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Cardiorespiratory Biology > ECG Arrhythmias > Flashcards

ECG Arrhythmias Flashcards

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1
Q

ECG provides info on

A

about rate, rhythm and the timing of events in the cardiac cycle
– arrhythmias, conduction blocks
heart muscle

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2
Q

what do increased voltage in ECG suggest

A

increased muscle mass - hypertrophy

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3
Q

what do wider waves suggest

A

slowed conduction

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4
Q

what does left axis deviation mean

A

left ventricle hypertrophy
more muscle mass pulls depolarisation to the left
deflections in lead I get bigger but aVF get smaller

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5
Q

what does right axis deviation mean

A

– right axis deviation
– right ventricle hypertrophy
– more muscle mass, pulls depolarisation to the right
– deflections in AvF get bigger, while lead I gets smaller

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6
Q

how is delayed conduction conveyed

A

elongated PR interval, QRS or QT

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7
Q

when is ST depression seen

A

– only seen in leads pointing towards damage ischaemia

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8
Q

when is ST elevation seen

A

(infarction)
– only seen in leads pointing towards damage
– acute infarction, full thickness of the myocardium

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9
Q

tachycardia

A

> 100 bpm

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10
Q

bradycardia

A

<60 bpm

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11
Q

name 2 types of irregular rhythms

A

regularly irregular - irregular pattern

irregularly irregular - does not repeat an irregular pattern

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12
Q

arrhythmia

A

It collectively describes a change in the normal sequence of electrical impulses

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13
Q

causes if arrhythmia

A

altered rate - too fast or too slow
irregular patterns
conduction problems

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14
Q

how does ischaemia affect the heart

A

disrupt individual membrane potential in individual myocytes

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15
Q

• Sinus tachycardia and cause

A

: increased rate but normal rhythm
– mainly sympathetic as in exercise or secondary to low blood pressure
– also increased high temperatures or cardiac toxicity

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16
Q

Sinus bradycardia

A

decreased rate but normal rhythm
– seen in athletes, low rate but larger stroke volume
– increased vagus (PNS) activity (e.g. carotid sinus syndrome)

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17
Q

Sinus arrhythmia:

A

a regularly irregular rhythm from the SA node
– Cross talk between cardiorespiratory signals
– heart rate increases on inspiration

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18
Q

Arrhythmias may arise due to a number of reasons

A
  1. Changes in automaticity
  2. Triggered activity (after depolarisation)
  3. Conduction delay and appearance of re-entry circuits
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19
Q

is the SA alone in its automaticity

A

The SA node is not alone in its automaticity

– but it is the fastest

20
Q

SA node depolarisation rate what does the its rate depend on?

A

depolarisation rate 60-100/min

– depends on the autonomic nervous system

21
Q

AV node depolarisation rate

A

depolarisation rate 40-50/min

22
Q

Purkinje fibres depolarisation rate

A

depolarisation rate ~35/min

23
Q

Afterdepolarisations

A

abnormal stimuli outwith the normal activity

24
Q

types of afterdepolarisations

A

early (EAD) or delayed afterdepolarisations (DAD

25
Q

when do EADs occur

A

EADs occur when stimulation occurs during the plateau (Phase 2) or repolarisation phase (Phase 3)

26
Q

when do DADs occurs

A

DADs occur during Phase 4 (resting) and trigger depolarisation, but
before the time normally expected
– due to elevated Ca2+
levels

27
Q

what parts of the heart DONT depolarise

A

blood vessels, damaged fibrotic tissue

28
Q

what happens when depolarisation in regions of heart that dont typically depolarise

A

When depolarisation hits these areas it cannot go through, but must go around
can be a problem if there new route is longer than typical path of conduction

29
Q

issues that can arise when typical path of conduction is deviated to longer path of conduction

A

– fibrous plaques or dilated heart increases path length
– ischaemia slows conduction, due to high K+ and depolarisation
– this goes back to the refractory period

30
Q

paroxysmal tachycardia

A

• Bursts of tachycardia due to re-entry pathways

– classified by origin: either ventricular or supraventricular

31
Q

types of paroxysmal tachycardia

A

ventricular and supraventricular

32
Q

what can ventricular paroxysmal tachycardia lead to?
what is ventricular paroxysmal tachycardia?
what are its causes?

A

may lead to fibrillation and death
– fibrillation is the uncoordinated depolarisation
– usually due to ischaemic damage or some drugs

33
Q

supraventricular paroxysmal tachycardia

A

it originates above the ventricles so is either atrial or AV node
– atrial (inverted P wave) or AV node (hidden P wave)
– more common in young, seldom has morbidity

34
Q

fibrillation

A

• Rather than the coordinated spread of depolaristion through the
heart this is uncoordinated and sporadic

35
Q

Atrial fibrillation

A

no coordinated depolarisation of the atria, so no P wave

– irregular transmission to ventricles, irregularly irregular tachycardia

36
Q

Ventricular fibrillation

A

individual myocytes depolarising so no discernible waveform

– no coordinated contraction, no cardiac output

37
Q

ectopic beats of the atria

A

These are premature contractions due to abnormal impluses from
ectopic (abnormal) foc

38
Q

causes of ectopic beats of atria

A

– areas of ischaemia (altered membrane potential)
– excessive stretch of muscle fibres
– drug actions

39
Q

what does ectopic beats of atria look like on ECG

A

– show up as extra P wave and weak pulse on the ectopic beat
Looks similar to premature AV node contraction
weak pulse no P wave

40
Q

ectopic beats of ventricle

A

premature ventricular contractions (PVCs)

41
Q

what does ectopic beats of ventricles look like on ECG

A

• Present as a widened and QRS and inverted T wave
– conduction through muscle is slower than conducting system
– the slow conduction means fibres that depolarised first also repolarise first

42
Q

causes of Ectopic beats

A

Minor PVCs caused by drugs (nicotine/coffee) but others are major
and may lead to fibrillation

43
Q

heart block

A

• Decreased or total block of AV conduction

– due to ischaemia/compression/inflammation of AV-node

44
Q

how is 1st degree heart block characterised

A

the delay in conduction

– characterised by an increased PR interval (>0.2 sec or one large box)

45
Q

how is 2nd degree heart block characterised

A

the increased delay

– so that now some QRS complexes are dropped (PQRS > P > PQRS > P…)

46
Q

how is 3rd degree heart block characterised

A

3rd Degree is the complete block
– ventricles contract (automaticity /”ventricular escape”) but slower (~40 bpm)
– SA node still firing but no relationship between P and QRS

Cardiorespiratory Biology (25 decks)

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