Flashcards in ECG Deck (98):
What is the normal PR interval?
= 3-5 small squares
If there are 5 squares between QRS complexes, what is the heart rate
What does the PR interval represent
Time taken for wave of depolarisation to spread from the SAN through the atrial muscle and AVN down the bundle of His and into the ventricular muscle (most of the time is taken up by delay at the AVN)
What is the normal duration of the QRS complex?
120ms (3 small squares)
Which leads look at the left lateral surface of the heart?
Leads I, II and aVL
Which surface do III and aVF look at?
Which areas of the heart to V1-V6 look at?
V1 and V2= right ventricle
V3 and V4= septum
V5 and V6= left ventricle
Which leads look at the right ventricle?
aVR, V1 and V2
Which of the six standard leads is mainly negative?
Which lead(s) are predominantly negative in right axis deviation? What happens to the other lead(s)?
Lead I is predominant negative. The deflection in lead III is more positive
Which lead(s) are negative in left axis deviation?
Lead 3 and sometimes lead 2
What pathologies may be suggested by right axis deviation?
Right ventricular hypertrophy
Congenital heart disease
What conditions are associated with left axis deviation?
Left ventricular hypertrophy
N.B. Left axis deviation is only significant when the QRS is predominantly negative in lead III AND lead II
Describe the QRS complex in a right ventricular chest lead (V1 and V2)
Deflection is first upward (R wave) as the septum is depolarised from left to right
There is then a downward S wave as the main muscle is depolarised. This is because the electrical effects in the LV outweigh those of the smaller RV so the predominant electrical activity is moving away from the RV leads
Describe the QRS complex in a left ventricular chest lead (V5 and V6)
The first deflection is downwards ('septal' Q wave) as the septum depolarises from left to right, away from the LV leads
The second deflection is upwards (R wave) due to the depolarisation of the left ventricular towards the LV leads
What is the transition point? Why is it important?
The transition point is the point at which R=S, which shows the position of the interventricular septum. It is normally at V3/V4.
This is important as if the RV is enlarged it occupies more of the precordium so the septum is shifted to the left and the transition point moves to V4/V5 or even V5/V6
Describe the features of first degree heart block on an ECG
One P wave per QRS complex
PR interval is prolonged (>220ms or 6 small squares)
Describe the characteristic ECG seen in Mobitz type I (Wenckebach) heart block
Progressive lengthening of the PR interval
One non-conducted P wave
Next conducted beat has a shorter PR interval than the previous conducted beat
Describe the characteristic features see in Mobitz type 2
Most beats are conducted with a constant PR interval but occasionally there is atrial depolarization without subsequent ventricular depolarization
Describe the characteristic features see in third degree (complete) heart block
No relationship between P waves and QRS complexes
QRS complex rate much less than P wave rate (e.g. 36/min vs 90/min)
Abnormally shaped QRS complexes because of abnormal spread of depolarization from a ventricular focus
What is the characteristic feature of RBBB
RSR1 pattern in V1
(Also observe deep S waves in V6)
What is the characteristic feature of LBBB
'M' pattern in V6 ('W' pattern in V1 may also be seen)
T waves are inverted in lateral leads (I, VL, V5, V6)
Causes of sinus bradycardia
Drugs (beta-blockers, digoxin, amioderone, verapamil)
Which three rhythms can be described as supraventricular?
Causes of sinus tachycardia
Sympathomimetic drugs (caffeine, adrenaline, nicotine)
What is the major difference between ECGs showing supraventricular rhythms to ECGS showing ventricular rhythms?
What is the exception to this rule?
Supraventricular rhythms have narrow QRS complexes
Ventricular rhythms have wide QRS complexes
The exception to this is when there is a supraventricular rhythm with right or left BBB (or Wolff-Parkinson-White WPW syndrome), where the QRS complexes will be wide
What is an escape rhythm?
The heart is usually controlled by the SAN as this is the region which spontaneously depolarises the most frequently, at a rate of around 70bpm. If the SAN fails to depolarise control is assumed by a focus either in the atrial muscle or in the region round the AV node (the junctional region), both of which depolarise at a rate of around 50bpm. If these fail or conduction through the bundle of His is blocked, a ventricular focus will take over with a rate of around 30 bpm. These slow, protective rhythms are called escape rhythms.
What are the four categories of abnormal rhythm?
Bradycardias- slow and sustained
Extrasystoles- occur as early single beats
Tachycardias- fast and sustained
Fibrillation- activation of the atria or ventricles which is totally disorganised
Describe the ECG seen in atrial escape
After one sinus beat the SAN fails to depolarise
After a delay, an abnormal P wave is seen because excitation of the atrium has begun somewhere other than the SAN
The abnormal P wave is followed by a normal QRS complex, because excitation has spread normally down the His bundle
The remaining beats show a return to sinus arrhythmia
What is the characteristic feature of the ECG seen in junctional escape
No P waves
Describe three types of ventricular escape
1. Complete heart block: Regular P waves due to normal atrial depolarization occurring at a rate of 145/min. QRS complexes are highly abnormal due to abnormal conduction through ventricular muscle and occur rarely at a rate off 15/min. No relationship between P waves and QRS
2. Single ventricular escape beat: after x number of normal sinus beats, the SA node fails to discharge. No atrial or junctional escape occurs. After a pause there is a single wide and abnormal QRS complex with an abnormal T-wave. A ventricular focus controls the heart for one beat before sinus rhythm is restored
3. Accelerated idioventricular rhythm: Ventricular focus has a faster intrinsic frequency than that seen in complete heart block. Often associated with acute MI. Appearence of ECG is similar to that of ventricular tachycardia but it is benign. Following failure of SAN to depolarize, escape focus in ventricle takes over causing a regular rhythm of 75 bpm with wide QRS complexes and abnormal T waves
Describe the appearance of a superventricular extrasystole
An atrial extrasystole has an abnormal P wave
A junctions extrasystole has no P wave at all, or the P wave appears immediately before or immediately after the QRS complex
QRS complexes are normal and the same as those of sinus rhythm
A superventricular systole resets the P wave cycle. No P wave is seen at the expected time and the next P wave is late
N.B. The ECG appearance of an extrasystole arising in the atrial muscle or junctional region is the same as that of the corresponding escape beat. The difference is that an extrasystole comes early and an escape beat comes late
Describe the appearance of an ECG showing ventricular extrasystole
Abnormal and wide QRS complexes
Abnormal T wave
Common and usually of no importance
Can occur at the peak of the T wave of the preceding sinus beat causing the R on T phenomenon. This can induce ventricular fibrillation so is potentially dangerous
A ventricular extrasystole does not affect the SA node so the next P wave appears at the expected time
What five questions should be asked to differentiate between atrial, junctional and ventricular extrasystole?
1. Is there an early P wave followed by an early QRS? If so it must be an atrial systole
2. Can a P wave been seen anywhere? If there is no P wave it must be junctional. However, a junctional extrasystole may also cause the appearence of a P wave very close to and even after the QRS because excitation is conducted both to the atria and to the ventricles
3. Is the QRS complex the same throughout? Yes= supraventricular extrasystole
No= ventricular extrasystole
4. Are the T waves normal or inverted?
Normal= supraventricular extrasystole
Inverted= ventricular extrasystole
5. Does the next P wave after the extrasystole appear at an expected time?
Supraventricular extrasystole= P wave is late (as the normal periodicty of the SAN is upset)
Ventricular extrasystole= P wave comes at the expected time
At what rate to the atria depolarize in atrial tachycardia?
At what rate does atrial tachycardia become atrial flutter?
What is the fastest rate of discharge that can be conducted by the AV node? What happens if the atrial rate is faster than this?
If the atrial rate is faster than this, atrioventricular block occurs with some P waves not followed by QRS complexes. This is different from 1st/2nd/3rd degree heart block as the AV node is functioning properly and is preventing the ventricles from being activated at a fast and therefore inefficient rate
Describe the ECG seen in atrial tachycardia
P waves are superimposed on the T waves of preceding beats
The QRS complexes have the same shape as those of the sinus beats
Describe the ECG seen in atrial flutter
No flat baseline between P waves giving a 'saw-tooth' appearance. Approx. 4 P waves per QRS complex
Describe the ECG seen in atrial flutter with a 2:1 block
Two P waves per QRS. If atrial rate is 250bpm, ventricular rate is 125bpm
The first of the 2 P waves associated with each QRS can be mistaken for the T wave of the preceding beat, but P waves can be identified by their regularity
T waves often cannot be clearly identified
Describe the ECG seen in junctional tachycardia
No P waves
Regular QRS complexes
Why is it useful to apply carotid sinus pressure (carotid sinus massage)
This helps to differentiate between supraventricular and ventricular tachycardia. This is because applying pressure to the carotid sinus may either abolish supraventricular tachycardia, or slow the ventricular rate. However, it has no effect on ventricular tachycardia
Describe the ECG seen in ventricular tachycardia
No P waves
Wide, abnormal QRS complexes seen in all 12 leads of the ECG
T waves are difficult to identify/unidentifiable
Give four ways of distinguishing between ventricular tachycardia and supraventricular tachycardia with bundle branch block
1. Compare the QRS complex during tachycardia with that during sinus rhythm. If the patient has bundle branch block when in sinus rhythm, the QRS complex during tachycardia will have the same shape as during sinus rhythm
2. If the QRS complex is wider than 4 squares (160bpm), the rhythm will probably be ventricular in origin
3. Left axis deviation during the tachycardia usually indicates a ventricular origin
4. If during tachycardia the QRS complex is very irregular, the rhythm is probably atrial fibrillation with bundle branch block
Describe the characteristic ECG seen in atrial fibrillation
No P waves and an irregular base line
QRS complexes occur irregularly (AV node conducts in an 'all or none' fashion so that the depolarization waves passing into the His bundle are of constant intensity. However, these waves are irregular so the ventricles contract irregularly)
QRS complexes are normally shaped (as conduction into and through the ventricles is by the normal route)
Normal T waves
Depressed ST segments in leads V5 and V6
Describe the characteristic ECG seen in ventricular fibrillation
No identifiable QRS
Completely disorganised ECG
Patient is likely to be unconcious
What is Wolff-Parkinson-White syndrome? What is its clinical significance?
The only normal electrical connection between the atria and ventricles is the His bundle. In WPW, however, there is an extra or accessory conducting bundle which forms a direct connection between the LA and LV, with no AV node to delay conduction. A depolarization wave therefore reaches the ventricle early and 'pre-excitation' occurs.
The only clinical importance of WPW is that it can cause paroxysmal tachycardia. This is because depolarization can spread down the His bundle and back up the accessory pathway and so reactivate the atrium. A re-entry circuit is thus set up and a sustained tachycardia occurs.
What is the distinguishing feature on the ECG of a patient with WPW
The QRS complex shows an early slurred upstroke called a delta wave (best seen in V3 and V4)
There is also a short PR interval
What causes a peaked P wave?
Right atrial hypertrophy due to tricuspid valve stenosis or pulmonary hypertension
What causes a broad, bifid P wave?
Left artial hypertrophy due to mitral valve stenosis
What are the three causes of a wide QRS complex?
1. Bundle branch block
2. Depolarization initiated by a ventricular focus
3. WPW syndrome
What effect does right ventricular hypertrophy have on an ECG?
QRS complex in V1 becomes upright as the left ventricle no longer has it's usual dominant effect. There will also be a deep S wave in V6
Right ventricular hypertrophy is usually accompanied by:
1. Right axis deviation
2. Peaked P wave (due to concurrent right atrial hypertrophy)
3. Inversion of T waves in leads V1, V2 and sometimes V3 or even V4 (severe hypertrophy)
What signs on an ECG may indicate pulmonary embolism?
1. Peaked P waves
2. Right axis deviation (inversion of QRS in lead I)
3. Tall R waves in V1
5. Inverted T waves in V1 (normal) spreading across to leads V2 and/or V3
6. Shift of transition point to the left, such that R=S in lead V5 or V6 rather than in V3 or V4
7. Q wave in III
What signs of left ventricular hypertrophy are seen on an ECG
Tall R wave (>25mm) in V5 or V6
Deep S wave in V1 or V2
Inverted T waves in I, aVL, V5 and V6 (necessary for diagnosis of LV hypertrophy)
May be left axis deviation
What causes small Q waves (<2mm) in the left ventricular leads (V6 and sometimes V5)
Depolarization of the septum from left to right
What is indicated by Q waves >1 small square in width and >2mm in depth?
What is indicated by Q-waves in leads aVF and III
Infarction of the inferior surface of the heart
Which leads would show Q waves if there was an infarction affecting both the anterior and lateral surface of the heart?
Lateral: I, aVL, V5 and V6
Describe the characteristics of an ECG showing posterior myocardial infarction
Dominant R waves in V1 (i.e. QRS complex is upwards)
N.B. appearance of ECG is therefore similar to that seen in right ventricular hypertrophy but other features of RV hypertrophy (right axis deviation, peaked P waves)
What are the causes of and elevated ST segment?
How can you tell from an ECG what has caused an elevated ST segment?
An elevated ST segment may be caused by MI or pericarditis
If ST elevation is caused by MI, the leads in which elevation occurs indicate the location of the infarct (V leads= anterior damage; aVF and III= inferior damage.
If ST elevation is caused by pericarditis, symptoms will not be localised so ST elevation is seen in most leads.
What are the causes of a horizontal depressed ST segment?
2. If the ECG is normal at rest, ST horizontal depression may appear during exercise, particularly when effort induces angina
What is the main cause of a downward sloping ST segment?
In which leads is the T wave normally inverted?
Normally inverted in leads aVR and V1
Sometimes inverted in leads III and V2
May be inverted in lead V3 in some black people
When might T wave inversion be seen abnormally?
2. Ventricular hypertrophy
3. Bundle branch block
4. Digoxin treatment
What is the first sign to appear following an STEMI? Is this sign permanent? What happens subsequently?
ST elevation. This sign is not permanent- return to baseline within 24-48 hours
Subsequently, Q waves develop and T wave inversion is seen. These changes are often permanent
How does a NSTEMI ECG differ from an STEMI ECG?
1. ST segment is not elevated.
2. No Q waves
T wave inversion is seen in V3-V4 and may be seen (or biphasic T waves may be seen) in V2 and V5
Which leads show T wave inversion in left ventricular hypertrophy?
The leads looking at the left ventricle- I, II, aVL, V5 and V6
Which leads show T wave inversion in right ventricular hypertrophy?
The leads looking at the RV- aVF, III, V1, V2 and V3. N.B inversion is normal in V1 and may be normal in V2 but is abnormal in V3 in white people
What changes to the ECG are caused by digoxin?
T wave inversion. Sloping of ST segment
What changes to the ECG are caused by hypokalaemia?
T wave flattening with the appearance of a hump on the end of the T wave called a U wave
What changes to the ECG are caused by hyperkalaemia?
Peaked T wave with disappearance of ST segment
What is the effect of hyper/hypocalcaemia on the ECG?
Hypercalcaemia shortens QT interval
Hypocalcaemia prolongs QT interval
Below what rate is the heart said to be in sinus bradycardia?
Above what rate is the heart said to be in sinus tachycardia
What four things may be indicated by total absence of P waves?
1. Sinus arrest
2. Junctional escape
3. Atrial fibrillation
What benign feature may be seen in the ECG of a tall, thin individual
Right axis deviation
What is meant by partial RBBB
RSR1 pattern in V1 but QRS duration is normal. Very common and of no significance
What variations may be seen in the ECG of a healthy athlete?
Variations in rhythm:
First degree block
Mobitz type 1- second degree block
Other variations in the ECG:
Tall P waves and QRS complexes
Prominent septal Q waves
Tall symmetrical T waves
Biphasic T waves
T wave inversion in lateral leads
Prominent U waves
What is meant by bifascicular block?
Left axis deviation + RBBB
Due to RBBB + left hemiblock (block of left bundle branch anterior fascicle)
What is meant by trifascicular block?
LAD (due to left anterior hemiblock) + RBBB + 1st degree heart block
How should you report/interpret an ECG?
1. Rate and rhythm
2. Cardiac axis and transition point
3. Conduction intervals- PR, QRS, QT
4. P waves (present/absent; peaked/bifascicular)
5. QRS complexes (broad or narrow)
6. ST segments and T waves
An ECG shows a fast heart rhythm with absent P waves and narrow QRS complexes. What is the diagnosis?
Which, of RBBB and LBBB is almost always pathological.
LBBB- often due to MI or LV pathology e.g. LV hypertrophy
Causes of left axis deviation?
Left anterior hemiblock
Left ventricular hypertrophy
Ventricular tachycardia from LV focus
WPW syndrome (some types)
Causes of right axis deviation?
Left posterior hemiblock (rare)
WPW syndrome (some types)
What drugs may prolong QT interval?
When might a J wave be seen?
What defines a pathological Q wave?
>0.04s wide and >2mm deep
In which leads may non-pathological Q waves occur?
I, aVL, V5 and V6
What is seen on an ECG showing pericarditis?
Global ST elevation
ST depression in aVR
How is QTc calculated?
QT/rootRR (because QT varies with heart rate
What are abnormal QTc values in males and females?
QTc>450 in males
QTc>470 in females
What treadmill protocol is used for ECG testing?
When is exercise ECG testing used?
1. To help confirm a suspected diagnosis of IHD. Should only be used when their is diagnostic uncertainty in peoples with known coronary artery disease e.g. previous MI or angioplasty, not to make a primary diagnosis.
2. Assessment of exercise induced arrhythmias
What are the six main contraindications for an exercise ECG?
1. Recent Q wave MI <5 days ago, or unstable angina
2. Severe aortic stenosis
3. Uncontrolled arrhythmia, hypertension or heart failure
4. Acute myocarditis or pericarditis
5. Acute aortic dissection
6. Acute PE
How do you calculate 90% of maximal heart rate?
What is a Holter monitor?
An ECG recorder given to patients to take home which they can activate themselves when they feel symptoms. Useful as in >70% of cases, 24h ECGs are not useful as patients do not experience symptoms during the period of monitoring.