ECG Flashcards
normal conduction pathway
SA AV bundle of his left and right bundle branches purkinjee branches
where is the sa node and whats it do
upper right part of Right atrium it sponetaneous generates (automaticity) current at 60-100 beats per min.
what does the AV node specialize in
slow conduction. As conduction flows down the atriums it hits the fibrous tissue and is neutralized at all points expect at the AV node which collects the current and slowly conducts it.
purkinjee cells specialization
fast conduction
how are myocardial cells connected
gap junctions. they are filled with flulid.
two types of myocardial cells. Specialized and contractile
Specialized 1.SA node 2.AV node 3.Purkinjee cells Contractile 1.Atrial 2.Ventricular
Resting membrane potential
myocardial genes make an mRNA that creates a transmembrane protein called to sodium potassium ATPases. Dumping out 3 Na and bringing in 2 K+. This creates about a -5 mV potential. Resting membrane potential is -90mV. The sodium would love to jump into the cell because of the concentration gradient and the electrical gradient that has been created but they cannot move through the non polar membrane. In resting cells you have potassium leaky channels that allow potassium to leave due to the concentration gradiant but the electrical gradiant is trying to hold the potassium in. When the concentration gradient taking the potassium out and the electrical gradient trying to keep the potassium in are in equilibrium it is called resting membrane potential.
how is action potential created
when a cell in resting membrane potential is stimulated by either pushing some cations in (sodium or calcium) as you throw in cations you decrease the electronegativity inside. Once you hit -70 mV(threshold potential) sodium gated channels open. rapid influx of sodium happens and electronegativity inside is gone. this is called depolarization. (((The sodium will take the electronegativity to like +10 mV this extra sodium will move through the gap junction and cause the neighboring cell to reach threshold potential.))))
depolarization opens up voltage gated potassium and calcium channels. This causes potassium to leak out causing slight electronegativity increase taking it from like 0 to -5. Calcium will try to jump in because the concentration outside is very high. the amount of calcium entering is = to the amount of potassium leaving therefore you reach what is called a plateau at -5mV. This phase does not last long because calcium channels eventually close. but the cell is still losing potassium until resting membrane potential is reached. (repolarization)
what is action potential
it is electrical activity that is moving unlike resting membrane potential which isnt moving.
why dont the sodium gated channels allow infinite sodium into the cell when they are activated
there are two levers one on the inside(activation channel) of the cell and one on the outside(inactivation channel). The one on the outside is open during rest and the one on the inside is closed during rest. When threshold potential is achieved the one inside opens very quickly allowing sodium to quickly influx in. The one outside begins to close but it is much slower during this time sodium is coming into the cell.
how does the SA node work
has the same ATPases as regular myocardial cells expect they also have leaky sodium channels too. but the gated sodium channels are perm closed. therefore it cannot have a super high electronegativity. (-60mV) you get influx of sodium causing electronegativity to drop to around -45mV which is the potential threshold. Instead of sodium channels opening we have calcium channels that open and cause depolarization. The extra calcium travels through the gap junction and stimulates the atrial cell to propagate the action potentials.
how is the AV node like the SA node
it is depolarized by calcium therefore it has automaticity.
what are the pros of sodium dependant depolarization vs calcium
sodium is almost instant depolarization (striaght line up) calcium is slower.
explain how G proteins work
beta 1 adrenergic receptor
norepi binds to a g receptor protein which then activates the alpha subunit of the gprotein(there is also beta and gamma subunits) the alpha subunit drops ADP for ATP and moves to activate adenlyl cyclase, once activated adenlyl cyclase will convert ATP to cAMP.
what is cAMP
it is an intracellular secondary messenger which activates protein kinase A (PKA) which leads to phosphorlyation of target proteins (calcium channels) which activates calcium channels. since extracellular calcium is more this causes calcium to move in. This increases the automaticity of the SA node.
