Origin of Self-Excitability

imissyou419's version from 2017-01-27 22:04

Section 1

Question Answer
SA node locationupper posterior wall of right atrium
What is so special about SA node?Self-excitation (spontaneous generation of AP) is fastest at SA node so it is the pacemaker (intrinsic rate = 100 times/min)
What happens if SA node is damaged?AV node and Purkinje fibers take over but discharge at slower rates
Speed of AP conductionslow AP velocity (SA node b/c slower rise in depol due to slow L-type Ca2+ channels), fast AP velocity (ventricular muscular fibers b/c faster rise in depol due to VG Na2+ channels)
Cardiac AP duration vs. Neuronal AP durationCardiac (s) vs. neuronal (1-2 ms)

Section 2

Question Answer
Slow spontaneous depolarization of SA nodal cells during diastole caused by:greater permeability to Na+ (funny) and Ca2+ (T-type VG and some slow L-type VG), decreased K+ permeability; (-60 -> -40)
SA nodal cell depolarization phaseNa+ (funny) and Ca (T-type VG) close, ALL slow L-type VG open, Ca2+ flows in slowly = slow response; (-40 -> +20)
SA nodal cell repolarization phase Slow L-type VG close, K+ VG channels open; (+20 -> -60)
Threshold of SA nodal cells-40 mV

Section 3

Question Answer
Interatrial myocardial bandpropagate AP from SA node to top of left atria so both atria contract at the same time
AV ringelectrically isolate atria from ventricles (do not want ventricles contracting from top down)
Internodal pathwaylinks SA node with AV node
AV nodeSLOWS AP conduction down! Makes sure atria finishes contracting before ventricles
Bundle of Hispropagate AP down to apex
Purkinje fibersPROPAGATE AP FASTEST to ventricle contractile cells
SA node conduction velocity0.05 m/s
Atrial muscle (gap junction) conduction velocity0.4-1.0 m/s
AV node conduction velocity0.05 m/s
Bundle of His conduction velocity1.0 m/s
Purkinje fibers conduction velocity2.0-4.0 m/s
Ventricular muscle (gap junctions) conduction velocity0.4-1.0 m/s

Section 4

Question Answer
P-wavedepolarization of atria
QRS-complexdepolarization of ventricles
T-waverepolarization of ventricles
U-waverepolarization of papillary muscles in ventricles
PR interval(beginning of P-wave to beginning of QRS) time AP takes from SA node through AV node to ventricles; if too short/long, AV node is damaged; decreased PR interval as heart rate decreases
QRS durationspeed of conduction through Bundle of His-Purkinje system; if narrow - fast and AP propagate through His-Purkinje, if wide - slow and AP jumping from ventricles through contractile cells
What happens if QRS duration is narrow?fast and AP propagation through His-Purkinje system
What happens if QRS duration is too wide?slow and AP jumping to ventricles through contractile cells
Wolf-Parkinson White SyndromePathway that allows AP to spread down directly from atria to ventricles so ventricles start contracting before AP got down to Purkinje fibers, therefore Q complex almost immediately after P-wave

Section 5

Question Answer
AP in ventricular contractile cells duration300 ms
Ventricular contractile cell depolarization phasecurrent from neighboring cells depolarize cell (gap junctions), opens fast Na+ VG channels and Na+ enters (-90 -> +20)
Ventricular contractile cell rapid repolarization phaseFast Na+ VG channels close, Cl- channels open and Cl- flows in briefly, K+ VG channels open and K+ moves out (outward + current)
Plateau phaseslow L-type Ca2+ channels open, Ca2+ moves in slowly (this inward Ca2+ current almost balances out the outward K+ current)
Restoration of Resting Potential phaseslow L-type Ca2+ channels close
Resting Potential phaseMembrane potential returns to -90 mV
Effective (absolute) refractory periodspans almost entire AP so can't add APs together, due to inactivation of Na+ and Ca+ channels
Relative refractory periodcaused by K+ efflux

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