ECG INTERPRETATION Flashcards
Which leads are ANTERIOR and which artery supplies the area represented by the anterior leads?
ANTERIOR LEADS: V3, V4
Supplied by LAD
Note: V1-V4 are often grouped together as ‘anteroseptal’
Which leads are LATERAL and which artery supplies the area represented by the lateral leads?
LATERAL LEADS: I, aVL, V5, V6
Supplied by left circumflex artery
Which leads are INFERIOR and which artery supplies the area represented by the inferior leads?
INFERIOR LEADS: II, III, aVF
Supplied by the right coronary artery
Which leads are SEPTAL and which artery supplies the area represented by the septal leads?
SEPTAL LEADS: V1, V2
Supplied by LAD
Note: V1-V4 are often grouped together as ‘anteroseptal’
What is the appearance of an ECG during atrial fibrillation?
Irregularly irregular R-R intervals with no discernible P waves
Describe what is represented by the P, Q, R, S, and T waves seen on an ECG.
P Wave = atrial depolarisation
Q Wave = 1st downward deflection after the P wave
R Wave = 1st upward deflection after a P wave
S Wave = downward deflection after an R wave
The QRS Complex represents ventricular depolarisation
T Wave = ventricular repolarisation
Using leads I and aVF, how can cardiac axis be determined?
- Positive in lead I and lead aVF: normal (0-90 degrees)
- Positive in lead I, negative in lead aVF: LEFT axis deviation (-90 to -30) OR normal (-30 to 0). Note: if lead II also has a negative QRS, then it is left axis deviation.
- Negative in lead I, positive in lead aVF: RIGHT axis deviation (90 - 180)
- Negative in lead I, negative in lead aVF: EXTREME right axis deviation (-180 to -90)
What is a normal cardiac axis?
-30 to 90 degrees
What does cardiac axis show?
Mean direction of ventricular depolarisation in the frontal plane
Why is cardiac axis important?
Can show myocardial and electrical abnormalities
In which lead is the QRS Complex / cardiac axis most positive? Why?
Lead II
The overall direction of electrical activity is towards leads I, II, and III. Lead II is most closely aligned with the direction of electrical spread.
In which lead is the QRS Complex / cardiac axis most negative? Why?
Lead aVR
It looks at the heart in the opposite direction
What is the most common cause of left axis deviation?
Conduction abnormalities
Left ventricular hypertrophy can cause cause LAD
What is the most common cause of right axis deviation?
Right ventricular hypertrophy
What is an escape beat?
Heartbeats that follow an extra-long pause and do not originate from the SA Node
2 EGC Principles
- Isoelectric line = depolarisation perpendicular to the lead
- The heart beats in time with the fastest pacemaker (most of the time, it’s the SA Node)
QRS complex in supraventricular vs. ventricular(?) disturbances
.
What is the difference in presentation and treatment of an anterior vs. inferior MI?
ANTERIOR: dyspnoea, tachycardia, cardiogenic shock, poorer prognosis. DON’T GIVE FLUID BECAUSE YOU’LL PUT THEM INTO PULMONARY OEDEMA.
LAD is biggest artery –> extensive necrosis w/anterior infarct (esp. if late presentation) –> significant LV dysfunction –> increased ED pressure –> transmitted to pulmonary vasculature –> because pressures have risen, they leak into the membranes –> extra fluid will just increase the pressure and send them into pulmonary oedema
INFERIOR: Nausea, bradycardia, hypovolemia (inferiors behave as though there’s vagal stimulation). GIVE SHITLOADS OF FLUID.
HYPOVOLEMIA DUE TO INFERIOR MI: Not enough fluid getting to the left side of the heart –> reduced preload
Classically, which leads have the best P waves?
Lead II
Lead V1
Why are there 12 leads and only 9 electrodes?
3 leads are imaginary (I, II, III): not reading a specific dot, just aggregating the electrical activity of aVL, aVF, and aVR
How many fascicles are on the left and right sides?
Left: 2 fascicles (anterior and posterior?)
Right: 1 fascicle
What is the clinical relevance of a long QT interval?
Long QT interval =
How can you spot sinus rhythm on an ECG?
Regular / correctly-oriented P waves
SPOT AF ON AN ECG (common exam question)
Anti-coagulation vs. no anti-coagulation
Counselling patients about this
SPOT ATRIAL FLUTTER ON AN ECG
Sawtooth pattern (up and down really quickly)
Especially in lead II
2 most common shockable rhythms
VT
VF
CO is nearly zero in these fatal arrhythmias
Name a non-shockable rhythm
Asystole
Describe the appearance of VT
Broad complex, monomorphic ventricular tachycardia
What is Torsad’s de pointes?
A type of VF
write more
Describe the appearance of an inferior STEMI on ECG
The following changes in V1-3:
- ST depression
- Tall, broad R waves (>30ms)
- Upright T waves
- Dominant R wave (R/S ratio > 1) in V2
Bradycardia MAY be present as the vessels supplying the posterior heart also supply the SA node.
First-degree heart block
PR interval > 200ms (five small squares)
SO MANY CAUSES. CAN ALSO BE NORMAL.
APPEARANCE ON ECG
Second-degree heart block / Mobick I / Wenckebach
Wenckebach: no syncope, no pacemaker
Mobitz II: fixed PR interval, drop beat, risk of syncope. Indication for pacemaker (but very rare)
Complete heart block requires…?
Needs a pacemaker
Supraventricular tachycardias
Any tachycardia above the ventricles
More common in younger people
Uncomfortable: rapid palpitations
SVT appearance on ECG
Most common types of SVTs
AVRT
AVNRT (9/10 times)
AVNRT
CONGENITAL
Need to be born with anomaly in AV Node: slow and fast pathway
Normal electrical activity goes down the ‘fast’ way
Some day, it goes down the fast pathway and swings back up the ‘slow’ pathway –> gets stuck in a loop which keeps repolarising itself
How do we terminate an SVT? (HIGH-YIELD)
Cardioversion (will always be a correct answer, but is almost never the first thing we do)
The thing that determines whether you shock someone is their BP. They will die from hypotension first before they die from a clot due to their AFib.
VAGAL MANEOUVER: Valsalva (blow: push the plunger back from a 10mL syringe. Impossible, but you need to get them to blow very hard). Do it twice. If it doesn’t work, do a carotid massage (worth trying, but often doesn’t work)
Trying to get a massive vagal response from the heart.
Guaranteed termination: adenosine (blocks AV node for a few seconds to reset everything). They will feel nauseous and like they’re going to die. Very uncomfortable.
If all else fails: DC Cardiovert
SVT
T waves, no p waves
Peaked P waves
Increased pressure in right heart
What is represented by the P wave?
Atrial depolarisation
What is represented by the QRS complex?
Ventricular depolarisation
and concurrent atrial repolarisation
What is represented by the ST segment?
Time during which ventricles are emptying and contracting
What is represented by the T wave?
Ventricular depolarisation
What is represented by the T-P segment?
Time during which the ventricles are relaxing and filling
Why is the ECG negative in some leads and positive in others? E.g. in lead I the P wave may be followed by a Q wave, whilst in lead aVF it may be followed by an R wave during septal depolarisation.
The resultant vector of electrical activity is reflected differently across different leads (since they are attached to different limbs/parts of the body).
Planar limb leads are oriented in a _______ plane.
Name the bipolar and unipolar leads.
Planar limb leads are oriented in a VERTICAL plane.
BIPOLAR LEADS: I, II, III
UNIPOLAR LEADS: aVF, aVL, aVR
Precordial leads are oriented in a _________ plane.
They are labelled V_ to V_.
Precordial leads are oriented in a HORIZONTAL plane.
They are labelled V1 to V6.
Which precordial leads give a more accurate view of the RIGHT ventricle?
V1 and V2
V3-V6 are more about the left ventricle
Where are the precordial limb leads places?
V1 - 4th intercostal space, right sternal edge
V2 - 4th intercostal space, left sternal edge
V4 - 5th intercostal space, MCL
V3 - Directly between leads V2 and V4
V5 - level with V4 (5th intercostal space) at the anterior axillary line
V6 - level with V5, MAL
What are some pathologies that can cause right-axis deviation (+105 - + 180 degrees)
The QRS complex tells us what is happening in the ventricles. Right-axis deviation can indicate:
- Right ventricular hypertrophy (the RV is much smaller than the left and will usually produce a smaller wave, but hypertrophy will change this)
- Wolff-Parkinson White syndrome
- Reversed arm electrodes
- Left posterior hemiblock
What are some pathologies that can cause left-axis deviation (-30 - to -120 degrees)?
- Left anterior hemiblock
- Inferior Q wave infarct
- Wolff-Parkinson White syndrome
Describe a systematic method of reading ECGs and what you would look for in each section.
- What is the RATE?
- P WAVE: is it absent or present?
- P-R INTERVAL: is it constant/consistent?
- QRS COMPLEX: is it present, with the same morphology?
Is is narrow or broad?
Is there a 1:1 ratio with the P waves? - ST SEGMENT / T WAVE:
- QT INTERVAL:
Describe the appearance of sinus arrhythmia on an ECG.
What is the physiology behind this?
Variations in the P-P interval. Otherwise, the ECG is normal.
Often seen in young, healthy patients due to changes in vagal tone during different stages of breathing.
Describe the appearance of a coronary sinus arrhythmia on an ECG.
What is the physiology behind this?
Inverted P-waves in inferior leads (especially II and III). Otherwise, the ECG is normal.
Caused by impulses that originate low in the atrium, causing it to travel retrograde as well as distally.
What is an escape beat?
An escape beat is a heart beat arising from an ectopic focus in the atria, the AV node, or the ventricles when the sinus node fails in its role as a pacemaker or when the sinus impulse fails to be conducted to the ventricles as in complete heart block.
What is the appearance of an escape beat on ECG?
Variable period of asystole followed by escape mechanisms
A narrower QRS complex can be seen if the escape beat is originating from the atria.
A broader QRS is present in ventricular escape beats.
What is an atrial ectopic beat?
Describe its appearance on an ECG.
Premature beat arising from ectopic pacemaking tissue within the atria.
Abnormal (non-sinus) P wave, usually followed by a normal QRS.
Other possible features:
- Camel hump appearance due to abnormal P wave being hidden in the preceding T wave
- Longer or shorter PR interval
- Longer RR interval after the ectopic beat
Describe the pathophysiology of atrial flutter.
Impulses travel a circular course in the atria, setting up regular, rapid flutter (F) waves.
It is a supra ventricular tachycardia caused by a re-entry circuit in the right atrium.
Describe the appearance of atrial flutter on an ECG (including the various P:QRS ratios)
Saw-tooth pattern of flutter (F) waves in leads II, III, and aVF
P rate is around 250-350bpm (usually 300bpm)
Variable P-R interval
Variable rate of QRS complexes with variable P:QRS ratio (e.g. 2:1, 3:1, 4:1)
https://litfl.com/atrial-flutter-ecg-library/
What is the most common AV conduction ratio in atrial flutter?
2:1
Results in a ventricular rate of ~150bpm
Describe the appearance of atrial fibrillation on an ECG?
Absent or chaotic P waves
Irregularly irregular
Variable R-R interval
Name 3 atrioventricular conduction abnormalities
First-degree
Second-degree
- Mobitz Type I (Wenckebach)
- Mobitz Type II
Third-degree (complete)
Name 2 intraventricular conduction abnormalities
Bundle branch blocks (right and left)
Fascicular blocks
Name 5 causes of first and second-degree heart block
- Drugs (e.g. digoxin, b-blockers, hyperkalemia)
- IHD
- Hyperthyroidism
- Addison’s disease
- Congenital
Name 5 causes of third-degree heart block
- Drugs (e.g. digoxin, b-blocker)
- Degenerative
- IHD
- Congenital
- Sarcoidosis
- Amyloid, RA, myeloma
tend to put in a pacemaker for third-degree
Name 4 causes of a right bundle branch block (RBBB)
- Normal/physiological (in young, healthy individuals)
- PE
- ASD (septal defect)
- IHD
- Myocarditis
Name 4 causes of a left bundle branch block (LBBB)
- IHD
- Hypertensive HD
- Cardiomyopathy
- Aortic valve disease
- Myocarditis
Describe the appearance of first-degree heart block on an ECG.
What is it usually caused by?
Prolonged P-R interval (PR interval of greater than 0.20 without disruption of atrial to ventricular conduction)
Usually caused by drugs (e.g. digoxin, b-blocker) which the patient actually needs. Doesn’t tend to cause them too many problems.
Can also occur in young, fit individuals.
Describe the appearance of second-degree Mobitz Type I / Wenckebach heart block on an ECG.
Is it usually pathological?
Progressive lengthening of P-R interval with intermittent dropped beats. P-R interval longest immediately before a dropped beat.
Usually not pathological. Can happen during sleep.
https://litfl.com/av-block-2nd-degree-mobitz-i-wenckebach-phenomenon/
Describe the appearance of second-degree Mobitz Type II / non-Wenckebach heart block on an ECG.
Sudden dropped QRS without prior PR lengthening
PR interval is constant except for the missed beat
- P waves regular, R waves IRREGULAR
https: //litfl.com/av-block-2nd-degree-mobitz-ii-hay-block/
What is the difference between a Mobitz Type I and Mobitz Type II heart block?
Which one is more likely to need a pacemaker?
Mobitz Type I: usually due to functional suppression of AV conduction (e.g. drugs)
Mobitz Type II: usually due to structural of the conduction system (e.g. ischaemia, infarct, fibrosis, necrosis). Would consider putting a pacemaker in if the patient was symptomatic.
Describe the appearance of third-degree / complete heart block on an ECG.
AV dissociation, with independent atrial and ventricular rates. QRS rates are slower than P waves.
- P waves and R waves are regular, BUT they are NOT related.
Impulses originate:
(a) at the SA node and either at the AV node (junctional rhythm) or in the ventricles (idioventricular rhythm)
Describe the appearance of a junctional rhythm and an idioventricular rhythm in third-degree/complete heart block
JUNCTIONAL RHYTHM: Atria and ventricles depolarise independently, with QRS complexes less frequent. Regular at 40-55bpm but NORMAL in shape.
IDIOVENTRICULAR RHYTHM: Atria and ventricles depolarise independently, with QRS complexes less frequent. Regular at 20-40bpm but WIDE and ABNORMAL in shape. (more dangerous)
Describe the appearance of a RIGHT bundle branch block on ECG.
QRS duration >0.12 secs
Secondary R wave in V1 (M-shape)
Deep slurred S wave in leads I, aVL, V4-6
Normal axis (involvement of the fascicles will cause an axis change)
Describe the appearance of a LEFT bundle branch block on ECG.
QRS duration >0.12 secs
No secondary R wave in V1
No septal Q wave in V5-6
Deep slurred S wave V1-3
ST/T wave: possible ST elevation in V1-3, depressed ST/T in I, aVL, and V4-6, ST/T vector opposite QRS
What are the normal durations of the following?
PR interval
QRS complex
PR interval: 0.12-0.20 secs
QRS complex: 0.08-0.10 secs
What duration is represented by the SMALL square on an ECG?
What duration is represented by the LARGE square on an ECG?
SMALL square: 0.04 secs
LARGE square: 0.20 secs
Describe the appearance of pericarditis on an ECG
Wide-spread saddle-shaped ST elevation
PR segment depression
(look out for recent viral illness in Hx)
Describe the appearance of a pulmonary embolism on an ECG
‘S1Q3T3’ = classic constellation of findings
It refers to a deep S wave in lead I, pathological Q wave in lead III and inverted T in V3 (and other anterior leads).
BUT THE MOST COMMON FINDING IS A SINUS TACHYCARDIA
There may also be RBBB or a RV strain pattern with T wave inversion in V1 to V4.
How can you tell whether there is left or right axis deviation by comparing leads I and aVF?
RIGHT AXIS DEVIATION = negative deflection in lead I, positive deflection in aVF
LEFT AXIS DEVIATION = positive deflection in lead I, negative deflection in aVF.
https://www.oxfordmedicaleducation.com/ecgs/ecg-interpretation/
Which characteristic wave is seen in Wolff-Parkinson-White syndrome?
Delta waves: a slurred upstroke in the QRS complex
Describe the appearance of WPW syndrome on an ECG
Delta waves
Shortened PR interval (<0.12 secs)
Broad QRS (>0.10 secs)
What is WPW syndrome caused by?
Refers to the presence of a congenital accessory pathway and episodes of tachyarrhythmias
Mobitz type II is usually due to a failure at which level of the cardiac conduction system?
Mobitz type II is usually due to a failure at the level of the His-Purkinje (below the AV node)
In around 75% of cases, the conduction block in Mobitz Type II is located _____ to the Bundle of His, producing _____ QRS complexes.
In around 75% of cases, the conduction block in Mobitz Type II is located DISTAL to the Bundle of His, producing BROAD QRS complexes.
How does the pathophysiology differ between atrial flutter and atrial fibrillation?
ATRIAL FIBRILLATION: impulses are being triggered from many different parts of the atria, causing them to quiver rather than contract.
CAUSES: hypertension, valvular HD, heart failure, obesity.
ATRIAL FLUTTER: coordinated electrical activity in the atria. They DO contract (unlike AF) but very rapidly (~300bpm).
CAUSES: anti arrhythmic drugs, disorders that also cause AF (e.g. hyperthyroidism, obesity, OSA), post-cardiac surgery.
What is the treatment for AV Nodal Re-entry Tachycardia (AVNRT)?
In which patient populations is it normally seen?
Adenosine
Young people. Typically presents with palpitations.
Narrow QRS complexes are ____________ in origin.
Broad QRS complexes (QRS>0.10secs) tend to be __________ in origin.
Narrow QRS complexes are SUPRAVENTRICULAR in origin.
Broad QRS complexes (QRS>0.10secs) tend to be VENTRICULAR in origin.
(But can also be due to aberrant conduction of supraventricular complexe, e.g. due to bundle branch block, hyperkalaemia or sodium-channel blockade)
