Interpreting ECGs Flashcards
Definitions
Depolarisation
Repolarisation
resting membrane potential
AP
Depolarisation : change within cell of electric charge distribution leading to less negative charge inside cell – happens through movement of ions - Na+;K+;Ca2 ions
Repolarisation: change within cell of electric charge distribution leading to more negative charge inside cells- happens through movement of – Na+ ;K+; Ca2 ions
(Resting) membrane potential: created by separation of charges across cell membrane – measures electrical imbalance between inside and outside of cells measured in mVolts – measures HOW much more negative inside of cell is c/w outside
Action potential: brief reversal of cell membrane electric polarity (ie depolarization) that is then propagated from cell to cell
Deflection: deviation from straight line – in ECG either an upward or downward wave/peak from the baseline
Overview of electrocardiogram
Contraction and relaxation of cardiac muscle results from the depolarisation and repolarisation of myocardial cells.
These electrical changes recorded via electrodes placed on the limbs and chest wall and transcribed to graph paper to produce an electrocardiogram (commonly known as an ECG)
ECG provides information about cardiac electrical activity from 12 separate views of the heart that are anatomically specific (though overlapping) – and if there is an abnormality in that activity we can localise which part of the heart is affected
The cardiac electrical conducting system - the beginning
Our heart has an intrinsic rhythm – remember our heart - if supported with ions and energy- can beat outside our body
Specialised cardiac myocytes- pacemaker cells of heart- spontaneously generate action potentials (APs) that initiate cardiac cycle.
APs are also influenced by external factors
The primary cardiac pacemaker cells is located in the Sinoatrial Node (SA node) in the right atrium
Action potentials result in depolarization wave that spreads through rest of myocardium in an organised manner (otherwise, chaos!) – all cardiac cells electrically connected through gap junctions
Depolarisation wave causes coordinated contraction of atria and ventricles- excitation-contraction coupling
Propagation of cell depolarisation from cell to cell
The wave of depolarisation spreads via gap junctions similar to a domino affect, with the ions entering one myocytes causing an AP leading to the generation of an AP in nearby cells
So, how does the electrical activity spread throughout the heart at the tissue level? - Part 1 – the atria
The AP is Initiated at the Sinoatrial (SA) Node - causing a sinus node impulse, which travels across both atria
This causes Depolarisation of both the right atrium and left atrium
Then it hits the atrioventricular (AV) node – located in inter-ATRIAL septum near the tricuspid valve (bottom-left of the right atrium)
The pulse slightly slows down in AV node (this delay occurs in order for the whole of the atria to have contracted before ventricular contraction occurs)
From AV node goes to the Bundle of His (located in the septum of the heart)- wide, fast, conducting muscle fibres that travel through Annulus Fibrosis
Annulus Fibrosus separates atria from ventricles
Part 2 – the ventricles
Bundle of His – enters the inter- VENTRICULAR septum where it divides into
– RIGHT bundle branch (RBB)– travels along right side of inter-VENTRICULAR septum – excites right ventricle
– LEFT bundle branch (LBB)- travels along left side of inter-VENTRICULAR septum – excites left ventricle
Right bundle branch and Left bundle branch terminate in extensive network of large conducting muscle fibres - Purkinje fibres - continue to conduct depolarization wave through the ventricles
Annulus fibrosis - fibrous skeleton of the heart
Anchors myocardium and cardiac valves – (also anchors muscles in the MSK system to bones)
Acts as an electrical insulator between atria and ventricles
Consists of four fibrous rings (left and right atrioventricular ring and fibrous ring of the aortic/ pulmonary valve)
Conducting system of heart and heart rate
ATRIA
Sinoatrial Node
Fastest rate of depolarisation in the heart
Intrinsic firing rate 60-100 times/minute
Sets heart rate and rhythm- SINUS rhythm
Atrioventricular Node
Slows conduction
Gives time for atria to contract before ventricles
Intrinsic firing rate without stimulation (such as from the SA node) 40-60 times/minute
Ventricle:
LBB and RBB
Ventricular electrical conducting system cells also have an intrinsic firing rate although this is NOT typically manifested
Intrinsic firing rate 20-40 times/minute – so slow!
The ECG
ECG measures changes in electrical potential (in mVolts) produced in successive areas of myocardium during cardiac cycle via a series of LEADS attached to body – measures & records these changes OVER TIME
ECG LEAD means TWO different things in this context
Cable used to connect electrode to ECG recorder
Electrical view of the heart obtained from any one combination of electrodes
Q: What’s an electrode?
A: Electrode is conductive pad - is attached to the skin and enables recording of electrical currents.
ECG records cardiac electrical activity as transmitted to chest wall and limbs
Q: Would ECG of someone with barrel chest from COPD potentially look abnormal not related to heart per se? How about someone with morbid obesity?
Depending on where electrode is positioned, the type of lead and what is happening to cell – depolarisation or repolarisation (and states in between, changes will be generated in ECG tracing – deflections – p QRS T
Recording the ECG
10 electrodes 4 on the limbs
6 on the chest
Connected by 10 cables (sometimes called leads) to ECG machine
Gives 12 views of heart
Views are also called leads - hence a 12 lead ECG
Right leg electrode grounding electrode - not used for any views
ECG limb leads (views 1,2,3)
Measure difference in voltage (i.e. membrane potential) of a pair of electrodes on skin surface
that pick up electrical activity of heart
Limb Leads I, II and III are Bipolar –negative and positive electrodes
Limb leads (views) created by electrodes attached to – Right “arm”(RA) – Left “arm”(LA) – Left “Leg” (LL) – Right “Leg” (RL)
1) Limb lead 1: voltage difference between electrode RA and LA; LA (+)electrode
2) Limb lead II: voltage difference between electrode RA and LL; LL (+)electrode
3) Limb Lead III: voltage difference between electrode LA and LL; LL (+)electrode
– Cables attach to electrodes
– Cables go to the recording device; device amplifies electrical signal so we can see it, and it also transcribes it onto ECG tracing (graph) paper
ECG - augmented limb leads aVR, aVL, AVF
Augmented Limb Leads aVR, aVL and aVF unipolar- only have a positive electrode
Other “electrode” actually represents the average of the remaining 2 electrodes and is designated “neutral” or reference – The positive electrodes for these augmented leads are located on
• Right arm for aVR • Left arm for aVL • Left leg aVF (F for foot)
Augmented unipolar leads use same electrodes used for standard limb leads - only thing changes is how these electrodes connected – ECG recorder does the actual switching and rearranging of the
electrode designations as positive, or negative, or averaged.
It also makes different connections for ALL leads - i.e. RA-LA; LA – (mean of RA+LL)
Understanding the concept of a positive electrode in the context of ECG
1) Cardiac view provided by a lead is from the perspective of the positive electrode
2) By convention – if electrical current (i.e. depolarisation current) of heart part being looked at is travelling to the positive electrode of lead – ECG wave will have positive deflection
Q: If the repolarization current is travelling towards the positive electrode will the deflection be positive (upwards) or negative (downwards)? Negative downwards
An impulse moving directly away from the negative electrode will be seen in reverse to the positive electrode, i.e. depolarisation will have a negative deflection and repolarisation will have a positive deflection
Shape of deflection and lead positioning
Looking at the heart from mVR to Lead 2
Depolarisation wave coming directly towards (+) electrode Tall upright QRS complex
Wave obliquely towards electrode smaller upright QRS complex
Wave At 90 degrees to electrode Biphasic or No complex
Depolarisation wave going directly away from electrode Deep -ve complex
Height (or depth) of deflection depends on how directly depolarisation wave is coming towards (or going away) from positive electrode
and the number of cells generating the signal
How are these views represented on the ECG
SA node
Atrial depolarisation
Delay at AV node
Bundle of His
Development of the AP in the IV septum
Depolarisation of apex and ventricular walls
Last part of depolarisation
Ventricular depolarisation
1) Sinoatrial (SA) node depolarisation
SA node top right hand corner of Right atrium (RA)
Near junction of SVC and RA
First electrical event of cardiac cycle
What change do we see on the ECG tracing – i.e. what deflection?
Nothing: insufficient signal to register on surface ECG
2) Atrial depolarisation
Spreads along atrial muscles fibres & internodal (SA-AV nodes) pathways
Throughout both right and left atria
Direction: Downwards & to the left (Towards AV node) - Will produce a small upward deflection - the p wave
Upward because towards recording (+ve) electrode
Lasts 80 – 100 ms
3) Delay at AV node
Conduction is slowed down at AV node
Allows time for atrial contraction to fill ventricle
Signal is very small
Isoelectric (flat line) segment – flat line on ECG after p wave
4) Bundle of His -Spread of depolarisation from atrium to ventricle
The Fibrous ring surrounding the atria and ventricles can only crossed by/at the Bundle of His
Therefore depolarisation can only reach ventricle via conduction through Bundle of His also gives an Isoelectric (flat) segment
Thereafter rapidly conducted through the ventricle via left bundle and right bundle branches (LBB & RBB) and the Purkinje system
120 – 200 ms from start of atrial depolarisation to start of ventricular muscle depolarisation
5) Depolarisation of the of the interventricular septum
First part to depolarise is muscle in interventricular septum
Depolarisation spreads from left to right
May produce a small downward deflection because moving obliquely away - to the sides (so not straight towards the +electrode)
(or no deflection may be seen)
Termed a Q wave = first downward deflection after p
6) Depolarisation of apex and free ventricular walls
Produces a large upward deflection
Termed the R wave
Upward because depolarisation moving directly towards electrode
Large because large muscle mass – more electrical activity
If left ventricle is hypertrophied – Then R wave will be correspondingly taller
7) Last part of depolarisation Depolarisation finally spreads upwards to the base of the ventricles Produces a small downward deflection Forms the‘S’ of the QRS It’s downward because moving away It’s small because not moving directly away Complete ventricular muscle depolarisation (QRS complex) takes 80 -120 ms
8) Ventricular repolarisation
Begins on the epicardial surface of the heart
Spreads in the opposite direction to depolarisation
Produces a medium upward deflection - The T wave
Upward because it is a wave of repolarisation moving away from electrode- when repolarisation moves AWAY from lead produces upward deflection – in comparison with when depolarisation moves away from lead produces a negative deflection
Limb leads - what they good for?
Leads I and aVL looking left side of heart
Best limb leads for looking problems lateral wall of left ventricle
E.g. seen in Muscle necrosis due occlusion branch left coronary artery - a lateral wall
myocardial infarction
Leads II, III and AVF looking at inferior surface of the heart.
best limb leads detect problems in the inferior surface of the heart (diaphragmatic surface )
e.g. muscle necrosis due occlusion right coronary artery - an inferior myocardial wall infarction
Precordial/chest leads - 6 views of the heart in horizontal plane
6 chest electrodes, V1 – V6
Leads V1 to V4 “ antero-septal” leads
V1 & V2 face the RV & septum (‘septal leads’)
V3 & V4 faces the apex and anterior wall of RV & LV
Leads V5 and V6 face the LV (‘lateral leads’)
Anterior cardiac wall necrosis - which leads, which artery?
Occlusion Left Anterior Descending Artery (LAD); this artery also known as Anterior Interventricular branch of left coronary artery
LAD/ AIBLCA - carries almost 50% of the blood carried by the coronary circulation
Common name: Widow maker
So which leads?
Major ECG changes will be seen precordial/chest leads – V3 and V4. and sometimes in limb leads – Q: which limb leads might show changes ? I and II
Which ECG leads face which parts of the ventricles
Leads facing (and giving views of): Inferior surface of ventricles = II, III and aVF
Septum and anterior surface of ventricles = V1,V2, V3,V4
Right ventricle and septum = V1 and V2 & aVR
Apex and anterior surface of ventricles = V3 and V4
Lateral surface of ventricle = Lead 1, aVL, V5, V6
ECG - calculating heart rates and intervals
1 small square = 40 milli seconds (msecs)
1 large square = 200 msecs (a large square consists of 5 small squares, 5 × 40 msecs = 200 msecs – remember 200 msecs ≡ 0.2 seconds ≡ 1/5 of a second)
5 large squares = 1 second (5 × 200 msecs = 1 second)
15 large squares = 3 seconds (15 × 200 msecs = 3 seconds)
30 large squares – 6 seconds (30 × 200 msecs = 6 seconds)
300 large squares = 1 minute = (300 × 200 msecs = 60 seconds = 1 minute)
Calculating the heart rate when the rhythm is regular:
Each cardiac cycle represents ONE heart beat i.e ONE P QRS T complex (P wave – to start of next P) equals ONE heart beat
Easier to count R – R interval than P – P interval – one R-R interval equals ONE heart beat
• Right ECG represents how many heart beats? - Four
Right ECG represents how much time?- Contains 16 big boxes (don’t count big boxes without a QRS complex if measuring R-R), remember one big box is equal to 200 milliseconds, or 0.2 seconds, or 1/5 of a second (all the same) so 16 × 0.2 seconds = 3.2 seconds
If there are four heart beats in 3.2 seconds, then how many heart beats in 60 seconds? - 60 divided by 3.2 ( how many times 3.2 goes into 60) = 18.75, multiply this by 4 beats = 75 beats in 60 seconds therefore HR = 75 bpm
Calculate heart rate if the rhythm is irregular:
if the rhythm is irregular - calculate heart rate by counting the number of QRS complexes in 6 seconds then multiply by 10 to get a total heart beats in 60 secs (this can be used for regular rhythms as well)
Intervals
Disease states of pharmaceutical, electrolyte, biochemical imbalances can all affect cardiac intervals - abnormal intervals predispose to arrhythmia
PR interval: - 0.12 – 0.20 seconds 3 – 5 small boxes Prolonged if > 1 large box
Prolonged PR interval: delayed conduction through AV node and bundle of His
QRS interval: - (width of QRS complex) Time taken for ventricular depolarisation < 0.12 seconds < 3 small boxes
Widened QRS: (usually) a depolarisation arising in ventricle; not spreading via the rapid conducting His-Purkinje system; hence takes more time
QT interval
QT interval time taken for depolarisation & repolarisation of ventricle
Varies with heart rate
Calculation to correct for heart rate (available in charts) - Corrected QT interval (QTc)
Upper limit of corrected QT (QTc) interval: ≤ 0.44 – 0.45 seconds (11 small boxes)
Prolonged QTc: indicates prolonged ventricular repolarisation
Prolonged QTc associated risk for dangerous arrythmias
Atrioventricular conduction blocks
Delay/ failure of conduction of impulses from atria to ventricles via the AV node and the Bundle of HIs
3 types - 1st degree heart block
2nd degreee heart block Mobitz type 1 second degree heart block Mobitz type 2 second degree heart block 3rd degree heart block
Causes of heart block - Degeneration of the electrical conduction system with age - e.g. sclerosis and fibrosis Acute myocardial ischaemia Medications Valvular heart disease
1st degree heart block
1st degree heart AV block - conduction is lowered without skipping betas
All normal P waves are followed by QRD complexes, but PR internal is longer than normal
Second degree block
Mobitz type 1:
Also called Wenkebach second degree heart block
Successively longer PR intervals until 1 QRS is dropped - i.e. electrical single not conducted through to ventricles - then cycles start again
Second degree AV block - Mobitz type 2:
PR intervals do not lengthen - sudden dropped QRS complex without prior PR changes
Atrial rhythm is regular
Ventricular rhythm is irregular
High risk progression to complete heart block
3rd degree heart block
Atria and ventricles are depolarising independently
Complete failure of AV conduction
Ventricular pacemaker tajes over - slow - 20-40 bpm
Typically too slow to maintain blood pressure
Usually wide QRS complex
Urgent pacemaker required
bundle branch block
Delayed conduction within the bundles branches - can be RBBB or LBBB
P wave and PR intervals are normals
Wide QRS complex (>3 small squares) - occurs as ventricular depolarisation takes longer
Arrhythmia overview
Arrhythmia overview:
Abnormal rhythms may arise from the Atria - above ventricles and therefore called supraventricular arrhythmia, Ventricles = ventricular arrythmias
Supraventricular vs ventricular arrhythmia
Supraventricular - heart beats around 150 BPM- narrows QRS complex
Ventricular - wide and bizarre QRS complexes
Afib - supraventricular arrhythmia
Arises from multiple atrial foci,
Rapid chaotic impulses,
no P waves - Just wavy baselines
irregular R to R intervals
Impulses reach AV node at rapid irregular rate
not all conducted
when the pulse is finally conducted the ventricles depolarised normally - so normal QRS
Usually can get blood to ventricles - may be hypotensive
Afib - ECG variations. - Afib can be - Slow - ventricular response <60bpm FAst - ventricular response <100 Normal rate - 61-99bpm Afib with coarse fibrillation or fine fibrillation - if coarse may sometimes be mistake for p waves
Afib - haemodynamic effects - Atrial contraction lost - atria just quiver
Ventricles contract normally
Heart and pulse are irregularly irregular
Loss of atrial contraction leads to increased blood stasis - most evident in the left atrium
Flow velocity is markedly reduced with impaired contractility of left atrial appendage - which leads to small clots in the LA - therefore atrial fibrillation is a well-established risk factor for ischaemic stroke
Significant problem because afib is the most common cardiac arrhythmia in the general population
Ventricular ectopic beats
Ectopic focus in ventricle muscles
Impulse does not spread via fast His-Purkinje system
Therefore much slower depolarisation of the ventricular muscles, therefore the patient has a wide QRS
Occurs premature as it occurs earlier than expected for the next sinus impulse
Ventricular tachycardia (VTACH): Run of more than 3 consecutive premature ventricular contractions (PVCs)
VTACH is broad complex tachycardia
Persistent VTACH is a dangerous rhythm, require urgent treatment
High risk progression to ventricular fibrillation
Ventricular fibrillation - Abnormal chaotic fast ventricular depolarisation, impulses from numerous ectopic sites in the ventricle
No coordinated contraction - Ventricles quiver
You get little to none cardiac output - If this is sustained then you can get cardiac arrest
ECG changes of ischaemia and MI
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
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
Myocardial ischaemia & infarction
Ischaemia: lack of oxygen but no muscle necrosis
– Blood tests will be negative for markers myocyte of necrosis (eg cardiac troponins)
Myocardial infarction:
Muscle necrosis present – therefore blood tests will be positive (eg cardiac troponins)
STEMI: ST Segment Elevation Myocardial Infarction (full thickness of cardiac wall)
Non-STEMI: non ST Segment Elevation
ST Segment elevation Myocardial infarction (STEMI)
ST Segment Elevation Myocardial Infarction (STEMI)
Due to complete occlusion of coronary artery
“Full thickness” of myocardium involved
Sub-epicardial injury causing ST Segment elevation in leads facing affected area is the earliest sign
STEMI – ECG changes - On ECG tracing behaves as if an abnormal current traversing damaged tissue is coming towards electrode – results in positive deflection (going up)
ST elevation earliest sign in a STEMI
Diagnostic of STEMI in conjunction with other criteria
Indication for intervention
Evolving ECG changes in a STEMI:
Due to the damaged tissue being repaired as scar tissue - i.e. not functional tissue
Usually after repair you get a Q wave forming on the ECG - Q waves can indicate pathology - they can be regular/normal q waves
ECG changes in non STEMI and ischaemia
Same changes in ECG for both severe ischaemia and Non-STEMI
Severe ischaemia ≡ unstable angina
BMJ Best Practice definition 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, longer in duration, or lower in threshold; or angina that occurs after a recent episode of myocardial infarction.”
Vs Non STEMI – actual cardiac muscle damage has occurred but NOT through entire wall of heart muscle- sub endocardial
Differentiate by blood tests for myocyte necrosis – eg troponin
ECG Changes in Non-STEMI and Ischaemia: ST segment
ECG changes due to subendocardial injury
ST segment DEPRESSION and T wave inversion
On ECG tracing behaves as if abnormal current traversing damaged tissue is moving AWAY from recording electrode
ECG Changes in Non-STEMI and Ischaemia: T waves
T waves: Normally upright in all leads except aVR and V1 –
New T wave inversion c/w old ECG must always be evaluated – no matter where it occurs!
Pathologic T wave inversion is usually symmetrical and deep(>3mm)
T-wave inversions due myocardial ischaemia or non STEMI occur leads consistent with anatomical regions perfused by specific coronary artery
For example, in majority patients the inferior wall of the heart is supplied by 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
ECG changes in Stable Angina
ST depression seen during exercise because of coronary disease – as “stable” atherosclerotic plaque causing fixed narrowing
“Exercise” can either be on a treadmill (Exercise stress test) or chemically induced (Dobutamine stress test)
ECG changes will REVERSE at rest
ECG: down sloping of ST-segment depression or elevation
PVCS occurring during recovery from excercise testing are associated with increased mortality
Hypokalaemia - signs and symptoms
Hypokalaemia: potassium level < 3.5 mmol/L
– Moderate hypokalaemia is a serum level of < 3.0 mmol/L
– Severe hypokalaemia is defined as a level < 2.5 mmol/L
Decreased extracellular potassium causes myocardial hyperexcitability
Symptoms - Generalised muscle weakness Respiratory depression Ascending paralysis (due to continuous stimulation) Ileus, constipation Palpitations, Arrhythmia, Cardiac arrest
ECG and HYPOkalaemia ECG: – Peaked P waves – T wave flattening and inversion – U waves start forming
Hyperkalaemia
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 critical
Resting membrane potential becomes less negative
Causes some voltage gated Na+ channels to be activated and remain inactivated, as the RMP hasn’t decreased enough
Heart becomes less excitable
Conduction problems occur
Can lead to – Generalised muscle weakness – Respiratory depression – Ascending paralysis – Palpitations, Arrhythmia, Cardiac arrest
Hyperkalaemia ECG - at 5.5-6.5mmol/L, tented T waves are present
6.5-7.5 - there is loss of P wave
7.5-8.5 - QRS complex widens
>8.5 QRS continues to wide approaching a SIN wave
