interpreting an ECG Flashcards

(40 cards)

1
Q

first thing you do Before taking an ECG

A

Confirm the name and date of birth of the patient matches the details on the ECG.

Confirm the date and time the ECG was performed.

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2
Q

12 step ECG algorithm

A
  1. rate
  2. rythm
  3. cardiac axis
  4. P waves
  5. PR interval
  6. QRS complex
  7. delta waves
  8. RS progression
  9. j point
  10. ST segment
  11. T wave
  12. U waves
    13.
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3
Q

1

normal heart rate

A

Normal = 60 – 100 bpm

Tachycardia > 100 bpm

Bradycardia < 60 bpm

Hint: If there are obviously P-waves present, check the ventricular rate and the atrial rate. The rates will be the same if there is 1:1 AV conduction.

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4
Q

1.1

how to measure HR if REGULAR

A

Count the number of large squares present within one R-R interval

Divide 300 by this number to calculate the heart rate

e.g. 4 large squares in an R-R interval: 300/4 = 75 beats per minute

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5
Q

how to calc HR if rythm is IRREGULAR

A

Count the number of QRS complexes on the rhythm strip (each rhythm strip is 10 seconds long)

Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute)

e.g. 10 complexes on a rhythm strip X 6 = 60 beats per minute

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6
Q

3

what are the two types of IRREGULAR heart rythms

how to measure irreg rythms

top for measurement of AV block

A
  1. Regularly irregular (i.e. a recurrent pattern of irregularity) 2nd degree AV block
  2. Irregularly irregular (i.e. completely disorganised) e.g. atrial fibrillation

measurement

Mark out several consecutive R-R intervals on a piece of paper, then move them along the rhythm strip to check if the subsequent intervals are the same.

  • Hint – if you are suspicious that there is some atrioventricular block,*
  • map out the atrial rate and the ventricular rhythm separately (i.e. mark the P waves and R waves). As you move along the rhythm strip, you can then see if the PR interval changes, if QRS complexes are missing or if there is complete dissociation between the two.
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7
Q

4

what is the cardiac axis

which leads determine it

A

Cardiac axis describes the overall direction of electrical spread within the heart.

In a healthy individual the axis should spread from 11 o’clock to 5 o’clock.

To determine the cardiac axis you need to look at leads I,II and III.

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8
Q

normal cardiac axis

which leads are positive which is negative

A

n normal cardiac axis:

Lead II has the most positive deflection compared to Leads I

Lead III has negative deflection usually

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9
Q

Right axis deviation ( opposite of normal)

common assoc patholigy

A

Lead III has the more positive deflection than Lead II

Lead I should be negative

This is commonly seen in individuals with right ventricular hypertrophy

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10
Q

Left axis deviation

assoc pathology

A

Lead I has the most positive deflection

Leads II and III are negative

Left axis deviation is seen in individuals with heart conduction defects

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11
Q

4

what to look for in the P waves

A
  1. Are P-waves present? = Sinus rythm
    • If so, is each P-wave followed by a QRS complex? = if not AV block
    • Do the P-waves look normal? (check duration, direction and shape)
  2. If not present, is there any atrial activity e.g.
    • sawtooth baseline → flutter waves
    • chaotic baseline → fibrillation waves
    • flat lineno atrial activity at all?

Hint – If P-waves are absent and there is an irregular rhythm it may suggest atrial fibrillation

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12
Q

normal duration of P wave

A

Normal duration: 0.12-2.0 seconds (3-5 horizontal boxes).

This is measured from the onset of the P wave to the onset of the QRS complex regardless if the initial wave is a Q or R wave.

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13
Q

5

P-R interval

normal duration

when is it pathological

A

The P-R interval should be between 120-200 ms/ 0.12-0.2 (3-5 small squares)

pathologies

  1. prolonged P-R (over 0.2 secs)= AV block
  2. shortened (below 0.12) = small atrium or accessory pw
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14
Q

types of Causes of prolonged P-R

how to remember them according to anatomical location

A
  • First degree AV block: Occurs between the SA node and the AV node (i.e. within the atrium)
  • Second degree AV block:
    • Mobitz I (Wenckebach) – occurs IN the AV node. This is the only piece of conductive tissue in the heart which exhibits the ability to conduct at different speeds
    • Mobitz II – occurs AFTER the AV node in the bundle of His or Purkinje fibres
  • Third degree AV block: Occurs anywhere from the AV node down causing complete blockage of conduction
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15
Q

First degree heart block

A

fixed prolonged PR interval (>200 ms)

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16
Q

Second degree heart block (Mobitz type 1)

A

PR interval slowly increases/widens then there is a dropped QRS complex (beat), this is MOBITZ TYPE I SECOND DEGREE AV BLOCK (Wenckebach)

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17
Q

Second degree heart block (Mobitz type 2)

A

PR interval is fixed but there are dropped beats,

MOBITZ TYPE 2 SECOND DEGREE HEART BLOCK

(clarify that by the frequency of dropped beats e.g 2:1, 3:1, 4:1)

18
Q

Third degree heart block (complete heart block)

A

If the P waves and QRS complexes are completely unrelated,

this is THIRD DEGREE AV BLOCK (complete heart block)

19
Q

causes of shortened PR interval

A
  • P-wave is originating from somewhere closer to the AV node so the conduction takes less time (the SA node is not in a fixed place and some people’s atria are smaller than others!)
  • 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 (see below which demonstrates an ECG of a patient with Wolff Parkinson White syndrome)
20
Q

6

What are the 3 properties of the QRS complex to assess

A
  1. Width ( narrow/ broad)
  2. Height (small/ tall)
  3. Morphology ( asses the individual components)
21
Q

Width of the QRS complex

normal width/ duration

A

normal QRS interval = below 0.12 seconds

NARROW (< 0.12 seconds)

  • occurs when the impulse is conducted down the bundle of His and the Purkinje fibre to the ventricles. This results in well organised synchronised ventricular depolarisation

BROAD (> 0.12 seconds)

  • occurs if there is an abnormal depolarisation sequence – e.g.
    • a ventricular ectopic where the impulse spreads slowly across the myocardium from the focus in the ventricle. In contrast, an atrial ectopic would result in a narrow QRS complex because it would conduct down the normal conduction system of the heart.
    • bundle branch block results in a broad QRS because the impulse gets to one ventricle rapidly down the intrinsic conduction system then has to spread slowly across the myocardium to the other ventricle.
22
Q

what are the individual waves of the QRS to be assesed

A
  • Q waves
  • step 7 = Delta wave
  • step 8 = R and S wave progression
  • step 9 = J point
23
Q

when is a q wave pathologically signifiant

what previous condition can be found by looking at Q waves

A

Isolated Q waves can be normal.

A pathological Q wave is

  • > 25% the size of the R wave that follows it or
  • > 2mm in height and > 40ms in width.
    • A single Q wave is not a cause for concern – look for Q waves in an entire territory (anterior / inferior) for evidence of previous MI.
24
Q

7

Delta waves

what causes it’s characteristic slurred upstroke

conditions for WPW

A

sign that the ventricles are being activated earlier than normal from a point distant to the AV node.

The early activation then spreads slowly across the myocardium causing the slurred upstroke of the QRS complex.

NB The presence of a delta wave does NOT diagnose Wolff-Parkinson-White syndrome.

WPW = This requires evidence of tachyarrhythmias AND a delta wave.

25
_8_ R WAVE progression which lead shows normal progession what leads does pathological progression indicate previous condition
Look for R wave progression across the _chest leads_ * from *small* in **V1** to L A R G E in **V6** * The transition from S \> R wave to R \> S wave should occur in **V3 or V4**. * Poor progression (if S is still \> R at through to leads V5 and V6) can be a sign of * **previous MI** * but can also occur in **very large people due to lead position**.
26
_9_ J point segment how does it relate to 'high take off" what does this get confused for
The J point is where the S wave joins the ST segment This point can be _elevated_ resulting in the _ST segment that_ follows it also being raised (this is known as “**High take off**”) High take off aka **benign early repolarisation** is a **_normal variant_** that causes a lot of angst and confusion as it *_LOOKS like **ST elevation**_*
27
4 ways to that _benign early repolarisation_ is different from _STEMI_
1. Benign early repolarisation occurs _mostly under the age of **50**_ * (over age of 50, **ischaemia** is more common and should be suspected first) 2. **J point is raised** with widespread ST elevation in **multiple territories** making ischaemia less likely 3. **T waves** are **also raised** * (in contrast to a STEMI where the _T wave remains the same size_ and **only** the **ST segment is raised)** 4. **The changes do not change**! * During a STEMI, the _changes will evolve_ – in benign early repolarisation, they will remain the same.
28
step 10
* In a healthy individual it should be an **_isoelectric line_** (neither elevated or depressed). * Abnormalities of the ST segment should be investigated to rule out pathology .e.g. 1. ST elevation 2. ST depression
29
Conditions for ST elevation what specific pathology does it suggest
ST elevation is significant when it is * greater than 1 mm (1 small square) in 2 or more contiguous **limb** leads or * \>2mm in 2 or more **chest leads.** It is most commonly caused by **acute FULL thickness myocardial infarction.**
30
Conditions for ST which pathology does it suggest
ST depression **≥ 0.5 mm** in **≥ 2 contiguous** leads indicates **myocardial _ischaemia_.**
31
_step 11_ T waves normal t wave pathological conditions
T waves represent *_repolarisation of the ventricles_* normal t waves : upright in all leads, except **aVR, aVL, III** and **V1** leads. Highest amplitude of T wave is found at **V2** and **V3 leads**. The shape of the T wave is usually **asymmetrical** with a **rounded peak** pathological T waves 1. Tall 2. inverted 3. biphasic 4. flat
32
Tall T waves criteria ( same as what?) pathological conditions
criteria * \> **5mm** in the _limb_ leads **AND** * \> 10mm in the _chest leads_ (the same criteria as ‘small’ QRS complexes) Pathological conditions 1. **Hyperkalaemia** (“_Tall tented T waves_”) 2. Hyperacute STEMI
33
When are T waves Inverted normally and pathologically what is important to comment about the T wave Inversion
normally * normally inverted in **V1** * normal variant inversion in **lead III** Pathological 1. **Ischaemia** 2. Bundle branch blocks * V1 – V3 in RBBB * V4 – 6 in LBBB 3. **Pulmonary embolism** 4. Left ventricular hypertrophy (in the lateral leads) 5. Hypertrophic cardiomyopathy (widespread) 6. General illness ( 50% of ICU pts) * Comment on the distribution of the T wave inversion * e.g. anterior / lateral / posterior leads
34
Inverted T waves in V1 – V3 indicate
LBBB
35
Inverted t waves in leads V1-V3
RBBB
36
Inverted T waves in Lateral leads ( I, aVL, V5, & V6)
Lateral ventricular Hypertrophy
37
widespread Inverted T waves on ECG
Cardiomyopathy
38
what are Biphasic T waves what 2 conditions does it indicate
Biphasic T waves have _two peaks_ and can be indicative of 1. _ischaemia_ 2. **hypokalaemia**
39
what is a flat T wave and what does it suggest
non-specific sign, this may represent _ischaemia_ or **electrolyte imbalance**.
40
_12_ what is a u wave which leads what axacerbates it 3mconditions it suggests which 3 drugs can cause it i DAP- U wave
The U wave is a **\> 0.5mm** deflection after the T wave best seen in **V2** or **V3**. * These become larger the slower the bradycardia * classically U waves are seen in 1. various electrolyte imbalances 2. hypothermia, 3. antiarrhythmic therapy * **D**igoxin, **A**miodarone, **P**rocainamide