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Semester 2 - CVS > 12. Interpreting ECGs : When things go wrong > Flashcards

12. Interpreting ECGs : When things go wrong Flashcards

1
Q

What are the questions to ask to determine if normal sinus rhythm

A

typically look lead II:
• Is the rhythm regular?sinus rhythm?
• Heart rate? (60 -100 bpm)
• Are there p waves?
• Are P waves upright in leads I, II ?
• Is PR interval normal (3 – 5 small boxes)?
– Prolonged if > 1 large box
• Is every p wave followed by QRS?
• Is every QRS preceded by a p wave?
• Is QRS width normal? – Prolonged if > 3 small boxes
• Is corrected QT interval normal? – Prolonged if > 44 small boxes

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2
Q

What are Atrioventricular conduction blocks?

A

Delay/failure of conduction of impulses from atria to ventricles via AV node (more than physiological) and Bundle of His

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3
Q

What are the 3 types of Atrioventricular conduction blocks

A

– First degree heart block
– Second degree heart block
• Mobitz type 1 second degree heart block
• Mobitz type 2 second degree heart black
– Third degree heart block

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4
Q

What are the causes of heart block?

A

– Degeneration electrical conducting system with age – sclerosis and fibrosis - doesn’t conduct as well
– Acute myocardial ischaemia
– Medications
– Valvular heart disease

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5
Q

What is a first degree heart block

A
  • conduction is slowed without skipped beats.
  • All normal P waves are followed by QRS complexes, but PR interval is longer than normal (> 0.2 second)
  • Caused by delayed conduction through the AV node
  • This is usually due to vagal activation, an electrolyte disturbance or an effect of medication e.g calcium channel blockers or beta blockers.
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6
Q

What is a second degree heart block, Mobitz type I

A

Successively longer PR intervals until one QRS is dropped – ie electrical signal not conducted through to ventricles – then cycle starts again with a normal PR interval which progressively lengthens.

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7
Q

What is a second degree heart block, mobitz type II

A

• PR intervals do not lengthen – sudden dropped QRS complex without prior PR changes
• Atrial rhythm (p waves) is regular,
• Ventricular rhythm is irregular
• the drop in QRS could be a regular pattern (may be a fixed ratio of P waves transmitted. For example in a 2:1 block only every second P wave is conducted to the
ventricles, but it can change over time because this type of block is unstable) or random
• symptomatic
• likely to be a problem in the His-Purkinje system

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8
Q

In second degree heart block, mobitz type II, what is there a high risk of?

A

HIGH RISK progression to COMPLETE heart block

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9
Q

What is a third degree heart block

A

• Complete failure of conduction between the atria and ventricles, they work independently - complete failure of AV conduction - No electrical activity conducts down the bundle of His and the ventricles end up depolarising at their own rate B
• No relationship between the P waves and QRS complexes.
• Often the ventricular pacemaker will take over as an escape rhythm, this makes the QRS complex wider because there isn’t use of the his-purkinje systems.
• ventricular pacemaker Typically too slow to maintain blood pressure
• ventricular rate slower than atrial rate as ventricular pacemakers are slow -20-40 bpm
NEED A PACEMAKER ASAP

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10
Q

What is a bundle branch block

A
  • A block in conduction of the right or left bundle – can be Right Bundle Branch Block (RBBB) or Left Bundle Branch Block (LBBB).
  • the blocked bundle delays the depolarisation to the ventricle it supplies.
  • P wave and pr intervals are normal but a wide QRS - – because ventricular depolarisation takes longer
  • There’s no block at the AV node or the bundle of His this explains why each QRS complex will be preceded by a P wave.
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11
Q

What is arrhythmia? How do you detect where it originates

A
  • irregular heart beat
  • Originating in the atria or ventricle
  • To determine where it is originating from, look at the width of the QRS complex (narrow=supraventricular, broad= ventricular)
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12
Q

What are arrhythmia that originate in the atria called?

A

– above the ventricles and therefore

called SUPRAVENTRICULAR Arrhythmia

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13
Q

Where are the 3 places that supraventricular arrhythmia can originate from?

A
  • Sinus node
  • Atrium itself
  • AV node
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14
Q

Where do ventricular arrhythmia originate from?

A

Various areas in the ventricular muscle wall

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15
Q

How is the QRS complex affected in ventricular arrhythmias and why

A

Wide & bizarre QRS complexes

- ventricular conduction pathway is abnormal

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16
Q

Explain what supraventricular tachycardia is

A

Supraventricular tachycardia (SVT) is an abnormally fast heart rhythm that’s due to improper electrical activity in the upper part of the heart (atria).

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17
Q

What are the 4 main types of supraventricular tachycardia

A

Atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff-Parkinson-White syndrome.

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18
Q

What is atrial fibrillation?

A
  • Rhythm arises from multiple atrial foci
  • rapid, chaotic impulses
  • rhythm is defined as irregularly irregular - occurs because of the chaotic electrical activity in the atria
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19
Q

What abnormality is seen in an ECG of atrial fibrillation?

A
  • no p waves, just wavy baseline - because depolarisation not arising from SAN
  • When conducted, ventricles depolarised normally – so normal narrow QRS
  • IRREGULAR R-R intervals
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20
Q

Why is there a variable R-R interval in AF?

A
  • Impulses from different ectopic atrial foci reach AV node at rapid irregular rate
  • Not all are conducted (because of AV node refractory period)
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21
Q

What is the rate like in AF?

A 
• The ventricular rhythm is irregular and the rate depends on how well the electrical activity passes through the AV node – bundle of His to the bundle branches, but is usually rapid (tachycardia).
• Afib can be
– SLOW – ventricular response < 60 bpm
– FAST – ventricular response >100
– Normal rate – 61-99 bpm
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22
Q

What are the haemodynamic effects of AF?

A
  • It means that the normal atrial contraction is lost and that the atria just quiver instead.
  • The loss of atrial contraction leads to increased blood stasis particularly in the left atrium. This can lead to small clots (thombus) in the left atria. This is why atrial fibrillation is a risk factor for ischaemic stroke.
  • The ventricles will contract normally.
  • Heart rate and pulse of the patient will be irregularly irregular.
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23
Q

Discuss Atrial flutter?

A
  • In atrial flutter there are distinct atrial depolarisations but these are happening at a very fast rate and produce a ‘saw-tooth’ appearance.
  • Again the ventricular rate depends on how much of the electrical activity passes to the ventricles.
  • This causes tachycardia but with a regular rhythm
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24
Q

What are premature ventricular ectopic heart beats?

A
  • A ventricular ectopic heart beat is an extra beat or depolarisation that originates in the ventricles rather than by the sinoatrial node.
  • The impulse doesn’t spread via the His- Purkinje system which causes a much slower depolarisation of the ventricular muscle.
  • This is why an ectopic heart beat shows a wide QRS on an ECG and an unusual shape.
  • It’s said to be premature as it occurs earlier than would be expected for the next sinuous impulse.
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25
Q

Are premature ventricular ectopic heart beats symptomatic?

A

May be asymptomatic or cause palpitations without haemodynamic consequences

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26
Q

Describe Ventricular Tachycardia (VTACH)

A
  • Ventricular tachycardia is a type of regular, fast heart rate that arises from improper electrical activity in the ventricles.
  • It’s classed as a sustained serious of 3 or more consecutive PVCs (ectopic heartbeats).
  • VTACH causes a broad QRS complex.
  • A persistent VTACH is dangerous and there’s a risk of progression to ventricular fibrillation.
  • Patients suffering from VTACH will present with lightheadedness, palpitations or chest pain.
27
Q

What is ventricular fibrillation?

A
  • Ventricular fibrillation is a type of cardiac arrhythmia where the heart quivers instead of pumping, this is due to disorganised electrical activity in the ventricles.
  • Abnormal, chaotic, fast ventricular depolarisation
  • You get impulses from numerous ectopic sites in the ventricles.
  • There’s no coordinated contraction.
  • It means that there’s no cardiac output.
  • If this is sustained it can lead to cardiac arrest and death.
28
Q

How do you classify arrythmias?

A
  • Organised into bradycardia and tachycardia
  • Bradycardia can be classified into heart block or simple bradycardia
  • Tachycardia can be classified into broad complex or narrow complex
  • narrow complex include AF, atrial flutter, SVT and sinus tachycardia
  • broad complex includes VT and VF
29
Q

Differentiate between Ischaemia and myocardial infarction.

Discuss the features of each condition that’ll be seen in a test

A

• Ischaemia refers to a restriction in blood supply to tissues which causes a lack of oxygen needed for metabolism.
As this condition doesn’t cause muscle necrosis it means that blood tests will be negative for markers for myocyte necrosis (e,g cardiac troponins)

• A myocardial infarction is a heart attack and it occurs when blood flow to the heart is severely reduced or completely stops. This causes damage to the heart muscle.
With an MI muscle necrosis will be present so therefore blood tests will be positive (e.g cardiac troponins)

30
Q

How can an ECG be used to detect changes due to cardiac Ischaemia or infarction?

A

• The ST segment on an ECG is particularly useful for doing this.

  • The ST segment represents the point at which the ventricular myocytes are all depolarised and that there’s no spread of electrical activity. As there’s no spread the ST segment should be on the baseline.
  • Deviation from the baseline suggests spread of depolarisation due to an ischaemic or infarction area of myocardium.
  • An ST segment depression indicates cardiac Ischaemia or infarction that hasn’t affected the full thickness of the ventricular wall.
  • An ST elevation indicates a full thickness MI.
31
Q

In an ECG of a heart with MI or ischaemia, in which leads will changes be seen?

A
  • Coronary artery narrowing or occlusion leads to ischaemia or infarction (necrosis) of the area supplied by that artery
  • Changes can be seen in leads facing the affected areas as necrotic tissue doesn’t conduct electricity at all and ischaemic tissue conducts differently
  • Need to look at P QRS T all 12 leads
  • Need to know which leads and groups of leads look at different parts of heart
32
Q

What is STEMI and non-STEMI?

A

– STEMI: ST Segment Elevation Myocardial
Infarction
– Non-STEMI: non ST Segment Elevation MI

33
Q

Explain what a STEMI is and the ECG changes that will be seen as a result

A

STEMI stands for ST Segment Elevation Myocardial Infarction.

It’s the most serious type of heart attack where there’s a long interruption to the blood supply. This is caused by a complete occlusion of the coronary artery.

This type of MI will affect the full thickness of the myocardium involved.

On an ECG you’ll see an elevation of the ST segment.

34
Q

What is the earliest sign of STEMI?

A

Sub-epicardial(full thickness) injury causing ST Segment elevation in leads facing affected area is the earliest sign

35
Q

Why does myocardial necrosis and scar tissue from evolving and old infarcts lead to pathologic Q waves?

A

A Q wave is defined as any negative deflection that precedes an R wave.
An abnormal Q wave is indicative of an ongoing or an old MI. The reason an MI can cause these abnormal waves is because there’s no electrical activity in dead tissue as well and thus you don’t get action potentials and electrical current through the damaged and dead tissues.Pathological Q waves persist because they are due to an electrically silent ‘window’ in the wall of the myocardium, effectively allowing the ECG leads to look through the silent region to the opposite wall

36
Q

What needs to be present for q wave to be classed as pathological?

A

For a Q wave to be classed as pathologic it has to be
- > 1 small square WIDE ( > 40 milliseconds)
- > 2 small squares DEEP (mV) - (except leads III & aVR - slightly bigger Q waves may be normal in these leads)
- It’s depth must be more than ¼ of height of subsequent R wave
You have to look at the Q wave in relation to the QRS

37
Q

Are all Q waves pathologic?

A

– NO
– Small Q waves represents normal left-to-right depolarisation of the interventricular septum – typically seen LATERAL leads – I, aVL, V5-V6
– Deeper Q waves (>2 mm) may be seen in leads III and aVR as normal variant (should NOT have any Q waves in leads V1-V3)

38
Q

Are all q waves a sign of an old infarct or depolarization of septum?

A

No.
A pulmonary embolism may also lead to Q waves in lead 3.
To identify that it is a pulmonary embolism you’d also expect to see:
- An S wave in lead 1
- Q wave in lead 3
- An inverted T wave in lead 3

39
Q

From what regions and what thickness of the myocardium is affected in a STEMI?

A

Transmural epicardial injury

  • transmural = full thickness
  • (major coronary arteries are epicaridal)
40
Q

What is a STEMI an indication for?

A

Urgent reperfusion (to prevent/minimise muscle necrosis)

41
Q

How does the ECG of a STEMI change with time?

A
  • acutely there is an ST elevation and the T wave becomes taller
  • few hours, a pathological Q wave develops as the R wave decreases in height
  • after 24 hours, raised troponin I and T showing myocytes death
  • 1-2 days, T eave inversion and Q wave becomes deeper, after a few days the St segment normalises but the Q wave remains decreased
42
Q

Explain what a Non-STEMI is

A

An NSTEMI is a non ST segment elevation MI.
This is when there’s damage to the myocardium due to the partial occlusion of a coronary artery but it doesn’t affect the full thickness of the myocardium. It’s known sub endocardial.
You’d use a blood test for myocyte necrosis (e.g troponins) to test for it.

43
Q

What ECG changes will be seen in Non-STEMI?

A
  • You’ll get ECG changes as a result of the sub endocardial injury.
  • It causes ST segment depression and T wave inversion.
  • On the ECG the area of damage behaves as if an abnormal current traversing damaged tissue is moving away from the recording electrode.
  • Same changes in ECG for both severe ischaemia and Non-STEMI
44
Q

How are T waves affected in Non-STEMI and Ischaemia

A
  • Usually T waves are upright in all leads apart from aVR and V1.
  • However these conditions will cause a symmetrical and deep inversion of the T wave.

• The T wave inversions due to myocardial Ischaemia or non-STEMI occur in leads consistent with anatomical regions perfused by specific coronary arteries.
• E.g In the majority of patients the inferior wall of the heart is supplied by the right coronary artery via posterior descending artery (PDA).
Ischaemia secondary to atherosclerosis in RCA will lead to changes in ECG leads facing inferior aspect of heart - II, III and aVF

45
Q

Explain what a stable angina is and the ECG changes that’ll be seen in this condition

A

Stable angina is chest pain or discomfort that most often occurs with activity and exercise. This is due to the presence of an atherosclerotic plaques that causes fixed narrowing.
On an ECG you’ll see down sloping of the ST-segment depression or elevation with exercise, however at rest these ECG changes will reverse.

46
Q

Explain what an unstable angina is

A

An unstable angina is an acute coronary syndrome that’s defined by the absence of biochemical evidence of myocadial damage. You just have the features of angina e.g prolonged angina at rest or new onset severe angina or angina that is increasing in frequency

Unstable angina means that atherosclerosis plaque has ruptured and there is occlusion of coronary artery but not complete so still some blood flow. Potential infarct of endocardium/ inside of heart. In unstable angina there hasn’t been any infarct of cardiac cells yet.
• Severe ischaemia ≡ unstable angina

47
Q

How is unstable angina shown on ECG?

A

Normal, inverted T waves or St depression - suggestion of ischaemia

48
Q

What is the difference between ischaemia and non-STENI?

A
  • Same changes in ECG for both severe ischaemia and Non-STEMI
  • Severe ischaemia ≡ unstable angina
  • “Unstable angina (UA) is an acute coronary syndrome that is defined by the absence of biochemical evidence of myocardial damage…characterised by specific clinical findings of prolonged (>20 minutes) angina at rest; new onset of severe angina; angina that is increasing in frequency
  • Vs Non STEMI – actual cardiac muscle damage has occurred but NOT though entire wall of heart muscle- sub endocardial
  • Differentiate by blood tests for myocyte necrosis – eg troponin
49
Q

What is hypokalaemia?

A

Hypokalemia is when the bloods potassium levels are too low.

50
Q

Describe the Different levels (baseline, moderate and severe) of hypokalaemia

A

It’s classed as hypokalemia when the potassium level is < 3.5 mmol/L
It’s moderate hypokalemia if the levels are < 3.0 mmol/L
It’s severe hypokalemia is the levels are < 2.5 mmol/L

51
Q

What are the effects of hypokalaemia?

A

Due to decreased extracellular potassium levels you’ll get myocardial hyperexcitability as the resting membrane potential is closer to threshold meaning that an action potential is more likely to be generated.
It can also result in:
- Generalised muscle weakness
- Respiratory depression
- Ascending paralysis
- Palpitations, Arrhythmia, Cardiac arrest

52
Q

Give the ECG changes that’ll be seen in a patient with hypokalemia

A

For a patient with hypokalemia their ECG a will show peaked P waves, T wave flattening and inversion and U waves.
The U wave indicates that it’s a medical emergency and that the patient is at severe risk of a cardiac arres

53
Q

What is hyperkalaemia?

A

Hyperkalemia is when the bloods potassium levels are too high.

54
Q

Describe the Different levels (baseline, moderate and severe) of hyperkalaemia

A
  • Hyperkalaemia: >5mmol/L (5.2 mmol/L in some labs)

* Problems usually develop at higher levels - 6.5 mEq/L to 7 mEq/L - BUT the rate of change also critica

55
Q

What are the effects of hyperkalaemia?

A

Hyperkalemia causes Resting membrane potential becomes less negative and also causes some voltage gated Na+ channels to be inactivated. This causes the heart to be less excitable and results in conduction problems.

This can then lead to:

  • Generalised muscle weakness
  • Respiratory depression
  • Ascending paralysis
  • Palpitations, Arrhythmia, Cardiac arrest
56
Q

What can also cause a change similar to a Non-STEMI in an ECG and how can they be differentiated?

A

Severe ischaemia
- Differentiated by a blood test for myocyte necrosis (e.g. Troponin) which would occur in non-stemi but not in ischaemia

57
Q

What is the earliest sign of hyperkalaemia in an ECG?

A

Tall, peaked T wave

58
Q

How does the ECG change as K+ levels increase from normal?

A
  • tall peaked T wave
  • tall peaked T wave, flattened P wave, prolonged PR interval
  • Tall, peaked T wave, absent p waves (atrial standstill), widened QRS
  • widened QRS, ST segment merges with T wave (to give “sine wave pattern”)
59
Q

How does the ECG change as K+ levels decrease from normal?

A
  • low T wave
  • Low T wave, high U wave
  • Low T wave, high U wave, low ST segment
60
Q

What is the first thing to check for in an ECG?

A

first thing to note is whether it is in sinus rhythm or not. In sinus rhythm each QRS complex is preceded by a P wave. This indicates that electrical activity is being initiated by the sino-atrial node and that atrial depolarization is spreading via the atrioventricular node and bundle of His to generate electrical activity in the ventricles

61
Q

What is the second thing to look for in an ECG?

A

you should assess if the rhythm is regular or irregular and also what the rate is. Is the heart rate unduly slow (bradycardia) or is it unduly fast (tachycardia)?

62
Q

What is the cause of sinus tachycardia?

A

Sinus tachycardia is due to an increased rate of depolarisation of the SA node (>100 bpm); this can be physiological (e.g. exercise), or due to conditions such as thyrotoxicosis or hypotension (sympathetic activation)

63
Q

What is the cause of sinus bradycardia?

A

sinus bradycardia is caused by a reduced rate of
depolarisation of the SA node (<60 bpm); while often present in healthy young athletes, it can be a sign of diseases such as hypothyroidism, ischaemia or the side effect of medication such as beta blockers.

Semester 2 - CVS (20 decks)

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