
b) lead II
c) lead III
each run between?

A

a) lead I is between left arm + right arm
b) lead II is between left leg and right arm
c) lead III is between left leg and left arm

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14
Q

where do you place the 6 chest leads?

A

V1 = 4th intercostal space next to sternum on right side

V2 = 4th intercostal space next to sternum on left side

V3 = in between V2 + V4

V4 = 5th intercostal space midclavicular line

V5 = same horizontal level as V5 but in anterior-axillary line

V6 = same horizontal level as V5 but in mid-axillary line

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15
Q

what leads look at left lateral surface of heart?

A

leads I, II and aVL

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16
Q

what leads look at inferior surface of heart?

A

leads III + aVF (lead II also can)

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17
Q

what leads look at right atrium?

A

lead aVR (which combines lead 1,2,3)

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18
Q

what does V1+V2 chest leads look at?

A

right ventricle

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19
Q

what does V3+V4 chest leads look at?

A

look at septum in between ventricles

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20
Q

what does V5+6 chest leads look at?

A

look at anterior and lateral walls of left ventricle

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21
Q

what direction does depolarisation spread to show positive deflection?

A

when depolarisation spreads towards a lead it shows a positive deflection and when away negative deflection

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22
Q

what is shape of QRS complex if mostly positive?

A

r wave greater than s (depolarisation moving toward that lead)

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23
Q

what shape is QRS complex if mostly negative?

A

s wave greater than r (depolarisation moving toward that lead)

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24
Q

what shape is QRS complex if depolarisation moving at right angles?

A

the r and s same is

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25
Q

what is right axis deviation?

A

happens for example when right ventricle hypertrophied so has more effect on QRS so depolarisation swings to right

lead I negative and lead III more positive than lead II

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26
Q

what is left axis deviation?

A

left ventricle hypertrophied so average depolarisation swings to left

lead III and lead II negative (lead I positive)

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27
Q

what is normal axis deviation?

A

is 11 o’clock to 5 o’clock axis so lead II greater positive deflection than I or III

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28
Q

what is shape of QRS in leads looking at right ventricle?

A

right ventricle leads = V1+2, aVR

lead deflection is 1st upwards ( R wave) due to septum depolarisation. then downward deflection (S wave) as main muscle mass depolarised (which bigger in left)

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29
Q

what is shape of QRS in leads looking at left ventricle?

A

left ventricle = V5+6

small downward deflection (septal Q wave) then upward deflection (R wave) as ventricular muscle depolarised. once whole myocardium depolarised it turns to baseline

30
Q

what is the steps of what to look for in a practical approach to analysing ECG?

A
  1. verify patient details - name & DOB
  2. check date & time ECG taken
  3. check calibration of ECG paper
  4. determine the axis
  5. workout heart rate & rhythm - use following rhythm strip ask yourself following questions
    a. is electrical activity present?
    b. is rhythm regular or irregular?
    c. what is heart rate? (300 / n.o large squares)
    d. P- waves present? tells you there is atria activity, makes you think if heart getting excited like normal
    e. what is the PR interval? should be 0.12 - 0.2 seconds
    f. is each P-wave followed by QRS complex?
    g. Is the QRS duration normal? no more than 0.1 seconds (100 ms)
  6. Look at individual leads for voltage criteria changes OR any ST or T-wave changes
31
Q

what is heart block and how many degrees/types is there?

A

heart block is a delay along conduction pathway from SA node to ventricles

there is 1st degree, 2nd degree (mobitz 1+2) and 3rd degree

32
Q

what is 1st degree heart block?

A

PR interval greater than 0.2 seconds (no need for treatment)

33
Q

what is 2nd degree heart block?

A

2 types:

mobitz 1 = progressive lengthening of PR interval until drop beat (no treatment as relatively stable)

mobitz 2 = constant PR interval with P wave associated with every QRS until random dropped beat (treat with atropine, adrenaline, pacing = random rhythm means dangerous)

34
Q

what is 3rd degree heart block?

A

P waves no relation to QRS complex (treat with atropine, adrenaline, pacemaker)

35
Q

what is bundle branch block?

A

reaches interventricular septum normally but problems in right or left bundle branch so delay in depolarisation of ventricles

36
Q

what is important signs of bundle branch block? where should you look?

A

look in chest leads V1-V6!

signs:
wide QRS →if conduction of QRS complex more than 0.12seconds then abnormal

right = MaRRoW
left = WiLLiaM

37
Q

what are the 3 options for causes of tachycardia?

A
  1. ectopic foci
  2. accessory/re-entrant pathways allowing electrical activity to flow back into circuit
  3. increased automaticity of heart
38
Q

what area of tachycardia does
a) narrow QRS suggest?
b) wide QRS suggest?

A

a) supraventricular
b) ventricular

39
Q

what is ventricular tachycardia?

A

= abnormal foci in ventricle, makes wide QRS as abnormal path. no p waves, regular QRS

40
Q

what causes sinus tachycardia?

A

= due to increased firing of SA node (treat underlying cause) - think about drugs, autonomic disorders (stress & caffeine)

41
Q

what is atrial flutter? what leads is it best seen in?

A

= irregularly regular, saw tooth like waves (best seen in lead II, III, aVF)

42
Q

how do you treat atrial flutter?

A

→treat with direct cardioversion (DCCV) where you restart areas of heart in certain specific areas but to completely get rid radiofrequency ablation (also antiarrhythmic drugs)

43
Q

what is atrial fibrillation? what leads is it best seen in?

A

= irregularly irregular rhythm with no P waves (best seen in lead 2 - if no p waves in lead II then none anywhere else)

44
Q

what causes the random QRS complexes in atrial fibrillation?

A

Afib caused by hundreds of ectopic foci and only some picked up by ventricles so just random QRS complex (but they’re normal when do occur)

45
Q

why can atrial fibrillation lead to clotting?

A

less blood flow due to confused contractions

46
Q

what is the PIRATES pneumonic to remember causes of AF?

A

P = Pulmonary embolism, pulmonary disease, post operative

I = ischaemic heart disease, idiopathic

R = rheumatic valvular disease (mitral stenosis or regurgitation)

A = anemia, alcohol, age, autonomic tone (vagal atrial fibrillation)

T = thyroid disease (hyperthyroidism)

E = elevated blood pressure (hypertension), electrocution

S = sleep apnoea, sepsis, surgery

*sepsis, electrolyte and age are common

47
Q

what is management of atrial fibrillation?

A
  1. if acute haemodynamic = emergency DCCV (direct current cardioversion)
  2. chronic - if can return back to normal then think about restoring like anti-arrhythmic, elective DCCV (planned cardioversion)
  3. chronic - if can’t return back to normal then rate control with beta blockers or calcium channel blockers (slowing heart rate minimises damage)
48
Q

what are 2 types of ventricular tachycardias?

A
  • monomorphic VT = regular and similar QRS amplitudes
  • polymorphic VT = irregular rhythm and QRS amplitudes
48
Q

what does Chad Vasc score measure?

A

→score to determine risk of stroke from atrial fibrillation
= need to use anti-coagulant if Chad Vasc score ≥2

49
Q

what is torsades de pointes?

A

twisting of points on ECG = = specific polymorphic VT associated with long QT syndrome

50
Q

what is ventricular fibrillation?

A

rapid & irregular ventricular activation progressing from VT

51
Q

what are the only 2 shockable rhythms?

A

ventricular fibrillation and ventricular tachycardia

52
Q

what are the 4 rhythms you can get when pulseless and what ones are shockable?

A

shockable:
- Ventricular tachycardia
- Ventricular fibrillation

non-shockable:
- Pulseless electrical activity(all electrical activity except VF/VT, including sinus rhythm without a pulse)
- Asystole(no significant electrical activity)

53
Q

what is sinus bradycardia?

A

= normal sinus rhythm can be physiological such as beta blockers or calcium channel blockers
(treat cause)

54
Q

what leads is wolff parkinson white syndrome best seen?

A

best seen in V3 + V4

55
Q

what is wolff parkinson white syndrome?

A

syndrome that - have extra bundle (as well as bundle of His) usually on left side of heart →in these bundles there are no AV nodes to make delay. depolarisation wave reaches ventricles early and pre-excitation occurs (delta wave)
- example of accessory pathway bundle is bundle of kent

56
Q

what is seen on ECG for wolff parkinson white syndrome?

A
  • has delta waves & short PR interval

delta waves = QRS has slurred on upstroke (but rest of QRS is normal as conduction through the his bundle catches up with pre-excitation)

57
Q

how do you treat wolff parkinson white syndrome?

A

treat with radiofrequency ablation (zap out cardiac tissue that’s causing arrhythmia)

58
Q

what is seen on ECG for
a) severe RV hypertrophy
b) severe LV hypertrophy

A

a) R wave much taller than S wave (especially V1,2,3)
b) R wave much taller than S wave (especially in V4,5,6)

59
Q

what are abnormalities with P wave that can be seen on ECG due to
a) RA hypertrophy
b) LA hypertrophy

A

a) peaked p wave
b) broad and bi-fed p wave

60
Q

what is STEMI and NSTEMI?

A

ST elevation = STEMI

non-ST elevation = NSTEMI

61
Q

how can you identify myocardial infarction when NSTEMI?

A

can be seen by lots of T wave inversion

62
Q

what is sign of past MI? (hint = Q wave)

A

if Q wave is wider than 1 small square and deeper than 2mm
*once Q wave developed it’s permanent

63
Q

where would large Q wave be if past MI in lateral part of heart?

A

large Q waves in V5,6

64
Q

where would large Q wave be if past MI in inferior part of heart?

A

large Q waves in lead III, aVF

65
Q

what should ST segment be?

A

should be iso-electric = in line with start of P wave

66
Q

what is ST elevation a sign of?

A

indication of acute MI, due to recent infarction or pericarditis (not localised ST elevation, in most leads)

67
Q

where would ST elevation be if anterior damage?

A

chest leads

68
Q

where would ST elevation be if inferior damage?

A

in leads III, aVF

69
Q

what is ST depression a sign of and when might you see it?

A

depression = sign of ischaemia, rather than infarction

(ST depression can occur during people with angina when they do exercise)

70
Q

when is T wave inversion seen?

A

normal, ischaemia, RV hypertrophy, bundle branch block, digoxin treatment

*take home point - T wave inversion doesn’t necessarily mean ischaemia