Arrhythmias (CV) Flashcards
What is an arrhythmia?
Any disturbance in the rate, rhythm, site of origin or conduction of the cardiac electrical impulse
What is sinus bradycardia?
- heart rate <50bpm
- due to SAN dysfunction and/or AV conduction abnormalities
- physiological in athletes, normal during sleep
Describe the rate, rhythm, P wave, PR interval and QRS complex in sinus bradycardia.
- rate: <50/60bpm
- rhythm: regular (sinus)
- P wave: before each QRS, identical
- PR interval: 0.12-0.20s
- QRS complex: <0.12s
What are the different types of causes of sinus bradycardia? (4)
- 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
What are some clinical features of sinus bradycardia? (5)
- dizziness + light-headedness
- syncope
- fatigue
- exercise intolerance
- shortness of breath
What might you see on examination of sinus bradycardia? (3)
- cannon a-waves in JVP
- JVP distension
- raised ICP
How do we manage acute sinus bradycardia? (4)
- IV atropine, adrenaline, theophylline - increase sympathetic drive/block parasympathetic influences
- temporary pacing (transcutaneous, transvenous)
- reverse causes of bradycardia
- consider permanent pacing
How do we manage asymptomatic sinus bradycardia? (2)
- reassurance, reverse potential causes
- consider fludrocortisone
What is sinus tachycardia?
- 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
Describe the rate, rhythm, P wave, PR interval and QRS complex in sinus tachycardia.
- rate: >100bpm
- rhythm: regular (sinus)
- P wave: before each QRS, identical
- PR interval: 0.12-0.20s
- QRS complex: <0.12s
What would ECG show in sinus tachycardia?
P-wave preceding each QRS interval, with a normal P-wave axis
What are some causes of sinus tachycardia? (6)
- sepsis
- hypovolaemia
- endocrine e.g. thyrotoxicosis, phaeochromocytoma
- anaemia
- anxiety
- drugs - cocaine
How do we manage sinus tachycardia? (2)
- treat underlying cause
- beta-blockers (propranolol, atenolol) or rate-limiting CCBs (diltiazem or verapamil)
What is sinus arrhythmia?
- normal phenomenon displaying the changes in heart rate during breathing - increases during inhalation, decreases during exhalation
- rhythm appears irregular but is normal
What is sinus arrest?
- SAN fails to fire
- appears as a flat line pause on ECG
- AVN or other myocytes can take over if SAN cannot reset
What are supraventricular arrhythmias (or tachycardias) inclusive of? (4)
- atrial fibrillation
- atrial flutter
- Wolff-Parkinson-White syndrome (WPW)
- paroxysmal supraventricular tachycardia (PSVT)
How do supraventricular arrhythmias differ to ventricular arrhythmias on ECG?
- 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
Define supraventricular tachycardia.
A regular, narrow-complex tachycardia with no P-waves and supraventricular origin
Supraventricular = abnormal rhythm starts in atria/AVN (above ventricles)
What is the distinguishing feature of supraventricular tachycardia from atrial fibrillation?
SVT has a regular rhythm
What is supraventricular tachycardia caused by?
- 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
What is atrioventricular re-entry tachycardia (AVRT) vs atrioventricular nodal re-entry tachycardia (AVNRT)?
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
Why does supraventricular tachycardia happen (for understanding purposes)?
- 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
What is characteristic of Wolff-Parkinson-White syndrome (AVRT supraventricular tachycardia)?
Delta waves (slurred upstroke in QRS) after SVT termination
What are some risk factors for supraventricular tachycardia? (5)
- nicotine
- alcohol
- caffeine
- previous MI
- digoxin toxicity
What are some clinical features of supraventricular tachycardia? (8)
- 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
When would you do an ECG in supraventricular tachycardia?
Once SVT has been terminated (usually lasts mins/hours at a time) and normal rate and rhythm is established
What are the ECG findings in supraventricular tachycardia? (8)
- 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) AKA slurred upstroke
- slurred upstroke (high risk of SVT)
How does AVNRT vs AVRT (supraventricular tachycardia) appear on ECG?
- 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
Describe the P-waves in supraventricular tachycardia.
Absent!! (Or inverted post-QRS)
Compare the QRS complexes seen in supraventricular tachycardia vs ventricular tachycardia.
- SVT: QRS<120ms (narrow complex)
- VT: QRS>120ms (broad complex)
What is the first and second-line management for haemodynamically stable patients with supraventricular tachycardia?
- 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
What is the mechanism of action of adenosine (given in supraventricular tachycardia)?
- causes transient heart block in AVN (makes patient feel like they are about to die) = reduces AVN conduction
- short acting: half-life <10s
What are some side effects of adenosine (given in supraventricular tachycardia)? (3)
- chest pain (brief and intense)
- bronchospasm (hence CI in asthmatics - give verapamil instead)
- flushing
What is the management for haemodynamically unstable patients with supraventricular tachycardia (SBP<90mmHg)?
DC cardioversion - defibrillator
How do we manage chronic supraventricular tachycardia?
Radiofrequency ablation + beta-blockers
What is the management for WPW/AVRT (supraventricular tachycardia)?
Radiofrequency ablation of accessory pathway
What is atrial fibrillation?
Common type of SVT characterised by uncoordinated atrial activation that results in irregular ventricular response - hundreds of re-entrant circuits scattered around the atria
What are some types of atrial fibrillation? (4)
- 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
What is acute atrial fibrillation?
<48h
What is paroxysmal atrial fibrillation? (2)
- if AF terminates spontaneously
- terminates within 7 days (most commonly occurs within 24 hours)
What is persistent atrial fibrillation?
Continues for >7 days but is amended with cardioversion
What is permanent atrial fibrillation?
Cannot achieve sinus rhythm - cannot be cardioverted
What are some causes of atrial fibrillation? (8)
- hypertension
- pre-existing CAD / ischaemic heart disease
- alcohol - binge drinking–>holiday heart syndrome
- heart failure
- PE
- valve disease
- hyperthyroidism
- pneumonia
In which group of people is atrial fibrillation very common in?
Elderly
What is atrial flutter?
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
Describe what you would see on ECG in atrial flutter. (2)
- sawtooth pattern
- 2:1 ratio of P-waves to QRS complexes
What are the clinical features of atrial fibrillation/flutter? (9)
- palpitations
- chest pain
- dyspnoea
- faintness / dizziness
- fatigue
- polyuria
- syncope
- apical beat shows greater difference than radial pulse
- thyroid and valvular disease
What is seen on examination of atrial fibrillation? (2)
- irregularly irregular rhythm
- tachycardia
What is seen on examination of atrial flutter? (2)
- regular rhythm
- tachycardia
How can fast atrial fibrillation present? (3)
- heart failure (SOB)
- pulmonary oedema
- peripheral oedema
What investigations are done for atrial fibrillation/flutter? (4)
- ECG
- Holter monitor
- cardiac enzymes
- bloods - TFTs, lipid profile, U&Es, Mg2+, Ca2+
What would you see on ECG in atrial fibrillation?
- 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
What is a broad complex tachycardia?
- > 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
What would you see on ECG in atrial flutter?
- 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)
How should palpitations (e.g. AF) be investigated after initial bloods and ECG?
- 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
When should you do a transthoracic echocardiogram in atrial fibrillation/flutter?
Rule out underlying cardiac structural disease like valvular disease
Why are TFTs done in atrial fibrillation/flutter?
Check for hyperthyroidism
How do we manage atrial fibrillation in a patient that is haemodynamically unstable (BP<90/60) / syncope / myocardial ischaemia / HF / WPW / precipitating illness?
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
What must patients have in order to do cardioversion of atrial fibrillation?
Patients MUST either be anticoagulated or have had symptoms for <48h to reduce the risk of stroke
How do we manage atrial fibrillation in haemodynamically stable patients with a clear reversible cause of AF?
- 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
What are some side effects of amiodarone (atrial fibrillation)?
- bradycardia
- hyper/hypothyroidism
- pulmonary fibrosis
- liver fibrosis / pneumonitis
- jaundice
- taste disturbance
- persistent slate grey skin discolouration
- raised serum transaminases
- nausea
- constipation (especially at start)
How do we manage chronic (paroxysmal) atrial fibrillation?
Consider pill in the pocket (sotalol/flecainide) + anticogulation
How do we manage stroke due to atrial fibrillation?
Aspirin for 2 weeks then long-term anticoagulation with warfarin/DOAC
What is the 1st and 2nd-line treatment for rate control in atrial fibrillation?
- 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
Who do we avoid propranolol in?
Asthmatics
What do we do if a patient with atrial fibrillation has been on >48h rate control then is considered for long-term rhythm control?
Delay cardioversion until they have been maintained on therapeutic anticoagulants for minimum 3 weeks
Why should you not use a beta-blocker and verapamil together?
Can lead to heart block
What other medication do we give in atrial fibrillation and why?
- 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
How do we determine the most appropriate anticoagulation strategy in atrial fibrillation?
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)
How do we interpret CHADSVASc score in atrial fibrillation?
- 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+
What is an ORBIT score for atrial fibrillation?
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
What are some complications of atrial fibrillation?
- 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
Describe the prognosis of chronic atrial fibrillation.
Chronic AF in a diseased heart does not usually return to sinus rhythm
How do we manage atrial flutter? (4)
- 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
What is Wolff-Parkinson-White syndrome?
Accessory conduction pathway (the bundle of Kent) between the atria and ventricles
What are the clinical features of Wolff-Parkinson-White syndrome? (6)
- palpitations
- dizziness
- SOB
- chest pain
- syncope
- atrial fibrillation
What are the ECG findings in Wolff-Parkinson-White syndrome? (4)
- 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
What is the management plan for Wolff-Parkinson-White syndrome?
- 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
What medications do you avoid in Wolff-Parkinson-White syndrome that develops into AF/atrial flutter?
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
Which cardiomyopathy is Wolff-Parkinson-White syndrome associated with?
HOCM
Which way does the axis deviate in Wolff-Parkinson-White syndrome?
Axis deviation on opposite side to accessory pathway:
- LAD if right-sided pathway
- RAD if left-sided pathway
How can you tell the difference between LAD & RAD on ECG?
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)
What is a complication of Wolff-Parkinson-White syndrome?
Sudden cardiac death
What is long QT syndrome?
Congenital or acquired (secondary to ingestion of QT interval-prolonging drugs, electrolyte imbalances e.g. low Ca/K/Mg, or bradyarrhythmias)
What drugs can cause long QT syndrome? (11)
- clarithromycin
- quinidine
- procainamide
- sotalol
- amiodarone
- disopyramide
- dofetilide
- phenothiazines
- TCAs
- SSRIs
- haloperidol
What are the clinical features of long QT syndrome? (7)
- syncope during heightened adrenergic tone
- arousal
- surprise
- palpitations
- arrhythmic symptoms postpartum
- dizziness
- angina
What do we see on ECG in long QT syndrome? (2)
- long QT interval
- broad-based/notched/late-appearing T wave
How do we manage long QT syndrome? (5)
- beta-blocker
- lifestyle, medication and monitoring
- implantable cardioverter defibrillator
- left cervicothoracic sympathetic denervation
- mexiletine (QT3)
Define ventricular tachycardia.
A regular broad-complex tachycardia originating from a ventricular ectopic focus (can result in hypotension, collapse and acute cardiac failure), HR usually >120bpm
What are some causes of ventricular tachycardia? (3)
- ischaemia
- electrolyte abnormalities (hypokalaemia, hypomagnesaemia)
- long QT interval
What are some risk factors for ventricular tachycardia? (5)
- CHD
- structural heart disease / cardiomyopathies
- hypokalaemia
- cocaine
- cardiac dysfunction
Is ventricular tachycardia a shockable rhythm?
Yes - this is one of the shockable rhythms that may be seen in cardiac arrest patients
What are the clinical features of ventricular tachycardia? (7)
- chest pain
- palpitations
- dyspnoea
- syncope
- dizziness + light-headedness
- bibasal crackles
- raised JVP
What would ECG show in ventricular tachycardia? (6)
- 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
What is the difference between monomorphic and polymorphic ventricular tachycardia?
- monomorphic VT: stable single QRS morphology
- polymorphic VT: changing QRS morphology e.g. Torsades de pointes
What is Torsades de pointes (ventricular tachycardia)?
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)
What are some causes of Torsades de pointes (ventricular tachycardia)? (6)
- macrolides - clarithromycin, azithromycin
- hypothermia
- hypokalaemia
- hypomagnesaemia
- hypocalcaemia
- secondary to subarachnoid haemorrhage - rare but important complication
What is Torsades de pointes (ventricular tachycardia) associated with on ECG?
Long QT interval
What may Torsades de pointes (ventricular tachycardia) deteriorate into and lead to?
VF and sudden death
What approach is used in treating ventricular tachycardia?
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
How do you manage patients with haemodynamically unstable ventricular tachycardia?
DC cardioversion (synchronised) + antiarrhythmics (amiodarone/lidocaine)
How do you manage patients with haemodynamically stable ventricular tachycardia?
- antiarrhythmics - IV amiodarone 300mg (baseline CXR due to risk of pulmonary fibrosis/pneumonitis in amiodarone)
- treatment of reversible cause
- synchronised cardioversion
How do you manage a stable patient with Torsades de pointes? (6)
- 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
How do you manage long-term ventricular tachycardia? (4)
- ICD (implantable cardioverter defibrillator)
- antiarrhythmics (mexiletine/flecainide/sotalol)
- catheter ablation
- beta-blockers
What medication is contraindicated in ventricular tachycardia?
CCBs e.g. verapamil, diltiazem, amlodipine
Define ventricular fibrillation.
Irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death
How does ventricular fibrillation occur?
- ventricular fibres contract randomly and rapidly causing complete failure of ventricular function
- most cases occur in patients with underlying heart disease
What are the clinical features of ventricular fibrillation? (6)
- sudden collapse and unconscious
- pulseless
- noisy/irregular breathing
- chest pain
- fatigue
- palpitations
How can ventricular fibrillation be excluded?
If patient is conscious
How would you diagnose ventricular fibrillation?
ECG
How does ventricular fibrillation ECG compare to ventricular tachycardia? (4)
- 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
Describe the rate, rhythm, P-wave, PR interval and QRS complex in ventricular fibrillation.
- HR: 300-600bpm
- rhythm: extremely irregular
- P-wave: absent
- PR interval: N/A
- QRS complex: fibrillatory baseline
What do you need to check for first in ventricular fibrillation?
- 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
How do we manage patients with ventricular fibrillation?
Urgent defibrillation AND cardioversion, and:
- myocardial perfusion and electrophysiological stability
- empirical beta-blockers
- ICD
- radiofrequency ablation
What do ventricular fibrillation survivors require?
Implantable cardioverter defibrillator (ICD)
Which cardiomyopathy is ICD the treatment of choice for and how does this relate to VT/VF?
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
What is ventricular fibrillation prognosis dependent on? (2)
- time between onset and medical intervention
- early defibrillation is essential - ideally within 4-6 minutes
What is 1st degree AV block?
Prolonged conduction through AVN
What are the two types of 2nd degree AV block?
- 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
What is 3rd degree (complete) AV block?
No relationship between atrial and ventricular contraction
What are some causes of heart block? (3)
- drugs e.g. digoxin
- metabolic e.g. hyperkalaemia
- MI –> complete AV block due to RCA occlusion which supplies AVN
What types of heart block are usually asymptomatic?
1st and 2nd degree AV block
What are Stokes-Adams attacks? (4+1)
- syncope
- dizziness
- palpitations
- chest pain
- ECG - bizarre, wide, inverted T waves
Which types of heart block can cause Stokes-Adams attacks?
Mobitz type II and 3rd degree AV block
What can Mobitz II and 3rd degree AV block show signs of?
Reduced cardiac output, hypotension
What are the clinical features of complete heart block? (3)
- JVP may show cannon A waves
- syncope
- regular bradycardia (30-50bpm)
What does ECG show in 1st degree AV block?
Fixed prolonged PR interval (>3-5 small squares - 1 small square = 0.04s/40ms)
What is a prolonged PR interval and prominent U waves a sign of?
Hypokalaemia (e.g. from thiazide diuretic - bendroflumethiazide):
- prolonged PR interval
- prominent U waves
- flattened T waves
- ST segment depression
What are some signs of hypokalaemia on ECG? (4)
- prolonged PR interval
- prominent U waves
- flattened T waves
- ST segment depression
What does ECG show in Mobitz type I (2nd degree AV block)?
Progressively prolonged PR interval, then eventually dropped beat
What does ECG show in Mobitz type II (2nd degree AV block)?
PR interval is constant but intermittently a P-wave is not followed by a QRS
What does ECG show in 3rd degree (complete) AV block?
No relationship between P waves and QRS complexes - complete AV dissociation
What is the definitive management for chronic AV block?
- permanent pacemaker
- Mobitz II is an indication for a pacemaker
- pacemaker ECG: vertical lines before QRS are pacing spikes delivered by pacemaker
What does pacemaker ECG look like (AV block)?
Vertical lines before QRS = pacing spikes delivered by pacemaker
What is the acute management for acute heart block?
- IV atropine - used for bradycardia to speed up heart, would be used in acute setting of symptomatic bradycardias/low BP
- max dose = 3mg
- transcutaneous pacing
- transvenous pacing
What are Mobitz II and 3rd degree AV block patients with a broad QRS at risk of?
Asystole in bradycardia - managed via transvenous pacing
Describe the prognosis of Mobitz type II and 3rd degree complete AV block.
Usually indicates serious underlying cardiac disease
What is arrhythmogenic right ventricular dysplasia?
Autosomal dominant inherited cardiac arrhythmia that is a common cause of sudden cardiac death in people <65y
Symptoms usually precipitated by exercise
What is arrhythmogenic right ventricular dysplasia characterised by on ECG? (4)
- epsilon wave
- widened QRS
- T wave inversion
- prolonged S upstroke in V1-V3
