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Cardiac > Making sense of the ECG > Flashcards

Making sense of the ECG Flashcards

1
Q

How much blood is pumped in 1 pump of the heart at rest?

A

Around 70ml

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2
Q

What cells is cardiac muscle comprised of?

A

Myocardial cells (myocytes)

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3
Q

What is the name for the cytoplasmic bridges between myocytes?

A

Synctia

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4
Q

What are the 3 types of myocardial cells?

A
  1. Pacemaker cells - mainly in SAN, produce spontaneous discharge.
  2. Conducting cells - found in AVN, bundle of His, and purkinje fibres
  3. Contractile cells - main type of cells
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5
Q

Where is the SA node located?

A

High in the right atrium

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6
Q

What is the general rate of:

a. the SA node
b. the AV node
c. ventricular contractile cells

A

a. 60 - 100 bpm
b. 40 - 60 bpm
c. 30 - 40 bpm

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7
Q

What are the cardiac action potential phases?

A
  1. at rest, little spontaneous depolarisation due to Na/K/ATPase. Stable potential of -90mV
  2. Rapid opening of Na Channels.
  3. Electrochemical gradient causes Na channel closure and K outflow
  4. Plateau phase, Ca influx while not all K channels open
  5. K channels fully open
  6. Ca, K, Na levels are restored by their respective ATPase pumps
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8
Q

What can influence the SA node?
(4 reasons)

A
  1. Parasympathetic NS (vagus), slows
  2. Sympathetic NS (T1-4), speeds up + increases contractility
  3. Serum concentration of electrolytes
  4. Hypoxia (causes severe bradycardia)

Cardiac drugs can also influence SAN

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9
Q

What is hyperkalaemia and what can it cause?

A

High plasma potassium concentration which can cause severe bradycardia

(note hypokalaemia can cause tachycardia)

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10
Q

What are negative chronotropes and examples?

A

Drugs that reduce heart rate, e.g. beta blockers and Ca channel blockers

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11
Q

What are positive chronotropes and examples?

A

Drugs that increase heart rate e.g. dopamine and dobutamine

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12
Q

What are negative ionotropes and examples?

A

Drugs that decrease heart force of contraction, e.g. beta blockers, calcium channel blockers and some anti-arrhythmic drugs such as flecainide and disopyramide

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13
Q

What are positive ionotropes and examples?

A

Drugs that increase heart force of contraction e.g. dopamine and dobutamine

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14
Q

How long does it usually take for ventricles to depolarise?

A

Less than 0.12 ms

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15
Q

After the bundle of His, what does the left bundle branch divide into?

A

The left anterior fascicle and the left posterior fascicle

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16
Q

What are the 4 phases of the cardiac cycle?

A
  1. Isovolumetric contraction
  2. Ventricular ejection
  3. Isovolumetric relaxation
  4. Ventricular filling

Phase 1&2 = ventricular systole
Phase 3&4 = ventricular diastole

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17
Q

Which side of the heart is the mitral valve in? and how how many cusps?

A

Left side and 2 cusps

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18
Q

Which nerve slows the heart rate (negative chronotrope)?

A

Vagus nerve (parasympathetic)

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19
Q

Which nerves increase the heart rate (positive chronotropes)?

A

Spinal nerves T1 - 4 (keep you off the floor)
sympathetic

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20
Q

What are the standard calibrations of the ECG?

A

10 mm/mV
25 mm/s

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21
Q

In what lead is the p wave and QRS negative?

A

aVR

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22
Q

How long is a normal PR interval?

A

0.12 - 0.2 s (3 - 5 small squares)

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23
Q

What is an R wave?

A

The first positive deflection of the ECG

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24
Q

Where is V4 positioned?

A

5th intercostal space, mid-clavicular line

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25
Q

Where is V3 positioned?

A

Inbetween V4 and V2

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26
Q

Where is V5 positioned?

A

Same horizontal orientation as V4, anterior axillary line

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27
Q

Where is V6 positioned?

A

Same horizontal orientation as V4, mid axillary line

28
Q

What is the purpose of the RL electrode?

A

Acts as a reference to reduce unwanted noise

29
Q

What should you do to the ECG leads when the patient has known dextrocardia?

A

Reverse all of the chest leads

30
Q

How can you calculate the HR for a regular rhythm?

A

300 / No. of large squares between QRS

31
Q

What classifies a QRS complex as broad?

A

> 3 small squares

32
Q

Why does inspiration increase HR?

A

There is an increased volume of blood returning to the heart

33
Q

When should you not treat tachycardia with beta blockers?

A

When the tachycardia is compensating for something e.g. low BP following blood loss
- never try to slow tachycardia until you know the cause

34
Q

What is persistent tachycardia indicative of?

A

It may not be tachycardia (e.g. could be flutter or AF)

35
Q

What is an ectopic beat?

A

A beat that arrives early

36
Q

What is the medical treatment for frequent ectopics causing symptoms?

A

Beta blockers

37
Q

What is paroxysmal AF?

A

Self-terminating episodes of AF usually lasting < 48 hours but can last up to 7 days

38
Q

What is persistent AF?

A

Continuous AF lasting >7 days or requiring DCCV

39
Q

What is long-standing AF?

A

AF lasting over 1 year, but still aim to treat

40
Q

What is permanent AF?

A

AF lasting > 1 year and no plan to restore sinus rhythm

41
Q

What are common symptoms of AF?

A

Breathlessness, palpitations, fatigue

42
Q

What percentage of strokes occur as a result of AF?

A

25%

43
Q

What medications should be used for AF patients?

A

Anticoagulants (if patients refuse these then consider antiplatelets)

44
Q

What are the 3 aspects of AF that need to be controlled and suitable medication examples for each?

A
  1. Reduce stroke risk - anticoagulants
  2. Control ventricular rate - beta/Ca channel blockers
  3. Rhythm control - DCCV (for recent onset, unstable AF)
45
Q

Why is digoxin not preferred as negative chronotrope in AF?

A

Works well at rest but not during exercise

46
Q

If patient is unsuitable for TOE, what should be done before DCCV?

A

Anticoagulation for 3 weeks

47
Q

How is sinus rhythm maintained following AF episode?

A

Prescribe beta blockers or Ca channel blockers (e.g. sotalol, proprafenodone)

Catheter ablation should also be considered

48
Q

What is INR?

A

Effectively clotting time - longer INR = longer for blood to clot

49
Q

What is the atrial rate in flutter?

A

Close to 300 bpm

50
Q

How do treatments differ for AF and flutter?

A

They are often the same

51
Q

How does atrial tachycardia differ from AF?

A

Tachycardia arises from an ectopic focus (can be uni-focus or multifocal)

52
Q

What can digoxin toxicity often cause?

A

Atrial tachycardia with AV block

53
Q

Which direction do most accessory pathways travel?

A

Antegrade - from atria to ventricles

54
Q

How is WPW disease diagnosed?

A

Short PR-interval and delta wave

55
Q

What is the difference between orthodromic and antidromic AVRT?

A

Orthodromic initially travels through AVN then back through AP
Antidromic initially travels through AP and then back through AVN

56
Q

What are 2 quick potential treatments for AVRT?

A

Carotid massage and valsalva manouevre

57
Q

Which drugs treat AVNRT?

A

IV Adenosine

58
Q

What is ventricular bigeminy?

A

Each normal beat is followed by a ventricular ectopic

59
Q

What is a ventricular couplet?

A

A run of 2 consecutive ventricular ectopics

60
Q

What is Brugada syndrome?

A

Abnormally fast heart rate (tachycardia) caused by sodium channelopathy

61
Q

How do you distinguish SA node block from sinus arrest?

A

In SA node block, the P waves reappear in phase

62
Q

What does a positive doppler shift mean?

A

A higher frequency wave is received and the object is moving towards the observer

63
Q

How can you distinguish NSTEMI from unstable angina?

A

NSTEMI are troponin positive

64
Q

How does the ECG evolve in STEMI?

A
  1. No Q wave, ST elevation, hyperacute T waves
  2. ST elevation
  3. T wave inversion
  4. Residual Q wave returns
65
Q

What 4 medications should patients be put on following STEMI?

A

Aspirin, clopidogrel, beta blocker, ACE inhibitor
+ also heparin and a statin

66
Q

How can you distinguish pericarditis from STEMI?

A

ST-elevation is widespread

Cardiac (7 decks)

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