Arrhythmias and ECG Changes Flashcards

1
Q

Describe the tachycardia algorithm

A

ABCDE assessment

If adverse features (shock, syncope, HF, MI) emergency synchronised direct current cardioversion

If haemodynamically stable, management defers on if the tachycardis is narrow (QRS>120) or broad complex (QRS<120)

For regular narrow, vagal manoeuvres is first line, followed by IV 6mg adenosine, followed by further 12mg

For irregular narrow, if <48 hours rhythm control and rate control if >48 hours

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2
Q

What is atrial fibrillation?

A

Disorganised atrial activity resulting in irregularly-irregular AV node stimulation and therefore disregular ventricular response

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3
Q

What are the types of AF?

A

First detected episode

Paroxysmal

  • <7 days, typically <24 hours
  • Episodes terminate spontaneously

Persistent

  • >7 days
  • Amenable to cardioversion

Permanent

  • >7 days
  • Not amenable to cardioversion
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4
Q

What are the causes of atrial fibrillation?

A

HTN

Lung disease

  • PE, Pneumonia

Ischaemic heart disease

Heart failure

Rheumatic heart disease

Hypoxia

Alcohol/Caffeine

Hypercapnia

Mitral stenosis

Atrial septal defect

Thyrotoxicosis

Sepsis

Metabolic abnormalities

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5
Q

Describe the presentation of atrial fibrillation

A

Palpitations

Fatigue

Chest pain

Dizziness

Dyspnoea

Irregularly Irregular pulse

Apical to radial pulse deficit

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6
Q

What ECG signs are seen in atrial fibrillation?

A

Absent P waves

Irregular QRS complex, but normal shape, so therefore an irregular rate

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7
Q

What is involved in rate control of AF?

A

ABCD

B Blocker, first line

  • Bisoprolol
  • Contraindicated in asthma, hypotension

CCB, first line

  • Verapamil
  • Contraindicated in HF

Digoxin, second line

  • Used in hypotension or co-existent HF
  • Contraindicated in younger patients because it increases cardiac mortality
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8
Q

When should rate control be offered in AF?

A

Offer rate control as the first-line strategy to people with AF, except in people

  • Whose AF has a reversible cause
  • Who have heart failure thought to be primarily caused by AF
  • With new-onset AF
  • For whom a rhythm control strategy would be more suitable based on clinical judgement
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9
Q

What is involved in rhythm control of AF?

A

AF = Amiodarone and Flecainide

Amiodarone

  • Older sedentary patients

Flecainide

  • Young patients with structurally normal hearts

Direct current cardioversion

  • If acute/<48 hours can be cardioverted with sedation
  • If >48 hours patient has to be anticoagulated for 3 weeks before cardioversion
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10
Q

What is the mechanism of amiodarone?

A

Blocking potassium channels which inhibits repolarisation and hence prolongs the action potential

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11
Q

Give adverse effects of amiodarone

A

Thyroid dysfunction, both hypothyroidism and hyper-thyroidism

Corneal deposits

Pulmonary fibrosis/pneumonitis

Liver fibrosis/hepatitis

Peripheral neuropathy, myopathy

Photosensitivity

‘Slate-grey’ appearance

Thrombophlebitis and injection site reactions

Bradycardia

Lengths QT interval

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12
Q

What score assesses the risk of stroke in AF?

A

CHAD VASC 2

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13
Q

What factors does the CHADS VAS score take into consideration?

A

C point for congestive cardiac failure

H 1 point for hypertension

A2 2 points if the patient is aged 75 or over.

D 1 point if the patient has diabetes mellitus.

S2 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA)

V 1 point if the patient has known vascular disease

A 1 point if the patient is aged 65-74

S 1 point if the patient is female

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14
Q

What are the groups of anticoagulants?

A

Vitamin K Antagonists

DOAC (direct oral anticoagulant)

  • Direct thrombin inhibitors
  • Direct factor Xa inhibitors

Low molecular weight heparins

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15
Q

When are anti-cogulants used in AF?

A

Males who score 1 or more or females who score 2 or more should be anticoagulated

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16
Q

What anticoagulants are used in AF?

A

Warfarin

  • Requires cover with LMWH for 5 days
  • Only drug lisenced for valvular AF

DOACS

  • Patients are not covered if they miss doses
  • Use if require anticoagulation but unable to carry out regular monitoring

LMWH

  • Rare option in those who cannot tolerate oral
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17
Q

When should anticoagulation be started for patients with AF after a stroke?

A

2 weeks

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18
Q

What is the mode of action of warfarin?

A

Inhibits thromboxane

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19
Q

Give side effect of warfarin

A

Haemorrhage

Teratogenic, although can be used in breastfeeding mothers

Skin necrosis

Purple toes

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20
Q

What has to be monitored with warfarin?

A

INR (International normalised ration)

The ratio of the prothrombin time for the patient over the normal prothrombin time

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21
Q

What is the INR target for AF?

A

2.5

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22
Q

What drugs can increase INR (inhibitors of P450 system)?

A

STICKFACE.COM

Sodium valproate

Ticlodipine

Isoniazid

Cimetidine

Ketoconazole

Fluconazole

Alcohol, Amiodarone

Ciprofloxacin

Erythomycin

Sulfonamides

Chlorampenicol

Omeprazole

Metronidazole

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23
Q

What drugs can decrease INR (inducers of the P450 system?)

A

BS CRAP GPS

Barbituates

St John’s wort

Carbamezapine

Rifampicin

Alcohol (chronic)

Phenytoin

Griseofluvin

Phenobarbital

Sulphonylureas

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24
Q

How do you manage INR of 5.0-8.0 with no bleeding?

A

Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose

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25
Q

How do you manage INR of 5.0-8.0 with minor bleeding?

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Restart when INR <5.0

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26
Q

How do you manage INR >8.0 with no bleeding?

A

Stop warfarin
Give vitamin K 1-5mg by mouth, using the intravenous preparation orally
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0

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27
Q

How do you manage INR >8.0 with minor bleeding?

A

Stop warfarin
Give intravenous vitamin K 1-3mg
Repeat dose of vitamin K if INR still too high after 24 hours
Restart warfarin when INR < 5.0

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28
Q

How do you manage major bleeding with high INR?

A

Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate,if not available then FFP

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29
Q

How do you manage INR <2?

A

Increase dose of warfarin and start LMWH

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30
Q

How long before surgery should warfarin be stopped?

A

In general, warfarin is usually stopped 5 days before planned surgery, and once the person’s INR is less than 1.5 surgery can go ahead

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31
Q

What is the preferred NOAC used in AF for renal impaired patients?

A

Apixaban

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32
Q

What is atrial flutter?

A

SVT characterised by a succession of rapid atrial depolarisation waves

33
Q

What ECG signs are present in atrial flutter?

A

Sawtooth P waves due to AV block

High QRS rate

Flutter waves may be visible following carotid sinus massage or adenosine

34
Q

How is atrial flutter managed?

A

Similar to AF although medication may be less effective

More sensitive to cardioversion however so lower energy levels may be used

Radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

35
Q

What are the two types of SVT?

A

Atrioventricular retentry tachtcardia (AVRT)

Atrioventricular nodal reentrant tachycardias (AVNRT)

36
Q

How can SVT be prevented?

A

B blockers

Radio-frequency ablation

37
Q

How are SVT managed?

A

Vagal manoeuvres

  • Valsalva manouvre
  • carotid sinus massage

IV 6mg Adenosine, infused via large cannula

Followed by further 12mg Adenosine

Later bolus can be repeated until a total of 30mg adenosine

38
Q

What is used instead of adenosine for SVT management in asthmatics?

A

Verapamil

39
Q

Give adverse affects of adenosine

A

Chest pain

Bronchospasm, avoid in asthmatics

Transient flushing

Can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

Infused via large calibre cannula due to short half life (8-10 seconds)

40
Q

What is wolf parkinson white syndrome?

A

Atrioventricular re-entry tachycardia (AVRT) caused by a congenital accessory pathway between the atria and ventricles

41
Q

What ECG signs are seen in WPW?

A

Short PR interval

Wide QRS complexes with a slurred upstroke, known asdelta wave

Left axis deviation if right-sided accessory pathway

Right axis deviation if left-sided accessory pathway

42
Q

What is the management of WPW?

A

Definitive management

  • Radiofrequency catheter ablation of accessory pathway

Medical therapy

  • Amiodarone
43
Q

What is ventricular tachycardia?

A

Broad-complex tachycardia in which heart rate originates in ventricles/does not start in SA node

44
Q

What ECG signs are seen in ventricular tachycardia?

A

Regular broad QRS complex

No P waves

45
Q

What are the types of ventricular tachycardia?

A

Monomorphic VT

  • Most commonly caused by myocardial infarction

Polymorphic VT

  • Prolongation of the QT interval
46
Q

How is ventricular tachycardia managed?

A

Emergency unsynchronised direct current cardioversion, if no palpable pulse (+chest compressions at 100-120bpm)

300mg IV amiodarone

  • Administered in shockable rhythms after delivery of 3rd shock
  • Once off dose

1mg IV adrenalin (1:10,000)

  • Administered in shockable rhythms after delivery of 3rd shock
  • Repeated every other cycle following a shock

Implantable Cardioverter Defibrillator

  • If drug therapy fails
47
Q

What drug is contraindicated in ventricular tachycardia?

A

Verapamil

48
Q

What is ventricular fibrillation?

A

Medical emergency in which there is chaotic depolarisation of ventricles, resulting in arrested pump function and CO

49
Q

What are the causes of ventricular fibrillation?

A

Hypoxia

Hypothermia

Metabolic

  • Hyperkalaemia
  • Hypokalaemia
  • Hypoglycaemia
  • Hypocalcaemia

Thrombosis, coronary or pulmonary

Tension pneumothorax

Cardiac tamponade

50
Q

What are the ECG signs in ventricular fibrillation?

A

Irregular rhythm

Unformed QRS

No P waves

51
Q

What is the management of ventricular fibrillation?

A

Emergency unsynchronised direct current cardioversion

  • Give up to 3 shots followed by CPR if no improvement

300mg IV amiodarone

  • Administered in shockable rhythms after delivery of 3rd shock
  • Once off dose

1mg IV adrenalin (1:10,000)

  • Administered in shockable rhythms after delivery of 3rd shock
  • Repeated every other cycle following a shock
52
Q

How are non shockable rhythms/pulseless electrical activity managed?

A

IV adrenalin immediately

53
Q

What is Torsade’s de Pointes?

A

Polymorphic ventricular tachycardia associated with a long QT interval, which may deteriorate into ventricular fibrillation and hence lead to sudden death

54
Q

What ECG signs are seen in Torsade’s de pointes?

A

Varied QRS in amplitude, axis and duration

Twisted QRS

55
Q

What is the management of Torsade’s de pointes?

A

IV magnesium sulphate

56
Q

What is long QT syndrome?

A

Inherited condition associated with delayed repolarization of the ventricles, which may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death

57
Q

What are the causes of long QT syndrome?

A

Congenital

Electrolyte disturbance

  • Hypokalaemia
  • Hypocalcaemia
  • Hypomagnesaemia

Drugs

  • Amiodarone
  • Erythromycin, Clarithromycin
  • TCA
  • Antipsychotics

MI

Myocarditis

Hypothermia

Subarachnoid haemorrhage

58
Q

How is long QT syndrome managed?

A

B Blockers

Implantable cardioverter defibrillator

59
Q

How is symptomatic bradycardia managed?

A

500mcg IV atropine, up to maximum 3mg

Transcutaneous/external pacing if atropine fails

Adrenaline infusion

60
Q

What is first degree heart block?

A

Delay in transmission of impulses between AV node to ventricles, causing a fixed prolonged PR interval

61
Q

What is second degree heart block type 1?

A

Progressive PR prolongation until p wave no longer conducts through and QRS is dropped

62
Q

What is second degree heart block type 2?

A

Normal/constant PR interval with randomly dropped QRS

63
Q

What is third degree heart block?

A

Complete AV node block, meaning p waves are not associated with QRS at all

64
Q

How is heart block managed?

A

IV atropine, acute setting with hypotension

Transcutaneous/external pacing if atropine fails

Mobitz type 2, pacemaker

65
Q

What is bundle branch block?

A

Block of electrical signal at one bundle branch, causing one ventricle to contract late

66
Q

What are the ECG signs of bundle branch block?

A

Right

  • Broad QRS

Left

  • Broad QRS
67
Q

What cause ST elevation?

A

MI

Pericarditis/myocarditis

Normal variant/’high take-off’

Left ventricular aneurysm

Prinzmetal’s angina/coronary artery spasm

Takotsubo cardiomyopathy

Subarachnoid haemorrhage, although rare

68
Q

What causes ST depression?

A

Secondary to abnormal QRS (LVH, LBBB, RBBB)

Ischaemia

Digoxin

Hypokalaemia

Syndrome X

69
Q

What causes peaked/tall t waves?

A

Hyperkalaemia

Myocardial ischaemia

70
Q

What causes inverted t waves?

A

BBB

Ischaemia/infRCT

PE

Ventricular cardiomyopathy

Digoxin toxicity

Subarachnoid haemorrhage

Brugada syndrome

Normal in children

71
Q

What caues prolonged PR interval?

A

Idiopathic

Ischaemic heart disease

Digoxin toxicity

Hyperkalaemia

Rheumatic fever

Aortic root pathology

Lyme disease

Sarcoidosis

Myotonic dystrophy

Athletes

72
Q

What causes shortened PR interval?

A

WPW syndrome

73
Q

What causes increased p wave amplitude?

A

Cor pulmonale

74
Q

What causes broad notched/bifid p waves?

A

Left atrial enlargement, mitral stenosis

75
Q

What ecg changes can be seen in hypothermia?

A

Bradycardia

‘J’ wave, small hump at the end of the QRS complex

First degree heart block

Long QT interval

Atrial and ventricular arrhythmias

76
Q

what ecg features can be seen in hypokalaemia?

A

U waves

Small or absent T waves, occasionally inversion/flattening

Prolonged PR interval

ST depression

Long QT

77
Q

What ecg signs are seen in hyperkalaemia?

A

Peaked t waves

Flat/abscent p waves

Increased pr interval

Abnormal QRS

78
Q

What ecg features can be seen with digoxin?

A

Down-sloping ST depression (‘reverse tick’, ‘scooped out’)

Flattened/inverted T waves

Short QT interval

Arrhythmias such as AV block, bradycardia

79
Q

What is seen in this ecg?

A

U waves