Mod D Tech 12 3 and 12-Lead ECG Placement and Acquisition Flashcards Preview

Technician Course MOD D 2016 > Mod D Tech 12 3 and 12-Lead ECG Placement and Acquisition > Flashcards

Flashcards in Mod D Tech 12 3 and 12-Lead ECG Placement and Acquisition Deck (61):
1

Basic considerations before ecg

To reduce artifact: Consider ambient temperature and patient dignity Ensure good electrode contact (How?) Shave off excessive hair Make sure electrodes are in date and gel is moist Ensure cable is not pulling on electrodes

2

Preparation for ecg

Expose the monitoring area Consider temperature and dignity Select and prepare the electrode site Shave excessively hairy areas Attach the electrodes Secure the patient cable Switch the machine on and take a recording Always explain to the patient what & why you are doing this procedure!

3

12 Views or Leads name groups of leads

3 Standard leads I, II and III

3 Augmented Voltage leads AVR, AVL and AVF

6 Precordial Leads V1,V2,V3,V4,V5 and V6

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4

Electrocardiogram

•A recording of electrical activity in the heart.

•The electrical activity is picked up by electrodes placed on the patients skin

•The positioning of these electrodes allows the ECG to look at the electrical activity from different directions

•Basic monitoring is carried out using three leads

•These leads are normally known as leads I, II, III.

•Lead II is commonly used as a rhythm strip and is normally sufficient to identify arrhythmia

5

•A normal ECG trace shows five deflections which are named?

P,Q, R, S, and T.

6

•The P wave arises when the impulse from the ______sweeps over the___and triggers contraction of the ____

The P wave arises when the impulse from the SA node sweeps over the atria and triggers contraction of the atria

7

•The QRS complex represents the very rapid spread of the impulse from the ____through the  ___   ___  and the ________and triggers contraction of the ventricles

•The QRS complex represents the very rapid spread of the impulse from the AV node through the AV bundle and the purkinje fibres and triggers contraction of the ventricles

8

•The T wave represents the _______ of the _______ muscle

•The T wave represents the relaxation of the ventricular muscle

9

•The normal ECG originates from the ____ ____ and is known as ____ ____ _____

•The normal ECG originates from the SA node and is known as normal sinus rhythm

10

PQRST Complex

 

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11

ECG Rate

lagre sq

•1 Sq  = 300 bpm

•2 Sq = 150 bpm

•3 Sq = 100 bpm

•4 Sq =  75 bpm

•5 Sq =  60 bpm

•6 Sq =  50 bpm

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12

13

ECG Electrical Deflection

•When an electrical impulse flows towards an electrode the ECG will record a _____ or _____ deflection (A)

•When an electrical impulse flows away from an electrode the ECG will record a _____ or _______ deflection (B)

•When an electrical impulse flows towards an electrode the ECG will record a positive or upward deflection (A)

•When an electrical impulse flows away from an electrode the ECG will record a negative or downward deflection (B)

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14

P Wave which part of the ecg

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15

Q wave which part of the ecg

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16

R Wave which part of the ecg

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17

S Wave which part of the ecg

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18

T wave which part of the ecg

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19

Normal Intervals ecg

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20

ST Segment

Denotes end of ventricular contraction to beginning of resting phase

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21

ST Segment

 

Normal  

ST Depression

(Ischaemia)

ST Elevation

(Injury/MI)

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22

Normal Parameters of

•P-R Interval = ___- ___seconds

•QRS Complex = ____seconds ___ – ___secs)

•P-R Interval = 0.12 - 0.2 seconds

•QRS Complex = <0.12 seconds (0.8 – 0.12 secs)

23

A 9-Point plan

1.Is there any electrical activity?

2.Has the patient got a pulse?

3.What is the ventricular rate?

4.Is the rhythm regular or irregular?

5.Is atrial activity present?

6.Is the PR interval within normal limits?

7.Is the QRS complex normal or prolonged?

8.How is atrial activity related to ventricular activity?

9.Is the ST Segment elevated or depressed?

24

10 rules of Chamberlain

1 The PR interval should be no longer than 0.12 – 0.2 seconds (3 to 5 small squares

2. The QRS should be no wider than 0.12 seconds (less than 3 small squares

3. The QRS should be predominantly positive (Upright) in leads I and II

4. The T waves should point in the same direction as the QRS in the limb leads (Standard leads)

5. All waves should be negative in aVR

6 The R wave should grow from V1 to at least V4

7. The ST segment should start isoelectric except in V1 and V2 where it may be slightly raised

8. The P wave should be upright in leads I and II and V2 – V6

9. There should be no Q wave greater than 0.03 secs (Less than 1 small square) in leads I, II and V2 – V6

10. The T wave should be upright in leads I,II and V2 – V6

25

Bradycardia - Treatment

No specific treatment if BP is maintained and no signs of hypoperfusion,

however if:

•Hypotension is evident

•Skin is pale, cold and clammy

•Pulse is below 40bpm with poor perfusion

Atropine should be administered by paramedics

Oxygen as per guidelines

26

what Rhythm

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Normal Sinus Rhythm

27

what Rhythm

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Sinus Bradycardia

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28

Sinus Bradycardia
Clinical Significance

•May be normal in fit healthy adults

•Increased parasympathetic tone

•Unopposed vagal tone (eg spinal cord injury)

•Damage to SA Node

•Hypoxia

•Excess of cardiosuppressant drugs (Digoxin, propranolol)

•May lower BP causing deterioration in tissue perfusion

29

Bradycardia - Treatment

No specific treatment if BP is maintained and no signs of hypoperfusion, however if:

•Hypotension is evident

•Skin is pale, cold and clammy

•Pulse is below 40bpm with poor perfusion

Atropine should be administered by paramedics

Oxygen as per guidelines

30

What Rhythem

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Sinus Tachycardia

31

Sinus Tachycardia
Clinical Significance

•Haemorrhage

•Hypoxia

•CHF, LVF

•Increased sympathetic stimulation

•Pain, anxiety, fear, exercise etc

•Over 120-140 bpm may result in lower BP, reduced tissue perfusion

32

What Rhythem

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Atrial Fibrillation

33

Atrial Fibrillation
Clinical Significance

•SA Node cell destruction

•Mitral valve disease

•Damage to atria due to organic heart disease

•Congestive cardiac failure

•If ventricular rate is rapid there may be lowering of cardiac output, hypotension and hypoperfusion

•Chest pain due to increased workload and reduced myocardial oxygenation

34

What Rhythem

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Atrial Flutter

35

Atrial Flutter
Clinical Significance

•Organic heart disease

•Damage to the atria

•May progress to atrial fibrillation, if due to disease

•If ventricular rate is above 140 could result in loss of cardiac output, lowered BP, lowered tissue perfusion.

•Chest pain due to inc. workload and reduced myocardial oxygenation

36

what rhythem

Premature Ventricular Contraction (PVC)

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37

PVC Clinical Significance

•Damage to ventricles (Ischaemic heart disease)

•Hypoxia

•Acidosis

•CCF

•Overdose of some drugs

May be precursor of more serious arrhythmias

Treat cause, closely monitor rhythm and record changes

38

What rhythem

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1st Degree Heart Block

39

1st Degree Heart Block
Clinical Significance

•May be damage to the AV node

•Increased parasympathetic tone on AV Node

•Hypoxia

•Overdose of some drugs (digoxin)

•Usually no serious clinical consequences but note and report rhythm

40

what rhythem

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2nd Degree Heart Block Mobitz Type 1 (Wenckeback)

41

2nd Degree Heart Block Mobitz Type 1 (Wenckeback)

•May be damage to the AV node

•Increased parasympathetic tone on AV Node

•Hypoxia

•Overdose of some drugs (digoxin)

•Inferior acute MI

•May be little or no clinical significance unless rate is slow, when cardiac output may be reduced.

•May progress to complete heart block

42

what rhythem

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2nd Degree Heart Block Type 2

43

2nd Degree Heart Block Type 2

•May be described as 2:1, 3:1 etc

•May be damage to the AV node

•Increased parasympathetic tone on AV Node

•Hypoxia

•Overdose of some drugs (digoxin)

•More serious than type 1 and more likely to progress to complete heart block

44

What Rhythem

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3rd Degree Heart Block (complete)

45

3rd Degree Heart Block (complete)

•Damage to AV Node, Bundle of His or Bundle branches

•Increased parasympathetic tone

•Ventricular rate low causing lowering of cardiac output

•Risk of deterioration to ventricular fibrillation or ventricular standstill

•No specific treatment if asymptomatic

•If hypotensive – atropine

•Oxygen as per guidelines

46

What Rhythem

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Ventricular Tachycardia

47

Ventricular Tachycardia
Clinical Significance

•Damage to conduction pathways

•Damage to ventricles

•Ischaemic heart disease

•Hypoxia

•Acidosis

•Low serum potassium

•Overdose of some drugs

Maybe precursor of ventricular fibrillation

Treat pulseless VT as VF

48

Torsades de pointes

•Form of VT where short periods cause dizziness and loss of consciousness

•Looks similar to VF but characterised by waves that seem to be pointing upwards at one moment and then twisting so that they are pointing downwards for a short spell, then reversed again and so on

•Conventional antiarrhythmic treatment can cause a serious reaction (may convert to VF)

•Do not treat this form of VT with drugs before arriving at hospital unless under medical direction

49

What rhythem

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Ventricular Fibrillation

50

Ventricular Fibrillation
Clinical Significance

•May have similar causes as other ventricular arrhythmias

•Result in loss of cardiac output and therefore cardiac arrest

•4 Hs

  • 4 Ts

51

what Rythem

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R on T Phenomenon

52

R on T Phenomenon
Clinical Significance

•Damage to ventricles (Ischaemic heart disease)

•Hypoxia

•Acidosis

•CCF

•Overdose of some drugs

Increased risk of ventricular fibrillation

53

What Rhythem

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Asystole

54

Asystole
Clinical Significance

•Absence of cardiac output

•Cardiac Arrest

•4 Hs

4 Ts

55

Supraventricular tachycardia

•Indicates pacemaker site above ventricles

•No identifiable P waves

•Maybe paroxymal ie occurs in brief episodes with normal periods in between

•Rate: 150 – 200 bpm (Up to 300 in infants)

•Rhythm: regular

•P waves: absent or abnormal

•QRS: usually normal

56

Supraventricular tachycardia

•Idiopathic

•Damage to SA Node, Atria or AV Node

•Drug overdose

•Sympathetic stimuli

•Reduced output

•Hypotension

•Hypoperfusion

•Cerebral hypoxia

•Chest pain

57

Bundle branch blocks

•Damage to one of the branches of the bundle of his

•Appears as a notch on the QRS

•Need a 12 lead to determine left or right

•Impulse spreads from one ventricle to the other by abnormal pathways producing distinct ECG waveforms altering the appearance and width of the QRS complex

•V1 QRS, when turned clockwise points right if RBBB and left if LBBB

•WiLLiam MoRRow (V1 and V6)

58

Causes of BBB

•Hypoxia

•AMI

•CHF

•Hypertension

•PE

59

Left bundle branch block (LBBB)

•Always implies significant disease

•QRS > 0.12 secs (3 small squares – usually wider)

•Diminutive R wave in V1 to V3

•V1 may take the form of small negative deflection followed by small positive deflection and then large negative deflection (Looks like QS complex)

•Often ST elevation

•Loss of septal Q wave and notching of the QRS

•M shaped deflection in V4-V6

T waves in opposite direction to QRS

60

Right bundle branch block (RBBB)

•QRS 0.12 secs occasionally wider

•S wave in lead I

•rSR in lead V1(Dominant R wave does not indicate RV hypertrophy

•Wide and slurred S wave in V6

•Not an indication for thrombolysis unless obvious ST elevation can be seen

61

Junctional Rhythms

•SA Node disease

•AV Node acts as pacemaker (40-60 bpm)

•High Nodal

•Mid Nodal

•Low Nodal