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NancyPHARM205 > Tut4: ECG > Flashcards

Tut4: ECG Flashcards

1
Q

What are the components of the conduction system of the heart

A 
Sino atrial node, 
Atrioventricular node
BUndle of his
Bacmann's bundle
Left posterior bundle
Right bundle 
Purkinje fibres
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2
Q

List the different waves of the ECG

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - Ventricular repolarisation
U wave - unknown

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3
Q

Where is the Atrial repolarisation wave?

A

It is masked by the QRS complex as ventricles have larger mass.

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4
Q

Where does the first heart sound occur?

A

at the QRS complex

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5
Q

where does the second heart sound occur?

A

at the end of the t wave

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6
Q

What is the wigger’s diagram?

A

Diagram that encomapses relative pressures of the aorta, ventricles and atria

Relative ventricular volume
Relative ECG and heart sounds
Relative valve activity

of a cardiac cycle against time.

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7
Q

What is normal sinus rhythm?

A

Regular rhythm of 60-100bpm
Normal QRS duration
P wave visible before each QRS complex
P-R interval normal (<5 squares)

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8
Q

What does normal sinus rhythm indicate?

A

That electrical signal is generated by the sinus node and travelling in a normal fashion in the heart

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9
Q

What reason could account for a P-R interval longer than usual (i.e. more than 5 squares)

A

1st degree block

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10
Q

What is sinus bradycardia?

A 
A heart rate less than 60bpm
Rhythm is regular
QRS duration is normal
P wave is visible before each QRS complex
P-R interval - normal
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11
Q

In what situation would sinus bradycardia be normal?

A

In a healthy athletic person.

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12
Q

What other reasons could cause sinus bradycardia?

A

Increased vagal tone from drug abuse,
Hypoglycaemia
Brain injury with increase intracranial pressure

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13
Q

What could benign sinus bradycardia be caused by?

A

patients on beta blockers

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14
Q

What features of the ECG would indicate a myocardial infarction?

A

S-T element does not go isoelectric which indicates infarction

Otherwise:
Regular rhythm
Rate: 80bpm
normal QRS duration
normal p wave
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15
Q

What is sinus tachycardia?

A 
excessive heart rate above 100bpm originating from the SA node
Regular rhythm
Normal QRS duration
P wave visible before each QRS complex
normal P-R interval

Impulse generating heart beats are normal but they occur at a faster pace than normal

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16
Q

In what situation would sinus tachycardia be considered normal?

A

During exercise

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17
Q

What are some other causes of sinus tachycardia?

A

stress
fright
illness and exercise

Not a surprise if triggered in response to regulatory changes like shock,

but if there is no apparent trigger some medications may be required to suppress the rhythm

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18
Q

What is atrial fibrillation?

A

Atria fire electrical impulses in an irregular fashion causing irregular heart rhythm.

Irregularly irregular rhythm
Rate: usually 100-160bpm (slower if on medication)
QRS duration usually normal
P wave not distinguishable as atria are firing off all over the place
P-R interval not measureable

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19
Q

What causes atrial fibrillation?

A

Many sites within atria generate their own electrical impulses, resulting in irregular conduction of impulses to ventricles that generate the heart beat.

Irregular rhythm can be felt when palpating a pulse

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20
Q

What is the significance of QT prolongation

A

Electrical disturbance of the heart is caused by lengthening of duration of ventricular repolarisation, detected by ECG

Increases risk of TORSADE DE POINTES - type of ventricular tachyarrhythmia which can lead to VT and sudden death

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21
Q

What are the boundaries for QT prolongation in adult males and females?

A

Adult males:
QTc(ms)
450 PROLONGED

Adult females:
QTc(ms)
470 PROLONGED

QTc >500ms or an increase in the Qtc of >60ms generally considered to confer a high risk of torsade de pointes in an individual patient

22
Q

What is QTc?

A

Corrected QT interval

23
Q

What is torsades de pointes?

A

A form of ventricular tachycardia where the QRS amplitude varies, and the QRS complexes appear to twist around the baseline

Associated with a prolonged QT interval which may be congenital or acquired (e.g. from medication)

Not usually sustained, terminates spontaenously, but frequently recurs unless the underlying cause is corrected

May degenerate into sustained ventricular tachycardia or ventricular fibrillation

Life threatening arrhythmia and may present as sudden cardiac death in patients with structurally normal hearts

24
Q

What is the Vaughan Williams Classification of Class I antiarhythmic drugs?

A

Class I- Sodium channel blockers
Reduces rate of depolarisation in phase 0
e.g. Lignocaine, Mexilitine

25
Q

What is the Vaughan Williams Classification of Class II antiarrhythmic drugs?

A

Class II- beta blockers
Reduces sympathetic tone (SNA normally increases intracellular Ca2+ availability)
e.g. Metoprolol, atenolol

26
Q

What is the Vaughan Williams Classification of Class III antiarrhythmic drugs? `

A

Class III- Potassium channel blockers
Prolongs the repolarisation but unclear
E.g. amiodarone

27
Q

What is the Vaughan Williams Classification of Class IV antiarrhythmic drugs?

A

Class IV- Calcium channel blockers
Block voltage sensitive L type calcium channels to slow conduction in SA and AV node
E.g. Verapamil and diltiazem

28
Q

What is the Vaughan Williams Classification of Other Class antiarrhythmic drugs?

A

e.g. Digoxin
Increases vagal tone - slows heart rate/ blocks AV conduction

Inhibits Na+/K+ ATPase
Na+ s retained in the cell, Ca2+ is retained
Increased contraction when triggered

29
Q

What is the Vaughan Williams Classification of Class I antiarhythmic drugs?

A

Class I- Sodium channel blockers
Reduces rate of depolarisation in phase 0
e.g. Lignocaine, Mexilitine

30
Q

What are the different types of atrial fibrillation?

A

Paroxysmal - self terminate in < 7 days
Persistent - Requiring therapy to cardiovert
Permanent - unable to maintain sinus rhythm

31
Q

What is the Vaughan Williams Classification of Class III antiarrhythmic drugs? `

A

Class III- Potassium channel blockers
Prolongs the repolarisation but unclear
E.g. amiodarone

32
Q

Despite both rhythm control and rate control strategies having the same survival advantage, what other findings were discovered about rhythm control?

A

All patients were on antiguagulation initially, but those in the
Rhythm control could stop anticoagulation discontinuation as they were thought to maintain sinus rhythm for 4 consecutive weeks

Increased hospitalisation- a nonsignificant trend was noted where those in the RATE control strategy had a decreased mortality.

ADE profile of class I and Class III agents

33
Q

What is the Vaughan Williams Classification of Other Class antiarrhythmic drugs?

A

e.g. Digoxin
Increases vagal tone - slows heart rate/ blocks AV conduction

Inhbits Na+/K+ ATPase
Na+ s retained in the cell, Ca2+ is retained
Increased contraction when triggered

34
Q

What is atrial fibrillation?

A

Most common cardiac arrhythmia

Increases risk of Stroke, Chronic heart failure, death

Causes remodelling of atria

35
Q

What is the ADE profile of Class III agents?

A

E.g. Amiodarone, sotalol
Effective (apporx 70% sinus rhythm in 1 year)
Multiple ADEs
torsade de pointes, pulmonary toxicity & thyroid dysfunction with amiodarone

36
Q

What is the AFFIRM trial?

A

Atrial fibrillation followup Investigation of Rhythm management

The first and largest trial to compare rate-control and rhythm-control strategies for treatment of atrial fibrillation

There was no survival advantage between rate-control by using betablockers, calcium channel blockers and/or digoxin, and rhythm control strategies.

Rhythm control is associated with a trend towards increased mortality

37
Q

Despite both rhythm control and rate control strategies having the same survival advantage, what other findings were discovered about rhythm control?

A

All patients were on antiguagulation initially, but those in the
Rhythm control could stop anticoagulation discontinuation as they were thought to maintain sinus rhythm for 4 consecutive weeks

Increased hospitalisation- a nonsignificant trend was noted where those in the RATE control strategy had a decreased mortality.

ADE profile of class I and Class III agents

38
Q

What are ADE

A

Adverse drug events

39
Q

What is the ADE profile of Class I agents?

A

E.g. Flecanide, Quinidine,
Minimal use due to safety profile
Anticholinergic effects (e.g. Glaucoma, dry eyes etc)
Torsade de pointes (polymorphic ventricular tachycardia, prolonged QT duration)

40
Q

What is the ADE profile of Class III agents?

A

E.g. Amiodarone, sotalol
Effective (apporix 70% sinus rhythm in 1 year)
Multiple ADEs
torsade depointes, pulmonary toxicity & thyroid dysfunction with amiodarone

41
Q

What are the two main components of Atrial Fibrillation management?

A

Rate control

Anticoagulation

42
Q

Describe the overview of Atrial Fibrillation Treatment

A

Newly detected Atrial Fibrillation leads to:

1) Thromboembolic Risk
- Assess and manage thromboemboic risk and cardioversion risk factors

2)Decide between Rate or Rhythm Control
Symptoms, age, paraxsmal/permanent AF, underlying heart disease are factors you should consider

Both outcomes lead to:
Follow up monitoring (as appropriate)
Reassess thromboembolic risk, consider warfarin (INR) control and ensure rate control.

43
Q

What is the QT period usually for?

A

Time for ventricular depolarisation and subsequent repolarisation

44
Q

What is widening of the QT interval usually caused by?

A

Factors impairing inward/outward ion movement
e.g. Na+ influx or K+ efflux
This prolongs repolarisation and QT Interval

45
Q

What does QT prolongation increase the risk of, and what drugs can be used to treat/prevent this?

A

Risk of torsade de pointes (type of ventricular tachyarrhythmia which can lead to VT)

  • Fluconazole (potent enzyme inhibitor)
  • Methadone - (HERG gene which blocks potassium)
46
Q

How does blood pressure affect arrhythmia?

A

Arrhythmias can be due to many things,
High blood pressure is one of these causes.
Other causes include
Simultaneous occurrence of a heart attack
scarring of heart tissue from prior heart attack
Changes to heart structure e.g. cardiomyopathy
Blocked arteries in your heart (Coronary heart disease)
Diabetes
Hyperthyroidism
Smoking
Excessive alcohol/caffeine consumption
Stress
Medications
Dietary supplements/herbal medicines
Electrical shock
Air pollution

From: mayo clinic

47
Q

Describe the overview of Atrial Fibrillation Treatment

A

Newly detected Atrial Fibrillation leads to:

1) Thromboembolic Risk
- Assess and manage thromboemboic risk and cardioversion risk factors

2)Decide between Rate or Rhythm Control
Symptoms, age, paraxsmal/permanent AF, underlying heart disease are factors you should consider

Both outcomes lead to:
Follow up monitoring (as appropriate)
Reassess thromboembolic risk, consider warfarin (INR) control and ensure rate control.

48
Q

What is the QT period usually for?

A

Time for ventricular depolarisation and subsequent repolarisation

49
Q

What is widening of the QT interval usually caused by?

A

Factors impairing inward/outward ion movement
e.g. Na+ influx or K+ efflux
This prolongs repolarisation and QT Interval

50
Q

What does QT prolongation increase the risk of, and what drugs can be used to treat/prevent this?

A

Risk of torsade de pointes (type of ventricular tachyarrhythmia which can lead to VT)

  • Fluconazole (potent enzyme inhibitor)
  • Methadone - (HERG gene which blocks potassium)
51
Q

How does blood pressure affect arrhythmia?

A

Arrhythmias can be due to many things,
High blood pressure is one of these causes.
Other causes include
Simultaneous occurrence of a heart attack
scarring of heart tissue from prior heart attack
Changes to heart structure e.g. cardiomyopathy
Blocked arteries in your heart (Coronary heart disease)
Diabetes
Hyperthyroidism
Smoking
Excessive alcohol/caffeine consumption
Stress
Medications
Dietary supplements/herbal medicines
Electrical shock
Air pollution

From: mayo clinic

52
Q

What are the two common arrhythmias that may be encountered in clinical practice?

A

Atrial Fibrillation,

QT interval prolongation

NancyPHARM205 (15 decks)

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