Cardiac Conduction And Action Potentials Flashcards
Bradycardia
RR is < 60/min
Tachycardia
RR > 100/min
First Degree AV Block
PR interval > 0.2
P is far from QRS complex
Long QT Syndrome
Q—> T is too far from
T wave is far from QRS complex
SA node
Major pacemaker
AV node passes to
through septa to Purkinjie Fibers
what makes A contract and V contract
A : SA node
V : AV node
which A contracts first
RA
What contracts first Endocardium or epicardium
Endocardium
which epicardium contracts first
RV epicardium
How are the AP speeds different
HIGHEST (largest D) Purkinje fibers Atrial and ventricular muscle fibers AV node SLOWEST
AP frequency in heart
HIGHEST SA node AV node Purkinje fibers LOWEST * to —I overdrive
What 2 places have spontaneous AP
- SA node : if it never gets signal to contract (40/min)
2. Purkinje fibers : if they dont get signal from AV node (20/min)
What happens in the primary AV block
The SA node sends signal to AV node and AV node holds on to it for too long
Secondary AV block
The SA node sends signal to AV node and it drops it and then SA node sends a second signal that causes AV node to send signal
= 2 p-waves , pretty spaced apart
AP Phases 0-4
For Ventricels and Atria and Purkfibers
Phase 0 : depolarization
Phase 1+ 2: keep Depolarization longer
Phase 3: Repolarization
Phase 4 : RMP (resting)
Phases of AP in SA node and AV node
More like
Slow APs and
Phase 4 : is at RMP——> rising slowly on its own
* no Phase 1 or 2
Phase 0
Na+ quick influx
Phase 1
NA+ channels close by inactivation gate
K+ channels open and K+efflux
*rapid small dip
Phase 2
Ca+2 channels then open = CA+ influx
= common always open (rectifying) K+ channels close
= closure of phase 1 K + channels
*MP stays + for a while
Phase 3
CA+2 closure
Rectifying K + channels open
Voltage K+ channels from phase 1 open (FULLY, started during phase 2)
What happens in Long OT syndrome
long time from phase 2 to phase 3
* Ikr(rapid K channels opening) and Iks (Slow K channels opening) channels don’t function right
= long QT interval (T wave is far from QRS)
Ik1
Ikr
Iks
Ito
Rectifying K+ channel (close phase 2)
Rapid voltage gated K + channel (O phase 3)
Slow voltage gated K + channels (O phase 3)
The voltage gated K + channels (O in phase 1)
When does ICa open
Phase 2
Phase 4 on slow AP
Gradual depolarization until threshold (spontaneous pacemaker)
= slow Na+ influx (If or INaf) funny voltage channels (closes at threshold and open during complete repolarization)
Phase 0 during slow AP
Ca+ channels open
K+ channels close
Phase 3 during slow AP
K+ channels open (rectifying)
Closure of Ca+ channels ——> opens Na+ funny voltage channels for phase 4
Parasympathetic stimulation by what N goes to
Vagus N —> ACH (M2/M3 receptors + special K+ ach channels)
SA node and AV node, and only very few to atrial myocytes
Slowing of heart rate has no influence on
Contractility (inotrophic)
Parasympathetic innervation on HR and how
Slows it (- chronotropic effect) Phase 4 : funny Na+ channels are slower = slow NA+ entry (decrease slope) Phase 3 : ACH causes K+ ACh receptors to keep K+ channels open longer = hyperpolarization
What does the sympathetic N innervates and what R and NT
The SA node, AV node, and ventricular myocytes
Norepinephrine——> B1 adrenergic Receptors
Sympathetic effect of HR and how
Increase it (+ chronotropic effect)
- Rapid influx of funny NA+ channels (phase 4)
- Increases CA+ into myocytes (phase 0) = increased contractility + slope
* + inotropic effect due to more Ca available for muscles
What does sympathetic n do to velocity and relaxation velocity on AP
Increases both
+ dromotropic : fast contraction
+ lusitropic : fast relaxation after contraction
Refractory period in heart
Are longer to allow all blood to get into A and V
ARP (Absolute Refractory Period)
X AP can be made no matter what
=All Na+ channels are inactive
RRP (Relative Refractory Period)
AP can be if the stimulus is great enough
= many of Na+ channels have reset
= makes an AP that’s not as big
Supranormal Period (SNP)
Cell is more excitable then normal (anything will)
= AP here will be abnormal and small
= close to threshold and mostNA+ channels are reset
Biggest reasons you get arrhythmia
ion concentrations aren’t right
Hyperkalemia
Excess K+ in ECM = RMP will get higher
SLOWS phase 0 + less steep slope
SPEEDS UP phase 3 + doesn’t go all the way back down to normal RMP = not normal refractory period
Hypokalemia
Low K+ in ECM = RMP gets lower
Need higher stimulus for AP (phase 0)
Hyperkalemia and Hypokalemia on HR
Makes some myocytes fire at different times - not normal rhythmic contractions
Isoelectrial point
When all myocytes are depolarized and contracting either in A or V
Ventricular AP happens at what point
Atrial AP happens at what point
End of T wave
End of P wave
Cardiac sounds: means what on the ECG S1 S2 S3 S4
S1 : Q wave starts when mitral valve closes
S2 : End of t wave, when the aortic valve closes
S3 : Mitral Valve opens and blood enters V
S4 : PR segment (atrial repolarization) blood fills the A
