Cardiac Electrophys Flashcards
Membrane potential
difference in movement of ions creating a charge separation across cell membrane
- measured on inside of cell
- electrical force
forces that drive ion movement
electrical force- membrane potential
and chemical force- due to difference in concentration of intra and extracellular fluid
nernst potential
ion’s individual chemical force depending on
- ratio of intra and extra concentrations
- valence of ion
magnitude of ion’s current depends on
forces during ion movement- nernst potential and membrane potential
and
conductance- how easily ion can move across membrane
conductance
ability of ion to cross cell membrane and related to:
- # of open ion channels
- leak channels
- ion concentration
Current
Iion= gion x (V - Eion)
g is conduction
I is current
V-E is electrochemical potential driving ion movement
V=E, no force driving movement and net current is 0
Larger V-Eion becomes
increases the force driving movement of ion
Fractional conductace
fgk= gk/ (gk+gNa)
Value of 0 if cell is impermeable, 1 is cell is only permeable to that ion
fgNa + fgK=1
Maximal limits for membrane potential set by
Ek and Ena
sequence of excitation in heart
SA node–> atrial muscle–> AV node–> common bundle–> bundle branches–> purkinje fibers–> ventricular muscle
Calcium dependent action potentials in
SA node and AV node
Intrinsic pacemaker
SA node
Sodium dependent action potential
atrial myocytes, bundle of his, purkinje fibers, ventricular myocytes
magnitude of depolarizing current during upstroke of AP will determine
- threshold potential
- amplitude of AP
- rate of rise of AP
- conduction velocity (propagation of AP down tissue)
ECG
P wave- atrial depol (sodium current) PR interval QRS complex- ventricular depol ST segment- phase 2 of ventricular AP T wave- vent repol QT interval
SA and AV node AP phases
Phase 4- funny sodium current is > Ik– depolarzing
Phase 0- upstroke of AP due to Ical
Phase 3- repolarizing phase where Ik is > depolarizing currents (delayed rectifier potassium current)
Maximum diastolic potential
most neg potential in SA node- normally -50 mV
Atrial and ventricular AP
Phase 4- stable resting potential (inward rectifier K channels)
Phase 0- upstroke due to Ina
Phase 1- transient repol due to K current
Phase 2- plateau due to balance between Ical and Ik (delayed rectifier channels)
Phase 3- repol due to Ik (delayed rectifier)
What phases determine duration of ventricular AP
phase 2 and phase 3
Effect of NE on SA and AV node
Released by SYM
Increase If (funny sodium channel)
Increase Ical
Increase heart rate primarily by increasing If in SA node - MDP less neg and phase 4 more steep
Increased SYM will increase IcaL and increase conduction velocity in AV node (dec PR interval)
Effect of ACh on SA and AV node
Released by PARA
Dec If
Dec IcaL
Effect of SYM on atrial and ventricular myocytes
- does not change Ina- no change in amp or width of QRS complex and P wave
- Inc IcaL and Inc Ik
Duration of vent AP determined by
Phase 2 and phase 3-
Ik inc- AP duration decreased as the rate of repol is increased- spiked T wave
Inc SYM firing will
increase inotropic state by increasing IcaL- make phase 2 more positive
common mediator of SYM and PARA that influences major cardiac ionic currents
adenylate cycase
- SYM acts via beta 1 to activate adenylate cyclase- enhances L type calcium, delayed rectifier potassium, and funny sodium currents
- PARA via vagus (ACh) acts via muscarinic receptor to inhibit adenylate cyclase and inhibits activation of above currents
Normal extracellular K concentration
3.5-5 mEq/L
Hypo and hyperkalemia cause
depolarization of resting membrane potential in cardiac muscle
- less negative than normal
- opp effects on K currents
Voltage gated Na channel
activation gate (rapid) inactivation gate (slow) -normal resting potential activation gate is closed and inactivation gate is opened -depolarization decreases # of resting Na channels in atria and ventricle--> decrease Ina during upstroke of AP
When Ina is decreased
- threshold potential is less negative (dec excitability)
- rate of rise of AP will be decreased
- amp of AP decerased (diminished height of P and QRS wave)
- dec conduction velocity (wider P and QRS)
Hypokalemia
-decreased gk–> decreased Ik–> longer AP duration (because phase 3 has gradual repol)- T wave is flat
decreased gk will increase fgNa- more neg Ek than normal
U wave may occur- delayed repolarizing wave
Hyperkalemia
inc gk–> inc Ik–> shorter AP duration (spiked T wave)
inc gk– less negative Ek than normal (more positive)
-less negative resting potential- fewer resting Na channels
Potassium effects on SA node- hypokalemia
MDP less negative
Phase 4 more steep
Tachycardia
Potassium effects on SA node- hyperkalemia
MDP more negative
Phase 4 less steep
Dec rate of firing of SA node (baroreflex may inc SYM firing)
Tx of hypokalemia
IV infusion of potassium
Tx of hyperkalemia
- inc plasma calcium to recover resting Na channels by shifting inactivation curve towards more positive potentials
- Sodium bicarb indirectly enhances Na K pump by inc Na influx via Na H exchanger
- Insulin stimulates Na-K pump, moving K into cell
- Lasix enhances K excretion by kidney
Absolute refractory period
During phase 2 and early phase 3- the time when Na channels are in inactive state
Relative refractory period
Later in phase 3 when membrane potential mecomes negative enough to allow convertion of inactive Na channels back to resting state
Functional refractory period
ARP + RRP
Decreases when duration of AP decreases- SYM activity
Reentrant loops
conduction velocity decreased (dec in voltage gated sodium current), duration of AP is decreased (inc potassium or dec calcium current), or both (high risk), inc size of tissue due to hypertrophy or dilatation (inc loop length, can’t depolarize simultaneously)
Length of loop occupied by AP= CV x Duration
Distance = rate x time
Conduction velocity reduced in conditions where
Ina is decreased
Ik increased
IcaL decreased
Early after depolarizations
If K+ current is suppressed, EAD can occur in late phase 2 or early phase 3 due to Ca++ window
- decreased rate of repol caused by hypokalemia or cocaine
- calcium window current due to opening of inactivation gates before activation gates have closed
Delayed after depolarizations
Can occur during phase 4
- high HR causes accumulation of Ca within myocytes (not enough time to pump ca out of cell)
- inc cystolic Ca levels activate- Na/Ca exchanger which causes net depolarizing current, or non specific cation channel which causes depolarizing current
Vfib
disorganized, chaotic ventricular rhythm due to multiple reentrant loops causing depol
- no effective cardiac contraction
- markedly reduced cardiac output
- requires defibrillation which will cause entire mass of myocardial cells to depolarize at same time and will be followed by spontaneous resumption of supraventricular rhythm
Afib
Multiple reentrant loops in atria (no P waves)
CO slightly reduced from normal
Results in stasis of blood in atria- inc risk of coagulation
