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103 theme 3 > Introduction to the ECG > Flashcards

Introduction to the ECG Flashcards

1
Q

What is the heart

A

a functional syncytium with gap junctions electrically coupling cells

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2
Q

what is a functional syncytium and a syncytium

A

Syncytium = one large cell having many nuclei that are not separated by cell membrane (eg skeletal muscle cells)
Functional syncytium = many cells functioning as one

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3
Q

what the 3 types of cardiac myocyte cells

A

Pacemaker cells – settle heart rhythm
Conducting cells – transmitting rhythm throughout heart
Contractile cells – contracting heart to the rhythm

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4
Q

how does speed of propagation vary

A

contractile – atrial and ventricular myocytes 0.3-0.5 m/s
Conducting system (modified cardiomyocytes) eg Purkinje fibres – up to 5m/s (compared fastest neurons about 100 m/s)
AV nodes 0.05 m/s slow

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5
Q

how is electrical impulse conducted through the heart

A

Signal starts in SA node
Travels to av bundles in atrium
Fibrous skeleton doesn’t allow for electrical signal to pass so has to pass through av node
Travels in conducting system (bundle of his, branches) to ventricles

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6
Q

how does impulse spread through the antra

A

Internodal bundles conduct impulse form SA node to AV node
4 specialised bundles in the atria (contain purkinje like cells – cardiomyocytes modified to conduct) in direct contact with atrial muscle

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7
Q

what do internodal bundles ensure in the atria

A

Bundles ensure synchronous contraction of the atria

Conducting via atrial muscle would be slow (0.3-0.5m/s) so conducts faster via bundles (1 m/s)

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8
Q

what happens to the impulse at the av node

A

only point where the wave of depolarisation passes from atria to ventricles (ventricles insulated by connective tissues from atria)
AV node delays wave of excitation from A to V by 1-2 s (V contract after, permit longer and more effective filling)
AP is conducted very slowly in AV node (composed of small modified cardiomyocytes, electrical conduction between adjoining cells is weaker)

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9
Q

how does the av node conduct action potential slowly

A

AP is conducted very slowly in AV node (as its composed of small modified cardiomyocytes and electrical conduction between adjoining cells is weaker)

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10
Q

how does ventricular propagation occur

A

AV nodes connects directly to bundle of his followed by purkinje fibres
Purkinje are very large myocytes – transmit the impulse faster (bigger diameter cells conduct faster)
Transmit the impulse rapidly to the main mass of ventricles (from there slower conduction between contractile myocytes can occur)
First part of v wall depolarised is septum apex and av groove

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11
Q

what is an ECG

A

Is a gross electrical measurement of the hearts electrical activity

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12
Q

How does an ECG work

A

The individual currents of cardiac myocytes are tiny (few nano amps)
Currents can be detected from wrist and ankle, nearly 1 metre from heart
Possible due to heart being functional syncytium so large groups of cells all make electrical changes simultaneously

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13
Q

what can an ECG diagnose

A

Excellent for rate (so is pulse, holter monitor (ECG) allows 24/7 rate det), esp useful when atrial is different to ventricular rate
Many subtleties (not a one stop diagnosis, patient history essential for interpretation)
Diagnosis req other techniques (but ecg fast and affordable)

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14
Q

what are leads

A

Seen on ecg depends on placement of electrodes

A lead is a configuration of the electrodes (usually a positive, negative and sometimes ground)

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15
Q

what is a standard 12 lead ECG

A

A standard 12-lead ECG looks at heart from 12 different angles, creating measurements for 12 leads with 10 electrodes
Lead II is a positive electrode on left leg, negative on right arm and ground on right leg (ground could be almost anywhere)
Lead II most shown/used in teaching

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16
Q

what are the 12 standard leads

A

3 bipolar leads I,II,III seen frontal plane (positive and negative opposite sides of heart)
3 augmented leads
6 precordial leads

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17
Q

what are the elements of a 12 lead ECG

A

Normal 12 lead ECG has
Switching leads shown by vertical lines (and small citations)
Bottom tracing (aqua) shows a long reading from a single lead (II) – consistency of rhythm in bottom strip

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18
Q

what is the P-wave

A

depolarisation of atria in response to SA node triggering

first bump

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19
Q

what is the PR segment

A

delay of AV node to allow ventricular filling (Start of P to start of QRS complex)

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20
Q

what is the QRS complex

A

depolarisation of ventricles, triggers main pumping contractions
Tall peak with two dips either side (Q R S)

21
Q

What is the ST segment

A

beginning of ventricle depolarisation, should be flat

end of QRS to start of t wave

22
Q

what is the t wave

A

ventricular depolarisation, last bump

23
Q

what is indicated with a wide and misshaped QRS complex

A

V conduction is abnormal eg ectopic pacemaker or bundle branch block
More cells give a bigger contribution – almost no conduction from His and conduction system
Large (deep) waves are a sign of dead tissue (old MI)

24
Q

what is sinus rhythm

A

When the heart rhythm is generated from SA node
Each P wave is followed by QRS complex (and vice versa)
When the PR interval must be normal (3-5 little boxes)
Sinus tachycardia – specifically driven by SA node beating too quickly
It has normal pr intervals, each p matched with a QRS

25
Q

what causes sinus tachycardia

A

specifically driven by SA node beating too quickly

It has normal pr intervals, each p matched with a QRS

26
Q

what is the QT interval

A

start of the QRS to end of T wave

27
Q

what are the boxies used on an ECG

A

Small - 0.04 sec and 0.1 mv

Large (5x5 small boxes)

28
Q

what are the normal durations of the PR interval

A

3-5 boxies (120-200 ms)

29
Q

what are the normal durations of the QRS complex

A

2-3 boxies (80-120 ms)

30
Q

what is the normal duration of the QT interval

A

9-11.5 boxies (360-460 ms)

31
Q

how is rate calculated on an ECG

A

Horizontal scale is 2.5cm/sec

To calculate rate count how many boxes between two P waves

32
Q

how is ventricular rate calculated on an ECG

A 
count between R waves
Rate = 300/big boxes or 
1 big box = 300 bpm
2 boxes = 150 bpm
3 =100
4=75
5=60
6=50
10=30
33
Q

How is CVS rate and contractility controlled autonomically

A 
The heart – parasympathetic input via vagus nerve (muscarinic stimulation decreases heart rate, contractility and conduction velocity 
Sympathetic input (sympathetic stimulation increases above)
34
Q

what is the effect of sympathetic/parasympathetic withdrawal

A

Parasympathetic withdrawal increases heart rate, contractility and conduction velocity
Can be caused by Atropine – muscarinic agonist
Vasculature not innervated by PS system
Sympathetic input to heart via Stellate nerves,
beta agonists increase rate and beta blockers decrease

35
Q

what are heart blocks

A

type of dysrhythmia, any kind of impulse conduction blocked (includes AV block, bundle branch block etc)

36
Q

what are AV heart blocks

A

A delay of failure of atrial signalling stimulating ventricle

37
Q

what are the causes of heart blocks

A 
Ischaemia of av node/bundle
Compression of AV bundle by scar or calcified tissue
Inflammation of av node or bundle 
Symptoms 
Asymptomatic 
Palpitations
Hypotension-like: dizziness, malaise, syncope
Risk of sudden death
38
Q

what is first degree heart block

A 
When pr interval is greater than 5 little boxes (200ms)
But all p’s followed by QRS 
Almost always asymptomatic
Often young people 
Delayed av node transmission
Rarely treated
39
Q

what is mobitz type 1

A

Second degree heart block some p waves blocked and not followed by QRS – some QRS missing
Mobitz type 1 (Wenckebach)
Pr interval gets longer until QRS wave fails to follow p wave
Likely cause is av node damage
Usually no treatment given

40
Q

what is mobitz type 2

A

Some P waves are blocked and not followed by QRS but Pr intervals always remain same
aka Hay
Likely bundle of His
High risk – can progress to 3rd degree HB
Treatment implant pacemaker

41
Q

what is 3rd degree heart block

A

Atrial systoles consistently fail to arrive at ventricles
V rate is consistent
Time between a beats and v beats is variable
Pr intervals varies radically – sometimes greater than 12 boxes (p and qrs very inconsistent)
Intrinsic v rate is slow (less than 60 bpm, eg 40)
A beats consistent (not always visible)

42
Q

what are ectopic beats

A

Escape beats and premature beats
Individual abnormal beats
These beats often triggered by ventricular tissue (or av node)

43
Q

what are premature beats

A

Premature beats triggered by irritable tissue

44
Q

what are escape beats

A

Escape beats (late) triggered by natural rhythmicity of non-atrial tissue, occur when signal is very delayed (wait for SA node but only so long)

45
Q

how is premature ventricular contraction characterised

A

Unusually wide (width determined by slow conduction velocity) and weird looking electrical activity
No S wave, instead a wide negative dip where t wave should be
Often beat triggered in middle of myocardium
The two ventricles electrically unsynchronised so delayed and ineffective conduction (non-purkinje)

46
Q

what is atrial fibrillation

A

Disorganised electrical activity in atria (no P wave, instead a flat or wiggly line)
Ventricular rate is fast and irregular (many signals reach AV node)
Very common in the elderly
Can lead to thrombus formation in atrium due to slow blood flow (stroke risk, need anti-coagulants)

47
Q

what is respiratory sinus arrhythmia

A

beat is slightly faster during inspiration, slightly slower during expiration
Normal: sign of healthy heart
Usually only in children and athletes
Caused by respiratory centres in medulla
Observe ventricular rate : inverse of RR interval

48
Q

what is is an interval and segment

A 
Interval= duration of start from one marker to end of another marker
Segment= the wave form between 2 other waves
49
Q

what is a ST segment elevation

A

is a sign of acute MI
Iso-electric baseline is from end of T to next P wave
ST elevation means ST segment doesn’t go back down to iso-electric baseline

103 theme 3 (20 decks)

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