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Phase 2a Sam > ECGs > Flashcards

ECGs Flashcards

1
Q

What is dipolarisation?

A

Depolarization of the heart is the orderly passage of electrical current sequentially through the heart muscle, changing it, cell by cell, from the resting polarized state to the depolarized. It is associated with contraction of the heart muscles

it can be detect by electrodes attached to the surface of the body

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2
Q

What is the intrinsic rate of
a) SA node
b) AV node
c) Ventricular Cells

A

a) 60-100 beats per minute, the dominate pacemaker
b) 40 - 60 beats a minute
c) 20 -45 beats a minute

AV node and Ventricular cells are both backup pacemakers

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3
Q

What is represented by
a) one small box
b) one large box

In terms of length and time?

A

Each (small) horizontal box corresponds to 0.04 sec (40 ms) and has a length of 1 mm

Heavier lines forming larger boxes (thatinclude five small boxes) hence represent 0.20 sec (200 ms) intervals and are therefore 5mm or 0.5 in length

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4
Q

What is the direction of impulse conduction through the heart, that is shown in an ECG?

A

SA node => AV node => Bundle of His (IV Septum) => Bundle Branches => Purkinje Fibres

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5
Q

What is shown by the PR interval?

A

P wave (So atrial depolarisation) and the delay in transmission at the AV node, so allows for ventricles to fill with blood

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6
Q

Explain what happens in myocytes when a wave of depolarisation is conducted through them.

What does Dipole mean

A

The wave of depolarisation is cells of the Myocardium (that are normally negative at rest) become briefly positive.

As this current flows through each cell, the cells that are depolarised at any given time will have a positive charge, while their neighbouring cells will be resting/negative. The difference in charge across the two cells can be referred to Dipole, as there are two electric poles

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7
Q

What does a wave of depolaristaion look like on an ECG?

A

This can be seen as a Vector, with Magnitude (size) and direction . The movement of charge from negative to positive creates a positive upwards deflection

Dipole always goes from Positive to Negative

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8
Q

On ECG paper,
What does one large box represent vertically?

A

Large box vertically - 0.5mV

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9
Q

What does the trace given on the ECG paper from each lead represent?

A

Vector sum of the electrical activity of all the cells in the heart, across the the two poles of each lead.

The ECG trace reflects the net electrical activity at a given moment. Consequently, activity in one direction is masked if there is more activity, eg, by a larger mass, in the other direction.

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10
Q

What does a postive deflection show?

A

Depolarisation waves moving towards an electrode

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11
Q

What does negative downwards deflection show?

A

Depolarisation waves moving away from an electrode

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12
Q

Where is the reference and exploring electrodes for
a) Lead I
b Lead II
c) Lead III

Draw it out

A

a) Runs from Right arm (-ve) to Left arm (+ve)

b) Runs form Right arm (-ve) to Left leg (+ve)

c) Runs from Left arm (-ve) to left leg (+ve)

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13
Q

Where do the augmented bipolar leads:

Where is the reference (negative) and exploratory (positive) for the
aVR, aVL, aVF leads?
In other words, where do they go from and to?

A

aVF lead - looks at the flow of charge going from the The computed average charge of arm electrodes to the left leg

avR lead - looks at the flow of charge going from the The computed average charge from the left arm and left leg going to the right arm

avL lead - looks at the flow of charge going from the The computed average charge from the right arm and left leg going to the left arm

Again, always negative to positive! See picutre

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14
Q

Where is the reference and exploratory terminals for the unipolar V1-6 leads?

A

The reference/negative terminal is approximately at the centre of the thorax, more precisely in the centre of Einthoven’s triangle. –> It represents the average of the electrical potentials record in the limb electrodes

The chest leads are derived by comparing the electrical potentials at the centre of Einthoven’s triangle to the potentials recorded by each of the V1-V6 electrodes placed on the chest wall, thus creating 6 chest leads

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15
Q

What ECG leads look at the lateral side of the heart?

A

Lead I,
Lead aVL
V5 and V6

Lateral = THEREFORE LOOKING AT THE CIRCUMFLEX ARTERY

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16
Q

What ECG leads look at the anterior side of the heart?

Therefore what vessel is predominantly looking at?

A

Leads V3 and V4

DRAW IT OUT

Therefore looking at right coronary artery

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17
Q

What ECG leads look at the Inferior side of the heart?

A

Leads II,
Leads III and
aVF lead

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18
Q

Which ECG leads look at the Septum of the heart?

What coronary artery would this be looking at?

A

leads V1 and V2

AKA LAD artery

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19
Q

ECG basic Rules - How long should a healthy PR interval last?

A

3 - 5 little squares - 0.12-0.2 seconconnds

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20
Q

ECG basic Rules - how long should a healthy QRS complex last?
Where does a QRS complex go from and to

A

No more than 3 little squares

It is from Q-S

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21
Q

ECG basic Rules - It what leads should the QRS complex be predominantly upright in?

A

Lead I and Lead II

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22
Q

ECG basic Rules - In what lead are all waves negative in?

A

Lead aVR

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23
Q

ECG basic Rules - In what leads should the R wave grow in? (the top wave of QRS complex)

A

R wave must grow from at least V1 to V4 leads

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24
Q

ECG basic Rules - In what leads should the P waves be upright?

A

Leads I, Leads II and Leads V2 through to V6

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25
Q

ECG basic Rules -In which leads should the T wave Must be upright?

A

Leads I, Leads II and Leads V2 - V6

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26
Q

What is the appearance of the P wave in Left atrial enlargement?

What leads would this be best seen?

A

Notched/Bifid P waves,
Like M, for Mitral, left atria

Best seen in Limb leads

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27
Q

What is the appearance of the P wave in right atrial enlargement?

What leads would this be best seen?

A

Tall, Pointed P waves, greater tahn 2.5mm

Think Right Atria - P for Pulmonale, P for pointed

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28
Q

What is reciprocal change on an ECG? In what condition would you see it?

A

Reciprocal change – sometimes seen in STEMI.

When here is ST DEPRESSION in some leads, in the presence of ST elevation in others.

Occurs as the ECG leads are viewing the heart from different angles.
ST depression will typically occur in leads viewing the heart at the opposite angle to those showing ST elevation.

Taken from almostadoctor

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29
Q

Exceeding what parameters would deem a Q wave to be pathological?

A

Greater than 2mm (Two small boxes deep)
as well as being greater than one small (1mm) box wide/ greater than 40milliseconds/0.04 seconds

or, Greater than 25% of the amplitude of the subsequent big R wave

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30
Q

What is the Axis?

A

The axis on an electrocardiogram (ECG) shows the direction of electrical current flow in the heart. It is determined by measuring the direction of the electrical vector of the QRS complex across the frontal plane.

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31
Q

What are some Pathological common causes of tachycardia?

A

Atrial fibrillation, Atrial Flutter
Supraventricular tachycardia
Focal atrial tachycardia

Ventricular tachycardia
Ventricular fibrillation

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32
Q

What are some common causes of bradycardia?

A

Conduction tissue fibrosis
Ischaemia
Inflammation/infiltrative disease
Drugs
AV conduction problems

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33
Q

Outline the normal conduction pathway of the heart.

A

Sinoatrial node (pacemaker)
Atrioventricular node
Bundle of His
Right and left bundle branches
Purkinje fibres

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34
Q

When would you see sinus tachycardias? What is it defined as?

A

HR >100 BPM

Physiological response to exercise and excitement

Also occurs in:
Anaemia
Fever
Heart failure
Thyrotoxicosis
Acute PE
Hypovolaemia
Atropine

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35
Q

What is the management of sinus tachycardia?

A

Management:
Correction of cause
Beta blockers e.g. bisoprolol to slow sinus rate

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36
Q

Define what a Supraventricular Tachycardia is. What are the 4 types? What is the most common?

A

Any tachycardia which arises from the atrium or AV junction

Atrial fibrillation
Atrial flutter
AV nodal re-entry tachycardia (AVNRT) MOST COMMON
AV reciprocating tachycardia (AVRT)

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37
Q

Supraventricular Tachycardias - What is atrial flutter? What things characterise it?

A

It is irregular ORGANSIED atrial firing, around 250 - 300BPM (conduction pathway typically from around opening of tricuspid valve
Often associated with AF
Atrial HR = 300 BPM
Ventricular rate = 150/100/75 BPM (due to AV node conducting every 2nd/3rd/4th beat “flutter beat” , so see at least 2 P waves for every QRS complex - but QRS complexes will be regular

ECG - see flutter waves, which are a saw-tooth pattern of atrial activation, most prominent in leads II, III, aVF, and V1

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38
Q

Supraventricular Tachycardias - Name some causes of atrial flutter

A
  • Idiopathic (30%)
  • Coronary heart disease
  • Thyrotoxicosis
  • COPD
  • Pericarditis
  • Acute excess alcohol intoxication
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39
Q

Supraventricular Tachycardias - Outline the pathophysiology behind atrial flutter.

A

It is caused by the electrical signal re-entering/ re-circulating back into the atrium, due to an extra electrical pathway

It goes round and round, without interruption, so Atrial contraction is at 300bpm

The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction.

Can be sudden and brief in episodes, or on going

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40
Q

Supraventricular Tachycardias - what would you see on an ECG that would indicate Atrial flutter?

A

ECG: regular sawtooth-like atrial flutter waves (F waves) with P-wave after P-wave

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41
Q

Supraventricular Tachycardias - what is the management of atrial flutter?

A
  • Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
  • Rate/rhythm controlwith beta blockers or cardioversion (*use of electric shock to put heart back into rhythm)
  • Radiofrequency ablationof the re-entrant rhythm (Uses heat generated by radio waves to destroy tissue)
  • Anticoagulationbased on CHA2DS2VASc score
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42
Q

Supraventricular Tachycardias - What characterises AV nodal re-entry tachycardia (AVNRT)?

A

Most common type of SVT - AV nodal re-entry tachycardia (AVNRT)
Twice as common in women than men

The electrical conduction of the atrium re enters back through the AV node, Due to the presence of a “ring” of conducting pathways in the AV node, of which the “limbs” have different conduction times and refractory periods
This allows a re-entry circuit and an impulse to produce a circus movement tachycardia

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43
Q

Supraventricular Tachycardias - What is AV reciprocating tachycardia? What is the best known type of this?

A

The eletrcial signals goes back in the atria via an accessory pathway.

The best known type of this is Wolff-Parkinson-White Syndrome, there is an accessory pathway (bundle of kent) between atria and ventricles

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44
Q

Supraventricular Tachycardias - what is the are the key presentations of someone with AV nodal re-entry tachycardia/AV reciprocating Tachycardia?

(What’s the slightly rogue one)

A

Presentation
Regular rapid palpitations – abrupt onset and sudden termination
Neck pulsation – JV pulsations
Polyuria – due to release of ANP in response to increased atrial pressure during tachycardia
Chest pain and SOB

Symptoms
Palpitations
Dizziness
Dyspnoea
Central chest pain
Syncope

45
Q

Supraventricular Tachycardias - What would you see on an ECG of someone with AV Nodal re-entry tachycardia?

A

P waves are either not visible, or are seen immediately before or after the QRS complex (short PR interval)
QRS complex is a normal shape because the ventricles are activated in the normal way (down bundle of His)

46
Q

Supraventricular Tachycardias - what would you see on an ECG for AV Nodal Reciprocating Tachycardia? (WPW syndrome)

A

The early depolarisation of part of the ventricle leads:

  • shortened PR interval
  • slurred start to the QRS (delta wave)
  • QRS is narrow
    Patients are also prone to atrial and occasionally ventricular fibrillation
47
Q

What is a Delta wave? Why does it occur?

A

“ A delta wave is slurring of the upstroke of the QRS complex.

Occurs because the action potential from the SA node is able to conduct to the ventricles very quickly through the accessory pathway

=> QRS occurs immediately after the P wave, making the delta wave.

48
Q

Supraventricular Tachycardias - What is the initial management of AV Nodal re-entry tachycardia and AV Reciprocating tachycardia?

A

Breath-holding
Carotid massage - massage the carotid on one side gently with two fingers.
Valsalva manoeuvre - Pt blows hard into resistance

49
Q

Supraventricular Tachycardias - if carotid massage and Valsalva manoeuvre are unsuccessful, what can you give to treat AVNRT and AVRT?

A

If manoeuvres unsuccessful, IV adenosine
Causes a complete heart block for a fraction of a second
Effective at terminating AVNRT and AVRT

50
Q

Supraventricular Tachycardias - What is Atrial fibrilation?

A

Atrial fibrillation is where the contraction of the atria is uncoordinated, rapid and irregular. This is due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node.

This disorganised electrical activity in the atria also leads to irregular conduction of electrical impulses to the ventricles.

51
Q

What does atrial fibrillation lead to?

A
  • Irregularly irregularventricular contractions
  • Tachycardia
  • Heart failuredue topoor fillingof the ventricles duringdiastole
  • Risk ofstroke
52
Q

What are some common causes of atrial fibrillation?

A

PE/COPD
IHD, Heart failure
Rheumatic heart disease, Valve abnormalities
Alcohol intake
Thyroid issues - Hyperthyroidism
Sleep Apnoea
Electrolyte disturbances - Hyper/Hypo Kalaemia, Hypo magnesia

PIRATE

53
Q

What are some signs and symptoms of AF?

A
  • Irregular irregular pulse
  • Hypotension:red flag; suggest haemodynamic instability
  • Evidence of heart failure:red flag; such as pulmonary oedema
  • Palpitations
  • Dyspnoea
  • Chest pain: red flag
  • Syncope: red flag

Can also be asymptomatic!

54
Q

What investigations would you carry out for AF

A

ECG

Tests to look for causes of AF:
Serum Electrolytes
Thyroid Function Tests
Cardiac biomarker - eg Troponin
Chest x-ray look for heart failure
Transthorasic Echo - look for functional heart disease

55
Q

What would you see on an ECG for someone in AF?

A

Irregularly irregular
F (Fibrillatory) waves
No clear P waves
Rapid QRS complex
absence of [isoelectric]
baseline
variable ventricular rate

56
Q

What is the management for someone who is haemodynamically unstable with AF? What signs could indicate that this is the case?

A

Emergency electrical synchronised DC cardioversion

  • Shock: hypotension (systolic blood pressure <90 mm Hg), pallor, sweating, cold, clammy extremities, confusion or impaired consciousness
  • Syncope
  • Myocardial ischaemia
  • Heart failure:
57
Q

What is the first line management for someone who is haemodynamically stable with AF? What signs could indicate that this is the case? What Rate control would you do?

A

Start by controlling either rate of rhythm

Rate control:
- First line: beta-blocker(e.g. bisoprolol) or arate-limiting calcium-channel blocker (e.g. verapamil)
- Digoxin: may be considered first-line in patients with AF and heart failure

OF HAEMODYNAICALLY STABLE, DO RATE CONTROL BEFORE RHYTHM CONTROL

58
Q

What Rhythm control would you do in AF?

A

Rhythm control: - either pharmacological or electrical cardioversion
- Pharmacological: - anti-arrhythmics
- Flecainide or amiodarone: if no evidence of structural/ischaemic heart disease
- Amiodarone: if structural/ischaemic heart disease is present
- Electrical cardioversion:rapidly shock the heart back into sinus rhythm

IF HAEMODYNAICALLY UNSTABLE, DO RHYTHM CONTROL BEFORE RATE CONTROL (aka Cardioveresion)

59
Q

What Further management might be necessary for persistent AF/ or AF that has not been treated with meds

A

Left atrial ablation - small burns/freezes to scar heart tissue to break up electrical signals that cause irregular heartbeats

Electrical DC cardioversion

Anticoagulants - DOACS - Apixaban to reduce risk of strokes, or Warafarin if DOACs are CI, (aka in Metal heart valves)

60
Q

Anticoagulants are often given to patient with AF to reduced their likelihood of developing clots that can cause strokes.
What scoring system is used to calculate stroke risk in AF? What types of factors are included on it?

A

CHADS2VASc score used to calculate stroke risk in AF

0 = no anticoagulation
1 = consider oral anticoagulation or aspirin
2 = Anticoagulants - DOACS - Apixaban to reduce risk of strokes

Congestive Heart failure = 1
Hypertension = 1
Age > 75 = 2
Age 65-74 = 1
Diabetes Mellitus = 1
Stroke or TIA = 2
Vascular disease = 1
Female sex = 1

61
Q

Where are the 2 places in which conduction of the heart can be blocked?

A

Block in AVN or bundle of His = AV block
Block in lower conduction system = Bundle Branch Block (RBBB or LBBB)

62
Q

What are the types of heart block?

A

First Degree Heart Block
Second Degree Heart Block Either Mobitz type I, (Wenckebach), or Mobitz Type II
Third Degree Heart Block

Bundle Branch Block

63
Q

Describe what first degree heart block is.

A

Occurs where there is delayed atrioventricular conduction through the AV node but every atrial impulse leads to a ventricular contraction.

A first-degree AV block is usually harmless and doesn’t need any treatment. It could be suggestive of a more serious AV block in the future, so depending on the PR interval, it might be wise to avoid taking medications that could cause blocking.

64
Q

What would first degree heart block look like on ECG?

A

It reflected by a prolonged PR interval (>0.20s) on the ECG, so greater than 5 small boxes

There is a 1/1 ratio between P waves and QRS complexes in first-degree AV block

65
Q

Name some causes of first degree heart block. What is the management for it?

A

Caused by:
LEV’s disease - idiopathic fibrosis and calcification of the electrical conduction system of the heart.
IHD – scar tissue from myocyte death blocks conduction pathway
Myocarditis
Hypokalaemia

Management – asymptomatic so no treatment required

66
Q

What is second degree AV block I? What characterises it?

A

Also known as Wenckebach Block

Generally caused by an AV node block, so conductions get weaker until a P wave fails to conduct down into a QRS complex, missing a beat.

At this point pacemaker cells in the ventricles kick in, and PR interval returns to normal

67
Q

What would you see on a an ECG for someone with Second degree heart block, Mobitz type I?

A

a growing PR interval until a P wave that does not send an electrical signal to the ventricles.

This is followed by an absent QRS complex, after which the PR interval returns to normal before gradually increasing again until another QRS complex is absent. This cycle can keep repeating.

68
Q

What characterises second degree Mobitz type II heart block?

A

This is where there is intermitted failure or interruption of AV conduction. This results in missing QRS complexes. There is usually a set ratio of P waves to QRS complexes ==> eg 3 P waves in a row that conduct to QRS, followed by a P wave with no QRS = a 3:1 block.

The PR interval remains normal.

There is a risk of asystole with Mobitz Type 2.

69
Q

What are the differences between Mobitz type I and type II heart blocks on an ECG?

A

The PR interval may be normal or prolonged, however it is constant in length unlike second-degree AV block Mobitz Type I (Wenckebach) in which the PR interval progressively lengthens until a P wave is not conducted.

A second-degree type II AV block indicates significant conduction disease in this His-Purkinje system and is irreversible (not subject to autonomic tone or AV blocking medications).

70
Q

What is third degree heart block?

A

No action potentials are conducting through the AV node, So atrial depolarisations are completely unrelated to ventricular depolarisations

Ventricles have to make action potentials on their own, so ventricular rate is slow, around 30-40 bpm

71
Q

What would you see on an ECG for someone with third degree AV heart block?

A

So you would have Regular P-P intervals and Regular R-R intervals
But a Lack of an apparent relationship between the P waves and QRS complexes.

72
Q

What is the management for AV blocks?

A
  • If stable: observe
  • If unstable or risk of asystole
    • First line: atropine500mcg IV
    • If no improvement:
      • Atropine500mcg IV repeated
      • Otherinotropes(such as noradrenalin)
      • Transcutaneous cardiac pacing(using a defibrillator)
  • In patients with high risk ofasystole
    • Temporary transvenous cardiac pacingusing an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
    • Permanent implantable pacemakerwhen available - needed in 3rd Degree heart block
73
Q

What are the common causes of a Left bundle branch block?

A

Causes: ischaemic heart disease, hypertension, cardiomyopathy, idiopathic fibrosis

74
Q

What heart block is this?

(I know recognising conditions off ECGs isn’t in the exam Shek but wouldn’t want this to get to easy) #hustle

A

Second degree heart block, Mobitz Type 2

2:1 ratio.

75
Q

What are the common causes of a right bundle branch block?

A

pulmonary embolism, cor pulmonale, ischaemic heart disease, atrial/ ventricular septal defect

76
Q

Bundle Branch blocks:
What is a
a) Bifascicular block?
b) Complete Block?

A
  • Bifascicular block: blockage of right bundle branch and left anterior fascicle
  • Complete block: failure of all bundle branches
77
Q

What happens in a right bundle branch block?

A

The left ventricular wall depolarises as normal, but
The right ventricular walls are eventually depolarised by the left bundle branch, this occurs by a slower, less efficient pathway. (late activation of the right ventricle)

78
Q

What happens in a left bundle branch block?

A

Depolarisation down the bundle of His occurs only via the right bundle branch. The septum is abnormally depolarised from right to left.

The right ventricular wall is depolarised as normal.
The left ventricular walls are eventually depolarised by the right bundle branch, this occurs by a slower, less efficient pathway.

It is always pathological

79
Q

What would a left bundle branch blockage look like on an ECG?

A
  • Deep S wave in V1 and a tall late R wave in V6
  • WilliaM: QRS looks like a W in V1 and V2, QRS looks like an M in V4-V6

When assessing whether a broad QRS complex is LBBB or RBBB, the appearances of V1 and V6 are often enough to provide the answer using the WiLliaM and MaRroW technique.

80
Q

What would a right bundle branch blockage look like on an ECG?

A
  • Wide, slurred S wave in V6 and as a tall late R wave in V1
    • MarroW: QRS looks like an M in V1, QRS looks like a W in V5 and V6

When assessing whether a broad QRS complex is LBBB or RBBB, the appearances of V1 and V6 are often enough to provide the answer using the WiLliaM and MaRroW technique.

81
Q

Define ventricular tachycardia - what could it lead to?

A

Rapid ventricular beating that may result in inadequate ventricular filling

Ventricular tachycardia (VT) occurs due to rapid, recurrent ventricular depolarisation from a focus within the ventricles. This is commonly due to scarring of the ventricles following myocardial infarction.

82
Q

What are the main causes of ventricular tachycardia?

A

Ischaemia and coronary artery disease (CAD)

Other forms of structural heart disease, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy

83
Q

What is the pathophysiology behind ventricular tachycardia?

A

areas previously scarred regions of slowed conduction due to ischaemia, or MI can lead to rapid, recurrent ventricular depolarisation from a focus within the ventricles

84
Q

What causes a prolonged QRS complex on an ECG?

A

Multiple depolarisations of the ventricles, originating not from the atria

85
Q

Do supraventricular tachycardias have wide or narrow QRS complexes?

A

Narrow unless present with bundle branch block

86
Q

What conditions do you see wide-complex QRS tachycardias?

A

Ventricular tachycardia,
Ventricular fibrillation
Torsades de pointes

87
Q

How would you treat a patient with VF?

A

Treatment if they are haemodynamically unstable with a pulse- do a cardioversion and look for underlying cause try and solve.

Consider using antiarrhythmic medication amiodarone

If stable then use adenosine/amiodarone then cardiovert if not successful

88
Q

What causes a QRS complex to be broad?

A

A broad QRS complex occurs if there is an abnormal depolarisation sequence – for example, a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle

89
Q

What is the pathophysiology behind Torsades de Pointes?

A

secondary due to long QT period

Due to long QT period, there a longer time before ventricular repolarisation - and in this time spontaneous depolarisations of the ventricles can occur

If this happens ventricles continue to stimulate recurrent contractions without normal repolarisation - known as Torsades De pointes

90
Q

What are ventricular ectopics?

A

Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria.

Can occur in healthy patients, but are more common in people with underlying heart conditions e.g. ischaemic heart disease or heart failure).
Can present with weird, brief palpitations

91
Q

What do ventricular ectopics look like on an ECG?

A

They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.

92
Q

Name some causes of prolonged QT

A

Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)

93
Q

What is the management of Torsades de Pointes

A

Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs

is the asynchronous delivery of energy, such as the shock is delivered randomly during the cardiac cycle

94
Q

What are the 2 shockable rhythms for a cardiac arrest?

A

Ventricular tachycardia
Ventricular fibrillation

If it has a V, give it the D ( for Defibrillator lol)

95
Q

What are the two non-shockable rhythms?

A

Asystole- when there is no electrical activity
Pulseless electrical activity

96
Q

What is the cardiac axis

A

Average direction of spread of depolarisation wave through the ventricles as seen from the front
- from -30 degrees to +90 degrees

97
Q

What angles of the cardiac axis are deemed to be
Left Axis deviation
Right Axis deviation

A

Anything less than -30 = Left axis deviation
Anything more than +90 = right axis deviation

98
Q

What condition is right axis deviation associated with?
What does it look like on an ECG?

A

Lead III has the most positive deflection and lead I should be negative.
Right axis deviation is associated with right ventricular hypertrophy.

99
Q

What conditions is left axis deviation associated with?
What does it look like on an ECG?

A

Lead I has the most positive deflection.
Leads II and III are negative.
Left axis deviation is associated with heart conduction abnormalities.

100
Q

in what condition would you see tall tented T waves

A

Hyperkalaemia (“tall tented T waves”)
Hyperacute STEMI

101
Q

What would Right atrial enlargement look like on an ECG?

A

Tall P wave

102
Q

What would left atrial enlargement look like on an ECG?

A

Broad notched Bifid P wave

103
Q

What would Hyperkalaemia look like on an ECG?

A

Flat P wave
Prolonged PR interval
Tall, Peaked T wave
Wide QRS

Go, Go long, Go tall, Go wide

104
Q

What would Hypokalaemia look like on an ECG?

A

ST Depression,
Flat, inverted T wave
presence of a U Wave

U Wave

Comes after T wave, - ‘U’ waves are thought to represent repolarization of the Purkinje fibres.

105
Q

What is a U wave?

A

The U wave is a small (0.5 mm) deflection immediately following the T wave, its polarity is the same as the T wave, meaning that they will both be in the same direction

may be a sign of hypokalemia or drug effect or toxicity

106
Q

What would Hypercalcaemia cause on an ECG?

A

Short ST segment, and Widened T wave, Shorted QT interval

107
Q

What would Hypocalcaemia cause on an ECG?

A

Prolonged ST segment
Prolonged QT interval

108
Q

What does a wave of depolaristaion look like on an ECG?

A

This can be seen as a Vector, with Magnitude (size) and direction . The movement of charge from negative to positive creates a positive upwards deflection

Dipole always goes from Positive to Negative

Phase 2a Sam (18 decks)

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