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ESA 2 > CVS session 7: electrocardiogram > Flashcards

CVS session 7: electrocardiogram Flashcards

1
Q

Why can electrodes on the surface of the body detect electrical changes in the myocardium?

A

The myocardium undergoes electrical changes at the same time, generating a large changing electrical field which can therefore be detected on the surface by EXTRACELLULAR RECORDING (so looks different to ventricular and pacemaker potentials as these are intracellular)

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2
Q

What do the electrodes “see”?

A

Two signals with each systole: one on depolarisation and one on repolarisation. Also detects the changing signal which the excitation produces.

These combine to give the ECG

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3
Q

Function of gap junctions?

A

Myocytes are connected by these to coordinate depolarisation, giving synchronous and rapid contraction
There is a pause between atrial and ventricular contraction

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4
Q

Describe the electrical pathway of the heart

A

SA node discharges depolarisation
Spreads via internodal tracts (specialised cells with gap junctions) across atria to AV node
Pause of 120ms at AV node before reaches bundle of His
Bundle of His divides the septum and spreads depolratisation as the atria are electrically isolated from the ventricles by AV valves
Reaches left bundle branch fractionally earlier than right bundle branch
Purkinje fibres depolarise the rest of the ventricles (more slowly)

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5
Q

In which direction does the heart repolarise?

A

From epicardium (outer) to endocardium (inner)

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6
Q

In which direction does the heart depolarise?

A

From endocardial to epicardial

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7
Q

What is an ECG lead?

A

An electrical picture of the heart, which inspects it in frontal (standard leads) and horizontal (chest leads). Each lead looks from a different direction, each with different electrical activity, therefore the ECG pattern in each lead is different. An imaginary line between two electrodes
10 electrodes are attached and computed into 12 leads

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8
Q

Which leads are unipolar and which are bipolar?

A

UNIPOLAR: read from the labelled positive electrode, and utilise several other electrodes as the negative. Chest leads (V1-V6) and augmented leads (AVR, AVL and AVF)

BIPOLAR: uses one positive-sensing electrode and one negative electrode from standard limb leads (I, II and III) in configuration of Einthoven’s triangle. Best readings from body aspects of limbs. Lead II looks from the apex of the heart so is best for looking at rhythm

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9
Q

How does the direction of depolarisation/repolarisation affect the ECG trace?

A

Depolarisation:

  • moving TOWARDS electrode=POSITIVE deflection
  • moving AWAY from electrode=NEGATIVE deflection

Repolarisation:

  • moving TOWARDS electrode=NEGATIVE deflection
  • moving AWAY from electrode=POSITIVE deflection
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10
Q

What determines amplitude of signal?

A 
How much muscle is depolarising
How directly towards the electrode this happens
-directly towards/away=big
-obliquely towards/away=smaller
-at right angle=no signal
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11
Q

What might confound the ECG trace?

A

Lead confounders
Muscle contraction (need to avoid movement, shivering, talking, coughing)
Interference e.g. alternating current
Poor electrode contact (sweat, cable pull, hair)

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12
Q

How does each lead view the heart?

A

DRAW DIAGRAM! To properly understand

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13
Q

Where are the electrodes placed?

A

Chest leads:
V1 – 4th intercostal space – right sternal edge
V2 – 4th intercostal space – left sternal edge
V3 – midway between V2 & V4
V4 – 5th intercostal space – mid clavicular line
V5 – anterior axillary line – same horizontal level as V4
V6 – mid-axillary – same horizontal level as V4

Limb leads:
Red-right arm (shoulder/wrist)
Yellow-left arm (shoulder/wrist)
Green-left leg (ASIS/ankle)
Black-right leg (ASIS/ankle)
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14
Q

Draw a typical ECG trace from lead II. What does each landmark represent?

A

Draw and where to measure
P: atrial depolarisation
Q: depolarisation of interventricular septum (laterally)
QRS: depolarisation spread through ventricle. This masks atrial repolarisation
S: depolarisation from apex upwards from ventricles (So downwards as moving away from lead II, which views from the bottom)
T: ventricular repolarisation, from epicardial to endocardial surface

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15
Q

What are the normal values for the intervals measured on an ECG?

A

P-R interval: 3-5 small squares (120-220 ms)
QRS complex: 3 small squares (120 ms)
QT interval: 9-11 small squares (360-440 ms)

ECG machine must be calibrated: standard signal of 1 mV should move the graph 1cm vertically (2 large squares), so calibration signal included in every graph

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16
Q

What do the squares on an ECG mean?

A

ECG standard speed at 25 mm/s
1 large square= 5 mm = 0.2 s = 200 ms
1 small square= 1 mm = 0.04 s = 40 ms
There are 5 large squares per second, so 300 large squares per minute

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17
Q

How is heart rate measured using an ECG?

A

If rhythm is REGULAR: count the number of large squares in 1 R-R interval, and divide 300 by this number

If rhythm is IRREGULAR: count the number of R-R complexes in 30 large squares (6 seconds), then multiply by 10

18
Q

Which lead is used to assess rhythm?

A

Lead II rhythm strip: a long (~10s) reading

19
Q

Describe a simple method to check rhythm

A

Mark on paper a few R waves, then move paper alongn and see if they still line up (if they do=regular).

Irregular:

  • pattern to irregularity=regularly irregular
  • no pattern to irregularly irregular
20
Q

Describe the factors that need to be looked at when assessing rhythm

A
  1. p waves
    - present/normal/absent
    - normally upright in leads I and II
    - no p waves and irregular QRS: probably AF
    - apparent absence of p waves and narrow QRS could be SVT
    - saw-toothed shaped p wave: atrial flutter (SAN firing v. fast, AVN only lets through every 2nd/3rd/4th impulse so HR predictable (150, 100 or 75 bpm)
  2. Cardiac axis-normal/left or right deviation
  3. PR interval
    - normal/long/short
    - estimates conduction in AV node and bundle of His
  4. Relationship between p wave and QRS: is every p followed by a QRS, and every QRS preceded by a p?
  5. QRS complexes
    - narrow means rhythm originating in atria (normal)
    - broad means rhythm originates in ventricles or there is a bundle branch block so depolarisation has to spread down a back route
  6. ST segment: elevated/depressed?
  7. T waves: present/inverted?
21
Q

What heart rate do the following, regular R-R intervals correspond to?

A 
Large squares vs. HR:
1-300
2-150
3-100
4-75
5-60
6-50
22
Q

Describe the sinus rhythms

A

SINUS RHYTHM:

  • normal
  • depolarisation initiated by SA node
  • rate 60-100 bpm
  • normal p wave followed by QRS and each QRS preceded by a p

SINUS BRADYCARDIA

  • sinus rhythm with a rate 100 bpm
  • associated with exercise, fear, pain, haemorrhage or thyrotoxicosis
23
Q

Atrial fibrillation

A

Multiple abnormal atrial pacemakers discharging randomly, so atrial depolarisation is chaotic and thus contraction is inefficient “quivering”. AV node continuously receives depolarisation waves of varying strength, so depolarisation spreads at irregular intervals down the bundle of His

ECG:

  • no p waves
  • irregularly irregular rhythm and HR
  • normal QRS (as conduction into and out of ventricles is by the normal route)
24
Q

First degree heart block

A

Each wave of depolarisation that originates in the SA node is conducted to the ventricles, but there is a delay somewhere in the pathway. This is not an issue in itself, but may be a sign of coronary heart disease or acute rheumatic carditis

ECG:

  • normal p wave and QRS
  • PR interval prolonged due to slow conduction in AV node and bundle of His due to ischaemia/degenerative change
25
Q

Second degree heart block

A

Excitation fails to pass through AV node/bundle of His

TYPE 1 (/Mobitz type 1/Wenkebach phenomenon):

  • progressive lengthening of PR interval, until 1 p wave isn’t conducted (allows time for AV node recovery), then cycle repeats
  • regularly irregular
  • due to problem at AV node
  • can be caused by beta blockers, reversible ischaemia

TYPE 2 (/Mobitz type 2)

  • intermittent non-conducted p waves without lengthening of PR interval. “all or nothing” unlike Mobitz 1, as suddenly don’t conduct an impulse
  • sudden lack of conduction of a beat: dropped QRS (a p is not followed by a QRS). Usually a bundle branch problem
  • usually caused by structural damage to conduction system e.g. fibrosis, necrosis
  • high risk of progression to complete hear block, so requires a pacemaker
  • if block distal to BoH produces wide QRS; if in His bundle produces narrow QRS
26
Q

How does the shape of an ECG change in chest leads compared to limb leads?

A

P wave and T wave still the same

27
Q

Third degree heart block

A

Complete heart block
Normal atrial contraction, but no beats conducted to ventricles. Ventricles excited by a slow “escape mechanism”, so only a few QRS complexes arise

ECG:

  • p waves normal but not related to QRS
  • QRS usually wide and abnormal shape

Causes:

  • acute phenomenon in MI
  • chronic due to fibrosis of BoH or block of both bundle branches
  • often a progression from type II

High risk of sudden death; need pacemaker urgently

28
Q

What are ectopic foci?

A

Abnormal pacemaker sites within the heart that display automaticity. Normally suppressed by the higher rate of the SA node. Can occur within the atria or ventricles

29
Q

Ventricular ectopic beats

A

Ectopic focus in ventricle, causing depolarisation to spread through muscle not Purkinje fibres (much slower). Abnormal QRS as ventricular extrasystole (usually no important)

30
Q

What is ventricular tachycardia?

A

A run of 3 or more ventricular ectopic beats. QRS becomes broad, excitation spreads through abnormal path in all 12 leads with no identifiable p or T waves. Is a shockable rhythm; can progress to VF

31
Q

Describe the differences between atrial and ventricular fibrillation

A

AF:

  • chaotic atrial depolarisation
  • impulses conducted irregularly to ventricles
  • ventricular depolarisation and contraction occur
  • pulse and HR irregularly irregular

VF:

  • ventricular muscle fibres contract independently causing abnormal, chaotic, fast ventricular depolarisation
  • very dangerous: cardiac arrest will happen and unconscious
  • no QRS complex; ECG completely irregular
  • no cardiac output: no pulse or heart beat –>cardiac arrest
32
Q

Ischaemic heart disease

A

Partial occlusion of coronary arteries:

  • poor myocardial perfusion esp. in exercise
  • pain on exercise : ANGINA
  • ECG often normal at rest but changes in exercise: horizontal depression of ST segment with upright T wave usually implies ischaemia (not infarction)

Acute occlusion by thrombus:

  • death of part of myocardium
  • myocardial infarction
33
Q

What is defibrillation?

A

The discharge of a high voltage field to depolarise the whole heart, allowing an organised rhythm to emerge

34
Q

Myocardial infarction

A

ECG features of a fully-evolved MI in leads facing infarcted area:

  • ST segment elevation due to sub-epicardial injury
  • pathological Q waves due to myocardial necrosis: >1 small square wide and >2mm deep presenti n full thickness MI. Once developed they’re permanent
  • T wave becomes inverted: often permanent. If not full thickness MI, T wave inverted but no path Q waves. Normally seen in VR and V1; sometimes in III, V2 andV3

Acute anterior MI: free wall of left ventricle. Marked ST elevation in V1-V4: very early sign of MI. Show injured but not dead; maybe can reperfuse heart

35
Q

What is the cardiac axis?

A

The average overall direction of spread of ventricular depolarisation, as seen from the front. See most easily in QRS complex of leads I, II and III

Normally is orientated downward and to the right (-30 to + 90 degrees). R wave should be tallest in lead II

36
Q

What is left axis deviation associated with, and how does it appear on an ECG?

A

Left ventricular hypertrophy (LV has more influence on QRS complex than RV so axis swings to left), conduction block in anterior part of left bundle branch (usual cause)

ECG: lead I upright (+ve), lead III inverted (-ve)
Lead I and III QRS are Leaving each other in Left axis deviation

37
Q

Tachycardia

A

Separated into supraventricular and ventricular:

Supraventricular

  • Atrial – caused by the SA node.
  • ‘Normal’ trace, just quicker

Ventricular

  • Caused by the ventricles
  • Abnormal QRS complexes (Wider and abnormal shape)
  • regular
38
Q

Right axis deviation

A

Associated with right ventricular hypertrophy: as when larger the RV will have more influence on QRS than LV

ECG: lead I inverted (-ve), lead III upright (+ve): lead I and III QRS are Reaching towards each other in Right axis deviation

39
Q

What is a bundle branch block?

A

Right tract is a single bundle branch; left has an anterior and posterior and either or both can be blocked

LBBB: V1 has W shaped peak and V6 has M shaped peak
RBBB: V1 has M shaped peak and V6 has W shaped peak

40
Q

What would differences in components of ECGs indicate?

A

Shorter R-R interval=faster heart rate

Wider QRS complex associated with ventricular depolarisations that are not initiated by the normal conduction mechanism, so longer depolarisation time

Longer P-R interval suggests slow conduction from atria to ventricle (first degree heart block)

ST segment should be isoelectric; if raised or depressed indicates MI or ischaemia

Prolonged Q-T interval suggests prolonged repolarisation of ventricles which can lead to arrhythmias. Commonly occurs as a result of medications which interact with K+ channels and prolong depolarisation; can also be due to long QT syndrome

ESA 2 (58 decks)

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