Arrhythmias

Occurs when a specific area of the cardiac tissue depolarises faster than the SA node, causing focal arrhythmia.

Normally, the AP travels through the myocardium via "fast" and "slow" pathways. In re-entry, the impulse finds the normal "fast" pathway refractory and is redirected to the "slow" pathway. It continues both distally and retrograde up the "fast" pathway and re-enters the loop.

The SA node contains special myocytes which depolarise faster than other cardiac tissue. This sets the pace for the other cells.

Abnormally high-amplitude oscillations in the myocardium lead to early triggering of an AP.

The SA node slows down or fails, causing the other myocytes to take over the pacemaking role. A similar problem can occur in the AV node.

- Previous MI
- LV aneurysm
- Valve disease
- Stimulant drugs
- Psychological (fear, pain, anxiety)

- Vagal maneuvers
- Drugs that block the AV node
- Antiarrhythmic drugs
- Electrical cardioversion
- Ablation of re-entry circuits

Generally a physiological response (normal). It originates in the SA node.

Ectopic tachycardia originates in a single area of the atrium and is characterised by early ectopic beats.

Multifocal tachycardia originates in multiples atrial areas and shows an irregularly irregular rhythm on ECG

In AF, the atria fibrillate at 400-600 bpm. The ECG shows a indiscernible P wave and highly irregular beat.

AF is dangerous because the high bpm produces no effective contraction and can also cause thrombi to form.

Atrial flutter is caused by a large re-entry circuit in the atrium. It shows a characteristic "sawtooth" appearance on the ECG.

A disturbance in the ventricular myocytes, e.g. from prior MI or ischaemia, is the main cause of VT. The ECG shows very wide QRS complexes which indicate slow repolarisation.

VT is dangerous because it can degenerate into ventricular fibrillation or sudden cardiac death.

- Increased vagal tone
- Decreased sympathetic tone
- Beta blockers
- Calcium channel blockers
- Digoxin
- SA or AV node fibrosis
- Ischaemia or MI

You would see long PR interval >200 ms

The two types are:
Mobitz I (wenckebach)
Mobitz II

Mobitz I - features progressive prologation of PR interval with each beat

Mobitz II - progressive PR is not seen

STRIDES
1. Structural abnormalities
2. Thyrotoxicosis
3. Rheumatic heart disease
4. Ischaemia
5. Drugs
6. Electrolyte disturbances
7. Social drugs

HARD
1. Heart block
2. Abnormal pacemaker
3. Reentry
3. Delayed after-depolarisation

Amiodarone is a potassium channel inhibitor. It prolongs phase 3 of the cardiac action potential, increasing the refractory period and thus slowing heart rate. It is used in shock-refractory VF, AF, and VT.

Classic syncopal episode caused by bradyarrhythmia.
- Brief loss of consciousness
- Very rapid recovery

Classic syncopal episode caused by bradyarrhythmia.
- Brief loss of consciousness
- Very rapid recovery