Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
1. What does ECG stand for?
Electrocardiogram
2. What diagnoses can we make from an ECG?
Cardiac:
1. MI
2. Pericarditis
3. AF
4. Heart block
5. ?PE
Non-cardiac:
1. Digoxin toxicity
2. Hyperkalaemia
3. Hypokalamiea
4. Hypercalcaemia
5. Hypocalcaemia
3. How many electrical leads do you need to record an ECG?
Need minimum of 3 but standard is a ’12-lead’, which actually uses 10 leads
Where on a patient do you attach them?
 V1 R sternum 4th IC space
 V2 L sternum 4th IC space
 V3 between V2 and V4
 V4 5th IC space at MCL
 V5 5th IC space at anterior axillary line
 V6 level with V4 at mid-axillary line
 aVr right hand (aV = augmented vector)
 aVl left hand
 aVf left foot
 1 dead lead right foot
 Lead 1, 2 and 3 show current moving between electrodes
4. What are the names of the leads on a 12 lead ECG?
How can we divide them up?
5. The ECG is a graph.
What is represented by the x axis? Time
What does a large square represent? 0.2s
What about a small square? 0.04s
What is represented by the y axis? mV
Isoelectric
line; Q and S
not always
seen
x
6. In the picture above,
what does P represent? Atrial depolarisation
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
What does QRS represent? Ventricular depolarisation
How many squares wide can it be? 0.8-0.12s normal (2-3 small squares); widened QRS >0.12s (= 3 small squares)
What does T represent? Ventricular repolarisation
What is x called? PR interval
What does it represent? Atrial impulse through AVN, bundle of His and bundle branches (conduction delay)
How long can it be? 0.12-2.0s normal; can be very long if have complete heart block! (3-5 small squares)
7. Draw a schematic representation of the conducting system of the heart.
8. What is the normal heart rate? 60-100bpm
Fill in the table below
Pg 84 ox handbook
Causes of tachycardia >100
Sinus bradycardia: anaemia, anxiety, exercise, pain,
fever, sepsis, hypovolaemia, HF, PE, pregnancy,
thyrotoxicosis, beri beri, hypoxia = CO2 retention,
autonomic retinopathy, sympathomimetics (caffeine,
adrenaline, nicotine), CCF
AF
Atrial flutter
Ventricular tachycardia
Ventricular fibrillation?
Causes of bradycardia <60
Sinus bradycardia: physical fitness, vasovagal attacks, sick
sinus syndrome, acute MI (esp inferior), drugs (βblockers, digoxin, amiodarone, verapamil)
hypothyroidism, hypothermia, increased ICP, cholestasis
Heart block
9. What cardiac dysrhythmias do you know of? Can you add them to the table above?
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
Background info:
Looks at the heart in 12 directions.
6 chest/precordial leads (V1-6) and 4 limb leads (I, II, III and aVR, aVL, aVF).
Note that the four limb leads give us six directions at looking at the heart.
 Lead V1: R sternum 4th IC space
o Shows P wave, QRS complex, ST segment
o Distinguishes between R/L ventricular ectopic beats that
Unipolar but
originate from myocardial irritation; monitors ventricular
biphasic , with
arrhythmias, ST segment changes, bundle-branch block
+ve and –ve
 Lead V2: L sternum 4th IC space
deflections
 Lead V3: between V2 and V4
o Monitor ST segment elevation
 Lead V4: 5th IC space at MCL
 Lead V5: 5th IC space at anterior axillary line
o +ve deflection
o changes in ST segment and T wave
 Lead V6: level with V4 at mid-axillary line
o +ve deflection
Leads V1-6 provide a view of the horizontal plane of the heart.
The opposing pole of these leads is the centre of the heart.
Current travelling towards the –ve pole
= waveform deflects downwards
Current travelling towards a +ve pole =
waveform deflects upwards
Biphasic (up and down) if current
travels perpendicular to the lead

Lead I: provides a view of the heart that shows the current
moving from R to L; +ve electrode placed on left limb/chest
and –ve electrode on right arm
o Produces a positive deflection
Bipolar leads:
o Monitors atrial rhythms and hemiblocks
axes form
‘Einthoven’s Lead II: positive electrode on left leg and negative electrode
on right arm
triangle
Arteries involved with
o Produces a positive deflection
readings from leads
o Monitoring sinus node and atrial
I aVR V1 V4
arrhythmias and MI
II aVL V2 V5
 Lead III: positive electrode on left leg and
III aVF V3 V6
negative electrode on left arm
Inferior
o Changes involved with MI
Circumflex
Leads I-III provide a view of the frontal plane of the heart.
Anterior
Right ankle = neutral lead
The ‘a’ leads: augmented leads
 aVR: positive electrode placed on right arm
o Produces a negative deflection In practice, leads I, II and III are the
Unipolar  aVL: positive electrode on left arm
same leads as aVR, aVL, aVF. (The
leads
ECG machine does the actual
o Produces a positive deflection
switching and rearranging of the
 aVF: positive electrode on left leg
electrode designations).
o Produces a positive deflection
Leads aVR, aVL, aVF provide a view of the frontal plane of the heart.
A lead provides a view of the heart between a positive and negative pole
(along which current flows)
The mean electrical axis for the heart normally lies between
A plane refers to the cross-sectional perspective: frontal
-30 and +90°. Less than -30° is termed a left axis deviation
plane (vertical cut) provides an A-P view of heart activity,
and greater than +90° is termed a right axis deviation. Axis
whilst horizontal plane (transverse cut) provides either a
deviations can be caused by increased cardiac muscle mass
(e.g., left ventricular hypertrophy), changes in the sequence
superior/inferior view
of ventricular activation (e.g., conduction defects), or
because of ventricular regions being incapable of being
activated (e.g., infarcted tissue).
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
***10 leads; 1 dead therefore 9 useful leads and we get 12 readings***
10 small squares vertically = 1 mV.
Flat line = no electrical activity
A standard ECG is printed at 25mm/s =
25 small squares/s
Direction which waves point = elec
activity towards/ away from a lead
Eg normal travel through the heart is a
downward diagonal line from the right
shoulder (SAN) to the left lower
abdomen (left ventricle = more
conduction).
Amplitude is due to muscle mass. LHS
heart is thicker so needs more elec
activity = bigger peaks. Even bigger in
hypertrophy!
Lead AVR (right shoulder/right
arm/wrist) will always see the electrical
stimulus travelling away from it = waves
in sinus rhythm will all point downwards;
V6 will always see activity coming
towards it (point up)
V1 and V2 lie directly over rt ventricle
V3 and V4 lie over the interventricular septum
V5 and V6 lie over lt ventricle
aVR
V1
V4
V
II
aVL
V2
V5
III
aVF
V3
V6
I
I
I
II
Rhythm
strip
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
Regions of the Heart each lead refers to:
 AVL is on the left wrist or shoulder and looks at the upper left side of the heart.
 Lead l travels towards AVL creating a second high lateral lead.
 AVf is on the left ankle or left lower abdomen and looks at the bottom, or inferior wall, of the heart.
 Lead ll travels from AVr towards AVf to become a 2nd inferior lead
 Lead lll travels from AVL towards AVf to become a 3rd inferior lead.
 V2 V3 and V4 look at the front of the heart and are the anterior leads.
 V1 is often ignored but if changes occur in V! and V2 only, these leads are referred to as Septal leads.
 V5 and V6 look at the left side of the heart and are the lateral leads.
The ECG below shows where these leads are when printed.
•
•
•
12 lead connection box
Right hand = red lead
Left foot = green like grass
Left hand = yellow like the sun
5 lead connection box
ANTERIOR:
– V1-V4
INFERIOR:
– II, III, and AVF
LEFT LATERAL:
– I, AVL, V5 AND V6
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
ECG Complex:
P wave: atrial depolarisation
Look at its
 Location: precedes QRS complex
 Amplitude: 2-3mm high
 Duration: 0.06-0.12s
 Configuration: usually rounded and upright
 Deflection: +ve/upright
o Peaked, notched, enlarged P waves = atrial hypertrophy associated with COPD, pulmonary emboli,
valvular disease, heart failure
o Inverted P waves = retrograde/reverse conduction
o Varying P waves = impulse coming from different sites (irritable atrial tissue; damage near SAN)
o Absent P waves = conduction by a route other than SAN (junctional or atrial fibrillation)
PR Interval: tracks atrial impulse through AVN, bundle of His and R/L bundle branches: delayed
 Location: from beginning of P wave to QRS complex
 Duration: 0.12-0.2s (3-5 small squares)
o Altered impulse formation or conduction delay: AV
block
o Short PR: impulse originated from somewhere else
other than SAN: pre-excitation syndromes, junctional
arrhythmias
o Prolonged PR: conduction delay through atria/AVN due
to heart block or digoxin toxicity (ischaemia or
conduction tissue disease)
QRS complex: ventricular depolarisation (represents intraventricular
contraction time); atrial repolarisation is buried in complex
 Location: follows PR interval
 Amplitude: 5-30mm
 Duration: 0.08-0.12s (2-3 small squares; ½ PR interval); measured from beginning of Q wave to end of S wave
 Configuration: Q (-ve deflection), R (+ve deflection), S (-ve deflection); may not always see waves
 Deflection: +ve in leads I, II, III, aVL, aVF and V4-6; -ve in aVR and V1-3
o If no P wave, then impulse may have originated in ventricles = ventricular arrhythmia
o Deep and wide Q waves (Q amplitude is 25% of R wave, or duration > 0.04s) = MI
o Notched R wave = bundle-branch block
o Widened QRS complex (>0.12s) = ventricular conduction
delay
o Missing QRS complex = AV block or ventricular standstill
o Note that in older adult ECGs, PR, QRS and QT intervals are
often increased, whilst amplitude of QRS is decreased and
there’s a shift of the QRS complex to the left
 Q wave = septal depolarisation and previous MI so not present in
20yo; Whilst the electrical stimulus passes through the bundle of His,
and before it separates down the two bundle branches, it starts to
depolarise the septum from left to right. This is only a small amount
of conduction (hence the Q wave is less than 2 small squares), and it
travels in the opposite direction to the main conduction (right to left)
so the Q wave points in the opposite direction to the large QRS
complex.
 R wave = electrical stimulus passing through bulk of ventricular walls.
Thick walls = more cells = more electricity needed = bigger wave produced
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php

S wave = Purkinje fibres depolarisation; travels in the opposite direction to the large R wave because
Purkinje fibres spread throughout the ventricles from top to bottom and then back up through the walls of
the ventricles.
ST segment: end of ventricular conduction/depolarisation and beginning of ventricular recovery/repolarisation
The point that marks the end of the QRS complex and beginning of the ST segment = J point
 Location: extends from S wave to beginning of wave
 Deflection: usually isoelectric (flat with baseline)
o Elevated (1mm above baseline) = MI or pericarditis
o Depressed (0.5mm below baseline) = myocardial ischaemia or digoxin toxicity
T wave: ventricular repolaristation (specifically repolarisation of AVN and bundle branches)
 Location: follows S wave
 Amplitude: 0.5mm in leads I, II, and III, and up to 10mm in precordial leads
 Configuration: typically round and smooth
 Deflection: upright in leads I, II, V3-6; inverted in aVR; variable in the rest
o T wave may be bumpy because P wave is hidden within it (note that T wave = relative refractory
period and cells are extra sensitive to extra stimuli)
o Tall, inverted or pointy ‘tented’ = MI or hyperkalaemia
o Inverted in leads I, II, V3-6 may = MI
o Heavily notched or pointed T waves = pericarditis
QT Interval: measures ventricular depolarisation and repolarisation; time varies with HR (faster HR = shorter QT)
 Location: extends from beginning of QRS complex to end of T wave
 Duration: varies according to age, sex and HR; usually 0.36-0.44s; should not be greater than half the
distance between consecutive R waves when rhythm is regular.
o Prolonged QT = relative refractory period is longer = increases the risk of life-threatening arrhythmia
known as torsades de points
o Class IA antiarrythmics
o Congenital conduction defect present in certain families
o Short QT = digoxin toxicity of hypercalcaemia
U wave: recovery period of the Purkinje or ventricular conduction fibres; not always present
 Location: follows T wave
 Configuration: typically upright and rounded
 Deflection: upright
o If prominent, may = hypercalcaemia, hypokalaemia, digoxin toxicity
Interference on an ECG:
1. Muscle Tremor
Muscle tremor is something that can occur for a number of reasons, such as:
 Shivering due to cold
 Rigors
 Parkinsons disease
2. Electrical Interference
Another disturbance emanating directly from the surrounding
environment is electrical interference.
The ECG machine is designed to pick up electrical activity within the
heart but it will pick up electrical activity from nearby machinery,
such as:
 Pumps, TV, Drills, Machinery
Correct problems and repeat ECG
 Comfort of the patient, Turn machines off, Drugs to control
symptoms, Warm the patient, Talk to the workmen
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
3. Artefact
Artefact is the name given to disturbances in rhythm monitoring caused by movement of the electrodes.(see below)
Correct problems and repeat ECG
 If the electrodes have been in place for a prolonged period
of time, the moist inner pad can dry up and the
connection becomes poor.
 Sometimes the weight of the leads can pull the electrode
away from the skin and contact is lost intermittently, such
as when the patient leans or roles over.
 Sometimes the electrode has come away from the skin
and is stuck to an item of clothing
 Sometimes, the patient is fiddling with the electrodes
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
# of small block
HR
Analysing an ECG:
1. Patient details
 Name, DOB, NHS number
2. Check ECG details
 Date taken, any chest pain at the time, patient uncooperative and moving
etc CHECK OLD ECG for chronic changes (old MI, known bundle block)
3. Rate: 25 small squares=5 large blocks/second (ie 1 small square = 0.04s); <3
blocks = sinus tachycardia; > 5 blocks = sinus bradycardia (sinus = 60-100)
Three ways:
 10x method: especially if rhythm is irregular. ECG paper is marked in
increments of 3 seconds (15 large boxes); obtain a 6 second strip, count
the P waves and multiply by 10 for atrial contraction rate (and R waves for
ventricular contraction rate)
 1,500 method: 1500 small squares = 1 min; divide 1,500 by the number o f
small squares
 300 method: same as for 1,500 method but 300 large blocks = 1 min
4. Rhythm: Regular/irregular? Paper and pencil method:
 For atrial rhythm use P-P intervals
 For ventricular rhythm use R-R intervals (or Q wave if R wave not present)
 Place ECG on a flat surface; position the straight edge of a piece of paper
on the baseline; mark two consecutive R-R intervals and compare to
successive R waves. If the distance is the same, then the rhythm is regular,
if not, then it is irregular.
5 (1 large block)
6
7
8
9
10 (2 large blocks)
11
12
13
14
15 (3 large blocks)
16
17
18
19
20 (4 large blocks)
21
22
23
24
25 (5 large blocks)
26
27
28
29
30 (6 large blocks)
31
32
33
34
35 (7 large blocks)
36
37
38
39
40 (8 large blocks)
300
250
214
187
166
150
136
125
115
107
100
94
88
83
79
75
71
68
65
63
60
58
56
54
52
50
48
47
45
44
43
41
40
39
38
37
5. Axis
 A) Quick method:
 Left axis deviation (<-30°): leads I and III are ‘leaving each other’
 Due to left ventricular hypertrophy (due to hypertension or MI for example) = conduction system problems
 Right axis deviation (>+90°): leads I and III are ‘reaching each other’
Hypertrophy = more muscle mass
 Due to right ventricular hypertrophy (due to pul oedema putting back
Dilation = increased size but not muscle
pressure on the R heart = cor pulmonale) = lung problems
mass (ie HF) so no change on ECG
 B) Longer method: look at leads I, II, III, aVf: do +ve deflection - -ve
deflection for each lead and use a pencil to plot each result in mm in this diagram
6. P wave (unlikely in 3rd year OSCE) best seen in lead 2 and V1
 Is there a p wave?
 Yes = sinus rhythm or conduction problem
o Is there 1 P wave/QRS complex? If no = heart block
o Tall? Right atrial hypertrophy due to tricuspid stenosis
o Broad? Left atrial hypertrophy due to mitral stenosis (may not be seen as pt may have AF too!)
 No = arrhythmia or hidden…is the pattern regular? Is the QRS complex wide? Skip to QRS
7. Duration of PR Interval
 Count # of small squares between start of P wave and start of QRS complex; multiply by 0.04s
 Is the duration within 0.12-0.2s? (3-5 small squares). Is it constant?
 If no, then will be heart block
8. Q wave = 1st –ve deflection
 Normally: not present or <1square
 Larger >1-2 small squares = previous MI
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
9. Duration of QRS Complex
 End of PR interval to end of S wave; beginning and end of QRS complex and multiply by 0.04s
 Is duration between 0.08 an 0.12s (2-3 small squares)? Are all complexes same size and shape? Does a QRS
complex appear after every P wave?
pattern
Irregular pattern
 Is it wide: > 0.12s (3 small squares) = VT or VF Normal QRS Regular
SVT or atrial flutter AF
o Is the pattern regular?
Wide QRS
VT
VF
 Are there R and R’ waves?
o left BBB = WiLLiaM
o right BBB = MaRRoW
 Is it tall? (V1 or V2; whichever is biggest overall)+(V5 or V6; whichever is biggest overall)
o Yes if >35 small squares = LVH due to hypertension, aortic stenosis, HOCM (in athletes)
10. ST segment – can not be seen if bundle branch block
 Elevated: artery occluded, plaque, clot, arrhythmias, areas downstream will die; acute MI (in
any lead) or pericarditis; treat with clot blusters (streptokinase; old) or primary angioplasty
 Depressed: artery critically narrowed; cardiac ischaemia or acute coronary syndrome (eg non
ST-elevation MI) or unstable angina). Treat with GTN spray, aspirin, O2, clopidogrel, angiogram,
?stent
 Distribution of infarct/ischaemia? Inferior (leads 1, 2, aVf); anterior (V1-4); lateral (leads 1, aVl,
V5-6)
 NB. If see elevation in some leads, may see depression in the rest
a. Changes to the ECG during MI process: normal ECG – then ST elevation (merges with T wave) =
having an MI – T waves inverted = 12-14hrs after MI – T wave inversion increases, Q wave increases
= MI 1 week ago – back to normal ECG but Q wave present = MI ages ago
MI: need 2 out of 3 for diagnosis
Ischaemia
 Increased troponin (partial MI)
 Use V2-6
 Chest pain
 ST depression
 ST elevation (full thickness MI)
 T wave flattening/inversion
 Increased troponin
11. Evaluate T Waves
 Are T waves present? Do the T waves have the same deflection as the QRS complex?
 Tall/tented (no set value – judgement call): hyperkalaemia (3.5-5.1 normal; >6 =
massively dangerous); artificially raised via sample waiting a long time to be processed,
haemolysed sample? Do ECG to confirm with tented T waves. Do ABG as this gives
an immediate reading too. Repeat bloods.
 Inverted: MI; ischaemia also (but not bad enough to cause ST depression)
 Flattened: MI, ischaemia
12. Determine duration of QT Interval (not for 3rd year OSCE)
 Count # of small squares between beginning of QRS complex and end of T wave;
multiply by 0.04s
 Is the duration between 0.36-0.44s? (>10 small squares/2 large = problem)
 Congenital problem: long QT syndrome => ventricular arrhythmias => die suddenly; so screen family
 Electrolytes: hypokalaemic, hypo Ca2+, hypo Mg2+ (Mg and Ca usually change together)
 Drug side effects? Eg statin + pneumonia + clarithromycin = usually stop statin as may prolong QT interval
13. Check aVR: should be –ve; if not, ECG taken badly so request another one
14. Summary
NB. A pacemaker usually sits in the right ventricle but may sit in left if there’s a septal defect
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
Conditions:
Arrhythmias: due to
 Conduction system: left bundle branches into two smaller ones in ventricle (anterior, posterior), then Purkinje
fibres are given off
 Heart itself
Conduction system:
When you look at an ECG, always look for P waves. If you can’t see any, it is most likely an arrhythmia.
Is there a p wave?
 Yes = sinus rhythm or conduction problem
 No = arrhythmia or hidden…is the pattern regular? Is the QRS complex wide?
1. Is it Sinus Rhythm?
To ascertain whether a rhythm is sinus or not you need to be able to identify key features.
 There must always be a p wave.
 The P wave should be a rounded shape
 Each P wave should be the same shape
 Each P wave should be followed by a QRS
 The P-R interval should be 3-5 small squares (<0.2s) and constant
 The rhythm should be regular.
You do not need to be able to recognise a "T wave" for it to be sinus rhythm. Many abnormalities obscure the t
wave. Suffice to say, if the patient is alive then the ventricles are definitely repolarising.
2. Sinus Arrhythmia
Sinus Arrhythmia, or "regularly irregular" sinus rhythm, is a variation on sinus rhythm where the P-P interval (the
distance between consecutive P waves) varies by more than 10%.
It can be naturally occurring or due to heart damage.
Causes can be:
 Respiratory-where the P-P interval lengthens and shortens
with inspiration and expiration.
 Non-respiratory - where the process occurs seemingly for
no reason.
 Sometimes seen in association with Complete Heart Block.
Sinus arrhythmia is not commonly seen but the same evaluation
procedure is used:
 Is there a P wave?
 Is each P wave the same shape?
 Is each P wave followed by a QRS complex?
 Is the P-R interval between 3-5 small squares?
 Is the rhythm regular?
If the answer to the first four questions is "yes", but the answer to the last is "no" then you have sinus arrhythmia.
3. Sinus bradycardia:
 R-R intervals constant and regular
 All waveforms are present, and there is 1 P-wave to each QRS
complex
 The rate is <60bpm but not usually <40bpm
 Patients usually asymptomatic and no treatment is required
 Bradycardia causes: sinus, athletes, meds (β-blockers, digoxin,
Ca2+ channel blockers), when asleep
4. Sinus tachycardia:
 R-R intervals constant and regular
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php




All waveforms are present, and there is 1 P-wave to each QRS complex
Rate is > 100bpm, but not usually > 130bpm at rest
Patient is usually asymptomatic.
Tachycardia causes: exercise, low BP (eg haemorrhage/hypocolaemia), MI, CCF, hypoxia, stress, drugs,
caffeine
The passage of conduction through the heart in both sinus tachycardia and sinus bradycardia is exactly the same
as in sinus rhythm.
5. Heart Block
1. 1st degree: PR interval prolonged as held up at AVN but steady; HR same; if asymptomatic, do nothing; early
sign that other problems may develop such as a 2nd degree block!
2. 2nd degree: dropped QRS
a. Mobitz type 1/Wenckebach: PR interval increases on each systole, then QRS dropped; possibly affect
HR
b. Mobitz type 2: Prolonged QT, constant: p-p-QRS (a 2:1 2nd degree heart block); p-p-p-QRS (a 3:1 2nd
degree heart block); HR will decrease as a result, and may be SOB, fatigue, angina; treatment is to
use a pacemaker
rd
3. 3 degree: complete
a. Regular p waves and QRS waves, but they are not co-ordinated with each other; ventricles rely on
own pacemaker cells (ventricular pulse = ~30-40/min) ?hypotensive and HR decreases (and QRS
complex may be wide too as pacemaker cells may be in left ventricle so left ventricle will contract
before the right ventricle)
4. Bundle Branch Block – left or right BBB
Left BBB: impulse travels down right bundle so right ventricle contracts before left
Right BBB: impulse travels down left bundle so left ventricle contracts before right
QRS is wide with secondary waves: cause an ‘M’ or ‘W’ shape: look at leads V1 and V6:
 If see W in V1 and M in V6 = wiLLiam = left BBB
 If see M in V1 and W in V6 = marrow = right BBB
Arrhythmias: in the heart itself:
When you look at an ECG, always look for P waves. If you can’t see any, it is most likely an arrhythmia.
Is there a p wave?
 Yes = sinus rhythm or conduction problem
 No = arrhythmia or hidden…is the pattern regular? Is the QRS complex wide?
Regular pattern
Irregular pattern
Normal QRS SVT or atrial flutter AF
Wide QRS
VT
VF
5. AF
No P wave; irregular irregular; often tachycardia
To put back into sinus rhythm = two methods
1. Cardiovert:
a. drugs: amiodarone or digoxin
b. DC electric shock
2. Induce a bradycardia using a Β-blocker: metoprolol
6. Atrial Flutter
Atria flutter at ~300/min; ventricles can only beat at ~220/min
In 2:1 (atrial contraction: ventricle contraction) conduction, HR = 150/min. can also have 3:1 and 4:1. Hence ECG
looks ‘sawtooth’
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
Adenosine slows the HR so a flutter may become visible.
If slower…see flutter wave
7. Supraventricular tachycardia (SVT)
Due to an accessory pathway from the AVN
HR usually 150-180/min and so look very much like sinus tachycardia or atrial flutter (Think: why does your pt have a
sinus tachycardia of 150 if they’re lying in the bed?! Anxiety = ~110/min; sepsis = ~120/min; exercise =
~150/min…normally need to do serious exercise for HR to be that high…so unlikely to be sinus tachycardia of atrial
flutter!)
What to do: adenosine (decreases HR and causes a mini-MI, then the heart begins in sinus rhythm again; if atrial
flutter, it’d go back to being a fast atrial flutter). Carotid sinus massage may also decrease HR as does pinch your
nose and blowing through your ears, both working by increasing vagal tone and so decreasing HR.
8. Ventricular fibrillation
A mess; no discernable pattern. Must be able to recognise immediately as it requires shocking the pt. the pt looks
dead and will not be in VF if they are sat upright in their chair (a lead may have fallen off instead).
9. Ventricular ectopics:
• VEs alternating with a normal QRS is called bigeminy
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
10. Ventricular tachycardia:
• VT is just a series of regular fast ectopics from a ventricular pacemaker
11. Defibrillator spike
A vertical line before the QRS complex
ALS information:
Shockable rhythms = ventricular fibrillation and pulseless ventricular tachycardia
Non-shockable rhythms = pulseless electrical activity and asystole
Reversible causes of unconscious and not breathing person that must be ruled out before stopping CPR
 Hypoxia
 Hypovolaemia/haemorrhage
 Hypo/hyperkalaemia/hypocalcaemia (metabolic)
 Hypothermia – suspect in any pt who has drowned




Toxicity/toxins
Thrombosis – coronary or pulmonary – give thrombolytic drug; may need to continue CPR >90mins
Tamponade – cardiac – typical signs = distended neck veins and hypotension
Tension pneumothorax
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
Practise on spotting rhythms:
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php
Practise on everything:
Electrocardiogram (ECG)
http://www.cvphysiology.com/Arrhythmias/A016.htm or ECGmadesimple.com or http://www.ecglibrary.com/ecghome.html
http://www.nottingham.ac.uk/nursing/practice/resources/cardiology/function/5_12_lead_placement.php