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What's so difficult about ECGs--a bundle of what?
In the first in a series of understanding ECGs Dominic Cox and Hamish Dougall take you through the basics Are electrocardiograms (ECGs) difficult? Should we believe the titles of numerous texts written on the subject, which proclaim "ECGs Made Easy," "ECGs Made Simple," or "ECGs So Simple Your Granny's Cat Could Do Them"? We'll let you into a secret. Reading ECGs is not that difficult. A medical student can make the majority of important diagnoses just as well as a cardiologist and probably far better than the average orthopaedic surgeon. (The definition of a double blind study is an orthopaedic surgeon and an ECG.) At present you may run for cover on seeing an ECG. We hope to show you that there is no need to do this. If you experience a combination of confusion, apathy, and palpitations on hearing strange words, like ECG mapping, signal averaging, and QT dispersion by a consultant cardiologist on a ward round, take heart. Such discussions are intellectual twaddle and completely unnecessary for the majority of practising doctors to understand. All you need is to understand the basics of the ECG and the rest is simple pattern recognition. We hope to show that, with a simple approach to ECGs, you will no longer fear these "squiggly lines" and that they will aid and enhance your understanding of patients on a daily basis in whatever area of medicine you practise. The engine itself, its control, and power supply The heart is a simple, robust, and clever machine that beats around 3.2 billion times during an average life. It adapts to its situation by becoming more efficient the more it is used. It never stops (we hope) and it takes quite a battering from our lifestyle. A reasonable analogy in understanding the heart and therefore ECGs is to think of the heart as the three separate and interlocking systems involved in running a motorcar. If you understand the basic function and physiology of the heart and apply this as you learn to read ECGs then the whole subject area should click effortlessly into place in your grey matter.
The pumps (the engine)
This is what delivers the end product. In this case, blood to vital organs and tissues in the body. Each contraction (ventricular systole) sends blood to the body from the left ventricle (LV) through the aorta and, via a lower pressure system, to the lungs via the pulmonary artery. Because the pulmonary circulation is in such close proximity to the heart, only relatively small pressures are required (15-30 mm Hg) for the right ventricle (RV) to service this. The left ventricle has to create much higher pressures (100-140 mmHg--that is, systolic blood pressure) to circulate blood to the four corners of the body. As such the muscle of the LV is much thicker and necessarily more powerful than that of the RV. From a basic understanding of this simple physiological fact you can then understand why people talk generally about LV failure rather than heart or RV failure, as you can see the obvious systemic impact of a malfunctioning left ventricle. (See figure 1.) Atrial contraction occurs during ventricular relaxation (diastole) and its sole function is to fill the ventricle with blood in preparation for ventricular contraction. The atria contribute roughly 30% to the filling of the ventricle. The rest occurs passively into the relaxing ventricular chambers after systole. In the absence of coordinated atrial activity--for example, atrial fibrillation--the 70% passive filling may be enough in many individuals to avoid haemodynamic compromise.
The electrics (the engine's control system)
and near synchronous activation of the ventricles. Simplistically. When there are short circuits in the system the heart's pumping may become disorganised. and divides into the left anterior descending (LAD) branch down the front of the heart and the circumflex branch around the left side of the heart. Once past the AV node the electrical activity passes on to the bundle of His. figure 5 The pipes (the fuel) figure 6 Without the fuel the car will not run. thereby pushing blood through the mitral and tricuspid valves into the left and right ventricles respectively. The cells of the SA node discharge spontaneously. The blood pumping through the chambers themselves does not really fulfil this need. The LCA supplies the bulk of the muscle of the LV and ventricular septum.The electrical conducting system (see figure 2. These fibres allow rapid. It also supplies most of the fuel for the electrical centres of the heart (SA and AV nodes). and is rapidly conducted by branches of this specialised fast conducting tissue through both ventricles. The atrial muscle fibres are separated from those of the ventricle by a fibrous insulating tissue ring.) of the heart conducts and coordinates the performance of the pumps. The heart requires its own fuel and nutrient supply to enable it to function. (See figure 4. The AV node has a major role in controlling the heart. The rate of this discharge determines the speed at which the heart beats. The heart therefore has its own blood supply that comes off the root of the aorta just after it leaves the heart. These "wires" are divided into two bundles supplying the left and right ventricles. the sinoatrial (SA) node. ranging from relatively minor to haemodynamically catastrophic. the right coronary artery (RCA) usually supplies the inferior or underside of the heart.) . The left system separates into anterior and posterior fascicles. This does not allow the passage of the atrial electrical impulse to continue to the ventricles except at the atrioventricular (AV) node. It delays conduction of the electrical impulse long enough so that the ventricles are filled by atrial contraction before they themselves contract. There are two principal systems (right and left coronary systems) that run over the external surface of the heart muscle and give the heart nutrients and oxygen. which can result in a variety of sequelae. This is seen as a P wave on the ECG and it causes the atrial muscle fibres to contract. (See figure 3. ordered. The starting point in the control system is the heart's spark plug.) The left coronary artery (LCA) starts with left main stem (LMS). The AV node funnels this impulse from the atria and leads it to the start of the specialised "electrical wires" in the ventricles. An electrical wave stems from this spark plug flooding across the atria.
if there is a blockage of the RCA then the changes on the ECG will be seen on the inferior surface of the heart. Because the RCA supplies the SA and AV nodes then clearly you can get problems with the formation and passage of electrical information in the heart. Answer: In principle. For example. there is only one precordial lead and you need to do an ECG on another patient urgently. the ECG is a simple recording of its performance: several microphones placed strategically around the race track to detect the sound. How many of your standard 12 lead ECG recordings could you do and would they look any different? The answer to this can be simply worked out from the principles described above. if you have a blockage within the LCA there tends to be greater damage to the left ventricle. Unfortunately. Question: It is 3 am in the morning and you arrive at an ECG machine on your ward. Thus you could have a nine lead ECG which is much better than nothing. and aVF could be obtained but would not be augmented so would appear normal in shape but smaller in size. This is electrical earth for the unipolar leads. some of the fancy jiggery pokery that exists in modern ECG machines might not let you print the results. you could position each of the precordial leads separately and get a normal recording. As we are actually recording electricity our "microphone" needs to compare the electricity passing it with a reference point. aVL. Understanding the squiggly lines Now that we have discussed some of the background information relevant to making ECG reading easy we will move on to look at some of the basic concepts to understanding the squiggly lines seen on the ECG. The bipolar leads I. II. particularly if the important anterior descending artery is involved. There are no other ECG machines within 50 miles of your current location. Unfortunately. The earth lead is customarily placed on the right leg of the patient. Leads aVR. There may be less damage to the left ventricle if your RCA is blocked as it supplies less of the total muscle. On the other hand. and III are calculated vectors so could not be obtained by this method.figure 8 figure 9 figure 10 From this simple understanding of the structure of the heart you can work out quite a lot of clinically important information. To extend the analogy of the motorcar. .
These compare differences in electrical signals in two limbs. and III were used before the nine unipolar leads were developed.) The three "standard" limb leads I. secondly. left arm. II. They are not true recordings but calculated recordings.) >figure 7 Finally. The field diminishes rapidly with distance from its centre. Therefore all electrodes placed more than 15 cm from the heart can be considered to be equidistant from the heart. once the distance is greater than 15 cm." The term "vectors" will bring back distant and perhaps painful memories of school maths so we will not labour the point that essentially leads I.) .The nine leads (unipolar) shown (figure 5) essentially act as "microphones" that detect the electrical sound as it approaches. An additional fact about these three leads. and left leg respectively. even if physically they are not. However. (See figure 8a. Thus six records are obtained from these three limb leads. (See figure 6. The heart is the centre of an electrical field that it generates. to record directly as a "microphone" and.) An electrical impulse travelling directly away from a sensor will have a maximal negative deflection. (See figure 7. and aVF are limb leads attached to the right arm. aVL. Thus the three limb leads are each used twice: firstly. (See figure 8b. Like the unipolar limb leads these are best at looking at differentiating right/left and inferior/superior "sounds. and another six records come from the chest lead--the 12 lead ECG. to compare cardiac electrical signals between limbs. the decrement is insignificant. is that they are "augmented" by recording between one limb and the other two--this does not affect how the ECG looks but makes the size of the waves about 50% larger. we will show you three key pieces of information that will enable you to understand ECGs with respect to the different leads. 1) An electrical impulse travelling directly towards a sensor will have the maximal positive deflection. (The earth lead is attached to the right leg. and III are cardiac vectors. V1-6 are the precordial (chest) leads that are essentially all at roughly the same level on a horizontal plane--that is.) They detect "sound" in essentially the same way as the precordial leads but this time are best at differentiating right/left and inferior/superior signals. II. that you really do not need to know or understand. right/left and anterior/posterior--and are therefore best at picking up "sounds" in this axis and are relatively poor at giving useful information in the vertical plane (inferior/superior). Leads aVR.
We would like to emphasise. An ECG is a two dimensional recording of a three dimensional process. It lies in the same direction as electricity flowing from the SA to the AV node and thus this will be emphasised in this lead. In this article we will go through the different parts that make up the ECG recording (see figure 1) in turn. They are good at looking at cardiac electrical features in this plane. however. that you treat patients and not ECGs.An impulse travelling half way between these--that is. It in fact spreads out in all directions across the heart. control (electrical supply). (See figure 8c. article may seem a little dry. Once you understand the basics you can always look these up when you need that information. (See figure 9. and how that in an ECG. In the first article we explained how the heart works as an engine and outlined the power supply (coronary arteries). however. worth trying to grasp the basic concepts without getting bogged down too much in the numbers or fancy syndrome names. It is. then moving away. We re-emphasise that a grasp of only a few rudimentary concepts will allow all of us. to understand the majority of clinically important ECGs.) 2) The limb leads and the six recordings made from them are in a vertical plane through the body. When it is heading directly away from it we will get the opposite: the largest negative response. A cardiac electrical impulse does not travel in a single direction down a straight line with an arrow on the end. University of Dundee PART 2 Understanding ECGs: Minding your Ps and Qs In the second article in our series Dominic Cox and Hamish Dougall discuss what you need to learn and what you need to understand In this series of articles on electrocardiograms (ECGs) we hope to convey the basic concepts of reading and using this simple clinical tool. in the vertical and horizontal planes. and the previous. general practitioner and research fellow in general practice. It would certainly be worth having our . the electrical supply is recorded as it moves across the heart by a series of detectors placed strategically around the body. not just the cardiologists. Dominic Cox.) 3) The chest leads look at the front of the heart in a horizontal plane. Newcastle upon Tyne Hamish Dougall.) In the next article we will show how you can work out what a P wave or QRS complex would look like on an ECG and begin to look at simple rhythm recognition. We appreciate that the material in this. one that travels at 90o will show a biphasic deflection as initially it is coming towards you. lead II is commonly used to look at the heart's rhythm. Leads looking at right angles to the wave front will see smaller biphasic responses as the wave passes them. (See figure 10. For example. specialist registrar in cardiology. Thus they will be useful in looking for heart attacks affecting the front wall of the heart. When the wave is heading towards a specific lead we will get the largest positive deflection in that lead. The ECG leads allow us to look at this depolarisation wave from different views--that is.
Thus the P-wave typically has a biphasic waveform in this particular lead.) As five of the six chest leads are mostly on the left side of the body and in approximately the same vertical plane there will generally not be much difference in the P-wave in these leads with small positive deflections seen in each. The P-wave This is a recording of atrial depolarisation. if there is damage to the SA node.) We point this out.first two articles to hand as you read the subsequent articles in this series.12sec and its height does not exceed 2. not because it is common or particularly important. In these circumstances P-wave deflections are in the opposite direction. and V2 to V6 The first part of the P-wave comes from the right atrium and the second . the initiation of the electrical activity can arise from other parts of the atria. apart from lead V1 with its different view on the heart. II. This generates a positive deflection in the leads that look at the heart from below. then the chest leads do not detect this well. (See figure 2. As one of the predominant movements of this depolarisation is downwards (inferiorly). As we have said before. Key facts about P-wave • • • • • • • Initiated at SA node Predominantly travels inferiorly and from right to left in the normal individual The rate of firing of the SA node normally determines the heart rate Limb lead II is the lead that normally best shows the P-wave. but because it is a simple example of seeing what the different leads record in changing circumstances. the chest leads are not good at looking at vertical movement. (See figure 3. Most of the time this starts in the sinoatrial (SA) node and the predominant direction of the impulse across the atria is inferiorly and from right to left. Occasionally. If this is lower down in the atria the impulse has to move in the opposite direction to normal. which will be much more clinically. Lead V1 looks across the atria and sees the atrial depolarisation pass across its view. and lead V1 provides an alternative view The normal P-wave does not exceed 0. and case study oriented.5mm The P-waves should be upright in I.
Enlargement of the left atrium causes exaggeration of second part of the P-wave. atrial tissues. and can thus be seen as affecting the PR interval. peaked P-wave. The AV node delays conduction of the electrical impulse long enough so that the ventricles are filled by atrial contraction before they themselves contract. There is then a flat segment as depolarisation reaches the AV node and there is an electrical interlude. This leads to the typical bifid "m" shape in lead II. (Lead II looks along the axis of the atria. Thus disease of the sinus node. (See figure 4. This is called P mitrale. the whole of atrial depolarisation. These two leads are typically used as rhythm strips as they emphasis the P-wave. Lung disease could lead to right atrial strain and thus this tall P-wave is known as P pulmonale. This gives a taller. and larger negative deflection in second part of the P-wave in lead V1.part from the left atrium The P-wave can be thought to have two components. and V1 looks across the atria. or AV node could affect the formation and passage of electricity prior to ventricular contraction.) The PR interval The PR interval starts from the beginning of the P-wave (SA node depolarisation). The best two leads to examine the Pwave are leads II and V1 as they look at the atria in opposite directions. The first half of the P-wave is made mainly by the right atrium. and includes the whole P-wave--that is. The PR interval ends as ventricular depolarisation begins (the start of the QRS complex). Key facts about PR interval • Represents the time it takes for the atria to depolarise and pass its message to the ventricles .) Disease processes that cause strain on the right atrium cause a typical enlargement of the first half of the P-wave. The second half comes from the left atrium.
pacemaker complexes. It is in fact quite remarkable that the whole of activation of the ventricle is so rapid. Wolf-Parkinson-White (WPW) and Lown-GanongLevine syndromes (will be discussed in later article) QRS-wave After traversing the AV node.08-0. a specialised conduction system is required to ensure the ventricular muscle all contracts in a synchronous. This may sound ominous at the moment but from the work covered in these first two articles you will be able to work out yourself very simply what you would expect to see in an ECG tracing in these different situations. Were the ventricles to be the same size as the atria and without a specialised path of conduction then the QRS complex would look similar to a P-wave.) The QRS complex represents ventricular contraction. as with the P-wave the complex looks different depending on where it is being recorded from. and life is just not that simple.12 to 0.12sec (three small squares) it suggests a defect in the . Key facts about QRS complex • • Spread of depolarisation from the AV node to all parts of the ventricles takes 0. (See figure 5. atrial tissue and AV node Is measured from the beginning of the P-wave to the beginning of the QRS complex (a better description would be PQ interval. Remember. A typical QRS complex is shown in figure 1. and broad complex tachycardias.) QRS complexes are not always so narrow. the impulse reaches the Bundle of His and thus its right and left bundle branches which rapidly conduct it to the ventricular myocardium through the Purkinje fibres. and efficient manner.• • • • • Is a function of the SA node.1 sec If QRS width is >0. rapid. (See figure 6. This rapid activation of such a bulk of muscle creates a large spiked complex. However because their size and relative bulk is much greater.21 sec (or three to five little squares) Prolonged in heart block (will be discussed in later article) Shortened in conditions where there is an abnormality in the fibrous insulating ring such that the electrical message gets past the AV node quicker--for example. We will look at this again in future articles when we discuss right and left bundle branch blocks. being as quick as the much smaller atria. but that would perhaps make medicine too easy to understand) PR interval should be 0.
There is no strict criteria for the size of the T-wave. figure 8 illustrates that the normal average direction of the QRS lies between aVL (-300) and aVF (+1200). (Note: the wave that would represent atrial repolarisation occurs during the QRS complex and is therefore not seen. of course. T-waves This wave represents repolarisation of the ventricles. Q-waves in the wrong place can be a sign of previous myocardial damage--for example. As a general rule the T-wave should not be less than one eighth and not more than two thirds of the height . Unfortunately. The mean QRS "axis" describes the average direction of the various electrical forces that develop during ventricular activation. V2 to V6 There is a fair amount of muscle in the interventricular septum. II. It returns along the outer ventricular walls towards the AV groove. From the arrow you can see that the initial movement is from left to right across the septum. The returning to normal of the ventricle after depolarisation.) The wave of depolarisation then spreads down the septum to the apex of the heart. Lead aVR will see the wave going directly away from it--a maximal negative deflection. II. the Qwaves are defined as pathological--meaning suggestive of a disease process. aVL is perpendicular to this wave front and thus has a smaller biphasic QRS. Similar to the direction shown for the P-wave in figure 2.wave and the ST segment are the most sensitive areas of the ECG in terms of looking at disease processes affecting the ventricle. However. But there are certain patterns which we can recognise.• • • • conduction system No precordial Q-wave must be greater or equal to 0. and is of course impelled by left ventricular energy. Generally the tallest precordial T-waves are found in V3 or V4 and the smallest in V1 and V2. Activation actually starts at the left side of the interventricular septum and crosses to the right. the changes are not always specific to a single disease.) It is normally positive in I. This axis is described in the standard vertical plane. The T. the first bit of the ventricle to be depolarised. We have already said that speed and mass of the left ventricular activation predominates the major deflection seen in the QRS complex. after a myocardial infarction. Where this deflection is greater than that outlined above.04 seconds in width in I. This is. (See figure 7.04 sec (one small square) Precordial Q-waves must not have a depth greater than a quarter of the height of the R-wave in the same lead The R-wave in the precordial leads must grow from V1 to at least V4 There should be no Q-wave or only a small q less than 0. Lastly. as we have seen you would normally expect to see an initial negative deflection in certain leads. Thus lead II will have a large positive QRS. V4-6 (see figure 9).
A little time spent understanding these concepts is the key to understanding the whole ECG. In subsequent articles we look at ECGs in clinical settings. Again we will return to this in future articles as this is one of the disease sensitive areas of the ECG.of the preceding R. The ECG in the disease state does become a matter of pattern recognition.wave in each of the leads V3-6. toxins. and some things you have to understand. University of Dundee . such as the way in which electricity moves in the heart and creates either an upward or downward deflection on the ECG. It is peaked in hyperkalaemia (high potassium) and flattened in hypokalaemia (low potassium). We should emphasise that these conditions are rare and a description is included in this article only for completeness.5mm implies ischaemia--for example. angina Widespread saddleshaped elevation occurs in pericarditis QT interval This is measured from the start of the QRS to the end of the T-wave. Romano-Ward and Jervell-Lange-Nielsen syndromes--or acquired--for example. Key facts about ST segments • • • Elevation of >1mm implies infarction Depression of >0. The length of this varies with rate. and electrolyte disturbances. secondary to drugs. Newcastle upon TyneHamish Dougall general practitioner and research fellow in general practice. The ST segment The ST segment lies between the QRS and the T-wave. This now completes our jaunt through the basics of the ECG. The normal ST segments do not deviate above or below the isoelectric line (see figure 1) by more than 1 mm. Prolongation of this parameter can be an inherited condition --for example. Grasping the fundamentals in these first two articles is the code to comprehending all ECGs. These conditions are rare but their significance is that they predispose such patients to potentially serious ventricular arrhythmias. The information we have discussed in this article is a mixture of some things you just have to remember such as the names of the waves on the ECG. Dominic Cox specialist registrar in cardiology.
Positive deflections if the wave is coming towards them and negative if going away. All the emergency treatment protocols are available from the European Resuscitation Council (website www.edu/). PART 3 Understanding ECGs: tachycardias In the third article in our series Dominic Cox and Hamish Dougall discuss the main types of tachycardia Tachycardias are the most exciting part of learning about ECGs. "Benign" arrhythmias can compromise a person. Whereas the impulse moves towards V1-3 resulting in an initial upward (positive) deflection: a small Rwave in these leads. It is useful to think of these as narrow complex (QRS complex <120ms) tachycardias (SVT) and broad complex (QRS >120 ms) tachycardias (VT).1 2 normally the atrium passes the sinoatrial (SA) node's signal to the atrioventricular (AV) node. The electrical wave moves leftward driven by left ventricular depolarisation. Answer Because the initial electrical movement is from left to right across the septum this means that it is away from leads V4-6 resulting in a small initial downward (negative) deflection: a small Q-wave in these leads. We are not going to try to explain the emergency treatment of arrhythmias. leads record large deflections if the wave front moves in the line of the way that they are looking. Why is the QRS complex narrow? As described in the previous articles. This then passes on through the ventricular specialised conducting . and "serious" arrhythmias can be asymptomatic. Then the bulk and speed of depolarisation of the left ventricle predominates what happens to the QRS. Leads on the left side (V4-6) have large positive deflections: an R-wave. Tachyarrhythmias can be divided into two broad categories: supraventricular tachycardias (SVT) and ventricular tachycardias (VT). rather than treating the ECG. Looking at figure 7.erc. It is of course important to understand the mechanism causing tachycardias. but it is equally important to remember to look at the patient first. Look at the patient and act with commonsense.Question From what we have discussed already you will already be able to predict what the shape of the QRS complex will be in each lead. can you work out in what direction the initial deflection (direction of depolarisation shown as a small arrow) of the QRS complex will be in each of the six chest leads (V16)? Remember. Thus the initial small septal depolarisation gives the first small deflection of the QRS complex. Thus leads on the right side of the heart (V1-3) have the large negative second deflections: an S-wave. but this should be something on all doctors' minds (and hearts).
see figure 1). The most common mechanism involves an abnormal electrical circuit which allows the heart beat to cycle around it.tissue. synchronous activation of the whole of the ventricle. ECG 1: Atrial fibrillation . Thus to get a narrow complex you must have an electrical signal that passes forward through the AV node. and you must have specialised conducting tissue. The other is where a focal area of the heart starts to "spark off" and send out a shower of extra heart beats (increased automaticity or triggered activity. that works. which gives rapid. A broad QRS complex means that either your conducting system is not working (bundle branch block) or the electrical circuit is not involving the AV node correctly. So what causes arrhythmias? Only two things cause abnormal heart rhythms. This is called re-entry.
atrial flutter Re-entrant mechanism. 5% over 75 years Associated with any disease affecting the heart Other narrow complex tachycardias can degenerate to AF--for example. baseline irregularities representing atrial activation (ECG 1). flecainide. Useful drugs: anticoagulation to prevent thromboembolism.ECG 2: Atrial flutter Narrow complex tachycardias Atrial fibrillation (AF) • • • • • The most common sustained arrhythmia of all Affects 2% of 65-75 year-olds. Arrhythmia anatomy: Typically involves a large circuit created by the structures in the right atrium (figure 3). Arrhythmia anatomy: Multiple wavelets of re-entry swashing around the atria. ß blockers. and verapamil (often in selected combinations) to control heart rate. . The AV node is inundated with cascades of chaotic activity (see figure 2). diltiazem. and amiodarone to prevent paroxysmal AF. propafenone. Atrial flutter • • • • Mistakenly thought of as a variant of atrial fibrillation Occurs at any age Can be difficult to control with drug therapy Re-entrant mechanism. digoxin ß blocker. sotalol. ECG: Irregular ventricular rate with no true P waves.
ECG 3: AV node re-entrant tachycardia during tachcardia .
The QRS complex in lead V1 no longer has a second small R wave. Atrioventricular nodal re-entry tachycardia (AVNRT) • Also known as AV nodal tachycardia (AVNT). which was due to backward atrial depolarisation occurring at the same time as the QRS during palpitations ECG: Saw tooth baseline with atrial rate of 300 and ventricular response of 150. You still get an atrial rate of 300 but hopefully a slower ventricular rate. Type 1c agents (propafenone or flecainide) can be used to stop the atrial circuit and terminate the tachycardia. Useful drugs: Digoxin and verapamil (or diltiazem) can be used to slow the response of the AV node. Flutter waves are seen before each QRS and after each QRS in the middle of each T wave.ECG 4: The same patient with AV node re-entrant tachycardia now in sinus rhythm. Always be suspicious of flutter if you see a narrow QRS tachycardia at a heart rate of 150(ECG 2). or AV junctional tachycardia (AVJRT) .
and verapamil. Useful drugs: ß blockers. as atrial and ventricular depolarisation occur at the same time. The QRS is . Useful drugs: Drugs which affect the AV node--that is. ECG: Narrow QRS tachycardia of about 180 bpm with P waves often absent: they are hidden in the QRS. These paths allow a circuit to be set up at the AV node itself. Wolff Parkinson White syndrome. adenosine can acutely stop the tachycardia as it transiently blocks the AV node (as can vagotonic manoeuvres). ECG 5). Atrial tachycardias • • • Second most common SVT Can occur at any age. digoxin. Arrhythmia anatomy: Varied anatomical basis (see figure 4): they can be due to a focal area in the atria with increased automaticity. back up the pathway. The early depolarisation of part of the ventricle leads to a shortened PR interval and a slurred start to the QRS (delta wave). pulmonary disease. or re-entry around an abnormal area of atrial tissue. previous cardiac surgery. You may see changes in the QRS complex in lead V1 as compared with the resting ECG: these are due to simultaneous P wave activation. It may even be you! Arrhythmia anatomy: Figure 5 shows that the re-entry mechanism is due to a congenital addition of a small piece of atrial tissue which crosses the isolating fibrous ring separating the atria and ventricles. diltiazem. This is a small positive deflection before the onset of the T wave and is shown in ECG 3 and 4. This illustrates why SVT is not such a good name for these arrhythmias: most of this tachycardia's circuit lies in the ventricle. may have different types of P waves on same ECG. type 1c agents (propafenone or flecainide). This gives a large circuit with the heart beat passing down through the AV node. Atrioventricular re-entrant tachycardia (AVRT) and Wolff-Parkinson-White syndrome • • • • Can occur from infancy onwards In infants it may be associated with congenital heart defects Re-entrant mechanism One to three people in every 1000 have an obvious extra pathway on the resting ECG--that is. Can have multiple foci of automatic activity.• • • Commonest type of narrow QRS Typically starts in the later teens and 20s Re-entrant mechanism. ß blockers. ECG: Abnormal looking P waves. amiodarone. giving rise to the arrhythmia. but increased likelihood if the atria are diseased (hypertension. ECG: The resting ECG can be normal but it can show evidence of the pathway's existence if the path allows some of the atrial depolarisation to pass quickly to the ventricle before it gets though the AV node (Wolff-Parkinson-White (WPW) syndrome. type 1c agents (propafenone or flecainide). Heart rate very variable from 140 to 240 bpm. etc) Either focal automatic activity (mainly) or due to re-entrant mechanism. and across the atrium back to the AV node. verapamil or diltiazem. Arrhythmia anatomy: The basis of this arrhythmia is that the AV node can have two pathways as part of it (see figure 3). around the ventricle. Look at the subtle difference in the QRS during tachycardia and during normal rhythm.
narrow. If the circuit is long or slow enough the P wave may occur at the end of the QRS and can be visible as a distortion in the T wave (this is best seen in lead V1). In patients with accessory paths there is a mechanism for this very fast heart rate to bypass the AV node and cause AF with a dangerously fast ventricular response (ECG 1). This is why the drugs are stated as being contraindicated in atrial fibrillation in the presence of an accessory pathway. The situation would be made a lot worse in this case. Fortunately. verapamil. Atrial fibrillation has an atrial rate of 300-600 bpm. adenosine can acutely stop the tachcardia as it transiently blocks the AV node (as can vagotonic manoeuvres). Treating this with drugs such as digoxin. ECG 5: Wolff-Parkinson-White syndrome . with P waves absent (hidden in the QRS). type 1a agents (procainamide or quinidine). or diltiazem would further block the AV node but not prevent the AF from passing down the accessory path. the AV node protects the ventricle from experiencing such a heart rate. the message via the AV node eventually predominates because it uses the rapid conducting system to depolarise most of the ventricle. The tachycardia ECG may be unremarkable. Useful drugs: ß blockers. type 1c agents (oropafenone or flecainide).
. So if you see a broad complex tachycardia look at the patient. The ECG is irregular and frighteningly quick (more than 300bpm in places) ECG 7: Ventricular tachycardia: AV dissociation ECG 8: Ventricular fibrillation Broad complex tachycardias To have a narrow complex you need functioning specialised conducting tissue. Always treat the patient and not the ECG. and the cardiac impulse must pass through the AV node normally.ECG 6: A patient with AF and an accessory pathway. To the majority of doctors it does not matter. All of the SVTs can give a broad complex tachycardia if bundle branch block is present. Think of it as VT and you will do little harm in the acute situation. Much time is spent by cardiologists considering ECGs and asking whether they show VT or SVT with bundle branch block.
totally uncoordinated contraction of ventricular myocardial fibres Causes circulatory arrest. bizarre QRS morphology.Ventricular tachycardia • • • Broad complex tachycardia means ventricular tachycardia until proved otherwise Likely in patients with established heart disease Mainly. Cox D. What's so difficult about ECGs--a bundle of what? studentBMJ 2001. The history can be very revealing. unconciousness develops within 10 to 20 seconds. Dougall H. and management Symptoms from slowing of the heart can be very varied. from sudden death. re-entrant mechanism (see figure 6). Ventricular fibrillation (VF) • • VF is the rapid.) Cox D. Useful treatment: Defibrillation. 2. If the patient is well there will be enough time to assess even the most serious rhythm disturbance. Dougall H. 9: 374-6. Understanding ECGS: minding your Ps and Qs.9:315-7. to much milder symptoms. significance. Some . The main message about tachycardias is at all times to assess the patient. etc. ECG: Broad complex >120 ms. ventricular arrhythmias cause most concern as they are most likely to upset the heart's ability to pump blood effectively. capture or fusion beats may be present (see ECG 7). abnormal axis.) PART 4 Understanding ECGs: bradycardias--fit and fitting In the fourth article in our series Dominic Cox and Hamish Dougall look at bradycardias--their diagnosis. chaotic electrical activity (ECG 8). Useful treatments: Check the patient. (October. These give everyone dealing with the situation a proper structure so that they can think and act together. but can also be very unreliable in those patients who truly lose consciousness. Obviously. If the patient is threatened by their heart rhythm then following life support protocols is essential. breathlessness. Newcastle upon Tyne Hamish Dougall general practitioner and research fellow in general practice. Dominic Cox specialist registrar in cardiology. no P waves preceding each QRS. But remember that relatively benign rhythms can be devastating if they are fast enough or in a patient with little physiological reserve. if the patient is pulseless get help and treat as per resuscitation guidelines. studentBMJ 2001. ECG: Irregular. not treat the ECG. and epileptic-type fits. recurrent syncope. but not exclusively. (September. University of Dundee 1. such as lethargy. concordant QRS (all point in the same direction).
Bradycardia is "slow" cardiac rhythm and results from either a failure of initiation of the heart beat or failure of passage of this electrical message through the heart--that is. Getting evidence of an intermittent problem can be very difficult. ECG 1: Patient who has gone into slow atrial fibrillation . young people. such as hypothyroidism. normal sinus node "spark plug" activity is disturbed or there is interruption of the passage of this activity to tell the pump to work. which controls the heart rate in normal circumstances. Identifying the important different types of bradycardias is relatively straightforward and will be considered in turn: sick sinus syndrome (sinoatrial disease). or during sleep. but it can be of profound clinical significance resulting from acute myocardial infarction. The first three conditions are predominantly problems with the SA node or its innervation. Likewise the treatment options are few in number and basically consist of removing or treating the underlying cause: (a) resuscitation with drugs to stop the heart slowing (atropine). This second type of failure usually occurs at the atrioventricular (AV) node. and raised intracranial pressure can also cause sinus bradycardia. hypothermia. The intrinsic rate of the sinoatrial (SA) node.bradycardias are only intermittent problems with bothersome recurrent blackouts but no abnormality found after many years of medical investigation. agonal rhythm. or from a variety of different drugs--for example. jaundice. (b) drugs to speed up the heart (isoprenaline). beta blockers. (c) pacing the heart electrically. Several non-cardiac disorders. sick sinus syndrome. Such a rate may be physiological (and therefore acceptable) in athletes. and a bradycardia is defined as a pulse rate of <60 beats per minute. asystole. AV heart block. vasovagal syndrome. carotid sinus hypersensitivity. is 60 to 70 beats per minute.
or sinus pauses. but there are periods when interval between P waves (P-P interval) is prolonged. dizziness. particularly that involving the right coronary artery. Note that in the tachy-brady syndrome once a PPM has been implanted medications which would normally slow the intrinsic cardiac rate can then be used to control the SVT--for example. . Patients may be completely asymptomatic. and symptoms. demonstrating a correlation between periods of bradycardia. although many of these patients have normal coronary arteries. Treatment: Removal of extrinsic causes of bradycardia and/or permanent pacemaker (PPM) implantation. Carotid sinus hypersensitivity Similar symptoms to SSS can occur due to a hypersensitive carotid sinus reflex. or syncope. There is lengthening of the PR interval and then complete loss of ventricular activity for over 3 and a half seconds ECG 3: First degree heart block: a constant prolonged PR interval Sick sinus syndrome (SSS) This is common in the elderly and is usually caused by idiopathic degeneration of the SA nodal cells. (ECG 1) Normal PR interval (because this is an SA node. Sinoatrial disease may be associated with coronary artery disease. They can present with symptomatic bradycardia. or supraventricular tachycardia (SVT) alternating with bradycardia ("tachy-brady syndrome"). The diagnosis is from 12 lead or 24 hour ambulatory ECG recording and. in which case usually no treatment is indicated.ECG 2: This ECG of a young patient undergoing cartoid sinus massage shows profound slowing of the P wave rate. It causes bradycardia that can be profound enough to cause arrest. problem). beta blockers. Again where an association is made between symptoms and ECG findings then PPM is indicated. Every P wave is followed by a normal QRS complex (unless dual pathology). SA block. not an AV node. importantly. It is diagnosed by finding either a sinus pause or of AV block greater than three seconds in response to five seconds of carotid sinus massage. It is accepted that a pause of over three seconds is significant.
calcific aortic stenosis First degree AV block The PR interval is prolonged (>0. and third degree AV blocks. verapamil. therefore as well as a sinus bradycardia the PR interval can also be prolonged resulting in AV block [ECG2] Vasovagal syndrome This is a common condition. rheumatic fever. It is the association between the two that is seen to be different. Class I antiarrhythmics Infection--diphtheria. second. Lyme disease Idiopathic fibrosis of the conducting system Infiltration--sarcoidosis.20 sec) but constant (ECG3). which as the names suggest. tumour. Causes of AV block • • • • • Acute myocardial infarction or ischaemia Drugs--beta blockers. endocarditis. syphilis. Because the problem is not with the SA node or the ventricular polarisation itself. ECG 4: Mobitz type I or Wenckebach block ECG 5: Mobitz type II second degree atrioventricular (2:1) AV heart block AV heart block is divided into first. This vagally mediated bradycardia can be treated by PPM. involve a problem at the AV node! All three variants involve the association between the P wave and the QRS complex. scleroderma.Note that carotid sinus massage affects both SA and AV nodes. digoxin.This does not produce any symptoms and does not require any active treatment. then both the P wave and QRS complex commonly look normal. Causes of AV block are shown in the box. . and a more malignant variety is recognised in the more elderly. particularly in younger people. and this is because they are connected via the AV node.
however. there is regular firing of the SA node giving regular P waves. Pacemaker implantation is not mandatory without evidence of correlated symptoms or undue bradycardia. Third degree AV block (complete heart block) In this. ECG 6: Third degree or complete heart block. It therefore takes longer to transmit across the ventricle and therefore the QRS complex looks wider. Möbitz type II is different in that the PR interval is constant but occasionally a P wave is not conducted through the AV node and is therefore not followed by a QRS complex--that is. leading to a narrow normal complex QRS." Regular non-conducted P waves may result in a high degree block. except in the context of an acutely reversible condition. there is a "dropped beat. (ECG 5) Type II AV block usually indicates an extensive infranodal abnormality and therefore. as there is a risk of sudden death. requires a permanent pacemaker. The P waves. If only every second or third P wave is followed by a QRS complex then there is said to be 2:1 block or 3:1 block respectively. ECG 7: Agonal rhythm Agonal rhythm . Most cardiac tissue can produce some spontaneous activity. do not get through the "broken" AV node. even if asymptomatic. There is clearly no association between the frequent P waves and narrow complex ventricular rhythm. Often this comes from near the start of the His Purkinje system.Second degree AV block There are two types of second degree block: Möbitz type I (also known as Wenckebach) has a progressively lengthening PR interval that eventually drops a QRS complex and starts over with a progressively lengthening PR interval before dropping a QRS complex again--need I go on? (ECG 4) This is normally associated with a reliable subsidiary pacemaker and a lower chance of progressing third degree block. If the complex arises more distally then the complex cannot be propagated in the normal manner. The lonely ventricle now electrically separated from the atrium usually produces its own slow heart rhythm. (ECG 6) A permanent pacemaker is essential.
This is a slow. irregular rhythm with wide ventricular complexes of varying morphology. These wires are the permanent part of the system. specialist registrar in cardiology. The need for treatment depends on the haemodynamic consequences of the arrhythmia. Newcastle upon Tyne Hamish Dougall. rather a complete cessation of both atrial and ventricular activity. Bradycardia can occur just because someone is fit. general practitioner and research fellow in general practice. many professional athletes will have a heart rate around 40 beats per minute. Most wires or leads are placed inside the heart via the subclavian or other vein. Patients who black out will not always be aware of truly losing consciousness and may even "remember" tripping over. If the heart beat changes they then step in to stimulate the heart appropriately. which is often seen during the later stages of unsuccessful resuscitation attempts as the heart dies. (ECG 7) Pacemakers Pacemakers treat all types of bradycardia and also interfere with and abort many tachycardias. a pacemaker. They can also be used to reco-ordinate ventricular function in patients with heart failure and damaged electrical conducting systems. Most pacemakers listen to the heart's own rhythm and leave things alone as long as things are working properly. and the computing system. or sympathomimetic drugs. The battery and computer are inside a can which attaches to the leads. and can be very difficult to diagnose if it occurs rarely and is intermittent. such as adrenaline or isoprenaline. which is not likely to be significant unless the rate drops below 40 beats per minute. University of Dundee . The complexes become progressively broader before all recognisable activity is lost. To do this the pacemaker is comprised of three parts: the wires. If there are persisting P waves but no ventricular activity then it is called ventricular standstill. Sometimes leads are placed on the surface of the heart (epicardial) via opening the chest in a more invasive procedure. the battery. If the ECG shows asystole and the patient is speaking to you then you need to check that your leads are properly attached. The emergency treatment of most bradycardias is atropine. Occasionally even the occasional case of epilepsy can be cured with a pacemaker! Dominic Cox. Asystole This is not really a bradycardia. Bradycardia is also a major cause of blackouts.
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