Cardiac physiology Flashcards
what is this and what is it used for
the nerst equation used to determine the Ex for a particular ion
what is the RMP of a cardiac myocyte
-90mV
what are two factors that generate RMP
unequal distribution of ions (Gibbs donnan)
relative permeability of ions (conductance)
how is RMP maintained
Na/K pump keeps and restores membrane to RMP
what is the difference in duration of AP between cardiac myocytes and pacemaker cells
cardiac myocytes are fast, pacemaker cells are slow
what current is at work in Phase 4 of a cardiac myocyte AP
IKir
what current is at work in Phase 0 of a cardiac myocyte AP
INa
what current is at work in Phase 1 of a cardiac myocyte AP
Ito (IKv1.4)
what current is at work in Phase 2 of a cardiac myocyte AP
ICaL
IKv1.4
IKv1.1
what current is at work in Phase 3 of a cardiac myocyte AP
IKv1.1
what are the 5 phases of a cardiac myocyte AP
Phase 4 (resting)
Phase 0 (upstroke)
Phase 1 (Early Repolarization)
Phase 2 (Plateau)
Phase 3 (final repolarization)
describe the process that produces Phase 2 (plateau)
L type calcium channels open at threshold (-50mV)
calcium enters the cell
creates a slow inward current
the movement of what two ions is balanced during phase 2
potassium intitally decreases in conductance, then increases as the AP transitions to phase 3
calcium increases in conductance then slowly decreases
what are the two advantages of the plateau period for cardiac function
maintenance of force generation (long contraction)
creation of a long absolute refractory period (allows for filling)
what happens when calcium is released from the sarcoplasmic reticulum in cardiac myocytes
calcium enters the L type calcium channel
it binds with ryanodine receptors on the SR
calcium induces calcium release from the SR
calcium binds to troponin C on tropomyson
ryanodine receptors
receptors on the SR of muscle cells that are triggered by calcium to release calcium into the cytoplasm
what is SERCA
what does it do
sarco/endoplasmic reticulum calcium ATPase
pulls calcium from the cytoplasm at the expense of ATP while the muscle is at rest
what causes the absolute refractory period
the closing of Na inactivation gates
what is different during relative and absolute refractory periods
during the relative refractory period some Na inactivation gates are open a second AP is possible
what is the supranormal period?
when does it occur?
a period where cells can be restimulated and threshold is lower than normal
only during phase 4
heart cells are particularly vulnerable to arrhythmias at what point in the cardiac cycle
the phase 4 supranormal period
how long does the absolute refractory period last in a cardiac myocyte AP
what are three advantages of this
almost as long as the twitch does
- no summation of APs
- no tetanus
- allows for filling
tetradotoxin
a volrage gated channel blocker derived from the venom of a puffer fish
what are three general symptoms of tetrotoxin poisoning
GI distress
CNS
Cardiovascular
three GI symptoms caused by tetrotoxin
nausea, vomitting, cramping
three CNS symptoms caused by tetrotoxin
muscle weakness
numbness
coma
three cardiovascular symptoms caused by tetrotoxin
decreased cardiac output
hypotension
bradycardia
automaticity
the ability of cardiac pacemaker cells to produce their own APs
two locations of nodal cells in the heart
SA node (right atria)
AV node (inferior posterior section of the intratrial septum)
what are the three phases of a pacemaker cell
Phase 4 (slow depolarization)
Phase 0 (upstroke)
Phase 3 (repolarization)
how are cardiac pacemaker cells able to produce a slow depolarization
they have an unstable resting membrane potential
what currents are at work in Phase 4 of a pacemaker cell
IF
ICaT
IKv1.1
what current is at work in phase 0 of a pacemaker cell
ICaL
what current is at work in phase 3 of a pacemaker cell
IKv1.1
what are two factors that determine the fire frequency of pacemaker cells
the rate of depolarization in phase 4
the maxium pacemaker potential
what causes a change in slope during phase 4 of a pacemaker AP
what will happen in each instance?
sympathetic/parasympathetic nerve stimulation
sym: slope increases and causes higher firing frequency
para: slope decreases = lower firing frequency
how does the maximum of the pacemaker potential effect firing rate
the more negative the pacemaker potential is, the slower the firing rate will be
describe the pathway of sympathetic stimulation on pacemaker cells up to PKA
Norepinephrine is release from the adrenal medulla
NE binds to beta 2 adrenergic receptor
B2 receptor releases G protein
alpha subunit activates adenylate cyclase
adenylate cyclase releases protein kinase A
what are the functions of protein kinase A in pacemaker cells
increasing Na conductance to allow If
phosphorylation of T-type calcium channels to increase Ca conductance and allow ICat
what is the end result of sympathetic stimulation of cardiac pacemaker cells
increase of Ca and Na influx which will increase the rate of depolarization, slope, and heart rate
describe the pathway of parasympathetic stimulation on HR (up to G protein release)
acetylcholine binds to muscarinic receptors
M receptors release G protein
G protein subunits beta and gamma induce intracellular response
describe the effect of G protein subunit ßy (parasympathetic) on heart rate
G protein subunit ßy binds to KAch channels
potassium influx increases
membrane is hyper polarized
pacemaker potential is more negative
describe the effect of G protein subunit Gαi on pacemaker cells
cAMP is decreased, causing a decrease in PKA
If, ICaL, IKv1.1 all decrease
slope/rate of depolarization are decreased
what is the end result of parasympathetic stimulation on pacemaker cells
decreased pacemaker potential and rate of depolarization, leading to a slower HR
which part of the autonomic nervous system dominates HR variability
parasympathetic
how does tonic stimulation apply to pacemaker cells
the parasympathetic nervous system displays tonicity by constantly having a inhibitory effect on heartrate
how do SNS and PsNS differ in terms of onset of effect after stimulus and decay of effect when the stimulus is with drawn
SNS: slow onset, slow decay
PsNS: fast onset, fast decay
which pacemaker node in the heart produces impulses at the highest frequency
the SA node
describe the path of an action potential through the heart
SA node
internodal pathways
AV node
bundle of His
bundle branches
purkinje fibers
what is the function of the AV node
delays ventricular excitiation to ensure filling
how long is an AP delayed at the AV node
0.1 second
what part of the cardiac conduction system has the slow conduction velocity?
the fastest?
the AV node
purkinje fibers
what is the function of the bundle of his, bundle branches, and purkinje fibers
ventricular excitation
T/F the slowest functional pacemaker dominates the heart
fast, the fastest pacemaker does
what is the firing rate range of the SA node?
AV node?
60-120
40
what would happen to HR if the SA node were nonfunctional due to injury
the AV node would take over and produce a HR around 40bpm
what would happen if the AV node were knocked out but the SA was still firing
the SA node AP would not be able to reach the purkinje fibers so the fibers would produce a HR of around 30
what would happen if the purkinje fibers began to fire at a rate of 140bpm even with a functional SA and AV node
the whole heart will be driven by the faster rate
what three factors determine the conduction velocity of pacemaker APs
diameter of fibers (decrease viscosity)
number of gap junctions (increase conductance)
rate of slow depolarization (increased slope)
why does the AV node have the lowest conduction velocity
small cell diameter and few gap junctions
why do the purkinje fibers have the highest conduction velocity
large diameter and many gap junctions
what is the physiological and clinical significance of delayed AV conduction
optimal ventricalr filling during atrial contraction
why does the AV node make the heart vulnerable
damage to the AV node will cause a loss of conduction to the ventricles
