CV a&p Flashcards
do skeletal myocytes or ventricular myocytes contain more mitochondria?
ventricular myocytes contain more mitochondria
normal ventricular RMP and what regulates it
-90mV, regulated by potassium
what does hypocalcemia and hypercalcemia do to threshold potential respectively?
hypocalcemia decreases TP (cells depol more easily bc its closer to RMP)
hypercalcemia increases TP
the wave of depolarization throughout the heart is regulated by gap junctions or t tubules?
gap junctions
equilibrium potential
no net movement across cell membrane. inside potential equals outside potential
which equation relates to equilibrium potential
nernst equation
automaticity
ability to generate AP spontaneously ex) SA node and HR
excitability
ability to respond to electrical stimulus by depolarizing and firing an AP. ex) conduction and contractile CV cells
conductance
ability to transmit electrical current. ions are charged and therefore require an open channel.
open ion channel increases conductance of that ion (duh)
lusitropy
rate of myocardial relaxation
dromotropy
conduction velocity through heart
RMP is determined by 3 things
chemical force (concentration gradient)
electrostatic counter force
Na/K/ATPase
what is the primary determinant for RMP
K. the nerve cell continually leaks this at rest
decreased serum K makes RMP more
negative, cells become more resistant to depol
increased serum K makes RMP more
positive, cells depol more easily
what is the primary determinant of threshold potential
calcium
a cell depolarizes when what enters the cell
Na or Ca2+
what happens during repolarization
K leaves the cell or Cl- enters the cell
resistant to subsequent depol during refractory period
hyperpolarization
movement of cells membrane potential to a more negative value beyond baseline RMP.
purpose of Na/K/ATPase
restores ionic balance towards RMP
1. removes Na that enters the cell during depol
2. returns K that has left the cell during repot
for every _______ ions the Na/K/ATPase pump removes, ___________ ions go back into the cell
for every 3 Na ions it removes, 2 K ions go back into cell
what happens during cardioplegia with high K
Na channels get locked in their closed inactive state
5 phases of myocyte AP
0: depol (Na in)
1: initial repol (K in, Cl- out)
2: plateau (K in, Ca2+ out)
3: repol (K out)
4: maintenance of trans membrane potential (K+ out and Na/K/ATPase fx
what’s the point of the plateau phase in a cardiac myocyte (that neurons dont have)
gives myocytes time to contract and eject SV
relation of myocyte AP to EKG
myocyte events during phase 0: depolarization
TP of -70 is met
activation of fast VgNa channels
slope indicates conduction velocity
myocyte events during phase 1: initial repolarization
inactivation of Na channels
K and Cl- channels open
myocyte events during phase 2: plateau
activation of slow VgCa channels counters loss of K to maintain depolarized state
delays repolarization
maintains fast Na channels in inactivated state
prolongs absolute refractory period
myocyte events during phase 3: final repol
k channels open, delayed rectifier
K leaves cell faster than Ca2+ enters- repol
slow Ca2+ channels deactivate
restores transmembrane potential to -90mV RMP
myocyte events during phase 4: resting phase
K leak channels open (to maintain RMP)
Na/K/ATPase (removes 3 Na gained during depol and replaces 2 K lost during repol)
channel that is the primary determinant of the pace makers intrinsic HR (SA node)
I-f (funny channels). sets rate of spontaneous phase 4 depol. funny channels are activated from hyper polarization
conduction of AP from SA node
SA–> internal tracts –> AV –> bundle of his –> left and right bundle branches –> purkinje fibers
RMP of SA node
-60mV (higher than cardiac myocytes)
SA node AP in relation to EKG
order of SA node AP
phase 4
phase 0
phase 3
SA node events during phase 4: spontaneous depolarization
Na in (via I-f channels) and Ca2+ out via T type channels
at -50mV, t type Ca2+ channels open to further depol the cell.
SA node events during phase 0: depolarization
Ca2+ in via L type channels
Na and T type Ca2+ channels close
SA node events during phase 3: repolarization
K channels open and K exits the cell making it more negative
K efflux repolarizes cell to return it to phase 4
repol decreases calcium conductance by closing L type calcium channels
intrinsic firing rate of SA node
70-80 (faster in denervated heart)
intrinsic firing rate of AV node
40-60
intrinsic firing rate of purkinje fibers
15-40
what 3 variables can we manipulate to alter HR?
rate of spontaneous phase 4 depolarization (slope increases like with NE admin)
threshold potential (TP becomes more negative, closer to RMP)
RMP (RMP becomes more positive, closer to TP)
how does Ach slow HR
stimulates M2 receptor, increases K conductance and hyper polarizes SA node. decreases slope of phase 4 conduction.
baseline CaO2
20 mL/O2/dL
baseline DO2
1000mL/min
baseline VO2
250mL/min or 3.5mL/kg/min
baseline CvO2
15mL/dL
DO2 equation
CO x [(Hgb x SaO2 x 1.34) + (PaO2 x 0.003)] x 10
=CO x CaO2 x 10