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Year 3 > Arrhythmias (CV) > Flashcards

Arrhythmias (CV) Flashcards

1
Q

What is an arrhythmia?

A

Any disturbance in the rate, rhythm, site of origin or conduction of the cardiac electrical impulse

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2
Q

What is sinus bradycardia?

A
  • heart rate <50bpm
  • due to SAN dysfunction and/or AV conduction abnormalities
  • physiological in athletes, normal during sleep
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3
Q

Describe the rate, rhythm, P wave, PR interval and QRS complex in sinus bradycardia.

A
  • rate: <50/60bpm
  • rhythm: regular (sinus)
  • P wave: before each QRS, identical
  • PR interval: 0.12-0.20s
  • QRS complex: <0.12s
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4
Q

What are the different types of causes of sinus bradycardia? (4)

A
  • intrinsic causes e.g. age-related, congenital abnormalities, valvular disease, inflammation/infection/AI
  • extrinsic causes e.g. toxins, drugs (BB, digoxin, CCBs, ivabradine, electrolyte abnormalities, hypothermia, opiates)
  • increased vagal tone e.g. vomiting, coughing, glottis stimulation, micturition, defecation
  • other causes e.g. hypothyroidism, anorexia nervosa
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5
Q

What are some clinical features of sinus bradycardia? (5)

A
  • dizziness + light-headedness
  • syncope
  • fatigue
  • exercise intolerance
  • shortness of breath
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6
Q

What might you see on examination of sinus bradycardia? (3)

A
  • cannon a-waves in JVP
  • JVP distension
  • raised ICP
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7
Q

How do we manage acute sinus bradycardia? (4)

A
  • IV atropine, adrenaline, theophylline - increase sympathetic drive/block parasympathetic influences
  • temporary pacing (transcutaneous, transvenous)
  • reverse causes of bradycardia
  • consider permanent pacing
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8
Q

How do we manage asymptomatic sinus bradycardia? (2)

A
  • reassurance, reverse potential causes
  • consider fludrocortisone
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9
Q

What is sinus tachycardia?

A
  • heart rate >100bpm
  • can be a normal physiological response to a systemic process (exercise) or can be a manifestation of underlying pathology
  • decreases diastolic filling time –> decreases stroke volume –> reduces CO
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10
Q

Describe the rate, rhythm, P wave, PR interval and QRS complex in sinus tachycardia.

A
  • rate: >100bpm
  • rhythm: regular (sinus)
  • P wave: before each QRS, identical
  • PR interval: 0.12-0.20s
  • QRS complex: <0.12s
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11
Q

What would ECG show in sinus tachycardia?

A

P-wave preceding each QRS interval, with a normal P-wave axis

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12
Q

What are some causes of sinus tachycardia? (6)

A
  • sepsis
  • hypovolaemia
  • endocrine e.g. thyrotoxicosis, phaeochromocytoma
  • anaemia
  • anxiety
  • drugs - cocaine
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13
Q

How do we manage sinus tachycardia? (2)

A
  • treat underlying cause
  • beta-blockers (propranolol, atenolol) or rate-limiting CCBs (diltiazem or verapamil)
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14
Q

What is sinus arrhythmia?

A
  • normal phenomenon displaying the changes in heart rate during breathing - increases during inhalation, decreases during exhalation
  • rhythm appears irregular but is normal
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15
Q

What is sinus arrest?

A
  • SAN fails to fire
  • appears as a flat line pause on ECG
  • AVN or other myocytes can take over if SAN cannot reset
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16
Q

What are supraventricular arrhythmias (or tachycardias) inclusive of? (4)

A
  • atrial fibrillation
  • atrial flutter
  • Wolff-Parkinson-White syndrome (WPW)
  • paroxysmal supraventricular tachycardia (PSVT)
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17
Q

How do supraventricular arrhythmias differ to ventricular arrhythmias on ECG?

A
  • supraventricular arrhythmias have very narrow QRS complexes - due to rapid excitation of ventricles
  • ventricular arrhythmias have broad QRS complexes - due to slower spread of ventricular depolarisation
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18
Q

Define supraventricular tachycardia.

A

A regular, narrow-complex tachycardia with no P-waves and supraventricular origin

Supraventricular = abnormal rhythm starts in atria/AVN (above ventricles)

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19
Q

What is the distinguishing feature of supraventricular tachycardia from atrial fibrillation?

A

SVT has a regular rhythm

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20
Q

What is supraventricular tachycardia caused by?

A
  • re-entry circuit caused by an accessory pathway which results in an AVRT (atrioventricular re-entry tachycardia = orthodromic; inverted P-wave post QRS) or AVNRT (atrioventricular nodal re-entry tachycardia; inverted P-wave immediately after QRS/buried)
  • increased automaticity –> more impulses fired by cardiomyocytes but IRREGULARLY –> increased HR
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21
Q

What is atrioventricular re-entry tachycardia (AVRT) vs atrioventricular nodal re-entry tachycardia (AVNRT)?

A

AVRT: re-entry circuit forms between atria and ventricles due to presence of accessory pathways (Bundle of Kent) - signals travel in loop via extra pathway outside AVN e.g. WPW syndrome

AVNRT: local re-entry circuit within AVN, signals travel in a loop within the AVN

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22
Q

Why does supraventricular tachycardia happen (for understanding purposes)?

A
  • Picture a single myocyte with two branches, triggering two adjoining pathways: 1 and 2. Under normal circumstances, electrical activity starts in SAN and travels from one myocyte to another
  • The wave of depolarisation should go through both 1 and 2 at the same speed - but let’s say pathway 2 was damaged in an MI
  • Pathway 2 is slowed down, the wave of depolarisation rushes through pathway 1 and then returns backwards through pathway 2
  • This creates an electrical loop that is now independent of the SAN - cluster of cells in atria/AVN start firing signals abnormally fast, overriding the SAN
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23
Q

What is characteristic of Wolff-Parkinson-White syndrome (AVRT supraventricular tachycardia)?

A

Delta waves (slurred upstroke in QRS) after SVT termination

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24
Q

What are some risk factors for supraventricular tachycardia? (5)

A
  • nicotine
  • alcohol
  • caffeine
  • previous MI
  • digoxin toxicity
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25
Q

What are some clinical features of supraventricular tachycardia? (8)

A
  • palpitations
  • light-headedness
  • syncope
  • chest pain
  • SOB
  • fatigue
  • polyuria - due to ANP secretion with increased atrial pressure (blood pools in atria due to ineffective contraction before release into ventricles)
  • tachycardic on examination
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26
Q

When would you do an ECG in supraventricular tachycardia?

A

Once SVT has been terminated (usually lasts mins/hours at a time) and normal rate and rhythm is established

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27
Q

What are the ECG findings in supraventricular tachycardia? (8)

A
  • absent P-waves (SAN no longer in control)
  • narrow QRS complexes
  • tachycardia 150-200bpm
  • short PR interval
  • regular rhythm
  • re-entrant circuit features - retrograde P-waves
    • AVNRT: close to/buried in QRS
    • AVRT: after QRS complex, long RP interval
  • presence of delta-wave (WPW)
  • slurred upstroke (high risk of SVT)
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28
Q

How does AVNRT vs AVRT (supraventricular tachycardia) appear on ECG?

A
  • AVNRT - normal, inverted P-waves in II, III, aVF close to/buried in QRS
  • AVRT - delta-waves (WPW - slurred upstroke in QRS), inverted P-waves in II, III, aVF after QRS complex, long RP interval
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29
Q

Describe the P-waves in supraventricular tachycardia.

A

Absent!! (Or inverted post-QRS)

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30
Q

Compare the QRS complexes seen in supraventricular tachycardia vs ventricular tachycardia.

A
  • SVT: QRS<120ms (narrow complex)
  • VT: QRS>120ms (broad complex)
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31
Q

What is the first and second-line management for haemodynamically stable patients with supraventricular tachycardia?

A
  • 1st line: vagal manoeuvres (AVNRT) - carotid sinus massage, Valsalva manoeuvre (exhalation against closed airway/blowing into syringe), cold water immersion, eyeball pressure
  • 2nd line: chemical cardioversion with IV adenosine as a rapid bolus - 6mg then 12mg then 18mg
    • adenosine reduces AVN conduction
    • contradiction in asthmatics - give verapamil
  • if unsuccessful, consider atrial flutter as the diagnosis and treat as appropriate
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32
Q

What is the mechanism of action of adenosine (given in supraventricular tachycardia)?

A
  • causes transient heart block in AVN (makes patient feel like they are about to die) = reduces AVN conduction
  • short acting: half-life <10s
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33
Q

What are some side effects of adenosine (given in supraventricular tachycardia)? (3)

A
  • chest pain (brief and intense)
  • bronchospasm (hence CI in asthmatics - give verapamil instead)
  • flushing
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34
Q

What is the management for haemodynamically unstable patients with supraventricular tachycardia (SBP<90mmHg)?

A

DC cardioversion - defibrillator

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35
Q

How do we manage chronic supraventricular tachycardia?

A

Radiofrequency ablation + beta-blockers

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36
Q

What is the management for WPW/AVRT (supraventricular tachycardia)?

A

Radiofrequency ablation of accessory pathway

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37
Q

What is atrial fibrillation?

A

Common type of SVT characterised by uncoordinated atrial activation that results in irregular ventricular response - hundreds of re-entrant circuits scattered around the atria

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38
Q

What are some types of atrial fibrillation? (4)

A
  • acute AF: <48h
  • paroxysmal AF: terminates spontaneously within 7d
  • persistent AF: >7d but amended with cardioversion
  • permanent AF: cannot achieve sinus rhythm, cannot be cardioverted
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39
Q

What is acute atrial fibrillation?

A

<48h

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40
Q

What is paroxysmal atrial fibrillation? (2)

A
  • if AF terminates spontaneously
  • terminates within 7 days (most commonly occurs within 24 hours)
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41
Q

What is persistent atrial fibrillation?

A

Continues for >7 days but is amended with cardioversion

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42
Q

What is permanent atrial fibrillation?

A

Cannot achieve sinus rhythm - cannot be cardioverted

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43
Q

What are some causes of atrial fibrillation? (8)

A
  • hypertension
  • pre-existing CAD / ischaemic heart disease
  • alcohol - binge drinking–>holiday heart syndrome
  • heart failure
  • PE
  • valve disease
  • hyperthyroidism
  • pneumonia
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44
Q

In which group of people is atrial fibrillation very common in?

A

Elderly

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45
Q

What is atrial flutter?

A

Form of SVT characterised by a succession of rapid atrial depolarisation - caused by a re-entrant circuit that runs around the annulus of the tricuspid valve

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46
Q

Describe what you would see on ECG in atrial flutter. (2)

A
  • sawtooth pattern
  • 2:1 ratio of P-waves to QRS complexes
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47
Q

What are the clinical features of atrial fibrillation/flutter? (9)

A
  • palpitations
  • chest pain
  • dyspnoea
  • faintness / dizziness
  • fatigue
  • polyuria
  • syncope
  • apical beat shows greater difference than radial pulse
  • thyroid and valvular disease
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48
Q

What is seen on examination of atrial fibrillation? (2)

A
  • irregularly irregular rhythm
  • tachycardia
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49
Q

What is seen on examination of atrial flutter? (2)

A
  • regular rhythm
  • tachycardia
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50
Q

How can fast atrial fibrillation present? (3)

A
  • heart failure (SOB)
  • pulmonary oedema
  • peripheral oedema
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51
Q

What investigations are done for atrial fibrillation/flutter? (4)

A
  • ECG
  • Holter monitor
  • cardiac enzymes
  • bloods - TFTs, lipid profile, U&Es, Mg2+, Ca2+
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52
Q

What would you see on ECG in atrial fibrillation?

A
  • absent P-waves (atrial HR too fast >500bpm)
  • irregular, small QRS complexes
  • irregularly irregular RR intervals (AVN overwhelmed = impulses pass through randomly and unpredictable)
  • ventricular HR 120-180bpm
  • no atrial contraction as atria are fibrillating
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53
Q

What is a broad complex tachycardia?

A
  • > 100bpm and QRS wider than 3 small squares on ECG (120ms)
  • AF with bundle branch block is the most likely cause in a stable patient
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54
Q

What would you see on ECG in atrial flutter?

A
  • regular rhythm
  • atrial HR 250-350bpm (too fast - not all impulses reach ventricles –> generates AV conduction ratio of 2:1 –> ventricular rate will be half e.g. 125-175)
  • sawtooth pattern (2:1 P:QRS)
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55
Q

How should palpitations (e.g. AF) be investigated after initial bloods and ECG?

A
  • Holter monitor
  • if dysrhythmia confirmed on Holter monitoring - consider echocardiogram
  • if Holter monitor normal but patient continues to have symptoms - external loop recorder should be considered
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56
Q

When should you do a transthoracic echocardiogram in atrial fibrillation/flutter?

A

Rule out underlying cardiac structural disease like valvular disease

57
Q

Why are TFTs done in atrial fibrillation/flutter?

A

Check for hyperthyroidism

58
Q

How do we manage atrial fibrillation in a patient that is haemodynamically unstable (BP<90/60) / syncope / myocardial ischaemia / HF / WPW / precipitating illness?

A

Emergency DC cardioversion - defibrillator

  • ABCDE assessment
  • anticoagulation with heparin - assess with CHADVASC score
  • consider pre-cardioversion heparin and IV amiodarone
  • treat reversible causes (thyrotoxicosis, chest infection)
  • beta-blockers if accompanied by HF
  • long-term anticoagulation with DOAC/heparin
59
Q

What must patients have in order to do cardioversion of atrial fibrillation?

A

Patients MUST either be anticoagulated or have had symptoms for <48h to reduce the risk of stroke

60
Q

How do we manage atrial fibrillation in haemodynamically stable patients with a clear reversible cause of AF?

A
  • rate control - verapamil, bisoprolol, diltiazem, digoxin (can be added as 2nd-line Rx for rate control)
  • THEN rhythm control - LMWH then DC cardioversion, or chemical cardioversion (amiodarone/flecainide)
    • done over rate control if age<65, first presentation of AF or symptomatic/HF
  • new AF <48h: DC cardioversion or chemical cardioversion (amiodarone/flecainide):
    • amiodarone or flecainide if no structural/IHD
    • amiodarone if SHD
  • if AF >48h: anticoagulation (DOAC/warfarin) should be given for at least 3 weeks prior to cardioversion
    • if CV unstable: transoesophageal echo to exclude a left atrial appendage (LAA) thrombus - if found, immediately heparinised and cardioverted
61
Q

What are some side effects of amiodarone (atrial fibrillation)?

A
  • bradycardia
  • hyper/hypothyroidism
  • pulmonary fibrosis
  • liver fibrosis / pneumonitis
  • jaundice
  • taste disturbance
  • persistent slate grey skin discolouration
  • raised serum transaminases
  • nausea
  • constipation (especially at start)
62
Q

How do we manage chronic (paroxysmal) atrial fibrillation?

A

Consider pill in the pocket (sotalol/flecainide) + anticogulation

63
Q

How do we manage stroke due to atrial fibrillation?

A

Aspirin for 2 weeks then long-term anticoagulation with warfarin/DOAC

64
Q

What is the 1st and 2nd-line treatment for rate control in atrial fibrillation?

A
  • 1st line: beta-blocker (propranolol - but avoid in asthmatics) OR rate-limiting CCB (diltiazem or verapamil)
  • 2nd line: digoxin - if patient is sedentary or other drugs unsuitable
65
Q

Who do we avoid propranolol in?

A

Asthmatics

66
Q

What do we do if a patient with atrial fibrillation has been on >48h rate control then is considered for long-term rhythm control?

A

Delay cardioversion until they have been maintained on therapeutic anticoagulants for minimum 3 weeks

67
Q

Why should you not use a beta-blocker and verapamil together?

A

Can lead to heart block

68
Q

What other medication do we give in atrial fibrillation and why?

A
  • anticoagulation (DOAC) due to stroke risk:
    • apixaban
    • rivaroxaban
    • dabigatran
    • edoxaban
  • do not need to monitor INR as you do with warfarin
  • if DOACs contraindicated –> give warfarin
69
Q

How do we determine the most appropriate anticoagulation strategy in atrial fibrillation?

A

CHA(2)DS(2)VASc (CHADS VASC) score for stroke risk in AF:

  • CHF/LV dysfunction
  • Hypertension
  • Age>75 (2)
  • Diabetes mellitus
  • Stroke/TIA/thromboembolism (2)
  • Vascular disease (prior MI, PAD, aortic plaque)
  • Age 65-74
  • Sex (female)
70
Q

How do we interpret CHADSVASc score in atrial fibrillation?

A
  • 2+ indicates anticoagulation
  • if score suggests no need for anticoagulation - do an echo to exclude valvular disease
  • after catheter ablation for AF:
    • 2 months if score 0
    • long term if score 1+
71
Q

What is an ORBIT score for atrial fibrillation?

A

Assesses bleeding risk in patient with AF who are being considered for anticoagulation:

  • age 75+
  • anaemia (Hb<130 in males, Hb<120 in females)
  • bleeding Hx
  • renal impairment (eGFR<60mL/min/1.73m2)
  • treatment with an antiplatelet agent
72
Q

What are some complications of atrial fibrillation?

A
  • lack of atrial contraction deprives heart of 10-20% output (blood stays in atria)
  • absence of contraction –> stasis of blood in atria –> increases risk of clot formation
    • in left atrial appendage
    • dislodges –> embolises into systemic circulation –> embolic stokes, acute limb ischaemia, central retinal artery occlusion, acute mesenteric ischaemia
73
Q

Describe the prognosis of chronic atrial fibrillation.

A

Chronic AF in a diseased heart does not usually return to sinus rhythm

74
Q

How do we manage atrial flutter? (4)

A
  • re-entrant circuit is not within AVN therefore vagal manoeuvres will not work - because vagal nerve is not innervating where arrhythmia started
  • medication
  • electrical cardioversion
  • catheter ablation for definitive management
75
Q

What is Wolff-Parkinson-White syndrome?

A

Accessory conduction pathway (the bundle of Kent) between the atria and ventricles

76
Q

What are the clinical features of Wolff-Parkinson-White syndrome? (6)

A
  • palpitations
  • dizziness
  • SOB
  • chest pain
  • syncope
  • atrial fibrillation
77
Q

What are the ECG findings in Wolff-Parkinson-White syndrome? (4)

A
  • broad QRS complex (>120ms)
  • biphasic/inverted T wave
  • short PR interval (<120ms)
  • delta-waves:
    • upward slurring/sloping of initial portion of QRS complex
    • pre-excitation of QRS complex - indicates ventricle being activated earlier than it normally should
78
Q

What is the management plan for Wolff-Parkinson-White syndrome?

A
  • initial: DC cardioversion (defibrillator)
  • acute: vagal manoeuvres (carotid sinus massage or Valsalva manoeuvre if narrow complex), IV adenosine, antiarrhythmics (if wide complex), rapid atrial pacing, DC cardioversion
  • ongoing: catheter ablation (of accessory AV pathway if symptomatic - Rx of choice), antiarrhythmics (flecainide), monitoring
79
Q

What medications do you avoid in Wolff-Parkinson-White syndrome that develops into AF/atrial flutter?

A

Most antiarrhythmic medications (BB, CCBs, adenosine) increase risk of polymorphic wide complex tachycardia by reducing conduction through AVN and so promoting conduction through accessory pathway = CI

80
Q

Which cardiomyopathy is Wolff-Parkinson-White syndrome associated with?

A

HOCM

81
Q

Which way does the axis deviate in Wolff-Parkinson-White syndrome?

A

Axis deviation on opposite side to accessory pathway:

  • LAD if right-sided pathway
  • RAD if left-sided pathway
82
Q

How can you tell the difference between LAD & RAD on ECG?

A

Look at lead I and aVF:

  • both positive in normal axis
  • lead I positive & aVF negative = LAD (Leaving)
  • lead I negative & aVF positive = RAD (Reaching)
83
Q

What is a complication of Wolff-Parkinson-White syndrome?

A

Sudden cardiac death

84
Q

What is long QT syndrome?

A

Congenital or acquired (secondary to ingestion of QT interval-prolonging drugs, electrolyte imbalances e.g. low Ca/K/Mg, or bradyarrhythmias)

85
Q

What drugs can cause long QT syndrome? (11)

A
  • clarithromycin
  • quinidine
  • procainamide
  • sotalol
  • amiodarone
  • disopyramide
  • dofetilide
  • phenothiazines
  • TCAs
  • SSRIs
  • haloperidol
86
Q

What are the clinical features of long QT syndrome? (7)

A
  • syncope during heightened adrenergic tone
  • arousal
  • surprise
  • palpitations
  • arrhythmic symptoms postpartum
  • dizziness
  • angina
87
Q

What do we see on ECG in long QT syndrome? (2)

A
  • long QT interval
  • broad-based/notched/late-appearing T wave
88
Q

How do we manage long QT syndrome? (5)

A
  • beta-blocker
  • lifestyle, medication and monitoring
  • implantable cardioverter defibrillator
  • left cervicothoracic sympathetic denervation
  • mexiletine (QT3)
89
Q

Define ventricular tachycardia.

A

A regular broad-complex tachycardia originating from a ventricular ectopic focus (can result in hypotension, collapse and acute cardiac failure), HR usually >120bpm

90
Q

What are some causes of ventricular tachycardia? (3)

A
  • ischaemia
  • electrolyte abnormalities (hypokalaemia, hypomagnesaemia)
  • long QT interval
91
Q

What are some risk factors for ventricular tachycardia? (5)

A
  • CHD
  • structural heart disease / cardiomyopathies
  • hypokalaemia
  • cocaine
  • cardiac dysfunction
92
Q

Is ventricular tachycardia a shockable rhythm?

A

Yes - this is one of the shockable rhythms that may be seen in cardiac arrest patients

93
Q

What are the clinical features of ventricular tachycardia? (7)

A
  • chest pain
  • palpitations
  • dyspnoea
  • syncope
  • dizziness + light-headedness
  • bibasal crackles
  • raised JVP
94
Q

What would ECG show in ventricular tachycardia? (6)

A
  • 3+ consecutive complexes originating in the ventricles at a rate >100bpm
  • rate >100bpm
  • broad QRS complexes
  • no P-waves
  • AV dissociation
  • sustained VT lasts >30s or results in haemodynamic compromise
95
Q

What is the difference between monomorphic and polymorphic ventricular tachycardia?

A
  • monomorphic VT: stable single QRS morphology
  • polymorphic VT: changing QRS morphology e.g. Torsades de pointes
96
Q

What is Torsades de pointes (ventricular tachycardia)?

A

Polymorphic VT, with gradual change in amplitude, and twisting around the axis (isoelectric line) - outline looks like a party streamer

VT in setting of a prolonged QT interval, with waxing and waning of QRS amplitude (oscillating about baselines)

97
Q

What are some causes of Torsades de pointes (ventricular tachycardia)? (6)

A
  • macrolides - clarithromycin, azithromycin
  • hypothermia
  • hypokalaemia
  • hypomagnesaemia
  • hypocalcaemia
  • secondary to subarachnoid haemorrhage - rare but important complication
98
Q

What is Torsades de pointes (ventricular tachycardia) associated with on ECG?

A

Long QT interval

99
Q

What may Torsades de pointes (ventricular tachycardia) deteriorate into and lead to?

A

VF and sudden death

100
Q

What approach is used in treating ventricular tachycardia?

A

ABC - check whether patient has a pulse or not –> if in cardiac arrest, may require defibrillation

Defibrillation different to DC cardioversion - larger shocks and done if no pulse vs DC cardioversion is smaller shocks when patient has a pulse but is haemodynamically unstable

101
Q

How do you manage patients with haemodynamically unstable ventricular tachycardia?

A

DC cardioversion (synchronised) + antiarrhythmics (amiodarone/lidocaine)

102
Q

How do you manage patients with haemodynamically stable ventricular tachycardia?

A
  • antiarrhythmics - IV amiodarone 300mg (baseline CXR due to risk of pulmonary fibrosis/pneumonitis in amiodarone)
  • treatment of reversible cause
  • synchronised cardioversion
103
Q

How do you manage a stable patient with Torsades de pointes? (6)

A
  • IV magnesium sulfate
  • withdraw offending drugs - clarithromycin/azithromycin
  • correct electrolyte abnormalities (hypo K/Mg/Ca)
  • isoprenaline (if recurrent)
  • temporary/permanent pacing
  • if unstable: DC cardioversion
104
Q

How do you manage long-term ventricular tachycardia? (4)

A
  • ICD (implantable cardioverter defibrillator)
  • antiarrhythmics (mexiletine/flecainide/sotalol)
  • catheter ablation
  • beta-blockers
105
Q

What medication is contraindicated in ventricular tachycardia?

A

CCBs e.g. verapamil, diltiazem, amlodipine

106
Q

Define ventricular fibrillation.

A

Irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death

107
Q

How does ventricular fibrillation occur?

A
  • ventricular fibres contract randomly and rapidly causing complete failure of ventricular function
  • most cases occur in patients with underlying heart disease
108
Q

What are the clinical features of ventricular fibrillation? (6)

A
  • sudden collapse and unconscious
  • pulseless
  • noisy/irregular breathing
  • chest pain
  • fatigue
  • palpitations
109
Q

How can ventricular fibrillation be excluded?

A

If patient is conscious

110
Q

How would you diagnose ventricular fibrillation?

A

ECG

111
Q

How does ventricular fibrillation ECG compare to ventricular tachycardia? (4)

A
  • VT is very tidy vs VF is very funny
  • VT regular vs VF irregular
  • VF has smaller QRS complexes vs Torsades de pointes
  • ventricular rate usually >300bpm
112
Q

Describe the rate, rhythm, P-wave, PR interval and QRS complex in ventricular fibrillation.

A
  • HR: 300-600bpm
  • rhythm: extremely irregular
  • P-wave: absent
  • PR interval: N/A
  • QRS complex: fibrillatory baseline
113
Q

What do you need to check for first in ventricular fibrillation?

A
  • pulse
  • if no pulse initiate ALS (advanced life support):
  • unwitnessed attacks: 1 shock –> 2min CPR
  • witnessed attacks: up to 3 shocks –> CPR –> amiodarone 300mg and 1mg adrenaline
    • adrenaline 1mg repeats every 3-5min + amiodarone 150mg can be given after 5 shocks
  • lidocaine can be used if amiodarone not available
114
Q

How do we manage patients with ventricular fibrillation?

A

Urgent defibrillation AND cardioversion, and:

  • myocardial perfusion and electrophysiological stability
  • empirical beta-blockers
  • ICD
  • radiofrequency ablation
115
Q

What do ventricular fibrillation survivors require?

A

Implantable cardioverter defibrillator (ICD)

116
Q

Which cardiomyopathy is ICD the treatment of choice for and how does this relate to VT/VF?

A

Hypertrophic obstructive cardiomyopathy (HOCM):

  • LV hypertrophy
  • deep T-wave inversion
  • S4 heart sound (think HOCM has 4 letters –> S4)

There is considerable risk of sudden cardiac death due to VT or VF in HOCM

117
Q

What is ventricular fibrillation prognosis dependent on? (2)

A
  • time between onset and medical intervention
  • early defibrillation is essential - ideally within 4-6 minutes
118
Q

What is 1st degree AV block?

A

Prolonged conduction through AVN

119
Q

What are the two types of 2nd degree AV block?

A
  • Mobitz type I - progressive prolongation of AVN conduction resulting in one atrial impulse failing to be conducted through AVN
  • Mobitz type II - intermittent or regular failure of conduction through AVN
120
Q

What is 3rd degree (complete) AV block?

A

No relationship between atrial and ventricular contraction

121
Q

What are some causes of heart block? (3)

A
  • drugs e.g. digoxin
  • metabolic e.g. hyperkalaemia
  • MI –> complete AV block due to RCA occlusion which supplies AVN
122
Q

What types of heart block are usually asymptomatic?

A

1st and 2nd degree AV block

123
Q

What are Stokes-Adams attacks? (4+1)

A
  • syncope
  • dizziness
  • palpitations
  • chest pain
  • ECG - bizarre, wide, inverted T waves
124
Q

Which types of heart block can cause Stokes-Adams attacks?

A

Mobitz type II and 3rd degree AV block

125
Q

What can Mobitz II and 3rd degree AV block show signs of?

A

Reduced cardiac output, hypotension

126
Q

What are the clinical features of complete heart block? (3)

A
  • JVP may show cannon A waves
  • syncope
  • regular bradycardia (30-50bpm)
127
Q

What does ECG show in 1st degree AV block?

A

Fixed prolonged PR interval (>3-5 small squares - 1 small square = 0.04s/40ms)

128
Q

What is a prolonged PR interval and prominent U waves a sign of?

A

Hypokalaemia (e.g. from thiazide diuretic - bendroflumethiazide):

  • prolonged PR interval
  • prominent U waves
  • flattened T waves
  • ST segment depression
129
Q

What are some signs of hypokalaemia on ECG? (4)

A
  • prolonged PR interval
  • prominent U waves
  • flattened T waves
  • ST segment depression
130
Q

What does ECG show in Mobitz type I (2nd degree AV block)?

A

Progressively prolonged PR interval, then eventually dropped beat

131
Q

What does ECG show in Mobitz type II (2nd degree AV block)?

A

PR interval is constant but intermittently a P-wave is not followed by a QRS

132
Q

What does ECG show in 3rd degree (complete) AV block?

A

No relationship between P waves and QRS complexes - complete AV dissociation

133
Q

What is the definitive management for chronic degree AV block?

A
  • permanent pacemaker
  • Mobitz II is an indication for a pacemaker
  • pacemaker ECG: vertical lines before QRS are pacing spikes delivered by pacemaker
134
Q

What does pacemaker ECG look like (AV block)?

A

Vertical lines before QRS = pacing spikes delivered by pacemaker

135
Q

What is the acute management for acute heart block?

A
  1. IV atropine - used for bradycardia to speed up heart, would be used in acute setting of symptomatic bradycardias/low BP
    • max dose = 3mg
  2. transcutaneous pacing
  3. transvenous pacing
136
Q

What are Mobitz II and 3rd degree AV block patients with a broad QRS at risk of?

A

Asystole in bradycardia - managed via transvenous pacing

137
Q

Describe the prognosis of Mobitz type II and 3rd degree complete AV block.

A

Usually indicates serious underlying cardiac disease

138
Q

What is arrhythmogenic right ventricular dysplasia?

A

Autosomal dominant inherited cardiac arrhythmia that is a common cause of sudden cardiac death in people <65y

Symptoms usually precipitated by exercise

139
Q

What is arrhythmogenic right ventricular dysplasia characterised by on ECG? (4)

A
  • epsilon wave
  • widened QRS
  • T wave inversion
  • prolonged S upstroke in V1-V3

Year 3 (108 decks)

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