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Cardiac > Making sense of the ECG > Flashcards

Making sense of the ECG Flashcards

(66 cards)

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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
Where is V3 positioned?
Inbetween V4 and V2
26
Where is V5 positioned?
Same horizontal orientation as V4, anterior axillary line
27
Where is V6 positioned?
Same horizontal orientation as V4, mid axillary line
28
What is the purpose of the RL electrode?
Acts as a reference to reduce unwanted noise
29
What should you do to the ECG leads when the patient has known dextrocardia?
Reverse all of the chest leads
30
How can you calculate the HR for a regular rhythm?
300 / No. of large squares between QRS
31
What classifies a QRS complex as broad?
> 3 small squares
32
Why does inspiration increase HR?
There is an increased volume of blood returning to the heart
33
When should you not treat tachycardia with beta blockers?
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
What is persistent tachycardia indicative of?
It may not be tachycardia (e.g. could be flutter or AF)
35
What is an ectopic beat?
A beat that arrives early
36
What is the medical treatment for frequent ectopics causing symptoms?
Beta blockers
37
What is paroxysmal AF?
Self-terminating episodes of AF usually lasting < 48 hours but can last up to 7 days
38
What is persistent AF?
Continuous AF lasting >7 days or requiring DCCV
39
What is long-standing AF?
AF lasting over 1 year, but still aim to treat
40
What is permanent AF?
AF lasting > 1 year and no plan to restore sinus rhythm
41
What are common symptoms of AF?
Breathlessness, palpitations, fatigue
42
What percentage of strokes occur as a result of AF?
25%
43
What medications should be used for AF patients?
Anticoagulants (if patients refuse these then consider antiplatelets)
44
What are the 3 aspects of AF that need to be controlled and suitable medication examples for each?
1. Reduce stroke risk - anticoagulants 2. Control ventricular rate - beta/Ca channel blockers 3. Rhythm control - DCCV (for recent onset, unstable AF)
45
Why is digoxin not preferred as negative chronotrope in AF?
Works well at rest but not during exercise
46
If patient is unsuitable for TOE, what should be done before DCCV?
Anticoagulation for 3 weeks
47
How is sinus rhythm maintained following AF episode?
Prescribe beta blockers or Ca channel blockers (e.g. sotalol, proprafenodone) Catheter ablation should also be considered
48
What is INR?
Effectively clotting time - longer INR = longer for blood to clot
49
What is the atrial rate in flutter?
Close to 300 bpm
50
How do treatments differ for AF and flutter?
They are often the same
51
How does atrial tachycardia differ from AF?
Tachycardia arises from an ectopic focus (can be uni-focus or multifocal)
52
What can digoxin toxicity often cause?
Atrial tachycardia with AV block
53
Which direction do most accessory pathways travel?
Antegrade - from atria to ventricles
54
How is WPW disease diagnosed?
Short PR-interval and delta wave
55
What is the difference between orthodromic and antidromic AVRT?
Orthodromic initially travels through AVN then back through AP Antidromic initially travels through AP and then back through AVN
56
What are 2 quick potential treatments for AVRT?
Carotid massage and valsalva manouevre
57
Which drugs treat AVNRT?
IV Adenosine
58
What is ventricular bigeminy?
Each normal beat is followed by a ventricular ectopic
59
What is a ventricular couplet?
A run of 2 consecutive ventricular ectopics
60
What is Brugada syndrome?
Abnormally fast heart rate (tachycardia) caused by sodium channelopathy
61
How do you distinguish SA node block from sinus arrest?
In SA node block, the P waves reappear in phase
62
What does a positive doppler shift mean?
A higher frequency wave is received and the object is moving towards the observer
63
How can you distinguish NSTEMI from unstable angina?
NSTEMI are troponin positive
64
How does the ECG evolve in STEMI?
1. No Q wave, ST elevation, hyperacute T waves 2. ST elevation 3. T wave inversion 4. Residual Q wave returns
65
What 4 medications should patients be put on following STEMI?
Aspirin, clopidogrel, beta blocker, ACE inhibitor + also heparin and a statin
66
How can you distinguish pericarditis from STEMI?
ST-elevation is widespread

Cardiac (7 decks)

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