ECG 2 Flashcards

1
Q

What type of abnormalities can the ECG detect

A

Conduction
Perfusion
Structural

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2
Q

Describe supraventricular abnormalities

A

Originates in atrium or AVN
o Atrial fibrillation.
o Atrial flutter.
o AVNRT – Atrio-Ventricular Nodal Reentrant Tachycardia.

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3
Q

Describe ventricular abnormalities

A

originate in the ventricles
o Ventricular tachycardia.
o Ventricular fibrillation

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4
Q

What are junctional arrhythmias

A

AVN and bundles

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5
Q

Describe conduction abnormalities

A

Not passing through the muscles effectively- not well insulated.

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6
Q

Describe structural abnormalities

A

Left hypertrophy

Left axis or right axis deviation

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7
Q

Describe perfusion abnormalities

A

Blocking or narrowing of arteries
Infarct/ischaemia
Myocytes cannot contract.

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8
Q

What is essential when performing the ECG

A

Reduce voluntary movements- creates noise- may be mistaken for pathology.

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9
Q

What are the first things you should consider when looking at the ECG

A

Correct recording?
Signal quality and leads? (movement can affect)
Voltage and paper speed?
Patient background? CVS/Resp disease? (axis moves to the right in patients with COPD- pulmonary hypotension-right ventricle has to work harder).

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10
Q

Describe a systematic approach for analysing the ECG parameters

A

Rate/Rhythm using R-R interval to calculate HR - regular? Divide 300 by the number of big squares to give HR
P-Wave and PR interval - tells you how long wave takes to pass through atrial myocardium and AVN
QRS duration - should be 120ms - is it broad/narrow?
Evaluate axis - -30 to 120o
ST segment elevation/depression?
QT interval
T wave - shape for electrolyte disturbances

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11
Q

What should you do when looking at rhythm

A

a. Determine the regularity of the rhythm.
i. Regular rhythm but fast/slow. E.G. Fast – tachycardia or slow – bradycardia.
ii. If irregular, determine type of irregularity.
b. Determine cardiac rhythm.
i. E.G. Sinus rhythm (normal cardiac rhythm).

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12
Q

What can the QRS axis tell you

A

a. Orientation in the chest – horizontal in obese patients, otherwise vertical.
b. Thickness of ventricular muscle – Left-shifted axis in left ventricular hypertrophy and right-shifted axis in right ventricular hypertrophy.
c. Abnormalities in direction of depolarisation – Disease in conduction pathways.

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13
Q

Describe the p wave

A

a. Determine amplitude and duration.

b. E.G. Long p wave, often with two peaks suggest left atrial enlargement.

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14
Q

Describe the PR interval

A

Time from atrial à ventricular depolarisation.

a. Time from atrial depolarisation to ventricular depolarisation.
b. E.G. Long PR interval but still with QRS following p wave could be first degree heart block due to delayed conduction through AV node.

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15
Q

Describe the QRS complex

A

Normal duration is <120ms.

a. Determine amplitude of QRS complex.
b. E.G. High amplitude predicts left ventricular hypertrophy.

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16
Q

Describe the QT interval

A

a. Length of time between onset of Q wave and end of T wave reduces as heart rate increases.
b. E.G. Interval can be increased by certain drugs.

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17
Q

Describe the T wave

A

a. Amplitude and duration of T wave and whether it is upright or inverted.
b. E.G. Inverted T wave is a sign of a previous MI.

18
Q

What should you always do when you find an abnormal ECG

A

Double-Check.

19
Q

Describe sinus rhythm

A

Each P-wave is followed by a QRS wave (1:1)
Rate is regular (even R-R intervals) and normal (83 bpm)
Otherwise unremarkable

20
Q

Describe sinus bradycardia

A

Each P-wave is followed by a QRS wave (1:1)
Rate is regular (even R-R intervals) and slow (56 bpm)
Can be healthy, caused by medication or vagal stimulation
Commonly occurs in:
Athletes
Raised Intracranial Pressure
Hypothermia

21
Q

Describe Sinus Tachycardia

A

Each P-wave is followed by a QRS wave (1:1)
Rate is regular (even R-R intervals) and fast (107 bpm)
No loss of conduction as P wave occurs before each QRS.
Is often a physiological response:
Exercise
Fever
Anxiety or excitement
Overactive adrenal gland
Hyperactive SNS
Decreased venous return lowering SV (blood loss).

22
Q

What is meant by an arrhythmia; describe briefly their classification based on an ECG

A

An arrhythmia is any deviation from the heart’s normal rhythm.
Classification:
Tachyarrhythmia (>100bpm) OR bradyarrthymia (<60 bpm)
Supraventricular OR ventricular
Narrow complex (supraventricular) OR broad complex (ventricular)
Persistent OR paroxysmal (intermittent attacks)
Heart block.

23
Q

What is meant by palpitations

A

An awareness of one’s own heart beat.

24
Q

What are sinus bradycardia and sinus tachycardia produced from

A

By autonomic nervous activity and they manifest as changes in rate with a regular rhythm and conduction.

25
Q

Describe Sinus Arrhythmia

A

Each P-wave is followed by a QRS wave
Rate is irregular (variable R-R intervals) and normal-ish (65-100 bpm)

R-R interval varies with breathing cycle
Look at long trace for lead 2- it won’t be continuous

26
Q

Describe how atrial fibrillation appears on an ECG

A

Oscillating baseline – atria contracting asynchronously
Rhythm can be irregular and rate may be slow
A rhythm composed of randomly contracting atria. Irregular-Irregular.
No P waves
QRS irregular but normal shape
V1 shows flutter waves

27
Q

What are the causes of AF

A

The chaotic activity is due to:
The presence of numerous ectopic foci for impulse generation
The presence of numerous re-entry circuits that become repeatedly excited with the atria.
Commonly caused by mitral valve disease, ischaemic heart disease, thyrotoxicosis, hypertension and excessive alcohol consumption.

28
Q

What are the consequences of AF

A

The lack of effective atrial contraction and resulting stasis of blood predisposes to the development of a thrombus in the left atrium, which can throw off emboli that can pass to the brain causing ischaemic stroke in elderly patients.

29
Q

Why does AF affect ventricular activity

A

Impulses are sporadically conducted through the AV node allowing variable time for ventricular filling between beats, producing a characteristic ‘irregularly irregular’ pulse in rate and volume.

30
Q

Describe atrial flutter

A

Regular saw-tooth pattern in baseline (II, III, aVF)

Atrial to ventricular beats at a 2:1 ratio, 3:1 ratio or higher

Saw-tooth not always visible in all leads

Numerous P waves produce ‘saw-tooth’ appearance

QRS complex rate is normal

  • NO isoelectric line due to constant atrial activity.
  • Nearly every third beat of the atrium conduct down to the ventricles as AV node blocks some depolarising wave from conducting.
31
Q

What is mean by heart block

A

Interruptions in the normal conduction through the atrioventricular conduction tissue- can lead to bradyarrhymias
Can be classified as first-, second- or third- degree.

32
Q

Describe first degree heart block

A

Prolonged PR segment/interval caused by slower AV conduction
Regular rhythm: 1:1 ratio of P-waves to QRS complexes
Most benign heart block, but a progressive disease of ageing
* The effects are fairly asymptomatic as cardiac output isn’t really affected

33
Q

Describe second degree heart block (Mobitz 1)

A

Gradual prolongation of the PR interval until beat skipped

Most P-waves followed by QRS; but some P-waves are not

Regularly irregular: caused by a diseased AV node

Also called Wenckebach

Some atrial impulses fail to reach the ventricles whilst others succeed

34
Q

Describe second degree heart block (Mobitz 2)

A

Unexpected non-conducted atrial impulse
P-R and R-R intervals between beats are constant
Analogous to a fracture in the His-Purkynje system which is about to become completely severed- can progress to complete heart block or even sudden cardiac death.
P-waves are regular, but only some are followed by QRS
No P-R prolongation
Regularly irregular: successes to failures (e.g. 2:1).

35
Q

Describe third degree heart block (complete)

A

P-waves are regular, QRS are regular, but no relationship
P waves can be hidden within bigger vectors
A truly non-sinus rhythm – back-up pacemaker in action
The atria and ventricles beat independently of each other
* AV node is not functioning à no conduction.
* The ventricles fire on their own as a back-up mechanism.
* P wave and QRS complexes completely dissociated.
* Notice the p wave follows the QRS, not other way round. This is wrong and very bad.
AVN/myocardium can be auto-rhythmic
Non-sinus with backup pacemakers
P waves regular and fast, QRS regular and slow

36
Q

Describe ventricular tachycardia

A

P-waves hidden – dissociated atrial rhythm
Rate is regular and fast (100-200 bpm

At high risk of deteriorating into fibrillation (cardiac arrest)

Shockable rhythm – defibrillators widely available
Ventricles contract faster than they can fill
* This has a broad QRS and can be deadly.
* Characterises as a rapid, regular, broad QRS complex pattern.

37
Q

What is the cause of ventricular tachycardia

A

When impulses originate from an ectopic focus or a re-entry within the ventricles.

38
Q

Describe ventricular fibrillation

A

Heart rate irregular and 250 bpm and above
Heart unable to generate an output
At high risk of deteriorating into fibrillation (cardiac arrest)
Shockable rhythm – defibrillators widely available
* Broad, irregular QRS complexes that are void of any such pattern.
* Irregular in terms of amplitude and rhythm.
* As the QRS is irregular à problem in ventricles
Vectors will change and do not all look same

39
Q

Describe the causes and consequences of VF

A

There is no effective Cardiac Output, leading to rapid loss of consciousness, as perfusion of the brain is interrupted. Death results unless effective treatment is initiated immediately. This often occurs secondary to MI and is thought to be the underlying arrhythmia in sudden cardiac death.

40
Q

Describe ST elevation

A

P waves visible and always followed by QRS
Rhythm is regular and rate is normal (85 bpm
ST-segment is elevated >2mm above the isoelectric line
Caused by infarction (tissue death caused by hypoperfusion

41
Q

Describe ST depression

A

P waves visible and always followed by QRS
Rhythm is regular and rate is normal (95 bpm
ST-segment is depressed >2mm below the isoelectric line
Caused by myocardial ischaemia (coronary insufficiency