Cardiac membrane potential Flashcards
What is the order of activation of the heart?
SA node (pacemaker) R & L atria AV node (slows down) His purkinje (super fast)- synchronize -bundle of his -bundle branches -purk cells: endo to epi
What is the function of the sodium-potassium pump?
takes 3 Na out
brings 2 K in
maintains the gradient
What is the function of the Na-Ca exchanger?
tries to keep calcium concentration low inside the cell
takes 1 ca out
brings 3 Na in
*driven by the sodium gradient set up by the pump
What is the normal concentr of extracellular potassium?
between 3 to 5 mM
What is anomalous rectification?
- Nerst equation predicts that at lower extracell [k] the K+ should be leaving the cell but it doesn’t
- there’s a decrease of K+ permeability whenever there is an increased driving force on K
e. g. hypokalemia or depol of membr
*via IK1 channel
What happens in hypokalemia?
extracell [K] is less than 3mM
incr gradient for K to leave the cell
doesn’t due to decr permeability (anomalous rectification)
result: no change in RMP
What happens in hyperkalamia?
extracell [K] is more than 5mM
causes membrane to be more permeable
but K stays inside -> more + RMP
-now got less Na channels available: fast AP upstroke decr and conduction slows
What happens in an MI?
RMP depolarizes (+) so Na channels are less available
no AP
infarcted regions can have K+ leaking out, local hyperkalemia
-slows conduction -> can lead to re-entry
How do potassium channels delay repolarization?
cuz rectification
when voltages are more positive than the K equilibrium (e.g. action potential plateau)
much outward K flow is not allowed
in other words, during the AP plateau K+ permeability decreases, delaying repolarization
What are fast responses?
Na channels!
have fast rate of rise and high amplitude
What are slow responses?
L type Ca channels!
have slow rate of rise and lower amplitude
*have short space constant cuz less gap junctions
plus have higher resistance cuz smaller cells
Describe the phases of the cardiac AP
Phase 0: upstroke- activation of fast sodium channels (membr potential approaches E-Na (+) [net inward]
Phase 1: Na channels close, K channel (I-TO) transiently open [net outward]
Phase 2: plateau phase- L type Ca channels open
background IK1 channel decrease (inward rectification) [net inward]
Phase 3: Ca channels close and iK1 conductance increases (reversal inward rectification) [decr outward]
Phase 4: repolarization- background K conductance (iK1) high, delayed iK channels deactivated
Ca channels closed and Na channels recover but remain closed [back to rest]
What is the effect of tetrodotoxin on purkinje fiber AP?
block fast Na channels (Phase 0)
slow Ca channels not affected so they carry phase 0
rest of phases unchanged
net result: slow response AP
Slow vs Fast response
Slow: SA & AV node
phases: 0, 3, 4
low membr potential, low threshold, slow upstroke, short duration, slow conduction!
Fast: atrial, His-Purk, ventricular
Phases: all
high membr potential, high threshold, fast upstroke, long duration, fast condition!
What are the characteristics of SA/AV node cells?
small! short space constant, few gap jnct = slow conduction
few myofibrils = weak contraction
function: pacemaker
What are characteristics of atrial and ventricular muscle?
medium! lotz of gap junct = rapid conduction
lotz myofibrils = strong contraction
function: conduction/contraction
What are characteristics of His-Purk cells?
large cells! lotzz gap junct = rapid conduction
few myofibrils = weak contraction
function: very rapid conduction
What is an intercalated disc?
Specialized region of intercellular connections b/w cardiac cells
- types of adhering junctions
1. fascia adherens: anchor site for actin
2. macula adherens (desmosomes): hold cells together during contraction by binding interm filaments
3. gap junctions: low resistance connections that allow current (AP) to conduct - primary determinant of internal resistance in cardiac tissue
- senstive to intracell [Ca] and [H+]
What is healing over?
increase in internal resistance due to decrease of open gap junctions
caused by increase of intracell [Ca] and [H+] after an MI
*electrical isolation fo damaged tissue
What are the factors that determine cardiac function?
- space constant!! (Rm/Ri)^1/2
Rm is inversely related to K+ permeability (low K causes decr K permeability which increases membr resistance)
Ri is inversely related to # of gap junctions & inv related to diameter - rate of rise and amplitude of AP
- lvl of resting membr potential (for fast responses) [rem the more positive, the less Na channels available]
- slow vs fast AP
- premature responses initiated during RRP
What conditions influence the AP upstroke?
those that change RMP (more + = inactivated Na channels)
e.g. hyperkalemia: make it more +
premature excitation during RRP- slower upstroke
ischemia/MI: damaged cells release K+ so depolarize RMP
What conductions can you see on an EKG?
P-R interval: conduction from atria to ventricles
QRS: conduction through ventricles
What can you tell me about AV node conduction?
delays conduction to allow ventricular filling
AP is slow response cuz slow inward Ca current
long refractory period (can’t get another AP)
-Protects ventricles from abnormally high atrial rates
*determined by P-R interval
What are examples of AV nodal conduction abnormalities
heart block!
1st degree: abnormal prolongation of PR (greater than 0.2s)
2nd degree: some atrial impulses fail to activate ventricles
-not all p waves followed by qrs (diff ratios)
Mobitz type I: progressive lengthening of PR then shortening, drop beats
Mobitz type II: same PR but still drop beats
3rd degree: complete AV nodal block
-no consistent PR interval
atrial flutter or fibrillation: when atrial rhythm is going way too fast
-thankfully long refractory period protect the ventricles
What can you tell me about ventricular conduction?
rapid conduction through His-Purk! endo to epi narrow QRS (less than 100msec) synchronized QRS interval!
What are some examples of abnormal ventricular conduction?
-slurred QRS= slowed intraventricular conduction. abnormal wall motion
causes? hyperkalemia, ischemia, ventricular tachy
-notched QRS= asynchronous activation of LV & RV
causes? L and/or R bundle branch blocks
-ventricular conduction through diff types of tachycardia
e.g. supraventricular tachycardia (SVT): conduction has normal pattern but just fast. coming from atria, normal wall motion, QRS duration normal, SV not sig compromised
e.g. ventricular tachycardia (VT): impulse originates from ventricular muscle- slower plus abnormal conduction pattern = abnormal wall motion, SV compromised
-slurred QRS
What can you tell me about atrial conduction? plus abnormalities
represented by p wave
atrial fibrillation: no discreet p wave
-not fatal cuz only contribute 5%
it can become ventricular fibrillation (conduction abnormality)
-asynchronous, cardiac output drops -> fatal
*both due to re-entry of excitation
What is the effect of parasympathetic innervation to the heart?
through Ach on muscarinic receptors
- incr K+ permeability: hyperpolarize membr
- inhibit adenylate cyclase activity + cAMP synth: dear slow inward Ca
- inhibit atrial muscle contraction: negative ionotropic effect
- inhibit SA node: slow HR, lengthen R-R
- inhibit AV node: lengthen P-R interval
What is the effect of sympathetics innervation to the heart?
affects all areas! via beta 1 -> incr cAMP -incr slow inward Ca current -incr atrial/ventri muscle contraction: + ionotropic effect -incr SA node rate: incr HR, decr R-R -incr AV node conduction: decr P-R
