Pacing Flashcards
Conduction system of the heart
- SAN originates generates action potential (automatic pacemaker)
- SAN to AVN with delay via internodal pathways to allow atrial contraction
AVN via Bundle of His to bundle branches and Purkinje fibres at the end (fast)
Where is the SAN?
Top of right atrium
How do ventrices polarise?
From bottom up (purkinje fibres)
SAN
From SVC to IVC
- central SAN tissue where rhythm originates
- peripheral SAN tissue where it exits
Origins of pacing in SAN
- unlike normal action potentials
- no true resting potential
- depolarised managed by sppecialised slow Na+ and Ca2+ channels making action potential different
Action potential of SAN
- unlike normal
- funny current (pacing controlled by slow Na+ channels)
- threshold reached = action potential (voltage gated Ca2+ channels)
- slower flow of calcium than in other cells so slower rate of depolarisation
3 phases of SAN action potentials
4 = funny current (constant changing as slow open Na+ channels), reaches -50 so transient calcium channels open so more flow in helping reach threshold 0 = depolarisation, increased calcium flow as long lasting channels open and transient close 3 = repolarisation (potassium channels open allowing depolarisation and calcium close)
What happens if there is failure with SAN?
- AVN will take over as have pacemaker cells here, similar action potentials, at slower rate of rhythmicity
- will be much slower rate than required
- = escape rhythm
Ventricular myocyte depolarisation
- much faster like nerve cells
- still significant difference with nerve cells however (heart cells have much greater time period)
- cause by fast sodium channels
- large plateau before repolarisation (caused by Calcium channels)
- have sudden rapid repolarisation which don’t get at nerve or pacemaker cells (transient potassium channels open and move out but calcium channels flooding in slows this repolarisation), increases absolute refractory period preventing building of action potentials (tetanus) so blood pumps out of ventricles
How is bradycardia treated?
Typically with pacemakers
How does bradycardia occur?
SAN = lack of sufficient electrical impulses AVN = heart block (3 degrees)
3 degrees of AVN heart blocks
1 - signal is travelling from SAN to AVN but is just slower
2 - some beats dropped so irregular
3 - no signal receieved at all = escape rhythm as AVN takes over
How is tachycardia treated?
Drugs or defibrillators
What do you get in tachycardia?
- AF
- atrial flutter
- SVT
- ventricular tachycardia
- VF
Reasons for pacing
- need something to sense slow/irregular beats and reinitiate standard rhythm for successful blood flow
SA block
- sudden stop of the P wave
SA pause or delay
- missing PQRST component
External pacemakers methods
- trans-thoracic
- transcutaneous
- external pacing
- emergency use only until transvenous pacing or other therapies applied
- after defibb
- for immediate bradycardia Tx
- should not be relied upon for extended time period
- use patch electrodes fixed to chest
Transvenous pacing
- temporary external pacing
- alternative to transcutaneous
- pacemaker wire is threaded through vein to enter RA or RV via subclavian or groin via x-ray guidance
- sedation is usually used
- issues = infection so guidance say avoid and put in permanent pacemaker instead
Implanted pacemakers
- local anaesthesia
- under skin
- pectoral muscle region
- battery life old issue but now lifetime guarantee mostly
- 1-2 hours surgery
- single or biventricular (bi = cardiac synchronisation therapy with you have HF with abnormal signals so have to stimulate both ventricles as not synchronised)