Sinus bradycardia
• SR <60bpm may occur in healthy people at rest or athletes
• Pathological causes – MI, sick sinus syndrome, hypothyroidism, drugs (BB, digoxin), carotid sinus pressure
• IV atropine [0.6-1.2mg] for symptomatic patients
Sinus tachycardia
• SR >100bpm
• Due to ↑sympathetic NS activity – exercise, emotion, pregnancy
• Pathologic causes – anxiety, fever, anaemia, thyrotoxicosis, heart failure, drugs (B-agonists)
Sick sinus syndrome
• MC in elderly people
• Fibrosis, degenerative changes or ischemia of the sino-atrial node (SAN)
• CF – sinus bradycardia, sinoatrial block, tachycardia
• Pacemakers indicated for pts symptoms due to spontaneous bradycardia
- ATRIAL TACHYARRHYTHMIAS
Atrial ectopic beats (extrasystoles, premature beats)
• Usually cause no symptoms. Sometimes a sensation of heaviness of the heart
• ECG- shows a premature but normal QRS
If visible, the P wave has a different morphology because the atria activate from an abnormal site
• Tx rarely needed – BB if sx are troubling
Atrial tachycardia
• May be due to ↑atrial automaticity, triggered activity or re-entry
• ECG – narrow QRS complex (<0.12s) with abnormal P waves
• Treatment
BB (which ↓automaticity) or class I or III antiarrhythmics
Ablation – to target the ectopic site
Atrial flutter
• Characterised by a large re-entry circuit within the right atrium, circling around the tricuspid annulus
• Atrial rate is 300bpm(if every beat conducts [rare])
• Usually associated with AV block – 2:1 is MC
Therefore every 2nd beat conducts – giving a ventricular rate of 150bpm
• ECG – saw toothed (flutter) waves
Can be difficult to see flutter waves in 2:1 block as they are buried in the QRS complex
Carotid sinus massage slows the AV block and reveal the flutter waves
• Treatment
DC cardioversion – to restore sinus rhythm
Catheter ablation
BB or amiodarone [200mg t.i.d] – to prevent recurrent episodes
Atrial fibrillation (AF)
• Characterised by
Accelerated automaticity
And multiple interacting re-entry circuits looping around the atria
• Episodes of AF are initiated by rapid bursts of ectopic beats arising from conducting tissue in the pulmonary veins or diseased atrial tissue
• Then AF becomes sustained because of re-entrant conduction
Re-entry is more likely to occur in enlarged atria e.g. in heart disease
• During episodes of AF the atria beat rapidly but uncoordinated and ineffectively
So the ventricles are activated irregularly – results in irregularly irregular pulse
• ECG – shows normal but irregular QRS. No p waves
Oscillations of the baseline
• AF can be paroxysmal (intermittent episodes that self-terminate within 7 days), persistent or permanent
• Long term AF leads structural remodelling – atrial fibrosis and dilation
Predisposes to further AF
• Causes of AF – CAD, valvular heart disease, HTN, hyperthyroidism, cardiomyopathy
• CF – palpitations, SOB, fatigue, chest pain
Can precipitate or aggravate HF
Associated with stroke and systemic embolism
Treatment
• Tx primary disorder
• Acute AF
Control ventricular rate – see below
Anticoagulation – warfarin
Cardioversion – with DC shock or drugs (IV flecainide, propafenone)
• Chronic AF
Rate control – digoxin, BB or NDP-CCB (verapamil/diltiazem)
Rhythm control
Patients with no heart disease – class Ia, Ic or III drugs
Patients with HF/Left ventricular hypertrophy – amiodarone
Patients with paroxysmal/early AF – LA ablation
Anticoagulation
Indicated in pts with AF related to rheumatic mitral stenosis or in patients with prosthetic heart valve
In patients with non-valvular AF, CHA2DS2VASc system is used to determine need for anticoagulation
Prophylaxis against ischemic stroke with anticoagulation must be balanced against risk of haemorrhage using the HAS-BLED score
Warfarin – INR 2-3
Direct thrombin inhibitor – dabigatran
Direct factor Xa inhibitor – rivaroxaban
- ATRIOVENTRICULAR JUNCTIONAL TACHYCARDIAS
AV nodal re-entrant tachycardia (AVNRT)
• MC in women
• CF – rapid, forceful, regular heart beat
• Characterised by 2 different pathways in the AVN
One with a short refractory period + slow conduction
Other with long refractory period + fast conduction
• In normal sinus rhythm, the atrial impulse that depolarises the ventricles conducts through the fast pathway
• If an atrial premature beat occurs early when the fast pathway is still refractory, the slow pathway takes over in propagating the impulse to the ventricles
It then travels back in a retrograde direction through the fast pathway, initiating the AVNRT
• ECG –normal QRS at 140-240bpm
P waves either invisible or are immediately before or after the QRS because of simultaneous atrial and ventricle activation
AV re-entrant tachycardia (AVRT)
• This circuit comprises the AVN, His bundle, ventricle and an abnormal connection of myocardial fibres (accessory pathway [AP])
Results from an incomplete separation of the atria and ventricles during fetal development
MC accessory pathway is the Kent bundles – in the septum
• Atrial activation occurs after ventricle activation – so P wave is seen between QRS and T wave
• Pathways that conduct in retrograde direction (ventricles→atria) are not seen on the ECG – concealed AP
• Bidirectional APs are seen on the ECG
• Conduction in sinus rhythm is mediated by both the AVN and the AP – this distorts the QRS
Premature ventricular activation (pre-excitation) via the AP shortens the PR interval and produces a slurred deflection of the QRS – called the delta wave
pts with a pre-excited ECG and palpitations have Wolff-Parkinson-White syndrome
Treatment
• DC cardioversion
• Carotid sinus massage or IV adenosine [6-12mg bolus] – for tachycardia
• Valsava manoeuvre