UNDERSTANDING ECGs

THE BASICS ECG stands for electrocardiogram. It is a method of measuring the efficiency of the conducting system of the heart.

P represents depolarisation of the atria QRS represents depolarisation of the ventricles T represents repolarisation of the ventricles There is no wave for repolarisation of the atria because this is covered up by the depolarisation of the ventricles. It is quite normal for no q wave to be present.

ECG paper Each large square represents 0.2s (200milliseconds) and each small square represents 40ms (5 small squares per large square). 1 big square is 0.5cm 1 small square is 1mm Five large squares represent 1 second. There are 300 large squares per minute. So, if a QRS occurs once every large square, the HR is 300.min. However, if they occur once only 4 squares, the heart rate is 300/4 = 75bpm. When you work this out, you say you are doing the R-R interval.

Segments and intervals

Segment This term is used to refer to a part of the ECG between the end of one wave and the start of the next. The two main segments are the PR segment and the ST segment. Intervals This term is more ambiguous and refers to various stretches of the ECG: PR Interval this is from the beginning of the P wave, until the beginning of the QRS complex. It measures the time taken for excitation to spread from the SA node (all the way through the AV node, and various bundles) to the ventricular muscle. Normal interval 0.12-0.2s i.e. it should be between 3-5 little squares. QT interval this is from the beginnings of the QRS complex until the end of the t wave. QRS duration this tells us the amount of time it took the signal to spread throughout the ventricles. Normal interval 0.12s (i.e. about 3 little squares) however various conditions can cause a lengthened QRS duration. Practicalities Normally you take a 12-lead ECG. This term is confusing because the word lead has two meanings.

It can mean the physical electrical cable that you use to connect the reader with the patient, or, more correctly it refers to an imaginary line between two ECG electrodes, along which electrical conductivity is measured.

So a 12-lead ECG has 12 of these lines along which conductivity is measure d, and thus 12 graphs can be produced. However, there are only 10 physical electrodes and leads that you attach to the patients body.

To try and avoid confusion here I will refer to the physical connections as electrodes It is important to attach your electrodes in the right place so they you get signals that can be properly interpreted. Calibrating the machine The height of the waves can be important in defining certain conditions. Thus it is important that the reader is calibrated correctly so we can interpret the wave height. A signal of 1mV should cause the graph to rise 1cm (2 large squares). At the start of each ECG trace, this calibration signal should be seen on the print out: Taking a reading

The patient should be laid down and relaxed (to prevent muscle tremors which may cause interference) Now connect the electrodes Calibrate the machine Make the recording!

Placing your electrodes You should connect the electrodes in the following order: V1 4 IC space on the right sternal edge V2 4 IC space on the left sternal edge V4 5 intercostal space at the midclavicular line- at the apex beat. V3 place this half way between II and IV so that it sits on the 5 rib. V6mid axillary line at the 5 intercostals space V5 anterior axillary line at the 5 intercostal space. LA should be connected to the left arm it can be done anywhere on the arm, but use your common sense for example if they have a tremor dont place it at the extremity. If they dont have an upper limb, you should try to still place the electrode distally to the shoulder joint on the stub (if they have one they will pretty much always have something there!). The electrode is yellow lemon left RA right arm. The electrode is Red red right RL right leg the electrode is black.
th th th th th th

LL left leg the electrode is green (spleen! just means put it on the left ankle put it over a bony prominence!) LA left arm the lead is yellow lemon left!

Note that the colouring scheme of leads varies. In cases of massive posterior MI there will be marked anterior ST depression, you have to take 4-6 off and put them on the back. this is to look if there is just anterior ischaemia (dont thrombolise) or if there is posterior MI. If there is just anterior ischaemia, there wont be ST elevation in 7-9. If there is posterior MI, there will be ST elevation in the posterior leads. 7- posterior axillary line, 5 IC space, left hand side 8 between 7 & 9 9 left spinal edge at the 5 IC space
th th

Leads There are three types of lead; bipolar (limb) leads, chest unipolar leads and augmented unipolar leads. Each type of lead basically measures the conductivity of the heart in a different plane, and thus this allows us to see the activity of different parts of the heart. Bipolar limb leads these comprise of a positive electrode and a single negative electrode, through which the conductivity of the heart are measured. Unipolar leads these utilise a single positive electrode, and then use a combination of other electrodes to represent a negative electrode. Bipolar limb leads Lead Lead I Lead II Lead III From RA (-) RA (-) LA (-) To LA(+) LL (+) LF (+) Plane Lateral Inferior Inferior

Viewing t

Lateral wall of le

Diaphragmatic

Diaphragmatic

You might wonder how the LA can operate as both a negative and a positive electrode simultaneously. Well so do I! I guess these voltages are relative, so it is relatively more positive than the Right arm, whilst still being more negative than the left leg. Also note that the inferior plane leads are viewing the heart from below, and thus looking at the diaphragmatic surface, which consists mainly of the left ventricle. Augmented Unipolar Limb leads Lead aVR From LA+LL (-) To RA (+) Plane Lateral (reversed) Viewing the
Right atrium*

aVL aVF

RA+LL (-) RA+ LA (-)

LA (+) LL (+)

Lateral Inferior

Lateral wall of left ventricle Diaphragmatic surface

*although the view is pretty non-specific

Some people find Einthovens triangle helpful in understanding the leads: (sorry about the captions in Dutch but Im sure you can understand!)

Just thought of a little trick to remember which goes where: aVF - Foot aVR - Right aVL - Left Unipolar chest leads These account for the other 6 leads of the 12-lead ECG. Each of the electrodes is positive. Lead V1 V2 V3 V4 Plane Septal Septal Anterior Anterior Viewing the Septal wall of ventricles Septal wall of ventricles Anterior surface* Anterior surface*

V5 V6

Lateral Lateral

Lateral wall of left ventricle Lateral wall of left ventricle

*note that this consists mainly of the right ventricle

You may notice that the Right Leg electrode is not mentioned, and this is because it is a NEUTRAL electrode, and thus not utilised in the measurements themselves. Graph Production When the graph is drawn, there is a positive line when the signal travels towards a particular lead, and a negative one, when the signal travels away from a lead. Depolarisation spreads throughout the heart in many directions at once, but the wave produced is the average of this. When the R wave is greater than the S wave, this means the signal is generally positive, and therefore moving towards the lead. When the S wave is greater than the R wave, it means the signal is negative and moving away from the lead. When the depolarisation wave is moving at right angles to the lead, then R and S waves will be of equal size.

Imagine looking at the heart from the front. From here, the waves of depolarisation generally spread through the heart from 11 oclock to 5 oclock. This direction of spread of the signal is known as the cardiac axis. Therefore, they head along lead II. This creates a nice positive R wave in lead II. aVR however has its positive and negative electrodes the other way around, and so the signal travels against this lead, and thus there is a negative signal produced in this lead. You can determine the direction of the cardiac axis (to check if it is normal or not) by looking at leads I-III. A normal cardiac axis will cause a positive signal in all 3 of these leads because between them these leads measure the lateral (right to left) and inferior dimensions and the signal is travelling laterally and inferiorly! The deflection is greatest in lead II because this lead measure both laterally and inferiorly.

However, in right ventricular hypertrophy the cardiac axis becomes displaced. The overall direction of charge is now from 1-7 oclock, because there is extra muscle, and therefore extra signal strength on the right side of the heart. This alters the signal, such that lead I will display a negative QRS, and lead III will now have the tallest QRS (not lead II). This axis shift is called right axis deviation. It is associated mainly with pulmonary conditions that put a strain on the heart. Left ventricular hypertrophy can also cause an axis deviation. We call this left axis deviation. In this, the lead I signal will become very weak, whilst leads II and III will become negative. This is often a result of a conduction defect rather than left ventricular hypertrophy. Basically, the cardiac axis points to any where the R is larger than the S, and points away from any lead where the S is larger than the R. however, it is unlikely that it will point directly towards any of the leads, and thus you only have an approximation thus this is why it is useful to have several leads! Where R and S are of equal size, the cardiac axis is at 90 to that particular lead. Deviations in the cardiac axis may not themselves be significant they can occur in normal people (often if they are very tall, or very thin or fat). However, they prompt you to look for other things. Also remember; right axis deviation is often a result of right ventricular hypertrophy (due to pulmonary disease) but in left axis deviation the most likely cause is NOT hypertrophy, but a conduction blockage.

QRS in the V leads

V1 and V2 look at the right ventricle V3 and V4 look at the septum V5 and V6 look at the left ventricle

There is more muscle on the left than the right therefore the ECG trace is biased towards the left of the heart. This means that for leads looking at the right of the heart, and to some extent at the septum, the overall flow of charge, is away from these leads thus leading to a negative QRS. The general rule is that V1 and V2 have a negative QRS, V3 and V4 have roughly equal sized R and S waves, and V5 and V6 have a positive QRS The point where R and S waves are equal indicates the site of the septum - it is called the transition point. Looking at these allows you to determine of there is right ventricular hypertrophy because if there is, then the transition pointwill not appear in lead V3/V4, but instead may appear in V5/V6, as the enlarged ventricle shifts the septum to the left.

Conduction Problems
Always remember the pattern of conduction: SA node AV node His Bundle bundle branches When looking at conduction problems, you are best to look at whichever lead shows p waves most clearly. This is usually lead II or V1. The PR interval the time taken for the depolarisation to spread from the SA node to the ventricular muscle. This should not be greater than 0.2s i.e. 1 big square.

First degree Heart block

If the PR interval is greater than 0.2s, then we call it first degree block. All the waves will still be present, there will just be a gap between the p wave and QRS complex. First degree heart block is not in itself very important it can be a sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance.

Second degree Heart block

This is where there is an intermittent absence of QRS complexes and thus an indication that there is a blockage somewhere between the AV nodes and the ventricles.

There are three types of this: Mobitz type 2 phenomenon this is where there is a regular rhythm, and a fairly constant PR interval, but every now and again there is an absent QRS (pictured above). basically for every QRS, there are 2 or 3 p waves.

Wenckebach phenomenon (aka Mobitz type 1) progressive lengthening of the PR interval followed by an absence of the QRS, then a shortened PR interval and normal QRS, and the cycle begins again. The cycle is variable in length, and the R-R interval shortens with the lengthening of the PR interval

2:1 and 3:1 conduction there is one normal cycle, then one cycle with an absent QRS (2:1) or there is one normal cycle, then two cycles without a QRS (3:1) pictured below

Causes Acute MI Chronic heart disease (CHD) Mobitz type 2 and Weckenbech dont require and specific treatment X:1 block may require a pacemaker (temporary or permanent), especially if the ventricular rate is slow

Third degree Heart block complete heart block

This occurs when atrial contraction is normal, but no beats are conducted to the ventricles. The ventricles are still excited by their own internal ectopic pacemaker system! Thus the definition of complete heart block is: P wave ~90/min (more p waves than QRS complexes)

QRS ~36/min Variable PR intervals No relationship between P wave and QRS complexes, but both are present. Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles QRS will generally be broad (~160ms as opposed to a maximum of 120ms in a normal heart 4 little squares as opposed to 3 little squares) Right axis deviation Escape rhythms present (more on these later) Causes:

MI it will occur acutely, and is often transient Chronic often due to fibrosis around the Bundle of His, or bundle branch block of both branches Always indicates underlying disease more often fibrosis then ischaemia Consider temporary or permanent pacemaker

More info about complete heart block: Patients with AV block can be haemodynamically stable; however they should still get a pacemaker because this situation can change at any time If the number of atrial and ventricular complexes is equal then we call it AV dissociation, and not AV block

Bundle Branch Block

If the wave of depolarisation can reach the intraventricular septum, then the PR interval will usually be normal. And in bundle branch block, this is still the case. However, the time taken for depolarisation to spread throughout the ventricles is altered because of the block, and thus thus duration of the QRS is lengthened. Thus, in bundle branch block there is: Normal PR interval Lengthened QRS duration (greater than 120ms - >3 little squares)

Thus to differentiate this from complete heart block, you should look at the P waves and the PR interval and the P waves will still be related to the PR interval.

Right Bundle Branch Block (RBBB)

In many people, this does not cause abnormalities of the ECG. It often indicates right sided heart disease. In the normal heart, the depolarisation of the septum occurs from right to left. In RBBB this still happens, but because the RBB is blocked, then the right ventricle does not depolarise at the same time as the left. So, left ventricular depolarisation continues as normal, and produces a normal R and a normal S wave. But after this has happened, the right ventricle then depolarises, and causes a second R wave (R1). This creates a distinctive pattern on the ECG: V1 creates an M shaped QRS because the R wave is positive, S is negative (and R1 is also positive). This is also known as an RSR pattern there is an up (R) then a down (S), then another up (R) V6 creates a W shaped QRS because the R wave is negative, and S is positive (and R1 is also negative) You can try to remember this with the word MarroW because V1 makes an M, and V6 makes a W Important the QRS complexes will also be wide greater than 120ms The axis of any BBB can be either normal, LAD or RAD. It is most commonly normal. There is no specific treatment and it may often be caused by an atrial septal defect

Left Bundle Branch Block (LBBB)

Usually indicates left sided heart disease. The QRS sign, and physiology behind LBBB is pretty much the exact opposite of that in RBBB, so the sign is opposite. You can use the word WillaM to try and remember this one! Causes Ischaemic disease if the patient has had recent chest pain, LBBB is likely to indicated MI, and thus thrombolysis should be considered. Aortic stenosis If the patient is asymptomatic, then no treatment is needed

But how do you know which side is which?! well, William has LL) in the middle for left, and Marrow has RR in the middle for right! You could also try the sentence William left his Marrow if this helps you remember the words and better. NB the William and marrow signs are not always that great;

RBBB - you may only see the M in lead V1 LBBB you may only see the W in lead V6

Bifascicular block
This refers to any situation in which two of the three main fascicles of the His/Purkinje system are blocked. These three fascicles are; the right fascicle, the left anterior fascicle and the left posterior fascicle. So there is one on the right and two on the left. Usually it refers to RBBB with either left anterior fascicular block (LAFB, sometimes called LAH left anterior hemiblock) or left posterior fascicular block (LPFB, sometimes called LPH left posterior hemiblock). Some people consider LBBB a bifascicular block because technically LBBB occurs above the bifurcation of the LAF and the LFP, and thus both are blocked. Treatment A new bifascicular block in a patient with acute MI needs emergency pacemaker placement A bifascicular block with RBBB and LAH is as stable condition that can go unchanged for years. You will need to look at old ECGs to establish how long it has been there A bifascicular block with RBBB and LPH should be considered for pacemaker therapy. If the pattern is new or old, the patient should be referred for emergency pacemaker. Note both LPH and LAH can cause left axis deviation

Rhythms
Rhythms can originate in 3 places in the heart the SA node, the region around the AV node (known as nodal, or junctional rhythm), or the ventricular muscle

Sinus Rhythm
This basically means that the rhythm of the heart is being controlled by the SA node i.e. this is the normal way the rhythm of the heart. You can have a sinus tachycardia, sinus bradycardia, and also sinus arrhythmias. The way to tell if it is sinus or not is There is one P wave per QRS There is a constant PR interval

Sinus arrhythmia

Sinus tachycardia Associated with; exercise, fear, pain, haemorrhage, thyrotoxicosis Sinus bradycardia Associated with; athletic training, fainting attacks, hypothermia, myxoedema, seen immediately after MI

Supraventricular rhythms
This is any rhythm that originates outside of the ventricles, and spreads to the ventricles in the normal manner; via the bundle of His, and left and right bundle branches. Thus, sinus rhythm is a supraventricular rhythm, as is junctional rhythm. These will produce: Normal QRS complexes because the part of the heart producing the QRS is not in the ventricles - so the conduction will still pass through the ventricles as if it was produced normally, no matter if the producing part of the heart was the SA node, junctional region, or atrial muscle. o Unless! there is also a right or left BBB, in which case the QRS may be wide

Ventricular rhythms the bradycardias

The spread of the electrical charge in this case is abnormal, and thus the QRS us abnormal. Repolarisation is also abnormal, and so the T wave is an abnormal shape. There will be: Wide QRS complexes

Atrial escape
This is a supraventricular rhythm. It occurs when the normal depolarisation of the SA node has not occurred, and some part of the atrium starts the depolarisation instead. On the ECG you can see atrial escape where there is:

An abnormal p wave - because the excitation has begun somewhere away from the SA node Normal QRS Normal beats after the abnormal one

Junctional escape
No p waves Normal QRS Slightly slower rate (~75bpm max)

Ventricular escape
Most commonly seen in complete heart block, although you may see it without complete heart block, and it may occur as a one off instance. Note there is no wave before the escape in this instance because in this case the escape is a result of the SA node failing to fire (and the junctional escape also failing to kick in), and not a result of a bundle block. Note that in this type of escape, normal rhythm is restored afterwards, whereas in branch block, normal rhythm is not restored.

Accelerated idioventricualr rhythm

Normally, the ventricular rhythm is slower than that of the SV node. However, in this particular instance, there is a rhythm of around 75pm, but it has been generated by the ventricles. This is often benign and need not be treated (although it is also associated with MI). You should not confuse it with ventricular tachycardia which requires a heart rate of over 120bpm

There are widened QRS complexes, as well as abnormal T waves

Extrasystoles
These basically have the same appearance as their corresponding escape beats, except that where an escape beat occurs later than expected, an extrasystole occurs earlier than expected.

Junctional extrasystole absent or misplaced P wave because the depolarisation travels towards the atria and the ventricles, not just away from the atria and towards the ventricles like a normal beat. Normal QRS

Atrial extrasystole Normal QRS, normal looking beat apart from it occurred earlier than expected.

The tachycardias
These are the result of foci either in the atria or in the junctional ( AV node) region depolarising quickly. To identify the origin of the tachycardia you have to look at the p wave. When tachycardias occur intermittently they are called paroxysmal.

SUPRAVENTRIUCLAR TACHYCARDIAS
Atrial tachycardia o o Atria depolarise >150bpm P waves superimposed on the t wave of the preceding beat QRS complexes are the same shape as normal The AV node cannot conduct faster than 200bpm. if the rate of atrial depolarisation is faster than this, then atrioventricular block occurs, where there are some p waves, not followed by QRS complexes. Differentiating from 2 In 1 and 2
st nd nd

degree heart block:

degree heart block, the rhythm is roughly sinus rhythm

In atrial tachycardia, the rhythm is fast

Atrial flutter Rate >250bpm No flat lines between P waves (saw tooth p waves) Often associated block remember the AV node cannot pass on rhythms of greater than about 125bpm. thus if there is an atrial rate of 250, the ventricular rate will be 125, and 2:1 block will be present. If the rate ventricular rate is 100, and the atrial rate is 300, then it is 3:1 block. P waves may be difficult to discern from T waves however you can tell if they are p waves because they occur regularly, even if they look like T waves. In the example below you cant see t waves they are all p waves.

Junctional (nodal) tachycardia Due to an area around the AV node causing depolarisation results in p waves very close to the QRS, or no p waves visible. QRS is normal because like all supraventricular arrhythmias the ventricles are still activated in the normal way. Basically there are probably no p waves, but a normal, regular QRS These are usually due to small re-entry circuits around the AV node- and are sometimes called atrioventricular nodal re-entry tachycardias (AVNRE).

Carotid sinus pressure By applying pressure to the carotid sinus you can stimulate the AV and SA nodes via vagal stimulation. This will reduce the frequency of discharge of the SA node, and increase the time of conduction across the AV node. Thus, by applying pressure to the carotid sinus you can: Reduce the rate of some arrhythmias Completely stop some arrhythmias It will have NO EFFECT ON VENTRICULAR TACHYCARDIAS thus is can help you differentiate. Applying the pressure basically reduces the frequency of QRS complexes, and allows the underlying atrial arrhythmia to become more visible.

VENTRICULAR TACHYCARDIAS
These are caused by a foci in the ventricles discharging at a high frequency. This causes an abnormal spread of charge through the ventricles, resulting in wide and abnormal QRS complexes.

QRS is broad T waves difficult to identify No p waves Regular QRS (~200bpm) REMEMBER you also see wide and abnormal QRS complexes in bundle branch block

Differentiating BBB with supraventricular tachycardia, from VT o o o o o o Remember the clinical state of the patient: If they have just had an MI it is most likely to be VT An isolated incidence of broad complex tachycardia is more difficult to differentiate: Look very carefully for p waves (only present in BBB not VT) Compare the tachycardia to the patients normal rhythm (if possible) if the QRS is the same shape in both then it is BBB with supra-v tachycardia If the QRS is >160ms (4 small squares) then it is most likely ventricular. Left axis deviation normally means ventricular in origin If the QRSs are irregular, it is most likely AF with BBB

FIBRILLATION
This occurs when individual muscle fibres contract of their own accord. So far all the rhythms we have looked at have involvedsynchronous muscle contraction. Atrial fibrillation No p waves just an irregular baseline Irregular QRS between 75-190bpm Normal shape QRS because conduction through the AV node is normal In V1 the trace resembles atrial flutter Normal T waves

Atrial fibrillation is a particularly common arrhythmia, and is discussed in more detail in the Atrial Fibrillation article

Ventricular fibrillation No discernable pattern no QRS, no P, no T Patient is very likely to lose consciousness thus the diagnosis is easy!

WOLFF-PARKINSON-WHITE SYNDROME (WPW syndrome)

In normal people the only route from the atria to the ventricles is through the AV bundle. However, in some people there exists anaccessory pathway through which conduction is able to travel. This is usually on the left side of the heart. Conduction is able to travel through this accessory pathway, and is not delayed by the AV node, and thus there is pre-excitation of the ventricles. The accessory pathway is known as the bundle of kent. The incidence of WPW syndrome is between 1-3% of the general population (i.e. very high!) The vast majority of patients will be asymptomatic, but there is a risk of sudden death. This occurs in about 0.6% of those with WPW. This sudden death can occur when there isparoxysmal tachycardia. When this occurs, the signal from the atria, travels down through the accessory pathway, and then back up the bundle of His, and back into the atria. This sets of a loop of depolarisation, sometimes called a re-entry circuit.

Findings in an asymptomatic individual: Sinus rhythm Right axis deviation Short PR interval Short QRS complex Delta wave this is a short upstroke that occurs just before the QRS. It basically looks like the upstroke of the R wave is a bit bent it starts off with a low gradient, and then increases to its normal gradient.

Findings during re-entry tachycardia: No p waves tachycardia

PACEMAKER
You should probably know what an ECG looks like when a pacemaker is present: Occasional P waves, not related to QRS QRS is preceded by a big spike which is the pacemaker stimulus. QRS complexes are broad because pacemakers usually stimulate the right ventricle and thus the depolarisation is ventricular in origin.

Q waves these show the spread of depolarisation of the ventricles travelling in the horizontal plane, thus they are often not present, because the charge travels equally in both directions and cancels itself out overall. Lead III is a good one to look at Q waves, and they are often normally present here. When pathological Q waves are present (basically big Q waves - see MI notes for definition), then this is basically a sign that part of the heart tissue is dead because it is no longer cancelling out the opposite side of the heart.

Abnormality Sinus rhythm (not an abnormality I know!)

ECG sign regular p waves, and each p wave is followed by a QRS. 60-100bpm Same as above, except>100bpm

Seen in All leads (best to look at the rhythm strip) All leads (best to look at the rhythm strip) All leads (best to look at the rhythm strip) Lead I

Pathology

Sinus Tachycardia

Could just be someone has done some exercise! Could be some sort of respiratory problem This is normal in young fit people

Sinus bradycardia

Same as above except<60bpm

Right ventricular hypertrophy

Negative QRS

Because the cardiac axis has shifted from 11-5 oclock to 1-7 oclock, thus lead I which measures laterally from right to left now gets a negative signal because the signal is going from left to right. This axis shift is called right axis deviation.

Right ventricular hypertrophy

Taller QRS

Lead III becomes taller than lead II

Because lead III measures vertically but also slightly left to right, and this is pretty much the exact direction of the new shifted axis. Lead II, measuring from right arm to left leg is no longer lined up as well. This axis shift is called right axis deviation.

Left Ventricular Hypertrophy

Transition point moved to the left equal sized R and S (normally seen in V3/V4) Small lead I QRS, negative leads II and lead III QRS

Equally sized R and S now seen in V5/V6 Leads I-III Left axis deviation this is often the results of a conduction defect, and not an increased bulk of left ventricular tissue.

Atrial fibrillation

Absent P waves just anirregular baseline. Irregularly Irregular, irregular QRS (but QRS is normal shape) Might look messy! E.g.

some? Rhythm strip

As well as no p waves, the rhythm will be irregularly irregular. There will be afibrillating baseline due to uncoordinated activity. The causes of atrial fibrillation are: 1. Ischaemic heart disease 2. Thyrotoxicosis (hyperthyroidism) 3. Sepsis 4. Valvular heart disease 5. Alcohol excess 6. PE

Generally

Note that AF can also co-exist with complete heart block, in which case Atrial Flutter Tachycardia Cant tell if T/P waves are present rhythm is too fast (250bpm). Often associated block; i.e. there are QRS complexes at a lower rate than the p waves Rhythm strip Lead where p waves are most easily visible you should use drugs to slow down the heart rate to see what is going on Any where p waves are best seen Anywhere the QRS will be regular! There will be saw tooth p waves that occur at 300bpm, but the QRS complexes will only be at 150, 100 or 75 bpm due to various blocks. The QRS can be regular or irregular. It can be very difficult to see t waves what looks like a T wave will probably just be a p wave. The p waves occur at very regular intervals. Caused by a foci of the atria (outside of the SA node) depolarising quickly Due to a re-entry loop; there is an area of depolarisation near the AV node; this not only transmits a signal throughout the rest of the ventricles to depolarise them This is an AV node block Can be caused by CAD, acute rheumatic carditis, digoxin toxicity, or electrolyte disturbance It is NOT an medical emergency 2 degree heart block Mobitz type 1 - Wencebach
nd

Atrial tachycardia

Junctional tachycardia

>150bpm, p waves superimposed over t waves of preceding beat, normal QRS P waves very close to QRS, or no QRS visible. QRS is normal PR interval >0.2s (one big square)

1 degree heart block

st

Allover best in I or V1

This can be an AV node block (nearly Progressive lengthening of the PR interval followed by absent QRS, then cycle repeats. Cycles are variable in Anywhere always), or an SA node block. usually benign and generally doesnt require specific treatment. can be caused by CHD or acute MI.

Mobitz type 2

length. R-R interval shortens with lengthening of PR interval Absent QRS every now and again Anywhere -

It is usually symptomless, but can present with: Dizziness / light-headedness / syncope This can be an SA node block, or far more commonly infra-Hisian block(distal block). It can progress to complete heart block, from which there is often no escape rhythm; and thus this needs treatment! the definitive treatment is an implanted pacemaker. Can be caused by CHD or MI

2:1 and 3:1 conduction

This is the ratio of P:QRS Complete (third degree) heart block 90 P waves/min, only about 38 QRS/min, and not relationship between the P waves and the QRS complexes. QRS will often have an abnormal shape, and be broad (>120ms). However, the P-P intervals will be regular, as will the R-R intervals they are just not in time with each other. The rhythm of the ventricles is the escape rhythm. ECG may appear normal.In some people there may be2 R waves. This creates a distinctive pattern: V1 there is an M shaped QRS this is sometimes called an RSR pattern V6 there is a W shaped QRS Wide QRS (120ms) LBBB left bundle branch block V1 there is an W shaped QRS V6 there is a M shaped QRS Wide QRS (>120ms) The axis can be deviated either way in BBBs, but it ismost commonly normal

Anywhere Best in II and V1

May require a pacemaker, particularly if the rate is slow This is an AV node block. Atrial activity will be completely normal, but this conductivity does not pass into the ventricles. This always indicates underlying disease the disease is often fibrosisrather than ischaemia, but it can occur in MI.

RBBB right bundle branch block

These are infra-Hisian blocks. In bundle branch blockages, the wave of depolarisation can still reach the IV septum, then the PR interval will be normal and it is. However, the time taken for the depolarisation to spread throughout the ventricles is longer thus QRS complex duration is lengthened. In the acute setting it may be caused by MI RBBB may indicate right sided disease. The two R waves indicate the depolarisation of the right and left sides of the heart at different times (the right depolarises after the left). You can remember the pattern with the word MarroW there is M in V1, and W in v6, and the rr tells you it is on the

right! There is NOT specific treatment, and it is often caused by an atrial septal defect. In the acute setting it may be caused by MI LBBB often indicates left sided heart disease. Remember the pattern withWillaM. Causes: Aortic stenosis, dilated cardiomyopathy, acute MI, CAD Symptoms: Syncope, and in more severe cases; heart failure. Those with syncope and / or heart failure will usually be treated Sinus bradycardia Normal rhythm <60bpm Anywhere with a pacemaker. Associated with; athletic training, fainting, hypothermia, myxedema (hypothyroidism), seen immediately after MI Associated with; exercise, fear, pain, haemorrhage, thyrotoxicosis Examples include: Ventricular rhythms (aka escape rhythms) Atrial escape Abnormal p wave (e.g.inverted) Normal QRS Some normal beats after Junctional escape the abnormal one Anywhere This occurs when the SA node fails to depolarise. Instead, some other part of the atrium depolarises and sends the signal to the ventricles. Wide QRS complexes Anywhere Sinus rhythms LBBB RBBB

Sinus Tachycardia Supraventricular rhythms

Normal rhythm >100bpm This is any rhythm that originates outside the ventricle

Anywhere

No p waves Normal QRS Slightly slow rate (max 75bpm)

The escape occurs somewhere at the AV junction. It occurs when the rate of depolarisation of the SA node falls below the rate of the AV node, thus the AV node starts the beat instead. The resulting bradycardia reduces cardiac outputand can cause symptoms similar to other bradycardias such as: Dizziness Light-headedness Syncope Hypotension Usually the bradycardia can be tolerated as long as it is above 50bpm

Ventricular escape

Accelerated idioventricular rhythm

Two types: Many p waves per QRS (complete heart block) Occasional missing p wave, followed by long gap, and then a ventricular QRS, then normal rhythm

Somewhere along the line the p waves isnt getting conducted to the ventricles, and thus the ventricles depolarise at their normal escape rate.

Wide QRS Rhythm of about 75bpm No p waves Abnormal T waves

Dont confuse this with ventricular tachycardia which requires a HR of >125pbm. Otherwise it looks very similar. Usually benign and does not need to be treated. Also associated with MI

Extrasystoles (aka ectopics)

These are easy they are the same as ventricular escapes, except that where in escapes the escape beat comes after a pause in the rhythm, in extrasystole, there is an abnormal beat earlier than expected. The QRS complexes are the same as those of sinus rhythm, but there are usually abnormal p waves that tend to come immediately before or immediately after the

QRS. Inferior MI (probably the right coronary artery) Anterior MI (probably the left anterior descending) Posterior MI ST depression, tall R waves ST elevation ST elevation II, III, aVF (theinferior leads) V2-5 the anterior leads V1-V3 The ST elevation in these leads is often accompanied by ST depression in the antero-lateral leads V1-V6, and possibly in lead I and aVL This will also cause deep q waves. The presence of Q waves implies a full thickness infarction. Posterior MI is unusual! The changes that occur are opposite to the changes of other type of MI. thus the tall R waves are the opposite of Q waves (remember Q waves are negative), and ST depression occurs in place of ST elevation Both factors, if they occur, are usually permanent. In a full thickness infarctionthen there are pathological Q waves, and T wave inversion, but in a non-full thickness MI then there is only T wave inversion. The differentiation between full /thickness and non full thickness is pretty much the same as ST elevation / non-ST elevation Can be difficult to differentiate from BBB. BBB has p waves, and a QRS generally 120-160ms. VT is more likely scenario after MI, and has QRS >160ms

ST elevation MI (STEMI)

ST elevation >2mm in 2+ chest leads OR >1mm in 2+ limb leads, T-wave inversion (after several hours) Pathological Q waves (24 hours +)

T wave inversion occurs within a few hours of MI, pathological Q waves occur several days after initial MI

NSTEMI Ventricular tachycardia

Pathological Q waves only Wide QRS, no p waves, T waves difficult to identify, rate >200bpm Narrow QRS No discernable pattern, no QRS, no P, no T Delta waves present, right axis deviation, short PR interval, short QRS ?

Supraventricular tachycardia Ventricular fibrillation

Patient is very likely to lose consciousness thus the diagnosis is easy! Accessory pathway, usually from the left atria to the left ventricle allows direct transition of the signal, bypassing the AV node, hence the shortened PR interval. It has a risk of mortality as it can cause re-entry tachycardia; however, most patients are symptomless and live with no problems. This causes a sloping ST segment that has a reversed tick look. This occurs because digoxin blocks the na/K pump, which increases intracellular Ca2+ concentrations. (similarly, ischaemia causes reduced production of ATP, and thus reduced pump activity)

Wolff-Parkinson-White SYndrome

The digoxin effect

Depression of ST, inverted T waves

widespread

Pericarditis

T wave inversion (rare: also ST elevation)

Widespread

P pulmonale

Tall ,peaked T waves, p wave height >2mm in lead II

Lead II

Bifid P waves (P-Mitrale)

Bi-phasic T waves Prolonged QT interval

P waves with two peaks, broad looks like an M; hence the name Mitrale T waves with t peaks Prolonged QT

If ST elevation does occur, then the ST waves will appear saddle shaped thus helping you to differentiate it from MI. also, the elevation in MI tends to be confined to a certain area, but in pericarditis, it is widespread Seen in cor pulmonale, or pretty muchanything that causes right atrial enlargement (or hypertrophy) such astricuspid stenosis or pulmonary hypertension Left ventricular hypertrophy

Can occur as a result of MI The corrected QT, is the QT interval as it would be at 60bpm. if this is long, then there is a risk of sudden cardiac death.It can be congenital, but also caused by drugs

Hyperkalaemia

Left ventricular hypertrophy

Pacemaker

Wide, tall, tented T ? Can lead to VF and AF waves, shortened/absent ST segment, small or absent p waves, wide QRS S wave in V1 or V2 >35mm AND R wave in V5 or V6 >35mm R in aVF >20mm R in aVL >11mm Any chest lead >45mm R in lead I >12mm ? Occasional P waves, not The large spike is pacemaker stimulus. related to QRS, QRS The QRSs are wide because the precede by large stimulus originates in the ventricles spike,QRS complexes broad

Axis deviation Lead I + + Lead II + Either Axis Normal LAD RAD

aVR should always be negative! If it is positive,it is called north-west axis. it could be due to incorrect limb lead placement, dextrocardia, or artificial pacing, due to the pacemaker wire - this enters the heart at the apex. Carotid sinus pressure By applying pressure to the carotid sinus you can stimulate the AV and SA nodes via vagal stimulation. This will reduce the frequency of discharge of the SA node, and increase the time of conduction across the AV node. Thus, by applying pressure to the carotid sinus you can: Reduce the rate of some arrhythmias Completely stop some arrhythmias It will have NO EFFECT ON VENTRICULAR TACHYCARDIAS thus is can help you differentiate. Applying the pressure basically reduces the frequency of QRS complexes, and allows the underlying atrial arrhythmia to become more visible.