Flashcards in Cardiology - ECG abnormalities Deck (52):
What causes changes to the shape of the P wave? In what leads is this best viewed?
The P wave shape is altered by atrial enlargement and arrhythmias. The normal P wave is the sum of the right and left atrial depolarization vectors and is best examined in leads II and V1.
What effect does it have on the ECG?
The ECG is not reliable in diagnosing right atrial enlargement. When the RA is enlarged depolarization takes longer (more distance to travel) and involves greater current flows (depolarizing atrial myocytes let more ions in, increasing current flow).
The vector directed towards lead II becomes larger, so the p wave in lead II becomes taller. V1 is less affected by atrial enlargement.
What is the effect of left atrial enlargement on the ECG?
In LA enlargement, the LA depolarization vector is prolonged and increased:
- in lead II there is a long late high voltage positive deflection after the initial RA P wave resulting in a bifid shape (called P mitrale from rheumatic mitral stenosis)
- as the vector of LA depolarization proceeds away from lead V1, after a small initial positive deflection arising from the normal right atria, the P wave is dominated by a late negative deflection which is a sensitive marker of LA enlargement
Causes of right atrial enlargement
COPD related pulmonary hypertension (often the cardiac axis is right shifted)
What causes left atrial enlargement?
Hypertension: look for ECG left ventricular hypertrophy
Aortic and mitral valve lesions: listen for murmurs
Cardiomyopathy: non specifically abnormal ECG or conducting tissue disease
What feature of the P wave shape would suggest a low atrial or AVN ectopic pacemaker?
If the pacemaker is situated other than in the sinus node then the P wave shape is altered. Inverted P waves in leads II, III and aVF can suggest ectopic pacemaker activity.
What determines the size of the QRS complex?
1) The number and activity of myocytes. Myocytes may become less numerous with age and are more electrically active in youth (< 40 years) and in ventricular hypertrophy.
2) The insulation between the heart and the observing electrodes. A pericardial effusion or obesity, diminishes the amount of electrical activity reaching the electrodes.
How does right ventricular hypertrophy affect the ECG?
Right ventricular hypertrophy results in greater voltages from the right ventricle, resulting in:
1) Right axis deviation
2) Leads looking at the right ventricle show a positive deflection. In particular, in lead V1 the size of the R waves increases - instead of the normal situation where there are small R waves followed by large negative S waves. The R wave can be the same height as the S wave and remains narrow
3) In severe RVH there can be T wave changes
4) Left sided chest leads are unchanged by RVH (the bulk of the right ventricle even when hypertrophied does not overshadow the influence of the left ventricle)
5) Signs of right atrial enlargement may be present, the the P wave becoming leaked early on in lead II and V1.
How does left ventricular hypertrophy affect the ECG?
In LVH greater voltages are generated by the left ventricle which results in:
1) Left axis deviation
2) Leads looking at the left ventricle show an increased deflection - i.e. leads I, II, aVL, and V5 and V6
3) Leads looking away from the left ventricle show increased negative deflections - i.e. increased size of the S wave in leads V2 and V3
4) May be signs of left atrial enlargement (bifid P wave in lead II and late negative deflection in V1)
What are pathological Q waves?
These are a key finding as they indicate cardiac damage. They must be distinguished from physiological Q waves which occur in:
- left sided chest leads where they reflect left to right septal depolarization
- lead aVR which "looks" directly through the AV valve at the endocardial surface of the heart
What is the mechanism underlying pathological Q waves?
Pathological Q waves indicate an "electrical window" in the part of the heart directly facing the electrode which allows current from the opposite wall to influence the electrode in an unopposed fashion. As depolarization proceeds from the endocardium to the epicardium, the electrode looking directly into the heart through this electrical window sees a Q wave rather than an R wave .
What causes pathological Q waves?
- an old transmural infarct; the Q wave distribution reflecting which artery has been occluded
- less commonly another pathology such as LVH (increased Q waves in left sided leads in association with large R waves) or occasionally hypertrophic cardiomyopathy (large Q waves in inferior leads without substantial R waves)
- myocarditis or dilated cardiomyopathy (rare)
What causes pathological loss of R wave height?
Damage insufficient to cause Q waves, but sufficient to cause death of some cells in the heart (i.e. sufficient numbers survive so that some electrical activity continues) leads to a decrease in R wave height without Q wave formation. Pathologically small R waves can be difficult to diagnose as there is normal variation in R wave height.
Pathological loss of R wave height usually follows regional distribution in coronary arteries.
What is meant by the term QRS axis?
The overall QRS vector shows the direction of depolarization of the bulk of ventricular mass. As such, it is mainly directed towards the main muscle mass being depolarised - i.e. in health towards the left ventricle.
What causes left axis deviation?
There are 2 main interpretation of left axis deviation:
1) More left ventricular muscle mass to depolarize - i.e. LVH is present which usually also causes left sided prominent R waves and deep right sided S waves
2) Left ventricular depolarization is delayed as the conducting system is damaged. The left anterior fascicle of the left bundle branch supplies much of the anterior part of the left ventricle. If this is damaged, the left anterior part of the left ventricle depolarizes late, which then predominates the depolarization vector, resulting in left axis deviation
What causes right axis deviation?
1) More right ventricular mass - i.e. RVH
2) The posterior lying bulk of the left ventricle is depolarized late due to disease in its conducting tissue - the posterior fascicle of the left bundle
What is the normal PR interval and what affects it?
The PR interval reflects the time between the start of the P wave and the first QRS deflection. On ECG paper it is <3 small squares. The normal PR interval is lengthened by high vagal tone/ low sympathetic tone and low heart rates and shortened by exercise and high heart rates.
PR interval prolongation can also result from diseases affecting the AVN, the bundle of His or both bundle branches
What is bundle branch block?
Disruption of the conducting system at any point from the SAN to the bundle of His can prolong the PR interval. Disruption below this level broadens the QRS complex resulting in bundle branch block.
What is right bundle branch block (RBBB)? How does it affect the ECG?
RBBB causes the right ventricle to be activated late, so right sided leads see unopposed activity late on resulting in a late deflection in lead V1. QRS complexes in leads looking directly at the left ventricle (i.e. I, II, aVL and V4-6) appear mostly normal.
An aide memoire is that RBBB causes a "MaRRoW" type pattern in the chest leads. The QRS complex is mostly above the isoelectric line in lead V1 and below it in lead V6.
What is left bundle branch block? How does it affect the ECG?
Full block of the left bundle gives rise to delayed and slowed activation of the left ventricle, so broadening the QRS complex in the left sided leads. Partial blockage of the left bundle results in axis deviation without QRS broadening.
The septum is depolarized right to left (rather than left to right) so there are:
i) no physiological Q waves in left sided chest leads and
ii) delayed activation of the left ventricle, resulting in a large late positive deflection in left ventricle (LV) leads
What does bi or trifascicular block mean?
Bi-fascicular block is the term used when any two of the following occur:
- PR interval prolongation
- right of left axis deviation.
Tri-fascicular block means all 3 and indicates serious conducting system disease that can progress to complete heart block.
What condition are delta waves associated with?
These are pathognomonic of the Wolf-Parkinson White syndrome, and are due to early ventricular activation from an accessory pathway bypassing the AVN.
What is the mechanism of delta waves?
In health the only connection between the atria and ventricle is the AVN. In WPW syndrome there is an extra electrical connection between the atria and ventricles (an accessory pathway) down which depolarization passes, bypassing normal AVN conduction.
Accessory pathways, unlike the normal AVN, do not delay conduction, so depolarization by this pathway reaches the ventricle before the normal current down the AVN. The premature arrival of depolarization in the ventricle causes an early start to the QRS complex resulting in a short PR interval. Depolarization spreads from its arrival site by cell to cell transmission, resulting in a "slurred" upstroke to the QRS complex - the delta wave.
How can the polarity of the delta wave be used to determine the location of the accessory pathway?
Most cases with a positive deflection in leads V1 have a left atrial to left ventricle pathway. Those with a negative deflection in V1 have a right atrial to right ventricular pathway.
What are the clinical features of WPW?
An accessory pathway provides a mechanism for tachyarrhythmias:
(i) Orthodromic tachyarrhythmia
(ii) Antidromic tachycarrhythmia
(iii) AF, which occassionally leads to
(iv) VF and sudden cardiac death
The annual incidence of SCD is 0.15% so most patients with WPW have a normal life expectancy. SCD in WPW occurs in those patients whose pathways have a short refractory period capable of generating very high heart rate during AF.
What are the causes of ST segment elevation?
1) Physiological - extremely common, usually in the anterior chest leads (V1-V3) and cardiac ultrasound shows no wall motion abnormalities; changes are not evolving
3) Bundle branch block
5) Brugada syndrome
6) Others - e.g. left ventricular aneurysm, hyperkalaemia, and hypothermia
What is the mechanism of ST segment elevation in the context of MI?
In STEMI, the sub-epicardial myocardium is more ischaemic than the sub-endocardial tissue. Ischaemic cells let in less positive charge from the extracellular space during depolarization, leading to an excess of external positive charge around the damaged cell. Electrons from less ischaemic areas to neutralize this charge and onto the observing electrode, causing ST elevation.
What are the features of ST segment elevation caused by STEMI that help it to be distinguished from other causes of ST segment elevation?
In STEMI the ST elevation is often "convex" upwards, whereas in pericarditis the ST elevation is more usually "concave" upwards. There are exception to this though.
In what leads does a posterior wall infarction causes ST segment changes?
Posterior wall infarcts are caused by circumflex artery occlusion, and causes ST depression in leads V1-V3. Circumflex artery occlusion is often associated with lateral infarcts showing ST segment elevation in leads V5/6 (although this could also be a distal RCA).
Inferior infarcts show ST segment changes in leads II, III, and aVF and are caused by occlusion of the RCA and sometimes the left circumflex.
Are the ST segment changes in MI permanent?
No. ST elevation only persists whilst the infarcting cells are still alive - when they have died (usually after 1-12h), the ST elevation disappears to be replaced by Q waves, T wave inversion (hours-days later) and days-weeks later as the remaining damaged cells are restored to health , re-inversion of the T waves back to normal polarity.
What is the mechanism of ST segment elevation in acute pericarditis?
Damaged myocardial cells adjacent to the pericardium let less positive charge in during depolarization, leaving excess external positive that are neutralized by by electrons flowing in from healthy sub-endocardial myocardial cells.
The volume of damaged sub-epicardial cells is less in pericarditis than STEMIs (so there is less external positive charge requiring neutralization) , so ST segment elevation is less substantial. It is often global as well (i.e. affecting many leads).
What causes ST segment depression?
ST depression has a large differential diagnosis, including:
- Ischaemia (NSTEMI)
- Drugs, especially digoxin
- Myocardial disease
- Bundle branch block
- Unknown (usually "fixed", i.e. does not change over time)
What is the mechanism underlying ischaemic related ST depression?
In angina due to epicardial coronary artery disease the sub-endocardium is more ischaemic than the sub-epicardium. ischaemic cells let in less positive charge during depolarization. This excess positive charge is neutralized in the plataeu phase by electrons flowing in from adjacent healthy sub-epicardial tissue away from an observing electrode. This causes ST depression.
What clues can help determine that the ST depression is ischaemic in origin?
- presence of typical angina pain at the time of recording
- regional distribution of the ST changes, reflecting the regional distribution of the coronary arteries
- dynamic ECG changes - i.e. ST depression comes and goes, rather than ST depression in LVH or in digoxin toxicity which is fixed
- in the resting ECG, ST dpression due to ischaemic heart disease is usually down-sloping
How does left ventricular hypertrophy cause ST depression?
LVH usually results in downsloping ST depression in the lateral leads (I, aVL, V5 and V6).
LVH prolongs epicardial action potentials more than endocardial ones, reversing the normal current flow during repolarization. Endocardial areas repolarize first, so reversing the repolarization wave which now passes endocardially to sub-epicardially producing T wave inversion.
The clue that ST segment depression is due to LVH is that the voltages in the left sided chest lead QRS complexes are increased, although this is not universal.
Why does digoxin cause ST depression?
Digoxin shortens sub-endocardial action potentials more than sub-epicardial ones, leading to "reverse -tick" ST segment depression in the lateral leads, mimiking the distribution of ST changes in LVH. The downslope is longer than the upstroke. It can be distinguished from ST segment changes of LVH by:
- knowing the patient is taking digoxin
- the absence of left sided QRS voltages
What are the features of ST depression caused by myocardial disease?
This is common. Any pathology affecting the myocardium can result in ST depression in any number of leads. Usually the ST depression is "fixed" - i.e. does not change over time. The ST depression is usually rather mild; cardiac angiography and ultrasound are diagnostic.
What are the features of normal T waves? What is T wave flattening?
The normal T wave:
- follows the polarity of the QRS complex i.e. where there is an R wave, the T wave is upright; where there is a Q wave the T wave is flat or negative
- is usually of substantial size with large R waves
Flattened T waves are a common ECG finding but are difficult to diagnose. Generally speaking T waves of <25% of the height of the R waves raise the suspicion of T wave flattening: the smaller they are in proportion to the height of the R wave the greater the suspicion that they are flattened. Flat T waves can mean almost anything!
What are some causes of T wave flattening in an otherwise normal ECG?
- Metabolic changes (esp low K+) and hyperventilation
- Drugs, including digoxin
- Myocardial disease, although often associated with quite abnormal ECGs, can occur with relatively mild ECG changes including isolated mild T wave flattening
- Coronary disease
- Pericardial disease
Outline a diagnostic approach to T waves
There are many causes of T wave flattening, including nothing! You should use the finding of flat T waves to consider that there may be either a cardiac problem or an electrolyte one. A sensible approach would be to (i) measure electrolytes, (ii) order a cardiac ultrasound, (iii) be guided by the clinical situation
What are the ECG features of T wave inversion?
Major T wave inversion is an important sign and usually points to serious illness.
The normal T wave follows the polarity of the R wave: in health leads with positive R waves have upright T waves, leads with equivocal R waves have flattened T waves and leads with deep S waves have inverted T waves.
T wave inversion can only be diagnosed when it occurs in a lead with a large R wave where an upright T wave is expected. T wave abnormalities include mild inversion/ flattening and major inversion.
What causes biphasic T wave inversion?
This is where the first part of the T wave goes up and the second part down. This is common in ACS and following myocardial infarction.
Biphasic T waves with the first part going down and the second part going up is common in coronary artery disease in the few minutes after exercise and represents the increased likelihood of coronary artery disease.
Name some causes of deep T wave inversion
1) Coronary disease
2) BBB, the clue is the wide QRS complex
3) LVH, the clue is large left sided QRS voltages
4) Other causes including drugs, e.g. psychotropics
What is the QT interval and what can alter it?
The QT interval reflects the time from onset of ventricular depolarization to the of offset of repolarization. It is altered by:
- heart rate: high heart rates shorten the QT interval
- autonomic nervous system activity: high vagal tone prolongs the QT interval; the opposite shortens the QT interval. Vagal tone has a diurnal rhythm, is high at night so lengthening the nocturnal QT interval by +/-20ms
- sex and age: small influence on QT interval (women and older subjects have longer QT intervals)
- genetic differences
How can the effect of heart rate on the QT interval be corrected?
The QT interval - heart rate relationship changes within an individual over time and between individuals in health, sickness and under certain drugs. This creates problems in correcting for heart rate, and makes using a single formula for correcting it unsound. The most common one is Bazett's correction: QTc = QT x square root of RR interval [the QTc = the QT interval corrected to its value at 60bpm]
Ideally, to correct for heart rate, the individuals QT-HR relationship should be determined (e.g. stress exercise test/ 24 hour ECG). If this is impossible, then the best formula to use as it removes the influence of heart rate on the QT interval is Fridericia's correction.
What pathological states can affect the QT interval?
1) The duration of depolarization (i.e. the QRS complex). Prolonged depolarization (e.g. LBBB) prolongs the QT interval
2) Myocyte action potential duration. If APD is prolonged, the QT interval is prolonged. Action potential duration can be prolonged throughout the heart, causing a long QT interval in all leads or prolonged regionally, causing increases in QT interval in some but not other leads.
Why is the QT interval important?
Some diseases and many drugs, prolong it, so a long QT interval is diagnostic.
QT interval prolongation can lead to life-threatening arrhythmias of torsade de pointes (TDP) type ventricular tachycardia.
What diseases can prolong the QT interval?
1) Left ventricular dysfunction - commonest cause, prolongation is proportional to severity of LV dysfunction
2) Critical myocardial ischaemia
3) Drugs - class III anti-arrhythmics (e.g. amiodarone and sotalol) universally prolong the QT interval. Non sedating anti-histamines, macrolide antibiotics, beta blockers and anti-fungals
4) Metabolic abnormalities - low K+ and Mg++
5) Endocrine disease - hypothyroidism
8) Genetics - hereditary long QT syndrome (HLQTS)
What ECG changes occur in PE?
Tachycardia and transient arrhythmias (particularly AF)
Right axis deviation
Right ventricular strain pattern - dominant R wave and inverted T waves in V1-4
Occassionally S1, Q3, T3 pattern
What is the ECG change in hypokalaemia?
Prolonged PR interval, depressed ST flattened T wave and prominant U waves.
ECG changes in hyperkalaemia
Flattened P wave, broad QRS complex, peaked T wave.