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Core clinical problems > 54. Palpitations/abnormal heart rhythm > Flashcards

54. Palpitations/abnormal heart rhythm Flashcards

1
Q

Assessment of new palpitations/abnormal ecg

A

ABCDE
A
B
C - IV access, VBG for electrolytes, ECG
D
E

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2
Q

when assessing someone with tachy or brady, what life threatening features do you need to check for?

A

Shock: SBP <90, pallor, sweating, cold, clammy, confused, <GCS
Syncope
Myocardial ischaemia
Severe HF

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3
Q

Management of tachycardia with life-threatening features

A
  • Synchronised DC shock up to 3x, with sedation or anaesthesia if conscious
  • If unsuccessful: amiodarone IV 300 mg over 10-20 mins, repeat DC shock
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4
Q

Management of bradycardia with lifethreating fetaures

A

Atropine 500 mcg IV

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5
Q

Hitsory taking palpitations

A

PC: palpitations? Associated with syncope?
Anxiety?

DHx: sympathomimetics eg amphetamines, beta-agonists eg salbutamol

SHx: caffeine, alcohol, stress?, RECREATIONAL DRUGS

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6
Q

what is normal sinus rhythm

A

Regular rhythm at a rate of 60-100 bpm (or age-appropriate rate in children)
Each QRS complex is preceded by a normal P wave
Normal P wave axis: P waves upright in leads I and II, inverted in aVR
The PR interval remains constant
QRS complexes < 100 ms wide (unless co-existent interventricular conduction delay present)

Pacemaking impulses arise from the sino-atrial node and are transmitted to the ventricles via the AV-node and His-Purkinje system

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7
Q

what is sinus arrythmia

A

sinus rhythm with a beat-to-beat variation in the P-P interval (the time between successive P waves), producing an irregular ventricular rate

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8
Q

management sinus tachycardia

A

treat cause eg pain, fear, infection

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9
Q

management SVT

A
  1. Vagal manourvres
  2. adenosine 6mg –> 12 –> 18
  3. Verapamil or beta blocker (control rate eg it might be atrial flutter)
  4. synchronised DC 3x
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10
Q

causes of narrow complex tachycardia

A

sinus tachycardia
SVT (AVNRT, AVRT)
atrial flutter
fast AF

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11
Q

who shouldn’t be given adenosine

A

Asthma
COPD
Heart failure
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation

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12
Q

what does SVT look like on ECG

A

Due to an area around the AV node causing depolarisation – results in p waves very close to the QRS, or no p waves visible.
On an ECG, SVT looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

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13
Q

management options for SVT recurrent

A

Long-term medication (e.g., beta blockers, calcium channel blockers or amiodarone)

Radiofrequency ablation

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14
Q

what is WPW

A

congenital accessory pathway (AP) and episodes of tachyarrhythmias

evidence of the accessory pathway can be seen on an ECG performed while in normal rhythm

The term is often used interchangeablely with pre-excitation syndrome

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15
Q

what tachyarrythmias can occur in WPW

A

Atrial fibrillation or flutter. Due to direct conduction from atria to ventricles via an AP, bypassing the AV node

Atrioventricular re-entry tachycardia (AVRT). Due to formation of a re-entry circuit involving the AP

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16
Q

ECG features of WPW during normal sinus rhythm

A

WPW

Wide qrs
PR narrow
Wave = delta wave : slurring slow rise of initial portion of the QRS

PR interval < 120ms
Delta wave: slurring slow rise of initial portion of the QRS
QRS prolongation > 110ms
Discordant ST-segment and T-wave changes (i.e. in the opposite direction to the major component of the QRS complex)
Pseudo-infarction pattern in up to 70% of patients — due to negatively deflected delta waves in inferior/anterior leads (“pseudo-Q waves”), or prominent R waves in V1-3 (mimicking posterior infarction)

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17
Q

commonest cause of palpitations in patients with structurally normal hearts

A

AVNRT

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18
Q

triggers AVNRT

A

exertion, caffeine, alcohol, beta-agonists (salbutamol) or sympathomimetics (amphetamines)

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19
Q

what drugs should people with WPW not have

A

should not have adenosine, verapamil or a beta blocker, as these block the atrioventricular node, promoting conduction of the atrial rhythm through the accessory pathway into the ventricles, causing potentially life-threatening ventricular rhythms.

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20
Q

ECG features atrial flutter

A

Rate: tachycardia
Rhythm: regular (can be irregular)
P waves: flutter waves present (sawtooth appearance )
PR interval: F waves are consistent, 2 for every QRS (2:1 or 3:1 is typical
QRS: <0.12 so narrow complex tachycardia

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21
Q

pathophysiology atrial flutter

A

reentrant rhythm through sinoatrial node in atrium

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22
Q

PResentation symptoms AF

A

Asymptomatic
Symptomatic: palpitations, SOB, dizziness or syncope
Symptoms of associated conditions (sepsis, stroke, thyrotoxicosis)

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23
Q

ECG fetaures AF

A

Rate: tachycardia
Rhythm: irregularly irregular
P: absent p waves
QRS: narrow QRS complex tachycardia

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24
Q

pathophysiology AF

A

Disorganised atrial activity. This chaotic electrical activity overrides the regular, organised activity from the sinoatrial node. It passes through to the ventricles, resulting in irregularly irregular ventricular contraction.

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25
Q

Commonest causes of AF

A

SMITH
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

Alcohol and caffeine are lifestyle causes worth remembering.

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26
Q

what is paroxysmal AF

A

Paroxysmal atrial fibrillation refers to episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.

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27
Q

invetsigations for patients ?paroxysmal AF with normal ECG

A

24-hour ambulatory ECG (Holter monitor) or

Cardiac event recorder lasting 1-2 weeks
- The device automatically detects and records any abnormal heart rhythm, but you can also ‘activate’ an ECG recording if you start to experience symptoms.

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28
Q

What is valvular AF

A

Valvular atrial fibrillation is AF with significant MITRAL STENOSIS or a MECHANICAL HEART VALVE. The assumption is that the valvular pathology has led to atrial fibrillation.

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29
Q

principles of treating AF

A

Rate or rhythm control
Anticoagulation to prevent strokes

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30
Q

most common combination drugs AF

A

Beta blocker bisoprolol for rate control
DOAC for anticoagulation

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31
Q

questions to ask yourself to see which approach to use treating AF

A

do they need immeidate cardioversion? <48 hrs, LT haemodynamic instability

do they need delayed cardioversion? reversible, HF, symptoms despite rate control

are there any CI to any of the drugs?

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32
Q

when should immediate cardioversion be used for AF management

A
  • Present for less than 48 hours
  • Causing life-threatening haemodynamic instability
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33
Q

options for immediate cardioversion in AF

A

Pharmacological cardioversion: flecainide or amiodarone

Electrical cardioversion

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34
Q

what is the drug of choice in patients with structural heart disease immediate cardioversion

A

amiodarone

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35
Q

when should delayed cardioversion be used as the treatment for AF

A

A reversible cause for their AF
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

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36
Q

how is delayed cardioversion carried out - prior, on the day, after

A

Prior
- rate controlled whilst waiting for cardioversion
- anticoagulated for at least 3 weeks before

On the day:
Electrical cardioversion is recommended.

After:
LT rhythm control is with:
1. Beta blockers
2. Dronedarone
3. Amiodarone is useful in patients with heart failure or left ventricular dysfunction

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37
Q

first line management of AF

A

Rate control is first line as long as they dont meet the above/below criteria:
A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

  1. Beta blocker first-line (e.g., atenolol or bisoprolol)
  2. Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
  3. Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)
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38
Q

Management paroxysmal AF

A
  1. Flecainide is usual pill-in-pocket drug
    + Anticoagulation based on chadsvasc as they would with normal AF
39
Q

management refractory AF

A

Left atrial ablation
Atrioventricular node ablation and a permanent pacemaker

40
Q

how much does anticoagualtion decrease risk of stroke AF? how much does it increase risk of bleed

A

Anticoagulation reduces the risk of stroke by about 2/3.

patients with atrial fibrillation have around a 5% risk of stroke each year, depending on individual factors. With anticoagulation, patients with atrial fibrillation have around a 1-2% risk of stroke each year

Anticoagulation treatment carries around a 2.5-8% risk of serious bleeding each year, depending on individual factors.

41
Q

interpretation of CHADSVASC score

A

0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation

42
Q

what is part of the orbit score?

A

O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication

43
Q

what is part of chadsvasc score

A

C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)

44
Q

anticoagulation for AF

A

Direct-acting oral anticoagulants (DOACs) first-line

Warfarin second-line, if DOACs are contraindicated

45
Q

reversal agent apixaban and rivaroxaban

A

Andexanet alfa

46
Q

DOAC advantages over warfarin

A

No monitoring is required
No issues with time in therapeutic range (provided they have good adherence)
No major interaction problems
Equal or slightly better than warfarin at preventing strokes in atrial fibrillation
Equal or slightly lower risk of bleeding than warfarin

47
Q

regular broad complex tachycardia - first ddx?

A

assume ventricular tachycardia (unless previously confirmed SVT with bundle branch block)

48
Q

regualr broad complex tachy - treatment?

A

assume ventricular tachycardia

loading dose of amiodarone followed by 24 hour infusion

amiodarone 300mg IV over 30-60 mins

49
Q

apart from VT, what is another cuase of broad complex tachy regualr?

A

SVT w BBB

50
Q

causes of irregualr broad complex tachycardia

A

atrial fibrillation with bundle branch block - the most likely cause in a stable patient

atrial fibrillation with ventricular pre-excitation

torsade de pointes

51
Q

management irregualr broad complex tachycardia

A

seek expert help

magnesium 2g over 10 mins

52
Q

what is polymorphic VT

A

is a form of ventricular tachycardia in which there are multiple ventricular foci with the resultant QRS complex varying in amplitude, axis, and duration. The most common cause of PVT is myocardial ischaemia/infarction.

53
Q

what is torsades?

A

is a specific form of PVT occurring in the context of QT prolongation — it has a characteristic morphology in which the QRS complexes “twist” around the isoelectric line.

54
Q

pathophysiology VT

A

These are caused by a foci in the ventricles discharging at a high frequency. This causes an abnormal spread of charge through the ventricles, resulting in wide and abnormal QRS complexes.

55
Q

ecg features VT

A

QRS is broad
T waves difficult to identify
No p waves
Regular QRS (~200bpm)

56
Q

how to ddx VT from BBB

A

supportive of BBB
- p waves
- qrs same shape as prev normal ecg
- qrs irregualr (AF w BBB)

supportive of VT
- wide qrs >160ms
- left axis deviation

57
Q

what acute thing may cause VT or PVT

A

myocardial infarction

58
Q

causes of prolonged QT

A

congenital

drugs
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)

other
hypocalcaemia, hypokalaemia, hypomagnesaemia
acute myocardial infarction
myocarditis
hypothermia
subarachnoid haemorrhage

59
Q

management long qt syndrome

A

avoid drugs which prolong the QT interval and other precipitants if appropriate (e.g. Strenuous exercise)

beta-blockers*** not sotalol

implantable cardioverter defibrillators in high risk cases

60
Q

what is long qt syndrome

A

an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death.

61
Q

features long qt syndrome eg symptoms

A

Long QT1 - usually associated with exertional syncope, often swimming

Long QT2 - often associated with syncope occurring following emotional stress, exercise or auditory stimuli

62
Q

bradycardia with life threatening symptoms. You have given atropine but not a good response, what next?

A
  • atropine 500mcg IV repeated up to 3g
  • transcutaneous pacing
  • other drugs eg adrenaline infusion
63
Q

bradycardia with life threatening symptoms. You have given atropine and there has been a goos response, what next?

A

Assess for any risk of asystole?
- recent asystole?
- mobitz type 2 AV block
- complete heart block with broad qrs
- ventricualr pause > 3 secs

If yes to risk: specialist help is indicated to consider the need for transvenous pacing

if no to risk: observe

64
Q

causes sinus bradycardia

A

athletic training, fainting attacks, hypothermia, myxoedema, seen immediately after MI

65
Q

life thretaening causes bradycardia

A
  • hyoxia in children
  • mobitz type 2 block
  • complete heart block
  • pause > 3s on ecg
66
Q

ecg features first degree heart block

A

PR interval is greater than 0.2s

67
Q

pathophysiology mobitz 1 vs 2

A

Mobitz I is usually due to a functional suppression of AV conduction (e.g. due to drugs, reversible ischaemia),

Mobitz II is more likely to be due to structural damage to the conducting system (e.g. infarction, fibrosis, necrosis)

68
Q

what is second degree heart block

A

This is where there is an intermittent absence of QRS complexes – and thus an indication that there is a blockage somewhere between the AV node and the ventricles.

69
Q

ecg features of mobitz 1

A

progressive lengthening of the PR interval followed by an absence of the QRS, then a shortened PR interval and normal QRS, and the cycle begins again. The cycle is variable in length, and the R-R interval shortens with the lengthening of the PR interval

70
Q

causes 1st degree heart block

A

First degree heart block is not in itself very important – it can be a sign of coronary artery disease, acute rheumatic carditis, digoxin toxicity or electrolyte disturbance, but does not usually require treatment.

71
Q

causes mobitz 1

A

Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
Increased vagal tone (e.g. athletes)
Inferior MI
Myocarditis
Following cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)

72
Q

what is mobitz 2, ecg features?

A

regular rhythm, and a fairly constant PR interval, but every now and again there is an absent QRS (pictured above). basically for every QRS, there are 2 or 3 p waves.

73
Q

are complexes narrow or broad in mobitz 2?

A

In around 75% of cases, the conduction block is located distal to the Bundle of His, producing broad QRS complexes.

In the remaining 25% of cases, the conduction block is located within the His Bundle itself, producing narrow QRS complexes.

74
Q

causes mobitz 2

A

Anterior MI (due to septal infarction with necrosis of the bundle branches)
Idiopathic fibrosis of the conducting system (Lenègre-Lev disease)
Cardiac surgery, especially surgery occurring close to the septum e.g. mitral valve repair
Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)
Autoimmune (SLE, systemic sclerosis)
Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)
Hyperkalaemia
Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone

75
Q

management mobitz 2

A

if causing bradycardia with LT features - atropine then transcutaenous pacing

if stable
immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker

76
Q

what are fixed conduction ratios?

A

there is one normal cycle, then one cycle with an absent QRS (2:1) or there is one normal cycle, then two cycles without a QRS (3:1)

Fixed ratio blocks can be the result of either Mobitz I or Mobitz II conduction.

77
Q

features complete heart block symptoms/signs

A

syncope
heart failure
regular bradycardia (30-50 bpm)
wide pulse pressure

JVP: cannon waves in neck
Cannon wave occurs in conditions with atrioventricular dissociation and right atrial contraction against a closed tricuspid valve.

variable intensity of S1

78
Q

pathophysiology complete heart block

A

atrial contraction is normal, but no beats are conducted to the ventricles.
The ventricles are still excited by their own internal ‘ectopic pacemaker’ system!

79
Q

ecg features complete heart block

A

P wave ~90/min (more p waves than QRS complexes)
QRS ~36/min
Variable PR intervals
No relationship between P wave and QRS complexes, but both are present.
Abnormally shaped QRS due to abnormal spread of conduction throughout ventricles
QRS will generally be broad (~160ms – as opposed to a maximum of 120ms in a normal heart – 4 little squares as opposed to 3 little squares)
Right axis deviation
Escape rhythms present

80
Q

causes complete heart block

A

MI – it will occur acutely, and is often transient
Chronic – often due to fibrosis around the Bundle of His, or bundle branch block of both branches
Always indicates underlying disease – more often fibrosis then ischaemia

81
Q

Management complete heart block

A

Patients with third degree heart block are at high risk of ventricular standstill and sudden cardiac death

They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker

82
Q

pathophysiology BBB

A

wave of depolarisation reaches intraventricualr septum fine = normal PR

block in the bundle branch –> the time taken for depolarisation to spread throughout the ventricles is prolonged = wide QRS

83
Q

why do you get RSR in RBBB V1

A

right bunder branch block. left ventricular depolarisation continues as normal, and produces a normal R and a normal S wave. But after this has happened, the right ventricle then depolarises, and causes a second R wave (R1).

84
Q

features ecg RBBB

A

MaRRoW

M in V1 RSR’

W in V6 Wide slurred S wave

85
Q

features ecg LBBB

A

WiLLiaM

W in V1 Wide slurred S wave

M in V6 RSR’

86
Q

causes RBBB

A

atrial septal defect

87
Q

causes LBBB

A

Ischaemic disease - if the patient has had recent chest pain, LBBB is likely to indicated MI, and thus thrombolysis should be considered.

Aortic stenosis

If the patient is asymptomatic, then no treatment is needed

88
Q

features ventric ectopic

A

Absence of P wave before the QRS
Wider, taller QRS complex (>120ms)
Often immediately follows a T wave
Has a discordant T wave (T wave point in opposite direction to major portion of QRS)

89
Q

management vent ectopics

A

Rule out structural heart disease with an echo
If present – refer to cardiology

assess FHx
If all the above is normal:
Reassure
Consider beta-blocker or calcium-channel blocker

90
Q

features ecg hypokalameia

A

U have no POT, you have no T, you have a long PR and a long QT

  • prominent u waves
  • T wave inversion
  • long QT
  • ST depression
91
Q

in any pt with arrythmia, what electrolytes in particualr should be checkeD?

A

Check both potassium and magnesium levels in any patient with an arrhythmia

Replace potassium to ≥ 4.0 mmol/L and magnesium to ≥ 1.0 mmol/L to stabilise the myocardium and protect against arrhythmias – this is standard practice in most CCUs and ICUs

92
Q

what other electrolyte abnormality is associated with hypokalaemia

A

hypomagnesaemia

93
Q

ecg changes hypomagnesia

A

Prolonged PR interval
Prolonged QT interval
Atrial and ventricular ectopy
Predisposition to ventricular tachycardia and torsades de pointes

94
Q

ecg features hypocalcaemia

A

prolonged QT and torsades

Core clinical problems (94 decks)

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