excitable heart Flashcards
SA node
- unstable phase 4
- automaticity
transmembrane conductance
- POTASSIUM
UNGATED POTASSIUM CHANNEL
- constant
- concentration dependent
- it is happening all the time
VOLTAGE GATED SODIUM CHANNELS
- not constant
- based on electrical charges
- affected by action potential
VOLTAGE GATED CALCIUM CHANNELS
- not constant
VOLTAGE GATED POTASSIUM CHANNELS
- not constant
Na+ permeability
- fast channel
Ca2+ permeability
- slow channel
K+ permeability
- slow channel
membrane potential (Inside the cell)
- 90mV due to potassium going out NORMALLY
- it becomes positive when sodium goes IN
Calcium2+ L type channels
- stays plateau positive
- going IN
Phase 0
- fast channels open gNa
- depolarization
- opens and close quickly
Phase 1
- slight repolarization
- due to transient Potassium current
- closing of the sodium channels
arrhythmia
treatment to lower mortality beta blockers not anti arrhythmic drugs because it is also a pro drug
Phase 2
- L-type Ca2+ are open
- Calcium influx (maintains the interior +)
- K channels are closed and leaving efflux
- CALCIUM channel antagonist shorten the plateau (NIFEDIPINE, NICARDIPINE, AMLODIPINE ETC) stops the calcium going IN
- POTASSIUM channel antagonist lengthen the plateau (
hyperpolarized
- becomes more negative from -70 to -90
lethal injection
- sudden depolarization of the heart
- K
Phase 3
- L type Ca2+ channel closes gCa
- large K efflux
- cells quickly repolarized
Phase 4
- gK high
- voltage gated and unrated potassium channels open
- relative refractory period
SA node
- top of the atrium
AV node
- bet the atria and ventricle
nodal channel
- no phase 1 and 2
acetylcholine
- vagal stimulation
beta blockers
- blocks the sympathetic stimulation
lightheadedness, pulse 40 what is the initial therapy
too slow speed up by
- atropine (anitcholinergic)
- anti vagal stimulation
- anti parasympathetic
- stimulate sympathetic
rapid atrial fibrillation initial therapy
too fast slow it down with
- beta blockers to slow down
- stimulate parasympathetic