Primary Care ECG Seminar

Primary Care ECG Seminar
Dr Sandeep Gandhi 8th May 2006

Learning Objectives Importance of ECG to the primary care health practitioner Understanding the normal ECG Learning a structured approach to ECG interpretation Interpreting the ECG in the clinical context

Why is the ECG important for GPs?
As a diagnostic aid in Chest pain SOB Syncope Presyncope Palpitations Electrolyte disorders hypothermia As a screening tool FH of SCD Looking for end organ damage in HT and diabetes

Why is the ECG important?

QOF2 Clinical Indicators
Total points CHD 89 Heart failure 20 AF 30 Total 139

Why bother when we have computer assisted interpretation?
Interpretative software is of variable accuracy Diagnosis of arrhythmias is the Achilles heel of software packages. Can over diagnose inferior and septal MI. Can over diagnose LVH in young black people with normal hearts.

Continued However one study showed how computer aided diagnosis actually improved the diagnostic accuracy when combined with physician evaluation The best approach is computer and physician evaluation combined

Action potentials and electrophysiology
+ + _ _ _ Resting Depolarised Repolarised Plateau _ + Na + _ Ca in(slow) ++ + + + Na in + + K out + K + Ca ++ _ + Action potentials and electrophysiology The heart is a hollow organ with walls made of specialised cardiac muscle. When excited, these muscles shorten, thicken and squeeze on the hollow cavities, forcing blood to flow in directions permitted by the valves (as described in the last slide). An action potential refers to the voltage changes occurring inside a cell when it is electrically depolarised, due to ionic movements into and out of the cell. Cardiac muscles can be electrically excited and show action potentials that propagate along the surface membrane, carrying excitation to all parts of the muscle. Cardiac muscle cells (cardiomyocytes) are interconnected by gap junctions, allowing action potentials to pass from one cell to the next. This ensures that the heart as a whole participates in each contraction, making the heartbeat an “all or none” response. The basic ventricular action potential is due to three voltage-dependent currents: sodium, potassium, and calcium. The very rapid rise of the initial spike of an action potential is due to the opening of the sodium channels, allowing sodium ions to rush into the cell from the outside, depolarising the cell further. The sodium channels then inactivate, and calcium channels activate. There is now a small flow of calcium ions flowing into the cell, balancing the small amounts of potassium ions leaking out. This results in the membrane potential being held in a suspended plateau. The potassium channels then open, and the calcium channels close, causing a rush of potassium ions out of the cell and the membrane being rapidly repolarised. The action potential does vary throughout the heart due to the presence of different ion channels. In the cells of the sino-atrial (SA node) and atrioventricular nodes (AV node) calcium channels, rather than sodium channels, are activated by membrane depolarisation, resulting in a different shape of the action potential. A recording of the electrical changes that accompany the cardiac cycle is called an electrocardiogram (ECG). Each cardiac cycle produces three distinct waves, designated P, QRS and T. It should be noted that these waves are not action potentials, they represent any electrical activity within the heart as a whole. + + + K + + + _ _ _ _ + 3.2

Understanding surface ECG recordings

Initiation and spread of electrical activation
Sino-atrial node Atrioventricular bundle (bundle of His) Atrioventricular node Initiation and spread of electrical activation; pacemaker function of the sino-atrial node The heart muscle, or myocardium, is a single functioning unit, or functional syncitium, since action potentials that originate in any cell can be transmitted to all other cells. This makes it important for the heart to have a single pacemaker, which is able to synchronise the electrical activity of the whole heart. It is the sino-atrial node (SA node) that carries out this function. The SA node is located in the right atrium, near the opening of the superior vena cava. It is this region of the heart that demonstrates dominant spontaneous electrical activity and by this means functions as a pacemaker. Each cell within the sinus node is an automatic cell that spontaneously generates slow potentials, but can be influenced by nervous and hormonal input. When the cell repolarises after an action potential, it never rests at a stable value. Instead, it reaches a maximum negative value at the end of repolarisation and then slow spontaneous diastolic (phase 4) depolarisation begins. When the membrane potential reaches a critical value, the threshold voltage, an action potential ensues. The normal automatic process in the sinus node is modulated by the autonomic nervous system. Many other cardiac cells are capable of independent action and hence depolarisation. However, the rate of spontaneous depolarisation of these cells is slower than that of the SA node. This means that the SA node normally controls the rate of contraction across the whole atrium, so acting as pacemaker. Right & left bundle branches Purkinje fibres 3.3

Spread of electrical activity through the atria
Spread of electrical activity through the atrial myocardium; relation to ECG Action potentials that originate in the SA node spread to adjacent myocardial cells of the atria and to the AV node. The action potentials are not transmitted into the ventricles as the walls of the atria and ventricles are separated by a band of connective tissue so that an action potential generated in the atrium can only pass to the ventricle via a specialised node. There are two routes for spread: cell to cell, and specialised internodal bands. The spread of the action potential causes the atrial cells to depolarise and so contract. This contraction of the muscle pumps the blood into the ventricles. This depolarisation of the atria is represented on the ECG by the P wave. The P wave is a relatively small wave as the atria have only a small muscle mass. Because the SA node is located in the right atrium near the vena cava, the cardiac impulse activates the right and left atria in the general direction from right to left, inferiorly and posteriorly. Initial activation of the right atrium, an anterior chamber, is directed to the front (anteriorly) and down (inferiorly) and is followed by activation of the left or posterior atrium, directed to the left, backwards (posteriorly), and inferiorly. 3.4

Atrioventricular node and the bundle of His
Atrioventricular node and the bundle of His; left and right bundle branches As described earlier, a fibrous skeleton separates the myocardium of the atria and ventricles. This means the action potential cannot be transmitted directly to the ventricles. There is therefore a specialised area for conducting the action potential, the atrioventricular node (AV node). Because of its location near the inferior portion of the interatrial septum, it is one of the last portions of the atria to be depolarised. The AV node, like the SA node, is also slow conducting. From the AV node, a tract of conducting fibres called the bundle of His runs through the cardiac skeleton to the top of the interventricular septum. The conducting pathway then continues down both sides of the septum as the right and left bundle branches. This slow conduction allows sufficient time for the entire atria to be depolarised and finish contracting (pushing the blood through into the ventricles), before the ventricles begin to contract. Therefore, the time from initiation of the depolarisation of the atria to the initiations of ventricular depolarisation corresponds to the PR interval on the ECG. A bundle branch block occurs when either the right bundle or the left bundle fails to conduct an impulse. In this situation the QRS complex is prolonged, showing that the ventricles are taking longer to depolarise. Because the affected bundle branch is unable to conduct the impulse, it is conducted into the ventricle from the unaffected side. It therefore takes longer for the ventricles to depolarise and contract. 3.5

Spread of electrical activity throughout the ventricle
Q S T Spread of electrical activity throughout the ventricular myocardium; Purkinje fibres and relation to ECG The Purkinje fibres lead from the AV node through the AV bundle into the ventricles. These fibres have very fast conduction velocities. Depolarisation of the ventricles is very rapid due to the Purkinje fibres. Because of this the cardiac impulse arrives at almost all portions of the ventricular muscle within a very small span of time, signalling all portions of the ventricular muscle in both ventricles to begin contracting at almost exactly the same time. This synchronous contraction is important in producing maximal thrust to the blood being pumped out of the heart. The contraction of the ventricles is shown by the QRS complex of waves on the ECG. There are three phases of ventricular depolarisation. The interventricular septum is depolarised first, then the free wall of the right ventricle and finally the free wall of the left ventricle. The QRS wave is usually, but not always, the largest deflection of the ECG, and is always spiky. It shows both positive and negative deflections representing the travel of the depolarisation to and away from the viewing electrode of the ECG. The ST segment represents the time between the spread of impulse through the ventricles and repolarisation of the ventricles. It is therefore a short interval during which the myocardium remains at rest in a depolarised state. You will remember this as the prolonged plateau phase of the action potential. This segment is often elevated in acute myocardial infarction. The T wave shows the repolarisation of the ventricles, which takes longer than the depolarisation. Repolarisation of the atria is hidden in the QRS complex due to the larger muscle mass of the ventricles. Depolarisation of Ventricles Repolarisation of Ventricle 3.6

The two planes of the 12-lead ECG
The 12 leads of the standard 12-lead ECG were selected to offer a wide variety of “views” of the heart. They do this by looking at the heart in two different planes. The limb leads look at the heart from the edges of the frontal plane. The six precordial leads are placed in defined positions over the heart. These leads look at the heart in the horizontal or transverse plane. Together these 12 leads allow the heart to be viewed from various angles, especially the anterior (front), anterolateral (front and side), lateral (side), and inferior portions of the heart. In particular this arrangement provides good detail about the left ventricle. This is important as the left ventricle is the most powerful part of the heart, and if damaged provides the most serious consequences. 7.3

Horizontal plane - the six chest leads
V1 V2 V3 V4 V5 V6 RA LA LV RV Horizontal plane - the six chest leads Each of the six chest leads has a fixed position. In order to place the precordial leads correctly the fourth intercostal space needs to be identified. The ribs form convenient horizontal landmarks. In order to count them, feel for the ridge with marks the junction of the manubrium and the body of the sternum. When this has been found, run the finger outwards until it reaches the second costal cartilage, which articulates with the sternum at this level. The space immediately above this is the first intercostal space. The spaces should then be counted downwards, well away from the sternum, as they are more easily felt here. V1 right sternal margin at fourth intercostal space V2 left sternal margin at fourth intercostal space V3 midway between V2 and V4 V4 intersection of left midclavicular line and fifth intercostal space V5 intersection of left anterior axillary line with a horizontal line through V4 V6 intersection of mid-axillary line with a horizontal line through V4 and V5. V1 and V2 face and lie close to the free wall of the right ventricle, V3 and V4 lie near to the interventricular septum with V4 usually at the cardiac apex, and V5 and V6 face the free wall of the left ventricle but are separated from it by a substantial distance. Together the chest leads observe changes in the anterior and lateral aspects of the heart, giving detailed information about the myocardium of the area they lie over. 6.5

Extending the horizontal plane with V7, V8, and V9
Extending the horizontal plane with V7, V8 and V9 to show posterior infarction Because the chest leads overlie the anterior and lateral aspects of the heart, it can often prove difficult to diagnose posterior infarcts. A patient may present with a history and physical examination that indicate myocardial infarction, but the ECG is normal. A patient may also show inferior lead changes or the reciprocal changes of ST segment depression for a posterior infarction. Recently these signs and symptoms have been approached in a new way. By using an extra three leads which extend around the back of the chest the posterior of the heart can be viewed. These leads are V7, V8, and V9. The procedure for using these leads is very simple. A standard 12-lead ECG is run first. Then an additional ECG is run using the precordial leads, and placing the additional electrodes in the appropriate locations. The posterior leads are located as follows: V7: left posterior axillary line, straight line from V6 (use V4 lead) V8: left midscapular line, straight line from V7 (use V5 lead) V9: left paraspinal line, straight line from V8 (use V6 lead) 6.6

Extending the Horizontal Plane to RV leads

The Vertical Plane

ECG paper 6.1 1 Small square = 0.04 second 1 Large square = 0.2 second
5 Large squares = 1 second ECG paper The electrocardiogram (ECG) is a recording of the electrical activity of the heart. It records the wave of depolarisation that spreads across the heart. The ECG is recorded from two or more simultaneous points of skin contact (electrodes). When cardiac activation proceeds towards the positive contact, an upward deflection is produced on the ECG. As the activation moves away from the electrode, a downward deflection is seen. The neutral position on the ECG is known as the isoelectric line, and is where the tracing rests when there is no electrical activity in the muscle. There are many types of ECG machine, including 3, 6, and 12 channel machines. The ECG trace is printed out on paper composed of a number of 1 and 5 mm squares. The height of each complex represents the amount of electrical potential involved in each complex and an impulse of 1 mV causes a deflection of 10 mm. Horizontally each millimetre represents 0.04 second and each 5 mm represents 0.2 second. Time 2 Large squares = 1 cm 6.1

ECG amplitude scale Normal amplitude 10 mm/mV Half amplitude 5 mm/mV
Double amplitude 20 mm/mV

The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s
QTc s

More on the QRS

Reading the ECG – The basics
Read name, date and time on ECG – make sure all of these are present Get old ECG for comparison eg is ST depression new, is LBBB new? Is the ECG recorded at full amplitude? Is the calibration mark a full 10 mm in height? Check speed of paper 25mm/s

Reading the ECG - The 3 Rs Rate Rhythm – sinus or not Regular or not
300/no. of squares between successive R-R intervals <60 bradycardia, >100 tachycardia Rhythm – sinus or not Regular or not

Rate Count number of large boxes between first and second R waves= /7.5 large boxes = rate 40

Rhythm To diagnose sinus (normal) rhythm
One P wave must be present before every QRS The PR interval must be normal and constant The P wave morphology remains constant If sinus rhythm is not present then the actual rhythm must be determined

Systematic Approach to Reading ECG
Cardiac axis P wave PR interval QRS complex ST segment T wave QTc

The electrical axis Normal Limits of QRS Axis in Adults: -30° to +90°.

Determining the Axis 2 simple methods
1. Look at leads I and II: QRS vector should be positive in both. If positive in I and negative in II then LAD; if negative in I RAD 2. Look for isopotential vector in limb leads: ie QRS with equal positive and negative deflections. The axis is 90 deg to this.

Left Axis Deviation

Right Axis Deviation

Causes of Axis Deviation
Right Axis Deviation Infancy RVH Cor pulmonale Acute RV strain Secundum ASD Fallot, severe PS Left posterior hemiblock Left Axis Deviation LVH LBBB Left anterior hemiblock Cardiomyopathies Primum ASD Inferior MI

The P wave <3 small squares in duration
<2.5 small squares in amplitude

PR interval Normal is between 3 and 5 little squares
PR > 200 ms = 1st degree HB PR < 120 ms may suggest accessory pathway (eg WPW) PR interval should be constant, if it varies this suggests some form of AV conduction block

AV block 1st degree 2nd degree 3rd degree HB Mobitz type 1
Mobitz type II 3rd degree HB

1st Degree HB PR interval > 200ms Asymptomatic

2nd Degree HB In second degree block there is intermittent failure of conduction between the atria and ventricles. Some P waves are not followed by a QRS complex. Mobitz type I block (Wenckebach phenomenon) Mobitz type II block The PR interval is identical before and after the P wave that is not conducted

Complete Heart Block Third degree heart block. A pacemaker in the bundle of His produces a narrow QRS complex (top), whereas more distal pacemakers tend to produce broader complexes (bottom). Arrows show P waves

QRS Complex Height LVH/RVH Width – should be <3 little squares. BBB>120 ms: either RBBB or LBBB (can be indeterminate sometimes)

LVH/RVH

Criteria for Ventricular Hypertrophy
RVH RAD > 900 RV1+SV6 > 11 mm RV1 or SV6 > 7 mm R/S V1 > 1 R/S V6 < 1 T inversion V1-V3 or V4, ST depression LVH LAD > -300 SV1 or V2+RV5 or V6 > 40 mm SV1 or RV5 or RV6 > 25 mm R1 or SIII > 25 mm R in I or aVL > 14 mm T inversion in I, aVL ST depression V4-V6

Causes of Ventricular Hypertrophy
LVH AS HOCM HT Coarctation of aorta RVH PS PHT Tetralogy of Fallot

Dominant R in V1 Other causes of tall R in V1 RBBB WPW (type A)
Posterior MI Muscular dystrophy Any cause of RVH

LVH and strain pattern Ventricular Strain
Strain is often associated with ventricular hypertrophy Characterized by moderate depression of the ST segment.

Small voltage QRS Defined as < 5 mm peak-to-peak in all limb leads or <10 mm in precordial leads. Chronic causes — pulmonary disease, hypothyroidism, obesity, cardiomyopathy. Acute causes — pleural and/or pericardial effusions

Bundle branch block

Causes of RBBB Can be normal ASD (and other congenital heart disease)
PE Cor pulmonale

Causes of LBBB IHD HT Cardiomyopathy Idiopathic fibrosis

The Q wave A Q wave is a negative deflection preceding the R wave
Normal (ie less than 1/4 of R wave height) allowed in I, aVL, V5-6. Represents septal depolarisation (L to R). Normal Q < 0.04 s wide Pathological Q is >1/4 R wave height and signifies old MI ‘Pathological’ Qs allowed in V1, III and aVR

ST segment ST segment should be an isoelectric line
Pathological ST segment manifest as ST segment depression or ST segment elevation

Characteristic changes in AMI
ST segment elevation over area of damage ST depression in leads opposite infarction Pathological Q waves Reduced R waves Inverted T waves Characteristic changes in AMI The 12-lead ECG is the most useful investigation for confirming the diagnosis of acute myocardial infarction, locating the site of the infarct and monitoring the progress. It is therefore very important to know the changes that occur in this situation. The only diagnostic evidence of a completed myocardial infarction seen on the ECG are those in the QRS complexes. In the early stages changes are also seen in the ST segment and the T wave, and these can be used to assist diagnosis of myocardial infarctions. Shortly after infarction there is an elevation of the ST segment seen over the area of damage, and opposite changes are seen in the opposite leads. Several hours later pathological Q waves begin to form, and tend to persist. Later the R wave becomes reduced in size, or completely lost. Later still, the ST segment returns to normal, and at this point the T wave also decreases, eventually becoming deeply and symmetrically inverted. Although these changes occur sequentially, it is very unlikely they will all be clearly observed by the paramedic or GP. A patient can present at any stage and a progression through the ECG changes will not be seen. It is important to recognise these features as they occur rather than in association with each other. All these changes imply myocardial infarction, and will be discussed in more detail over the next few slides. 7.13

Sequence of changes in evolving AMI
R R R ST T ST P P P T Q S Q Q 1 minute after onset 1 hour or so after onset A few hours after onset R Sequence of changes in evolving AMI The ECG changes that occur due to myocardial infarction do not all occur at the same time. There is a progression of changes correlating to the progression of infarction. Within minutes of the clinical onset of infarction, there are no changes in the QRS complexes and therefore no definitive evidence of infarction. However, there is ST elevation providing evidence of myocardial damage. The next stage is the development of a new pathological Q wave and loss of the r wave. These changes occur at variable times and so can occur within minutes or can be delayed. Development of a pathological Q wave is the only proof of infarction. As the Q wave forms the ST elevation is reduced and after 1 week the ST changes tend to revert to normal, but the reduction in R wave voltage and the abnormal Q waves usually persist. The late change is the inversion of the T wave and in a non-Q wave myocardial infarct, when there is no pathological Q wave, this T wave change may be the only sign of infarction. Months after an MI the T waves may gradually revert to normal, but the abnormal Q waves and reduced voltage R waves persist. In terms of diagnosing AMI in time to make thrombolysis a life-saving possibility, the main change to look for on the ECG is ST segment elevation. ST P P ST T P T T Q Q Q A day or so after onset Later changes A few months after AMI 7.18

Anterior infarction Anterior infarction I II III aVR aVL aVF V1 V2 V3
Location of infarction and its relation to the ECG: anterior infarction As was discussed in the previous module, the different leads look at different aspects of the heart, and so infarctions can be located by noting the changes that occur in different leads. The precordial leads (V1–6) each lie over part of the ventricular myocardium and can therefore give detailed information about this local area. aVL, I, V5 and V6 all reflect the anterolateral part of the heart and will therefore often show similar appearances to each other. II, aVF and III record the inferior part of the heart, and so will also show similar appearances to each other. Using these we can define where the changes will be seen for infarctions in different locations. Anterior infarctions usually occur due to occlusion of the left anterior descending coronary artery resulting in infarction of the anterior wall of the left ventricle and the intraventricular septum. It may result in pump failure due to loss of myocardium, ventricular septal defect, aneurysm or rupture and arrhythmias. ST elevation in I, aVL, and V2–6, with ST depression in II, III and aVF are indicative of an anterior (front) infarction. Extensive anterior infarctions show changes in V1–6 , I, and aVL. Left coronary artery 7.19

Inferior infarction Inferior infarction I II III aVR aVL aVF V1 V2 V3
Location of infarction and its relation to the ECG: inferior infarction ST elevation in leads II, III and aVF, and often ST depression in I, aVL, and precordial leads are signs of an inferior (lower) infarction. Inferior infarctions may occur due to occlusion of the right circumflex coronary arteries resulting in infarction of the inferior surface of the left ventricle, although damage can be made to the right ventricle and interventricular septum. This type of infarction often results in bradycardia due to damage to the atrioventricular node. Right coronary artery 7.20

Lateral infarction Lateral infarction I II III aVR aVL aVF V1 V2 V3
Location of infarction and its relation to the ECG: lateral infarction Occlusion of the left circumflex artery may cause lateral infarctions. Lateral infarctions are diagnosed by ST elevation in leads I and aVL. Left circumflex coronary artery 7.21

ST depression in unstable angina/NSTEMI
Subtle changes Dramatic ST depression

Other causes of ST segment shift
ST depression Digoxin effect LVH and strain pattern WPW LBBB Intracerbral bleed ST elevation LV aneurysm Pericarditis High take off Intracerbral bleed Coronary vasospasm (cocaine abuse)

T wave Represents ventricular repolarisation
T wave should have the same polarity as the QRS complex Normal Tall Flat/inverted

Examples of T wave abnormalities
Channer, K. et al. BMJ 2002;324: Copyright ©2002 BMJ Publishing Group Ltd.

T waves Tall Ts Inverted Ts Normal variant Hyperacute phase of AMI
Hyperkalaemia Inverted Ts Ischaemia Drugs Post tachycardia Electrolyte disturbances Cerebral bleed BBB LVH and strain Normal variant

QTc interval The QT interval represents the total duration of ventricular depolarisation and repolarisation. It represents the period of ventricular refractoriness QT interval increases normally with slower heart rates. QTc is the interval corrected for heart rate, calculated by the Bazell Formula It should be less than ½ of preceding R-R interval as a rule of thumb

QTc Normal QTc Men < 0.43 Women < 0.43 borderline 0.43-0.45
prolonged >0.45 Women < 0.43 borderline prolonged >0.47

Causes of Long QTc Congenital Drugs Electrolyte disturbances
Romano Ward Jervell and Lange Nielson Drugs Antiarrhythmics Class Ia and III Antibacterials Erythromycin Other drugs Terfanidine, cisapride, TCA Electrolyte disturbances Low K and Mg Other causes IHD SAH Bradycardia due to SSS or AV block Hypothyroidism

Sick sinus syndrome Disease of the sino-atrial node, usually due to age related fibrosis Risk of cardioembolic phenomena Can cause syncope/presyncope ECG shows Sinus bradycardia Sinoatrial block Sinus arrest Infranodal escape rhythms PAF/flutter

Sick Sinus Syndrome Sinoatrial block (note the pause
is twice the P-P interval) Sinus arrest with pause of 4.4 s before generation and conduction of a junctional escape beat Severe sinus bradycardia

What you should know… All patterns of myocardial infarction
Including true posterior infarction Distinguish this from acute pericarditis Recognise ST depression/ T wave inversion and know their causes AF, VT/VF All forms of AV block The BBBs Digoxin effect

Some clinical vignettes

Patients presenting with chest pain

A 48 year old male smoker with positive FH, HT and 2 week history of exertional chest pain
Cholesterol 7.2 BP 170/98 Commence aspirin 75 mg od, statin, GTN spray, beta blocker Smoking cessation advice Family screening Advise about MI warning symptoms and what to do Refer to RACPC Rate: 70 Rhythm: Sinus Intervals: Normal Axis: Normal Hypertrophy: None Infarct: None

A 56 year old male presents to Sittingbourne Hospital with chest pain
Rate: 44 Rhythm: Sinus Intervals: RBBB Axis: Normal Hypertrophy: None Infarct: ST elevation II, III, aVF = Acute inferior MI Administer 300 mg aspirin, GTN, iv morphine. Give high flow oxygen. Insert an iv line and attach to defib with monitor. Transfer urgently to Medway A+E, preferably with paramedics trained in thrombolysis. If not, then alert A+E about this patient. ALS trained ECG competency

You make a home visit to a 73 year old lady with pleuritic chest pain 2 weeks post THR
Rate: 100 Rhythm: Sinus Intervals: Normal Axis: Borderline LAD Hypertrophy: None Infarct: None Likely diagnosis is acute PE. Admit directly to hospital via 999

A further patient with PE
Sinus tachycardia S1, QIII, TIII. RBBB.

An 83 year old male with exertional chest pain, BP 110/80 and systolic murmur
Rate: 64 Rhythm: Sinus Intervals: Normal Axis: Normal Hypertrophy: LVH and strain; Left atrial hypertrophy Infarct: None Likely diagnosis is critical aortic stenosis +/- CAD. Urgent referral to cardiologist, NOT RACPC. Commence aspirin 75 mg od (avoid vasodilators)

A 64 year old female with typical exertional chest pain
A 64 year old female with typical exertional chest pain. Recently started on voltarol for back pain. This is the ECG during ETT. It shows ST depression I, II, III, aVF, V5-6. Hb came back as 4 g/dL. Her angina was due to severe anaemia. Repeat ETT once her Hb was corrected was normal.

Lessons… These last 2 cases demonstrate that angina is a syndrome and not a diagnosis It is caused by a mismatch in O2 demand and supply. In patients presenting with angina always check pulse for arrhythmia, look for pallor and listen for murmur of aortic stenosis Always check FBC and U+Es (as well as glucose and cholesterol).

SOB cases

A 78 year old female complaining of shortness of breath for 1 week.
Rate: About 40 Rhythm: Type 2 2nd degree AV block Intervals:Prolonged QRS consistent with RBBB Axis: Left axis deviation Hypertrophy: None Infarct: None This patient has bifascicular block and Mobitz type II: this is likely to progress to complete heart block Common aetiologies: IHD, degenerative disease of conducting system, drugs. This patient was admitted to hospital; MI was r/o. PPM fitted.

A 64 year old smoker with SOB
Rate: 150 Rhythm: Sinus tachycardia Intervals: Normal Axis: Normal Hypertrophy: RVH and RAH Infarct: None

A 72 year old hypertensive male with SOB
Rate: Rhythm: AF Intervals: Normal Axis: Normal Hypertrophy: LVH and strain Infarct: None This patient has developed heart failure secondary to AF on background of hypertensive heart disease

Previous case continued
Commence digoxin and warfarin if no contraindication Arrange U+E, FBC and TFT Diuretics if fluid overloaded Refer urgently to cardiologist or heart failure clinic.

A 63 year old woman with SOB, reduced exercise capacity and PND
Rate: Rhythm: AF Intervals: LBBB Axis: N/A Hypertrophy: N/A Infarct: N/A This patient also has CCF. The LBBB suggests structural heart disease which in this case was secondary to previous MI. Arrange bloods (including BNP) and refer to heart failure clinic. You could commence ACEI once BNP taken as CCF seems likely

Some palpitation cases

A 24 year old male with palpitations
Rate: 140 Rhythm: SVT (AVNRT) Intervals: Normal Axis: Normal Hypertrophy: None Infarct: None This shows a regular narrow complex tachycardia rate 140. No atrial activity seen. This is most likely to be SVT (AVNRT variety). Treatment and referral will depend on clinical circumstance.

Previous case continued
First of all try and eliminate potential triggers eg alcohol, caffeine, stress, sleep deprivation, chocolate) If symptoms persist treatment may be warranted Verapamil, beta blockers 2nd line agents : sotalol, flecainide Consider radio frequency ablation for failure of medical treatment (or drug SE).

A 48 year old female with palpitations
Rate: 75 Rhythm: Sinus with atrial premature beat (PAC) Intervals: Normal Axis: Normal Hypertrophy: None Infarct: None Take a full history of the palpitations and carry out CVS examination If normal then simply reassure the patient

More on tachycardias 3 important questions:
Broad or narrow complex (ie more or less than 3 little squares) Regular or irregular Is the patient compromised or not? Chest pain Low GCS Low BP SOB/HF

Some syncopal cases

A 90 year old woman with syncope
Rate: 64 Rhythm: Sinus Intervals: Normal Axis: Normal Hypertrophy: LVH and strain, LAH Infarct: None Consider the causes of LVH and strain: HT, HOCM, AS, coarctation. Of these only aortic stenosis is a probable diagnosis Avoid physical activity Urgent cardiology referral

A 70 year old man intermittent ‘falls’
Rate: 38 Rhythm: Complete heart block Intervals: CHB Axis: N/A Hypertrophy: N/A Infarct: None Diagnosis: CHB with syncope. Action: Admit directly to hospital for PPM

An 83 Year Old Lady with 2 Syncopal episodes in 1 month
Rate:50 Rhythm: Sinus Intervals: PR interval 240 ms; QRS duration 160 ms (RBBB) Axis: Left axis deviation Hypertrophy: None Infarct: None This is trifascicular block which probably leads to intermittent CHB Refer urgently for permanent pacemaker

A 56 year old man with CCF and frequent episodes of presyncope
You organise an event recorder: Rate: 140 Rhythm: VT High risk for sudden death Arrange urgent admission to CCU

A 29 year old man with syncope
SR RBBB pattern V1-3 ST elevation V1-3 The diagnosis is Brugada syndrome Admit for ICD Family screening

A 28 year old woman with depression and syncope after starting treatment for a chest infection
Rate: 67 bpm Rhythm: Sinus Intervals: QTc 0.61s Axis: Normal Hypertrophy: None Infarct: None

Long QT interval

ECG for screening purposes

A 42 year old man requiring medical clearance for an exercise program
A 42 year old man requiring medical clearance for an exercise program. He is a smoker, hypertensive and has a cholesterol of 6.8 Rate: 70 Rhythm: Sinus Interval: Borderline PR prolongation (1st degree AVB) Axis: Normal Hypertrophy: LVH and strain Infarct: Q waves V1-3 This ECG shows an old septal MI (silent) and LVH and strain pattern He cannot be cleared for his exercise program He needs referral to cardiology for ETT and further assessment In meantime commence aspirin, statin, ACEI, advice re MI signs.

An asymptomatic 35 year old male with a BP of 155/100
An asymptomatic 35 year old male with a BP of 155/100. He is registering as a new patient. Rate: 100 Rhythm: Sinus Intervals: Normal Axis: Normal Hypertrophy: LVH, LAH Infarct: None This man has an elevated BP with evidence of end organ damage. He requires investigation for 20 causes of HT; other end-organ damage He requires treatment (commence ACEI or ARB). Check for other CVS risk factors. If clinical examination is normal, he does not need cardiology referral at this stage

A 38 year old man whose brother died suddenly playing squash
Rate: 90 Rhythm: Sinus Intervals: Normal Axis: Normal Hypertrophy: LVH and strain Infarct: None Diagnosis: HOCM Avoid physical exertion, commence beta-blocker Urgent cardiology referral Family screening (ECG and echo)

A 32 year old woman with a FH SCD
Rate: 60 Rhythm: SR with 2 PVCs Intervals: Long QTc Axis: Normal Hypertrophy: None Infarct: None This is a case of Romano Ward syndrome: an autosomal dominantly inherited form of long QT. Urgent cardiology referral for consideration of ICD.

Now try some cases yourselves…
Remember Rate Rhythm Intervals (PR, QRS, QTc) Axis Hypertrophy (ventricles and atria) Infarct/ischaemia

Normal Findings in Healthy Individuals
Tall R waves Prominent u waves ST elevation – high take-off Wenkebach AV block Exaggerated sinus arrhythmia Sinus bradycardia Junctional rhythm Atrial and ventricular ectopics in setting of normal heart 1st degree heart block Wandering atrial pacemaker

Summing up ECG is a very valuable tool in primary care
The ECG, like any other test, must always be interpreted with the clinical scenario Computer aided diagnosis and trained physician/nurse evaluation are complementary Adopt a systematic approach to ECG evaluation

Summing up Look at 5 areas in turn: Rate Rhythm (intervals) Axis
Hypertrophy Infarction/ischaemia

The Normal ECG Normal Intervals: PR 0.12-0.20s QRS duration <0.12s
QTc s Normal P wave parameters: P wave width < 0.12s P wave height <2.5 mm

Primary Care ECG Seminar

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Primary Care ECG Seminar

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Presentation on theme: "Primary Care ECG Seminar"— Presentation transcript:

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