3. Interpretation of ECG Flashcards
Briefly describe electrical conduction of the heart.
What does 1 small and 1 big square represent on a normal ECG wave form?
How long should the following take in a normal ECG:
a) PR
b) QRS
c) QTc
SAN (R atrium wall) initiates electrical excitation via spontaneous rhythmic depolarisation. AVN (atrial septum) slows conduction of impulses, allowing atria to contract before ventricles. BoH transmits it along interventricular septum, dividing into anterior and posterior branch bundles to Purkinje fibres.
Small: 40 msec. Big: 200 msec.
a) 120 - 200 msec (3-5 small squares)
b) < 120 msec (< 3 small squares)
c) < 440 msec (QTc = QT/√RR) (RR= interval from onset of one QRS complex to next)
Describe the 12 lead ECG including lead placement.
What would you look at when assessing rhythm on an ECG trace?
What is sinus arrhythmia?
10 electrodes give 12 tracings. Paper speed 25mm/s. 1mV = 10mm.
6 electrodes = 6 chest leads: V1 R side of sternum, 4th ICS, V2 L side of sternum 4th ICS, V4 mid clavicular 5th ICS. V3 midway between V2 and V4. V5 axilla 5th ICS. V6 mid axilla 5th ICs).
4 electrodes: (R (R arm),Y (L arm),G (L leg), B (R leg)) = 6 standard (limb) leads: (I, II, III, aVR, aVL, aVF).
Regular QRS complexes? P wave before every QRS? If yes: normal sinus rhythm.
Variation of R-R interval with respiration, normal variant in young and athletes.
What can you deduce from the following 2 ECG traces?
How do you calculate the heart rate on an ECG trace?
1) Deep, slow respirations - sinus arrhythmia.
2) Sinus rhythm with ectopics (v. common and generally benign). Narrow complex: supra-ventricular (i.e. somewhere in atria) ectopics. Broad complex: ventricular ectopics.
Number of big squares between an R-R interval. 1 = 300bpm, 2 = 150bpm, 3 = 100bpm, 4 = 75bpm, 5 = 60bpm, 6 = 50bpm. Normal = 50-100bpm.
Use the rhythm strip to deduce this patient’s heart rate.
R-R = 4 big squares so rate = 75bpm.
Massive anterolateral infarct.
Use the rhythm strip to deduce this patient’s heart rate. What is the condition?
R-R = 1.5 big squares, so rate = 200bpm.
Broad complex tachycardia. Life threatening.
What is the ECG axis?
Why is lead II important, and what is the general assumption about net deflection?
The net electrical vector of the heart. It refers to the overall depolarisation through the ventricular myocardium in the coronal plane. Heart depolarises from aVR -> II. 0o is the horizontal line to the L of the heart (lead I = 0). Normal cardiac axis between -30 to +120o - anything outside this may suggest pathology. L axis deviation = axis > -30o. R axis deviation = axis > +120o.
- Lead II** is the centre of the normal axis range. General assumption: lead II +ve = normal axis *so don’t have to think about axis anymore. BUT if:
- *Lead II -ve = abnormal axis**. Therefore lead III (and lead II) -ve = LAD. Lead I (and lead II) -ve = RAD.
What can you deduce from this ECG - any axis deviation?
Lead II -ve so abnormal axis. Lead III (and lead II) are -ve thus:
Left axis deviation. (+ rhythm strip shows atrial flutter - sawtooth QRS).
(NB normal = below)
What can you deduce from this ECG?
Lead II is -ve (R up (5 sq) and S down (7 sq), and R-S is -ve overall). Lead I also -ve so:
Right axis deviation. (Normal ECG below)
What are some causes of:
a) RAD?
b) LAD?
What do the following 2 P wave morphologies show and suggest?
a) Children and tall, thin adults. RVH, chronic lung disease/PE, L posterior hemiblock, ASD/VSD, Wolff-Parkinson-White syndrome (L sided accessory pathway)
b) LVH, LBBB and L anterior hemiblock, Q waves of inferior MI, Wolff-Parkinson-White syndrome (R sided accessory pathway)
1) P pulmonale - P wave height >2.5mm (R atrial hypertrophy)
2) P. mitrale (L atrial hypertrophy) see bifid P waves (pic)
What are the 3 types of heart block?
What do you see in bundle branch block?
What does this rhythm strip show?
1st degree (long, but QRS), 2nd degree (Mobitz I and II. Every now and then no QRS), complete heart block (no QRS)
PR normal, QRS > 120 msec, LBBB and RBBB.
SR (sinus rhythm) + 1st degree heart block. P wave before every QRS but PR > 5 small squares (200 msec). Benign in young person
What does this rhythm strip show?
2nd degree heart block. Mobitz type I/Wenkebach. Progressive increase in P-R interval followed by non-conducted QRS.
Normally due to autonomic system - inhibition of vagus, so get this occasioanlly, benign.
What can you deduce from this ECG?
2nd degree heart block/Mobitz II.
Non conducted QRS after every 2nd P wave. Note: broad QRS complex. Would normally need pacemaker b/c such widespread problems. Rhythm strip: AVN only works every 2 beats. Broad BBB.
What can you deduce from this ECG?
- *Complete** heart block.
- *A-V dissociation**. P waves unrelated to QRS. (pic)
Escape rhythm, maybe in BoH - 2 electrical conductances, not related.
What can you deduce from this ECG?
How would you treat the condition?
Complete heart block followed by ventricular standstill (P wave there but V given up). Run of non-conducted P waves with no QRS activity.
Want to increase sympathetic and decrease parasymp, so give atropine and adrenaline.
What does this P-R interval suggest?
Wolff-Parkinson-White syndrome. Pre-excitation through accessory pathway. Short P-R interval. Delta wave. Wide QRS.
NB: WPW: extra conducting ‘accessory’ pathway between atria and ventricles (bundle of Kent). It isn’t specialised for conducting impulses so doesn’t delay the impulse as the AVN does. It is not linked to normal conduction pathways and BoH. During normal contraction impulses reach the AVN and accessory path at the same time. It is held up temporarily at the AVN but passes through accessory and starts to depolarise the ventricles, distorting the first part of the R wave and giving a short PR interval. Normal conduction via BoH then supervenes giving a slurred uptroke of the QRS complex called the delta wave. *pic*
What can you deduce from this ECG?
- *Supra-ventricular tachycardia** (SVT) due to accessory pathway e.g. WPW. Regular, narrow complex tachycardia, no P waves or electrical activity.
- NB: 4 main types of SVT:* atrial fibrillation, paroxysmal supraventricular tachycardia (PSVT), atrial flutter, and Wolff-Parkinson-White syndrome.
If electricity goes back up fast pathway can get reentry -> arrhythmia.
What can you deduce from this ECG?
If QRS duration is normal (<120ms/3 small sq) then don’t worry about LBBB/RBBB (due to abnormal electricity flow through heart). Here the QRS is >120:
QRS > 120 msec/3 small squares. WiLLiaM morphology (LBBB) and LAD.
The QRS complex in V1 looks like a W and an M in V6. WiLLiaM (W at start, M at end and L in middle = left)
Always look in V1 and V2, and V5 and V6! See if you can see a W or M first. In V2 it doesn’t really look like a W, but in V6 it looks like an M, so if there’s an M at the end it must be WiLLiaM!
What can you deduce from this ECG?
QRS >120 msec/3 small squares.
Looks more like an M in V1 (than a W in V6) so must be MaRRoW morphology (RBBB). And RAD.
QRS in V1 looks like an M and a W in V6 = MaRRoW
What would you observe on an ECG of LVH (left ventricular hypertrophy)?
Many different criteria e.g.
- Deep S in V1 or V2 + Tall R in V5 or V6 (which ever is larger) ≥ 35 mm (≥ 7 large squares).
- R > 25 mm (> 5 squares) in V6. (pic)
May be assocaited with ‘strain pattern’ of ST depression and T wave inversion.
QRS/ST and T waves are analysed by region of the heart. What leads would show you the inferior, anterior and lateral views of the heart’s electrical activity?
What regions of the heart do the red, blue and green boxes correspond to?
Inferior: II, III, aVF
Anterior: V2 - 4
Lateral: V5 - 6, I, aVL
Red: inferior
Blue: anterior
Green: lateral
ECG changes with MI. What is the feature show in the following ECG sections, and time frame after a MI?
What are the 2 different classifications of acute MI?
a) Peaked T waves (minutes) - also due to hyperkalaemia
b) ST elevation (mins-hours) - completely blocked artery
c) ST depression (mins-hours) - high grade stenosis
d) Q waves (> hours fixed), inverted T waves (hours may reverse)
1) STEMI (ST elevation, mins-hours -> ambulance!)
2) NSTEMI (ST depression, get angiogram if settles) (pic)
What can you deduce from this ECG?
Inferior ST elevation/Q wave lead III. Anterior and lateral ST depression (v6). Acute inferior STEMI.
What can you deduce from this ECG?
See ‘tombstoning’ - blocked LAD. Whole ant. and lat. wall infarcted:
Antero-lateral ST elevation. Acute anterior STEMI.
What can you deduce from this ECG?
Antero-lateral ST elevation. Acute anterior STEMI. Tombstoning in V6!
What can you deduce from this ECG?
Antero-lateral Q waves and T wave inversion. Old anterior Q wave infarct.
≥25% height of the partner R wave and/or >0.04 seconds in width and >2 mm (2 small squares) in depth.
What can you deduce from this ECG?
Antero-lateral ST depression, widespread. Probable anterior NSTEMI (pending Troponin).
Certain subtypes of troponin (cardiac I and T) are very sensitive and specific indicators of damage to heart muscle (myocardium). They are measured in the blood to differentiate between unstable angina and myocardial infarction. A recent MI would have an area of damaged heart muscle and elevated cardiac troponin levels in the blood.
What can you deduce from this ECG?
Antero-lateral T wave insertion on V5. Probable anterior NSTEMI (pending Troponin) ‘LAD syndrome’.
Wellens’ syndrome: electrocardiographic manifestation of critical proximal LAD coronary artery stenosis in patients with unstable angina. Characterized by symmetrical, often deep (>2 mm), T wave inversions in the anterior precordial leads.
What can you deduce from this ECG?
Antero-lateral ST elevation, V2. Established anterio-lateral STEMI with established Q waves.
What is AF?
Atrial fibrillation - disordered electrical activity in atrium. Irregularly irregular ventricular rhythm. No P waves.
What is atrial flutter?
Abnormally rapid contraction of atria. Contractions not disorganised/random ulike AF, but are fast and inadequate for normal blood movement. Re-entrant circuit in RA, flutter rate 300 bpm.
Baseline has typical saw tooth appearance (F/flutter waves). V rate depends on degree of transmission of F waves.
What is atrial tachycardia?
What are the different categories of broad complex tachycardias?
What is VT defined as?
Abnormal focus of atrial depolarisation. Abnormal P wave morphology. Unexplained tachycardia.
Ventricular tachycardia
Supraventricular tachycardia with aberrant conduction
WPW conducted via accessory pathway
Broad complex tachycardia is VT until proven otherwise.
3 or more sucessive ventricular extrasystoles at a rate of >120/min. ‘Sustained’ VTs last for > 30 secs. (pic)
What can you deduce from this ECG?
Atrial flutter. Re-entrant circuit in RA. Fluttter rate 300 bpm. Flutter waves. V rate 100 bpm (3:1 transmission)
What can you deduce from this ECG?
Broad complex tachycardia VT.
What can you deduce from this ECG?
Narrow complex tachycardia. SVT (AVNRT or AVRT - WPW)
What can you deduce from this ECG?
Broad complex tachycardia VT.
What can you deduce from this ECG?
Narrow complex tachycardia SVT.
What can you deduce from this ECG?
Irregularly irregular, tachycardia, no P waves/fibrillation waves in V1, AF.
What can you deduce from this ECG?
Irregularly irregular, no P waves/fibrillation waves in V1, broad complex QRS. AF and LBBB.
What can you deduce from this ECG?
Disordered ventricular depolarisation. VF.
