How to read an ECG Flashcards
what is a normal adult heart rate
Normal: 60-100 bpm
Tachycardia: > 100 bpm
Bradycardia: < 60 bpm
how to calculate heart rate
Count the number of large squares present within one R-R interval.
Divide 300 by this number to calculate heart rate.
how to calculate heart rate if there is an irregular rhythm
if the R-R intervals differ throughout the ECG, you should:
Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long).
Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)
heart rhythm
a patients heart rhythm may be regular or irregular
regularly irregular (ie. recurrent pattern of irregularity)
irregularly irregular (ie. completely disorganised)
typical ECG finding for a normal cardiac axis
lead II has the most positive deflection compared to leads I and III
right axis deviation
lead II has the most positive deflection and lead I should be negative
right axis deviation is associated with
right ventricular hypertrophy
typical ECG finding for left axis deviation
Typical ECG findings for left axis deviation:
Lead I has the most positive deflection.
Leads II and III are negative.
left axis deviation is associated with
conduction abnormalities
what should you look for when looking at P waves
- Are P waves present?
- If so, is each P wave followed by a QRS complex?
- Do the P waves look normal? – check duration, direction and shape
- If P waves are absent, is there any atrial activity?
how long should the PR interval be
120-200ms (3-5 small squares)
how long is a prolonged PR interval
> 0.2 seconds (200ms)
what does a prolonged PR interval indicate
atrioventricular delay (AV block)
first degree heart block (AV block)
fixed prolonged PR interval >200ms
second degree heart block (type 1)
Typical ECG findings in Mobitz type 1 AV block include progressive prolongation of the PR interval until eventually the atrial impulse is not conducted and the QRS complex is dropped.
AV nodal conduction resumes with the next beat and the sequence of progressive PR interval prolongation and the eventual dropping of a QRS complex repeats itself.
second degree heart block type 1 is also called
Second-degree AV block (type 1) is also known as Mobitz type 1 AV block or Wenckebach phenomenon.
ECG findings of second degree heart block (type 2)
Typical ECG findings in Mobitz type 2 AV block include a consistent PR interval duration with intermittently dropped QRS complexes due to a failure of conduction.
The intermittent dropping of the QRS complexes typically follows a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wave.
third degree heart block occurs when
complete heart block
Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction.
Cardiac function is maintained by a junctional or ventricular pacemaker
typical ECG findings of third-degree heart block
Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently.
what is the anatomical location of first degree block
between the SA node and the AV node
what is the anatomical location of second degree block
type 1 occurs IN the AV node
type 2 occurs AFTER the AV node in the bundle of His or pukinje fibres
what is the anatomical location of third degree AV block
occurs at or after the AV node resulting in a complete blockade of distal conduction
shortened PR interval
can mean one of two things:
1. the P wave is originating from somewhere closer to the AV node so conduction takes less time
2. the atrial impulse is getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. this is an accessory pathway and can be associated with a delta wave
what should the width of the QRS complex be
it is narrow if it is <0.12 seconds
broad if it is >0.12 seconds
how does a narrow QRS complex occur
when the impulse is conducted down the bundle of His and the Purkinje fibre to the ventricles
this results in a well organised synchronised ventricular depolarisation
how does a broad QRS complex occur
occurs if there is an abnormal depolarisation sequence – for example, a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle.
height of the QRS complex
Height can be described as either SMALL or TALL:
Small complexes are defined as < 5mm in the limb leads or < 10 mm in the chest leads.
Tall complexes imply ventricular hypertrophy (although can be due to body habitus e.g. tall slim people).
tall complexes imply
ventricular hypertrophy
what is a Delta wave
a sign that ventricles are being activated earlier than normal from a point distant from the AV node
the early activation then spreads slowly across the myocardium causing the slurred upstroke of the QRS complex
what is a delta wave associated with
wolff parkinson white syndrome
but it is not diagnostic of this
Q-waves
isolated Q waves may be normal - a single Q wave is not a cause for concern
a pathological Q wave is >25% the size of the R wave that follows it or >2mm in height and >40ms in width
look for Q waves in an entire territory for evidence of previous myocardial infarction
R wave progression
assess the R wave progression across the chest leads (from small in V1 to large in V6)
the transition from S > R wave to R > S wave should occur in V3 or V4
poor R wave progression is when the S wave continues to be larger than the R wave (ie. through to leads V5 and V6)
what is poor R wave progression a sign of
can be a sign of previous MI but can also occur in very large people due to poor lead position
where is the J point
where the S wave joins the ST segment
what if the J point is elevated
this will mean the ST segment that follows it will also be raised
(this is called ‘high take off” or ‘benign early repolarisation’)
what does benign early repolarisation mean
this is a normal variant
can cause unnecessary concern because it looks like ST elevation
how should you assess the J point to figure out whether there is ischaemia or benign early repolarisation
- benign early repolarisation occurs mostly under the age of 50 (over 50, ischaemia should be considered first)
- typically, the J point is raised with widespread ST elevation in multiple territories making ischaemia less likely
- the T waves are also raised (in contrast with STEMI where the T wave remains the same size and the ST segment is raised)
- the ECG abnormalities do not change - in STEMI, the changes will evolve, but in benign early repolarisation, they will remain the same
in a healthy individual, what should the ST segment look like
it should be an isoelectric line (neither elevated or depressed)
ST elevation is significant when
it is greater than 1mm (1 small square) in two or more contiguous limb leads
OR
>2mm in 2 or more chest leads
ST elevation is most commonly caused by
acute full-thickness myocardial infarction
what defines ST depression
> or equal to 0.5mm in > or equal to 2 contiguous leads
ST depression indicates
myocardial ischaemia
T waves represent
repolarisation of the ventricles
T waves are considered tall if they are
> 5mm in the limb leads
AND
10mm in the chest leads
(the same criteria as small QRS complexes)
tall T waves may be associated with
hyperkalaemia (tall tented T waves)
hyperacute STEMI
can inverted T waves be normal
T waves are normally inverted in V1 and inversion in lead III is a normal variant
when are inverted T waves not normal
if they are inverted anywhere except leads V1 and III this is a non-specific sign of a wide variety of conditions
- ischaemia
- bundle branch blocks
- pulmonary embolism
- left ventricular hypertrophy (in the lateral leads)
- hypertrophic cardiomyopathy
- general illness
biphasic T waves
have two peaks and can be indicative of ischaemia and hyperkalaemia
flattened T waves
non-specific sign, may represent ischaemia or electrolyte imbalance
can U waves be normal?
U waves are not a common finding
what is a U wave
> 0.5mm deflection after the T wave best seen in V2 or V3
what causes a U wave
they become larger the slower the bradycardia
they are seen in various electrolyte imbalances, hypothermia, and secondary to antiarrhythmic therapy (such as digoxin, procainamide or amiodarone)
