Introduction to the ECG Flashcards
Complete the diagram of the heart
Draw a coronal section of the heart showing the conduction system.
You do not need to include the valves or the vena cava
What is a functional syncytium?
Functional syncytium = many cells acting as one
What is a precordial lead?
There are six precordial (or chest) unipolar leads: V1, V2, V3, V4, V5, V6.
A “chest” lead. It is a configuration in an ECG of electrodes such that one electrode in placed on the chest and the negative “electrode” being Wilson’s central terminal.
Wilson’s central terminal is a combination of electrodes that act together as if they were a reference electrode positioned in the centre of the heart.
Precordial leads make measurements of electrical activity in the transverse plane
What are the approximate conduction velocities (including units) for: the fastest neurons/axons, His-Purkinje system, contractile cardiomyocytes, the AV node?
- Purkinje fibres up to 5 m/s
- fastest neurons ~100 m/s
- AV node 0.05 m/s
- ventricular myocytes 0.3-0.5 m/s
How and why does the AV node delay conduction of waves of depolarisation?
30 ms to AV node
90 ms delay before enters penetrating portion of AV bundle
40 ms delay in penetrating bundle
•Total of 160 ms delay in AV network.
Mostly due to increased resistance
•(i) diminished numbers of gap junctions between modified myocytes per cross sectional area, (ii) smaller fibres, (iii) more cell junctions per length distance travelled
Draw what a single lead of a normal ECG should look like (for 2 heart beats), and label the following on it: T wave, QRS complex, P wave, PR interval, ST segment, QT interval.
List four different forms of heart block, and how they are differentiated.
1st Degree Block - PR interval > 5 little boxes (200 ms), Asymptomatic, Often young people (adolescents), Delayed AV node transmission, Rarely treated
2nd Degree Block Type I – é PR interval, AV damage, no treatment
2nd Degree Block Type II – PR interval stable, Bundle of His, high risk, leads to third degree heart block, implant pacemaker
•3rd Degree Block – atrial signals do not arrive at ventricles, ventricles beat at their own pace: 30-40 bpm
What is the normal range (or a normal value) for QT interval?
From start of P-wave to start of QRS complex (name is misleading)
300-460 milliseconds
What is the normal range (or a normal value) for PR interval?
Under 200 ms ( 5 boxes)
Usually over 120 ms
What is the normal range (or a normal value) for RR interval?
RR interval is the reciprocal of heart rate per second
For 60 bpm, RR = 1000 milliseconds, for
Normal = 75 bpm RR = 800 milliseconds
Accept 50 -90 bpm = 1200 ms to 667 ms
What is the normal range (or a normal value) for PP interval?
PP interval is the reciprocal of atrial heart rate per second
For 60 bpm, PP = 1000 milliseconds, for
Normal sinus rhythm = 75 bpm PP = 800 milliseconds
Accept 50 - 90 bpm = 1200 ms to 667 ms
Draw an ECG showing the end of the PR interval clearly?
Draw an ECG showing both ends of the Q interval clearly?
What is clinically relevant about this rhythm, and what is the mostly likely form of treatment?
The P waves are not coordinated with the QRS complexes. The atria and ventricles are beating independently of one another. Note that the ventricular rate is less than half of the atrial rate; there are 11 big boxes between QRS complexes (the ventricular rate is less than 30 beats per minute). This is complete (third degree) heart block. It is usually symptomatic. The patient will not be exercise tolerant, may be haemodynamically unstable, and may be unconscious due to low cardiac output. This patient will be treated with a pacemaker.
What is clinically relevant about this rhythm, and what is the mostly likely form of treatment?
PR interval lasts too long. It should last for less than 5 little boxes. This is First degree heart block. Often there is no treatment except to monitor the patient for problems.
What is clinically relevant about this rhythm, and what is the mostly likely form of treatment?
There are no P waves, except before the the second QRS complex from left. These are fibrillatory waves instead of a P wave. This is atrial fibrillation. Note the highly irregular RR intervals (ie not consistent ventricular rate, but the ventricular rate is definitely fast).
This is likely to be treated with anticoagulants to prevent stroke
It may also be treated (depending on other aspects of history) with electrical cardioversion, digoxin, etc
What is clinically relevant about this rhythm, and what is the mostly likely form of treatment?
Skipped QRS complexes, varying PR interval. This is Mobitz type I second degree heart block (Wenckebach), it might not be treated.
What is clinically relevant about this rhythm, and what is the mostly likely form of treatment?
ST segment is elevated. This is an acute myocardial infarct.
This is most likely to be treated with immediate revascularisation using PCI or clot busting drugs (tPA)
The patient would also be treated with morphine, oxygen, nitrates, and aspirin
What is clinically relevant about this rhythm, and what is the mostly likely form of treatment?
Missed QRS complex. Consistent PR interval. This is Mobitz type II second degree heart block (Hay). It is potentially very dangerous, as it could degenerate into 3rd degree heart block. This may be treated with an implantable pacemaker.
What is clinically relevant about this rhythm, and how might it come about?
It is very slow. The RR interval is ~ 9 big boxes, so the rate is about ~ 33 beats per minute. However, there are normal QRS complexes, and normal P and T waves. This is Sinus bradycardia
Causes include: high doses of beta blockers or calcium channel blockers, as well as sick sinus syndrome, hypothermia and sleep apnoea
What is the cellular basis of the P wave, the QRS complex, and the T wave
P wave: depolarisation of atria as wave travels from SA node inferiorly to rest of atria.
QRS complex: depolarisation of ventricles – note that this masks the signal of the atria repolarising.
T wave: repolarisation of the ventricles starting from the apex and going superiorly.
Describe the progression of electrical activity through the heart during a single beat.
Impulse begins in SA node. 4 internodal bundles relay depolarisation from SA node. 3 (anterior, middle, and posterior tracts) go to AV node; Bachmann’s bundle goes to the left atrium. By the time it has emerged from the AV node impulse has been delayed ~ 160 ms. Impulse exits AV node and enters ventricles at bundle of His. This splits into the left bundle branch and right bundle branch (which also continue to have smaller branches), which travel down the septum. At the septum the two branching systems go in opposite directions, superiorly to the right ventricle and superiorly to the left ventricle.
In ECGs, what is a lead?
A lead is one of the twelve configurations of electrodes used for detecting the heart’s electrical activity. Sometimes the word “lead” is used to refer to one of the wires connecting to an electrode
What is a 12 lead ECG, and why is it used?
A twelve lead ECG is an ECG based on 10 electrodes arranged in 12 different configurations. There are three standard bipolar leads: I, II, and III. There are 3 augmented leads: aVR, aVF, and aVL. There are six precordial (or chest) unipolar leads based on the negative “electrode” being Wilson’s central terminal: V1, V2, V3, V4, V5, V6. Each lead detects a different vectorial element of the cardiac conduction cycle (ie each lead “sees the heart from a different angle”), so some leads are better placed to detect particular abnormalities or particular damage. In particular, the augmented and bipolar leads detect conduction in the coronal plane, whereas the chest leads detect conduction in the transverse plan.
What is atropine, and what does it do to the heart rate.
Atropine is an anticholinergic drug that reduces parasympathetic activity. It acts at muscarinic acetylcholine receptors. Until recently it was medically used to treat asystole and extreme bradycardia, but contemporary medicine no longer accepts this as a first line treatment; it remains used in opthalmology as a mydriatic (to dilate pupils to reduce painful ciliary muscle spasm (e.g. cycloplegia). Historically it was derived from plants such as deadly nightshade (Atropa belladonna), and it was used by women to increase their beauty by applying belladona to their eyes to cause pupil dilatation (bella donna = beautiful woman).
What is the difference in cardiovascular effects between infusing adrenaline vs. noradrenaline?
- Adrenaline is hormonal, noradrenaline is primarily a sympathetic neurotransmitter. Receptors: Alpha1 prefers NA. Beta1 NA and Adr are equal. Beta2 greatly prefer Adr.
- Sensitivity to plasma levels of noradrenaline is comparatively weak, and when noradrenaline is infused, it acts at alpha receptors leading to increased peripheral resistance, and then to a compensatory net DECREASE in heart rate (via baroreceptor activity) and thus a net decrease in cardiac output; note that noradrenaline will tend to make the heart beat faster and with greater force, but during plasma infusion the effect on pressure is masked by the effects on blood vessels.
- Sensitivity to plasma levels of adrenaline is comparatively high, and it acts at beta1 receptors to increase heart rate and force of contraction; it will also act via the beta2 receptor to vasodilate vessels in muscles and skin. As a result, adrenaline will increase cardiac output, with both rate and stroke volume increased – and systolic pressure will be increased, but diastolic pressure will be slightly DEcreased, due to a small net decrease in peripheral resistance.
Compare and contrast the advantages of the ECG vs taking a pulse.
- Pulse is fast and cheap, you only need a watch to take it, you can get information about pressure outflow as well as electrical activity (ECG does not give you pressure information).
- ECG gives detailed electrical information, it can reveal much about the state of the conduction system, and therefore also about tissue damage. The ECG can also be used for long term measurements (such as Holter monitoring), and the ECG can detect differences in rate between atria and ventricles (eg atrial flutter and atrial fib)
What is a U wave on an ECG?
•By definition, a U wave is a wave that occurs after the T wave; in most normal ECGs it is not visible, but it is not by definition pathological. The U wave is typically smaller than the T wave, and rounded like a T wave. The electrical substrate of the U wave remains controversial.
