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Cardiovascular Medicine > Arrhythmias and Conduction Defects > Flashcards

Arrhythmias and Conduction Defects Flashcards

1
Q

What is an arrhythmia?

A
  • any deviation from the normal cardiac rhythm
  • due to abnormal electrical activity of heart
  • arise from disturbance of generation or conduction of normal cardiac impulses
  • can be intermittent or continuous
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2
Q

What are cardiac causes of arrhythmias?

A
  • Ischaemic heart disease
  • Structural changes
  • Cardiomyopathy
  • Pericarditis
  • Myocarditis
  • Aberrant conduction pathways
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3
Q

What are non-cardiac causes of arrhythmias?

A
  • Caffeine
  • Smoking
  • Alcohol
  • Pneumonia
  • Drugs (beta blockers, digoxin, tricyclics)
  • Metabolic imbalance (eg. hyperkalaemia)
  • Phaeochromocytoma
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4
Q

What are the various types of ECG monitoring?

A
  • ECG → simple 12-lead, snapshot of heart, may miss
  • Telemetry → inpatient, signals shown on screen and watched continuously, reserved for high risk dangerous arrythmias
  • Exercise ECGs → pts exercise, BP and ECG monitored looking for changes (eg. delta waves) and arrhythmias
  • Holter monitors → pt wears monitor, records rhythm for 24h-7d whilst they go about normal life, analysed later
  • Loop recorders → record only when activated, planted under skin and useful in pts w/ infrequent episodes
  • Pacemakers & ICDs → record details of cardiac electrical activity, also therapeutic
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5
Q

Disturbances of cardiac rhythm are common, often benign, often intermittent and occasionally severe.

What are the two main types of arrhythmia?

A
  • bradycardia - HR slow, <60 during day or <50 during night
  • tachycardia - HR fast, >100
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6
Q

What are the bradycardias?

A
  • Sinus bradycardia
  • 1st degree (AV) block
  • 2nd degree (AV) block
    • Mobitz I / Wenkebach
    • Mobitz II
  • Complete (AV) heart block
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7
Q

What are causes of sinus bradycardia?

A
  • normal - esp in athletes + elderly
  • inc vagal tone - cushing’s reflex*
  • drugs - bblockers, ccbs, digoxin, etc
  • ischaemia/infarction - right coronary artery

*cushing’s reflex is bradycardia, hypertension and irregular RR - caused by a raised ICP, inc pressure in skull -> inc vagal tone

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8
Q

What is 1st degree heart block?

A
  • prolonged PR interval (> 200ms / 0.2s)
  • Every atrial depolarisation is followed by conduction to the ventricles, but with delay
  • eg. if AVN or bundle of His damaged -> prolonged PR interval
  • common in healthy adults, asymptomatic
  • no specific treatment required
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9
Q

What is Mobitz type 1?

A
  • Type 1 (2o) AKA Wenkebach
  • Progressive PR interval prolongation, until a P wave fails to conduct
  • No treatment required
  • Where the QRS is dropped, the PR interval after is short but the one before is much longer
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10
Q

What is Mobitz type 2?

A
  • PR interval is constant but the P wave is often not followed by a QRS complex
  • Signifies block at an infranodal level such as the bundle of His
  • There is a greater risk of this type to progress into complete heart block
  • Consider pacemaker due to risk of developing CHB
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11
Q

What is complete heart block?

A
  • No synchrony between P and QRS AKA complete atrioventricular dissociation
  • Regular P waves, regular QRS complexes but NO associated between the two
  • By chance, the atria and ventricles may contract at same time → atrial blood occurs against a closed tricuspid → blood refluxes back up the jugular veins → cannon waves
  • Ventricles can pace themselves
  • Rx: permanent pacemaker
  • URGENT specialist referral!
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12
Q

What are the clinical features of complete heart block?

A
  • Syncope
  • Heart failure
  • Regular bradycardia (30-50 bpm)
  • Wide pulse pressure
  • JVP: cannon waves in neck
  • Variable intensity of S1
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13
Q

What 4 adverse clinical presentations are important to recognise in severe bradycardia and what should be the management if any of these arise?

A

Manage based on adverse signs:

  • shock
  • syncope
  • myocardial ischaemia
  • heart failure

If any of these 4 arise -> TREAT -> atropine 500mcg x 6

  • ?betablocker overdose —-> glucagon
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14
Q

The diagram shows typical features of left bundle branch block (LBBB).

What is the most common way to remember the difference (on ECG) between LBBB and RBBB?

A

WiLLiam vs MaRRow

  • LBBB → ‘W’ in V1 and ‘M’ in V6
  • RBBB → ‘M’ in V1 and ‘W’ in V6
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15
Q

What are causes of LBBB?

A
  • Ischaemic heart disease
  • HTN
  • Aortic stenosis
  • Cardiomyopathy
  • Rare → idiopathic fibrosis, digoxin toxicity, hyperkalaemia

New LBBB is always pathological + may be sign of MI. Diagnosing MI for pts with existing LBBB is tricky. The Sgarbossa criteria can help with this.

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16
Q

What are the causes of RBBB?

A
  • Normal variant - more common w/ increasing age
  • Right ventricular hypertrophy
  • Chronically increased right ventricular pressure eg. cor pulmonale
  • Pulmonary embolism
  • Myocardial infarction
  • Atrial septal defect
  • Cardiomyopathy or myocarditis
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17
Q

Tachyarrhythmias are when the heart is beating >100bpm. How can tachyarrhythmias be classified?

A
  • Broad complex (QRS >120ms) -> Ventricular tachycardias
    • arise from ventricles
    • reflect disorganised, delayed depolarisation (hence broad QRS)
  • Narrow complex (QRS <120ms) -> Supraventricular tachycardias
    • arise from atrium or atrioventricular junction
    • reflect organised efficient electrical activity originating above AV node (hence narrow QRS)
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18
Q

What is atrial fibrillation?

A
  • Technically an SVT
  • Characterised by uncoordinated atrial activity on surface eCG
  • With fibrillatory waves of varying shapes, amplitudes and timing
  • Associated with an irregularly irregular ventricular response when AV conduction is in tact
  • Cardiac output drops by 10-20% as ventricles aren’t primed reliably by atria
  • AF is common in elderly (~9%)
  • Main risk = embolic stroke
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19
Q

What are the cardiac causes of AF?

A
  • Heart failure (24%)
  • IHD (33%)
  • Hypertension (26%)
  • Valvular heart disease (7%)
  • MI
  • Cardiomyopathy
  • Sick sinus syndrome
  • Constrictive pericarditis
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20
Q

What are non-cardiac causes of AF?

A
  • Alcohol intoxication or withdrawal
  • Hyperthyroidism
  • PE
  • Electrolyte abnormalities (hypokalaemia)
  • Pneumonia
  • Caffeine
  • Lone AF (no cause, probably genetic)
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21
Q

What are clinical features of AF?

A
  • May be asymptomatic
  • Chest pain
  • Palpitations
  • Dyspnoea
  • Faintness
  • Signs → irregularly irregular pulse, apical pulse rate greater than radial, signs of LVF (pulm oedema)
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22
Q

What investigations can be done for AF?

A
  • Bedside → ECG looking for absent P waves, irregularly irregular QRS complexes
  • Bloods → FBC, U+Es, TFTs, cardiac biomarkers, CRP
  • Imaging → CXR (HF, pulm oedema), Echo (left atrial enlargement, mitral valve disease, poor LV function)
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23
Q

AF can broadly categorised into different types.

When is a ‘first detected episode’ of AF diagnosed?

A

Irrespective of whether it is symptomatic or self-terminating

24
Q

What is persistent AF?

A
  • Recurrent episodes of AF
  • Not self-terminating
  • Typically last greater than 7 days
25
Q

What is paroxysmal AF?

A
  • Recurrent episodes of AF
  • Spontaneously terminate
  • Episodes last less than 7 days (typically <24 hrs)
  • Can sometimes occur in fit athletes
26
Q

What is permanent AF?

A
  • Continuous AF
  • Cannot be cardioverted or if attempts to do so are deemed inappropriate
27
Q

There are two key parts of managing patients with AF: 1) Rate/rhythm control and 2) reducing stroke risk.

What is meant by rate vs rhythm control?

A
  • Rate control → accept that the pulse will be irregular, but slow the rate down to avoid negative effects on cardiac function
  • Rhythm control → try to get pt back into, and maintain, normal sinus rhythm. This is termed cardioversion. Drugs (pharm cardioversion) and synchronised DC electrical shocks (electrical cardioversion) may be used for this purpose

For many years, predominant approach was to maintain pt in sinus rhythm - changed in early 00s and now majority of pts are managed with a rate control strategy. NICE advocate using a rate control strategy except in a number of specific situs eg. coexistent heart failure, firs tonset AF or where there is an obvious reversible cause

28
Q

Factors favouring rate control include being older than 65yrs and a history of IHD. What are the options for rate control?

A
  • First line → beta-blocker eg. bisoprolol
  • Second line → rate-limiting calcium channel blocker eg. diltiazem
  • If one drug does not control rate adequately, NICE recommend combo therapy with any 2 of: beta-blocker, diltiazem & digoxin. Use digoxin only if pt sedentary.
29
Q

Factors favouring rhythm control include being younger than 65y, symptomatic, first presentation, lone AF or 2o to a correct precipitant (eg. alcohol), and congestive heart failure.

What are the options for rhythm control?

A
  • If AF < 48 hrs:
    • pts should be heparinised
    • immediate cardioversion can take place
    • electrical → DC cardioversion
    • pharm → amiodarone (structural heart disease) or flecainide/amiodarone (without structural heart disease)
  • If AF > 48 hrs / timing uncertain
    • anticoag required 3wks prior to cardioversion, or
    • perform TOE to exclude thrombus → then heparin + DC cardioversion immediately
    • continue anticoag for 4 wks after DC
30
Q

When cardioverting, why do patients need to have presented with <48 hrs of symptoms or to be anticoagulated before?

A

When considering cardioversion it is very important to remember that the moment a patient switches from AF to sinus rhythm presents the highest risk for embolism leading to stroke. Imagine the thrombus formed in the fibrillating atrium suddenly being pushed out when sinus rhythm is restored. For this reason patients must either have had a short duration of symptoms (less than 48 hours) or be anticoagulated for a period of time prior to attempting cardioversion.

31
Q

When do you acutely treat AF and what needs to be done?

A
  • If the patient has adverse signs (shock, MI, syncope, heart failure):
    • ABCDE
    • Get senior help
    • DC Cardioversion (synchronised shock, start at 120-150J) +/- amiodarone if unsuccessful
  • If pt stable and AF started <48hrs ago → rate or rhythm control; rhythm control @ SGH:
    • IV flecainide (1-2 mg/kg over 10 mins; max dose 150mg)
    • In presence of HF or acute ischaemia, amiodarone should be used (300mg bolus via large bore cannula in large vein or centrally, then a 900mg 24hr infusion)
  • If pt stable and AF started >48hrs ago or unclear time of onset → RATE control (eg. w/ bisoprolol or diltiazem). If rhythm control chosen, the patient MUST be anticoagulated for >3wks first!
32
Q

How is paroxysmal AF managed?

A

‘Pill in the pocket’ (eg. Sotalol or flecainide PRN) may be tried if:

  • Infrequent AF
  • BP >100 mmHg
  • No past LV dysfunction

Anti-coagulate if needed and consider ablation of symptomatic or frequent episodes

33
Q

How is anticoagulation used in acute AF?

A
  • Use HEPARIN until full risk assessment for emboli made
  • E.g: AF started <48hr ago and elective cardioversion planned, if >48hr, ensure >3wks of therapeutic anticoagulation before elective cardioversion
  • Use DOAC (eg. apixaban) or warfarin (target INR 2-3) if high risk of emboli (eg. past ischaemic stroke, TIA or emboli, high BP and >75yrs, coronary disease)
34
Q

How is anticoagulation used for chronic AF?

A
  • May be paroxysmal, persistent or permanent
  • In all cases, need for anticoag should be assessed using the CHA2DS2-VASC score to assess embolic stroke risk and balancing this against risk of anticoagulation to the patient, assessed with the HAS-BLED score
35
Q

How do DOACs work?

A
  • Examples: Rivaroxaban, apixaban
  • Factor Xa inhibitors
  • Do not require regular monitoring and dose adjustment, just a quarterly assessment and annual blood test
  • They offer an attractive alternative to warfarin
  • CIs: severe renal/liver impairment, active bleeding, reduced clotting factors
36
Q

How does warfarin work?

A
  • Inhibits reductase enzyme responsible for regenerating active form of Vit K
  • Produces a state analogous to Vit K deficiency
  • In UK, warfarin tablets are 0.5mg (white), 1mg (brown), 3mg (blue) or 5mg (pink)
37
Q

What is atrial flutter?

A
  • Form of SVT characterised by a succession of rapid atrial depolarisation waves
  • Generally results from structural or functional conduction abnormalities of atria
  • It can be precipitated by toxic and metabolic conditions such as thyrotoxicosis or pericarditis
  • Patients taking anti-arrhythmics for AF may convert to atrial flutter
38
Q

What are ECG findings for atrial flutter?

A
  • Classic ‘sawtooth’ appearance
  • As underlying rate is often around 300/min, the ventricular or HR is dependent on the degree of AV block
  • For example, if there is a 2:1 block the ventricular rate will be 150bpm
  • Flutter waves may be visible following carotid sinus massage or adenosine
39
Q

What is the management of atrial flutter?

A
  • Similar to AF although meds may be less effective
  • Atrial flutter is more sensitive to cardioversion, DC > pharm; start with 70-120J
  • Recurrence rates are high so radiofrequency ablation often recommended for long-term management
40
Q

Whilst strictly speaking the term supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin, the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

What is AVNRT?

A
  • Most common cause of SVT (~80%)
  • Caused by small re-entry circuit involving AVN and surrounding atrial tissue
  • 2x common in women
  • Often strikes suddenly w/out obvious provocation
  • Triggers → coffee / alcohol / exertion
41
Q

What are the two pathways in AVNRT?

A

Both predominantly within AV node:

  • Short effective refractory period and slow conduction
  • Long effective refractory period and fast conduction

In sinus rhythm, the atrial impulse that depolarises the ventricle usually conducts through the fast pathway. If the atrial impulse occurs early when the fast pathway is still refractory, the slow pathway takes over. It then travels back through the fast pathway which has already recovered excitability, thus initiating the most common ‘slow-fast’, or typical AVNRT.

42
Q

AVRT occurs when electrical signal conducts abnormally between the atria and ventricles usually by accessory pathways.

Which condition is AVRT almost always seen in?

A
  • Wolff-Parkinson-White syndrome (WPWS)
  • Most of the time, pts w/ WPWS have a normal sinus rhythm
  • Tendency for pre-excitation is apparent in the form of delta waves → slow depolarisation preceding the R wave
  • This represents spread of action potential ‘leaking down’ accessory pathway, where it’s conducted more slowly than action potentials carried by bundle of his
  • Type A → left-sided pathway, dominant R wave in V1
  • Type B → right-sided pathway, no dominant R wave in V1
43
Q

What are associations of Wolff-Parkinson-White?

A
  • HOCM
  • Mitral valve prolapse
  • Ebstein’s anomaly
  • Thyrotoxicosis
  • Secundum ASD
44
Q

For management of AVNRT and AVRT, how can AVN blockade be achieved?

A
  • Vagal manoeuvres → carotid sinus massage / valsalva manoeuvre
  • IV adenosine if vagal manoeuvres don’t work: 6mg → 12mg → 12mg
    • verapamil preferred in asthmatics
  • Electrical cardioversion

Can prevent episodes with beta-blockers and radiofrequency ablation

45
Q

How are broad-complex tachycardias identified on ECG?

A
  • Rate > 100
  • QRS > 120ms

If no clear QRS complexes → VF or asystole

46
Q

Monomorphic ventricular tachycardia is very common. What symptoms may it present with?

A
  • Moderate discomfort (haemodynamically stable tachycardia)
    to. ..
  • Profound collapse or arrest (haemodynamically unstable tachycardia)
47
Q

What are the commonest causes of monomorphic ventricular tachycardia?

A
  • Acute infarction / ischaemia
  • Chronic LV scarring after infarction
48
Q

Monomorphic VT - first get the diagnosis correct and identify the underlying rhythm, if this cannot be obtained bc of collapse then urgent DC shock is required.

What are the ECG features of VT?

A
  • Wide QRS complexes (>0.14s or >3.5 small sq)
  • AV dissociation sometimes w/ capture and fusion beats
    • capture beat → normal QRS complex between abnormal beats
    • fusion beats → ‘normal beat’ fuses w/ VT complex to create an unusual complex
  • A leftward axis shift compared to sinus rhythm
  • Any previous history of IHD (MI, PTCA, CABG)

Most instances of VT can be correctly diagnosed but if in doubt treat broad complex tachycardia as VT

49
Q

What is the management of VT?

A
  • Connect pt to cardiac monitor + have defib to hand
  • O2 sats, if < 90% → supplemental oxygen
  • Correct electrolyte abnormalities, esp K+ and Mg+
  • Check for adverse signs (shock, MI, syncope, HF)
  • Obtain 12-lead ECG and obtain IV access
50
Q

How do you treat haemodynamically unstable VT?

A
  • Synchronised DC shock
  • Follow arrest protocol
51
Q

How do you treat VT if haemodynamically stable?

A
  • Lidocaine 1.5mg/kg IV → if this terminates tachycardia continue as an infusion at 2mg/min for up to 24hrs (use w/ caution in severe left ventricular impairment)
  • If tachycardia continues → additional lidocaine bolus of 0.5-0.75 mg/kg
  • Otherwise consider giving amiodarone (300mg bolus via large bore cannulae in large vein or centrally, then a 900mg 24hr infusion)
  • If drug therapy fails, or pt has poor cardiac fxn → DC cardioversion (150-200L biphasic) under sedation is the best therapy
52
Q

How is polymorphic VT different to monomorphic VT?

A
  • Less common than monomorphic VT
  • Causes presyncope, syncope or cardiac arrest
53
Q

What is Torsade de pointes?

A
  • ‘Twisting of the points’
  • Polymorphic VT assoc w/ long QT interval
  • Causes: acquired vs congenital
54
Q

What is the management of Torsade de pointes?

A
  • Congenital → high dose beta-blockers
  • Acquired → stop all predisposing drugs, correct hypokalaemia and give magnesium sulfate (2g IV / 10 mins)
55
Q

What is long QT syndrome (LQTS)?

A
  • Inherited condition associated w/ delayed repolarisation of ventricles
  • May lead to ventricular tachycardia / TdP → sudden death
  • Most common variants caused by defects in alpha subunit of slow delayed rectifier potassium channel
  • Normal corrected QT interval is less than 430 ms in males and 450 ms in females
56
Q

What are the causes of a prolonged QT interval?

A
  • Long QT 1 → exertional syncope, often swimming
  • Long QT 2 → syncope following emotional stress, exercise or auditory stimuli
  • Long QT 3 → after night or at rest

Tx → avoid drugs which prolong QT interval and other preciptants; beta-blockers; implantable cardioverter defibs in high risk cases

57
Q

What is ventricular fibrilation?

A
  • Life-threatening cardiac arrhythmia
  • Most often associated w/ coronary artery disease
  • VF can result from acute MI/ischaemia, or from myocardial scarring from an old infarct
  • Ventricular tachycardia may degenerate into VF
  • Most common cause of death following MI

Cardiovascular Medicine (10 decks)

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