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Year 2 - BRS > 5.8 - Electrocardiography and rhythm disorders > Flashcards

5.8 - Electrocardiography and rhythm disorders Flashcards

1
Q

What are the kinds of abnormalities ECG can tell us about? (3)

A
  • conduction abnormalities
  • structural abnormalities (e.g. ventricular hypertrophy)
  • perfusion abnormalities (e.g. whether muscle is ischaemic or infarct/MI)
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2
Q

What are the advantages of an ECG? (3)

A
  • relatively cheap and easy to undertake
  • reproducible between people and centres
  • quick turnaround on results/report
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3
Q

What is ECG nomenclature? (3)

A
  • electrodes - sticky pads that stick to person, connecting human to machine
  • cables/wires - insulated metal connecting electrodes to machine
  • leads - not a physical entity, view of heart
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4
Q

What is a vector?

A
  • a quantity that has both magnitude and direction
  • typically represented by an arrow in the net direction of movement, whose size reflects magnitude
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5
Q

What do the deflections on an ECG mean?

A
  • upward deflections are towards the +ve electrode
  • downward deflections are towards the -ve electrode
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6
Q

What does the isoelectric line represent?

A

No net change in voltage i.e. vectors are perpendicular to the lead

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7
Q

What is each wave composed of?

A

Both the upstrokes and downstrokes (but does not always have to end on the isoelectric line)

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8
Q

What does the steepness of the deflection mean?

A

The velocity of the action potential

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9
Q

What does the width of the deflection mean?

A

The duration of the event

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10
Q

What is the P wave?

A

The electrical signal that stimulates contraction of the atria (atrial systole)

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11
Q

What is the QRS complex?

A

The electrical signal that stimulates the contraction of the ventricles (ventricular systole)

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12
Q

What is the T wave?

A

The electrical signal that signifies relaxation of the ventricles (ventricular repolarisation)

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13
Q

Where in the ECG does atrial repolarisation occur?

A

Hidden in QRS complex

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14
Q

What happens at the sinoatrial node (SAN - step 1)?

A
  • autorhythmic myocytes
  • atrial depolarisation
  • slow and not a lot of muscle –> wide and small P-wave
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15
Q

What happens at the atrioventricular node (step 2)?

A
  • AVN depolarisation
  • isoelectric ECG (between P and QRS)
  • slow signal transduction (atria empty)
  • protective
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16
Q

What happens at the Bundle of His (step 3)?

A
  • rapid conduction
  • insulated
  • ECG still flat (last part before QRS)
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17
Q

What happens at the bundle branches (step 4)?

A
  • septal depolarisation
    • bundle branches are insulated but bottom of left branch has gaps and lets excitation escape –> septum is innervated
  • small deflection towards -ve electrode (Q-wave)
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18
Q

What happens at the Purkinje fibres (steps 5&6)?

A
  • ventricular depolarisation (big up and down R bit)
  • late ventricular depolarisation (small negative S bit) - as current travels up the Purkinje fibres towards negative electrode
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19
Q

What happens at fully depolarised ventricle (step 7)?

A

Isoelectric ECG

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20
Q

What happens during repolarisation (step 8)?

A
  • ventricular repolarisation
  • slow positive deflection (T wave) - going in same negative direction as S-wave but repolarising not depolarising
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21
Q

What is important to keep in mind about the timing of the ECG wave and the actual heart contraction?

A
  • electrical activity happens first and is quicker - heart muscle takes a little longer to react and pump
  • e.g. P wave triggers atrial systole but it does not reflect it
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22
Q

What are the 6 limb leads?

A
  • lead I
  • lead II
  • lead III
  • aVF
  • aVL
  • aVR
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23
Q

What are the 6 chest leads?

A

V1-V6

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24
Q

What is the rule of Ls for limb leads?

A
  • lead I (1L) –> right arm to Left arm
  • lead II (2L) –> right arm to Left Leg
  • lead III (3L) –> Left arm to Left Leg
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25
Q

How do we read the positive and negative directions of limb leads?

A
  • left to right & top to bottom
  • drawn as a triangle and reading left to right and top to bottom the first electrode of each bipolar pair you reach is the -ve electrode
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26
Q

What does aVL read?

A

Compares electrical activity between a positive electrode on the left arm with the average electrical activity between right arm and left leg (lead II) - think aVL = goes towards Left arm

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27
Q

What does aVF read?

A

Compares electrical activity between a positive electrode on the left leg with the average electrical activity between right arm and left arm (lead I) - think aVF = goes towards Foot (left leg)

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28
Q

What does aVR read?

A

Compares electrical activity between a positive electrode on the right arm with the average electrical activity between left arm and left leg (lead III) - think aVR = goes towards Right arm

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29
Q

How are chest lead electrodes placed on the body?

A
  1. V1 - right sternal border in the 4th intercostal space
  2. V2 - left sternal border in the 4th intercostal space
  3. V4 - mid-clavicular line in the 5th intercostal space
  4. V3 - halfway between V2 and V4
  5. V5 - anterior axillary line at the level of V4
  6. V6 - mid-axillary line at the level of V4
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30
Q

What do each of the leads give?

A

Each of the leads gives a view from one angle of the heart and also of the muscles that a certain heart artery supplies (e.g. ST elevation in leads II, III and aVF suggests RCA blockage)

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31
Q

What are the unipolar vs bipolar leads?

A
  • bipolar - lead I, lead II, lead III
  • unipolar - aVF, aVL, aVR, V1, V2, V3, V4, V5, V6
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32
Q

What plane are the limb leads in?

A

Coronal

33
Q

What plane are the chest leads in?

A

Horizontal

34
Q

Where are the positive and negative electrodes (respectively) for the 12 leads?

A
  • lead I: LA and RA
  • lead II: LL and RA
  • lead III: LL and LA
  • aVR: RA and 1/2(LA+LL)
  • aVL: LA and 1/2(RA+LL)
  • aVF: LL and 1/2(RA+LA)
  • V1: V1 and 1/3(RA+LA+LL)
  • V2: V2 and 1/3(RA+LA+LL)
  • V3: V3 and 1/3(RA+LA+LL)
  • V4: V4 and 1/3(RA+LA+LL)
  • V5: V5 and 1/3(RA+LA+LL)
  • V6: V6 and 1/3(RA+LA+LL)
35
Q

What leads give a lateral view of the heart, and are supplied by the left circumflex artery? (4)

A
  • lead I
  • aVL
  • V5
  • V6
36
Q

What leads give an inferior view of the heart, and are supplied by the right coronary artery? (3)

A
  • lead II
  • lead III
  • aVF
  • (L-shape on LHS of ECG, like anatomical position of RCA in heart)
37
Q

What leads give an anteroseptal / anterior view of the heart, and are supplied by the left anterior descending artery? (4)

A
  • V1 and V2 (anteroseptal, LAD)
  • V3 and V4 (anterior, LAD)
  • (RHS flipped upside down L, like anatomical position of LAD in heart)
38
Q

What lead do we tend to ignore?

A

aVR - upside down

39
Q

How do you calculate heart rate from ECG?

A

300 / big squares

40
Q

How do you calculate cardiac axis from an ECG using trigonometry?

A
  1. calculate the net deflections of both leads II and aVL
    • lead II: +6.5mm positive deflection, -2mm negative deflection = +4.5mm net deflection
    • aVL: +4.5mm positive deflection, -2.5mm negative deflection = +2mm net deflection
  2. draw out lines of the same length as the deflection and in the same directions as the lead (e.g. lead II down at 60, aVL perpendicular)
  3. align them and use trigonometry to work out the angle between:
    • tan(theta) = 2/4.5
    • theta = tan^-1(2/4.5) = 24 degrees
  4. use that angle to find the actual heart axis (by taking away/adding it to the nearest known angle on the diagram)
    • angle = 60 - 24 = 36 degrees
41
Q

What is the ECG reporting procedure? (4)

A
  1. is it the correct recording?
  2. review the signal quality and leads
  3. verify the voltage and paper speed
  4. review the patient background if available
42
Q

What do we review on the ECG? (5)

A
  1. rate and rhythm - normal RR interval?
  2. P-wave and PR interval
  3. QRS duration
  4. QRS axis (normal range -30 to 90)
  5. ST segment (duration, elevation/depression?)
43
Q

What do you do if there is a flatlined asystolic rhythm?

A
  • do not defibrillate - not a shockable rhythm as there is no electrical activity to reset
  • administer adrenaline - can help spontaneously restore shockable rhythm to this asystole (flatline) to get heart working again
44
Q

What is sinus rhythm and what are its features?

A
  • standard heart rhythm
  • each P-wave followed by a QRS wave (1:1)
  • rate is regular (even RR intervals) and normal (60-100bpm)
  • otherwise unremarkable
45
Q

What is sinus bradycardia and what are its features?

A
  • each P-wave followed by a QRS wave (1:1)
  • rate is regular (even R-R intervals) and slow (<60bpm)
  • can be healthy, caused by medication or vagal stimulation
46
Q

What is sinus tachycardia and what are its features?

A
  • each P-wave is followed by a QRS wave (1:1)
  • rate is regular (even R-R) and fast (>100bpm)
  • often a physiological response (i.e. secondary)
47
Q

What is sinus arrhythmia and what are its features?

A
  • each P-wave is followed by a QRS wave
  • rate is irregular (variable R-R interval) and normal-ish (65-100bpm)
  • R-R interval varies with breathing cycle
48
Q

Why can the R-R interval change with breathing cycle in sinus arrhythmia?

A
  • heart wants to natively beat at 110bpm but vagal nerve (through parasympathetic stimulation) slows it down to 70bpm
  • as we breathe in, many adults have vagal stimulation turned down –> small and big gaps in ECG between heart beats = varying heart rate
  • very common and often not pathological
49
Q

What is atrial fibrillation and what are its features?

A
  • oscillating baseline - atria contracting asynchronously
  • rhythm can be irregular and rate can be slow
  • turbulent flow pattern increases clot risk
  • atria not essential for cardiac cycle
50
Q

What is atrial flutter and what are its features?

A
  • regular saw-tooth pattern in baseline (II, III, aVF - RCA leads)
  • atrial to ventricular contractions are at a 2:1, 3:1 or higher ratio
  • saw-tooth not always visible in all leads
51
Q

What is first degree heart block and what are its features?

A
  • prolonged PR interval caused by slower AV conduction
  • regular rhythm - 1:1 ratio of P-waves to QRS complexes
  • most are benign heart block, but some can be a progressive disease of ageing
52
Q

What are the two types of second degree heart block?

A
  • Mobitz I
  • Mobitz II
53
Q

What is second degree heart block (Mobitz I) and what are its features?

A
  • gradual prolongation of the PR interval until beat skipped (normal, slow, slower, beat missed)
  • most P-waves followed by QRS but some P-waves are not
  • regularly irregular (caused by diseased AV node)
  • also called Wenckebach phenomenon
54
Q

What is second degree heart block (Mobitz II) and what are its features?

A
  • P-waves are regular, but only some are followed by QRS
  • no PR prolongation
  • regularly irregular - successes to failures (e.g. 2:1) or random
  • can rapidly deteriorate into 3rd degree heart block (if untreated)
55
Q

What is third degree (complete) heart block and what are its features?

A
  • P-waves are regular (PP interval standard), QRS are regular (RR interval standard), but no relationship
    • P-waves do not lead to QRS complexes (work independently of one another)
  • P-waves can be hidden within bigger vectors
  • a truly non-sinus rhythm –> backup pacemaker needs to be in action
56
Q

What is ventricular tachycardia and what are its features?

A
  • P-waves hidden - dissociated atrial rhythm
  • rate is regular and fast (100-200bpm)
  • at high risk of deteriorating into fibrillation (cardiac arrest)
  • shockable rhythm - defibrillators needed
57
Q

What is ventricular fibrillation and what are its features?

A
  • heart rate irregular and 250bpm and above
  • heart unable to generate an output
  • shockable rhythm - defibrillators needed
58
Q

What is ST elevation and what are its features?

A
  • P-waves visible and always followed by QRS (1:1)
  • rhythm is regular and rate is normal (60-100bpm)
  • ST segment is elevated >2mm above isoelectric line
  • caused by infarction (tissue death caused by hypoperfusion) - MI
59
Q

What is ST depression and what are its features?

A
  • P-waves visible and always followed by QRS (1:1)
  • rhythm is regular and rate is normal (60-100bpm)
  • ST segment is depressed >2mm below isoelectric line
  • caused by myocardial ischaemia (coronary insufficiency)
60
Q

What angles are the limb leads at?

A
  • I: 0
  • II: +60
  • III: +120
  • aVF: +90
  • aVL: -30
  • aVR: -150
61
Q

What can cause axis deviation?

A
  • ventricular hypertrophy (deviates in same direction as hypertrophy) - increased mass of muscle in one side causes bigger deflections and will move axis to same side
  • infarction in muscle in opposite side which disables it and pushes axis to other side
62
Q

What can cause a right axis deviation?

A
  • when the functional myocardium is more heavily concentrated on right hand side of heart
  • right ventricular hypertrophy (as a result of another condition e.g. COPD where increased pulmonary hypertension causes RV hypertrophy and afterload)
  • infarction of muscle in LV
63
Q

What angles make up the normal QRS axis?

A

-30 to +90 degrees

64
Q

What angles are classed as right axis deviation?

A

+90 to +180 degrees

65
Q

What angles are classed as left axis deviation?

A

-30 to -90 degrees

66
Q

What angles are classed as extreme axis deviation?

A

-90 to +/-180 degrees

67
Q

How can leads I and aVF (perpendicular) be used to find the axis of the heart?

A
  • look for net neutrals (means it is perpendicular)
    • if none, not at 3/6/9/12 o’clock
    • if yes, near 3/6/9/12 o’clock
  • compare size of QRS complexes and use it and diagram to figure out depending on size of complexes and whether positive or negative
  • if identical size, near 45 degrees
68
Q

What does ST elevation in leads II, III, aVF indicate?

A

Point to a STEMI in right coronary artery (which those leads are associated with)

69
Q

What diagnostic imaging is needed for third degree heart block and what would you see?

A
  • angiogram - release dye during diastole because that is when heart muscle is perfused
  • would see RCA being tapered at one point and thinner - blockage here
  • most likely atherosclerotic plaque
70
Q

How is third degree heart block treated?

A
  • stent - put balloon to distend artery and put in metal mesh stent to support and keep artery patent
  • bypass - obstruction is still there but you are getting blood supply from a different vessel
71
Q

What are the characteristics of a lateral STEMI? (elevation, reciprocal changes, coronary artery territory involved)

A
  • ST-segment elevation in leads I, aVL and V6
  • reciprocal changes - ST depression in the inferior leads (III and aVF)
  • left circumflex artery involved
72
Q

What are the characteristics of an anterior STEMI? (elevation, reciprocal changes, coronary artery territory involved)

A
  • ST-segment elevation in leads V1, V2, V3, V4
  • no reciprocal changes
  • left coronary artery and left anterior descending artery (LAD)
73
Q

What are the characteristics of an inferior STEMI? (elevation, reciprocal changes, coronary artery territory involved)

A
  • ST-segment elevation in leads II, III, aVF
  • reciprocal changes (ST depression) in leads I, aVL
  • right coronary artery involved
74
Q

What are the characteristics of a posterior STEMI? (elevation, reciprocal changes, coronary artery territory involved)

A
  • ST-segment elevation in leads V7, V8, V9
  • no reciprocal changes
  • right coronary artery and circumflex involved
75
Q

What are the characteristics of a septal STEMI? (elevation, reciprocal changes, coronary artery territory involved)

A
  • ST-segment elevation in leads V1, V2
  • no reciprocal changes
  • left anterior descending artery involved
76
Q

What is the ECG like for NSTEMI/unstable angina?

A
  • ST depression in leads II, III
  • T-wave inversions
77
Q

What is the difference in the pathophysiology between STEMI, NSTEMI, and unstable angina?

A
  • STEMI - nearly always coronary plaque rupture resulting in thrombosis formation occluding a coronary artery, there are several potential causes of this mismatch in NSTEMI
  • NSTEMI - incomplete thrombus formation - this does not stop blood and oxygen completely but the restriction is so great that the oxygen content is used up quickly and, in the distal arteries and arterioles, tissue death occurs as a result of oxygen starvation
    • area affected is small, not enough to cause ST elevation but enough to cause minor ST/T wave changes and troponin elevation
  • unstable angina - plaque becomes unstable, fibrous cap disrupts and thrombus is formed but still enough lumen to meet the demand during rest
78
Q

What is the difference between NSTEMI and unstable angina clinically?

A
  • unstable angina - normal troponins
  • NSTEMI - raised troponins
79
Q

How do you treat unstable angina/NSTEMI?

A
  • risk assessment (aspirin, clopidogrel, heparin, nitrates, b-blockers)
  • low risk - conservative management
    • stress test
    • if negative - discharge
    • if positive - coronary angiography (PCI, CABG, medical treatment)
  • high risk (positive troponin, ST changes, unstable patient) - invasive management (CA, CABG, PCI)

Year 2 - BRS (84 decks)

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