Cardiac Lecture 1 Flashcards
which type of cells have gap junctions
cardiac muscle cells
where are gap junctions located
within the intercalated discs
what do gap junctions do?
help carry the action potential through the cell
draw the action potential of a contractile cell
n
Phase 0 of a contractile cell
voltage-gated Na+ channels open
Na+ floods into the cell
start of depolarization
Phase1 of contractile cell
initial depolarization due to closure of the voltage gated Na+ inactivation gate
phase 2 of contractile cell
- plateau phase
- voltage gated Ca++ channels open and Ca++ rushes into the cell
- maintains depolarization (positive charge entering the cell)
phase 3 of contractile cell
- repolarization
- K+ leaves the cell and inside of cell becomes more negative- down to resting membrane potential
- resembles skeletal muscle
phase 4 of contractile cell
- leak K+ channels help keep cell at resting membrane potential
- 90mV
type of voltage-gated Ca++ channels in contractile cell
L-type
-slow to open, slow to close
what is the time of the absolute refractory period in
cardiac muscle cells
.2-.25 seconds
- good to have long absolute refractory period that lasts as long as cardiac muscle contraction
- allows muscle to relax for adequate filling of blood before next contraction
what is the time of the relative refractory period in cardiac muscle cells
.05 seconds
- will require a bigger stimulus to initiate contraction
- weaker contraction
how long does the action potential last in a cardiac muscle cell
almost as long as the entire contraction
-good because you do not want tetanus in cardiac muscle
how is cardiac muscle contraction different from skeletal muscle contraction
some of the Ca++ came from outside the cell
- 25% is from the outside
- 75% is from SR
how is cardiac muscle contraction different from skeletal muscle contraction
some of the Ca++ came from outside the cell
- 25% is from the outside
- 75% is from SR
three ways Ca++ can be excreted from the cell to get ride of contraction
- SERCA pump
- Ca++ ATP-ase pump on the membrane
- Na+/ Ca++ exchanger- uses the natural gradient of Na= to pump Ca++ against its gradient
what does the enzyme phospholambin do?
puts the brakes on the SERCA pump to slow it from pumping Ca++ back into the SR
what are the mutations involved with genetic Hypertrophic cardiomyopathy
- myosin heavy chain involved w/ contraction
- mutations in sarcomere proteins in the heart
- troponin, tropomyosin, titin, actin, myosin
what are the effects of genetic hypertrophic cardiomyopathy?
- obstructs outflow of blood through the aorta
- reduces filling volume of the ventricle
- prone to arrhythmia
- takes longer for the action potential to spread throughout the heart because of increased muscle
- changing the refractory period
what are 2 ways to augment (increase) the force of contraction of contractile cells
- beta agonists
- epi and NE on b1 receptors on heart
- increases the amount of Ca++ in the cell by phosphorylation of voltage gated Ca++ channels( cAMP to pKA) - phosphorylate actin and myosin to get stronger contractions
one way to decrease the force of contraction of contractile cells
- decrease Ca++
- beta-blockers
- verapamil, nifedipine-block the voltage gated- Ca++ channels
difference of pacemaker cells than muscle cells
- few contractile cells- does not contribute to contraction
2 faster conduction rate - no sarcomeres (t-tubules)
what leads to automatic depolarization in pacemaker cells
funny current- leaky Na+ channels
-Na+ moves into cell slowly and depolarizes it
in cardiac muscle cell, action potential is led by _____ while in pacemaker cells, the action potential is carried by ____
Na+ , Ca++
what happens when pacemaker hits threshold by funny current
voltage gated Ca++ channels open
what type of voltage gated Ca++ channels do pacemaker cells have
T-type: fast to open and fast to close
in pacemaker cells what happens after opening of voltage gated Ca++ channels
voltage gated K+ channels open and K+ leaves the cell and repolarizes the cell membrane
what is the resting membrane potential of a pacemaker cell
-60 mV
drug that reduces the funny current without changing contractility
ivabradine
what had the fastest depolarization rate from the funny current
SA node- 60-80/min
AV node- 40-60/ min
perkinjie fibers- 15-30 bpm
3 ways to alter the heart rate by the sympathetic (adrenergic) nervous system ( increase HR)
- activate the B1 receptors with epi or NE
- increase cAMP which activates the funny current
- more Na+ leaks into the cell and depolarizes it faster and you get a faster HR (chronotropic) - activate PKA which will block the enzyme phospholambin
- inhibits the SERCA pump and more Ca++ can be pumped into the SR to increase muscle relaxation (lusitropic) - Caffeine allows more cAMP to be around
ways to alter the heart rate by parasympathetic (muscarinic) nervous system (decrease HR)
- ach binds to muscarinic receptors (increases K+)
- stimulates GI which inhibits AC and decreases cAMP and PKA (decreases funny current and Ca++ influx) - Adenosine stimulates GI
what nerve is the parasympathetic nervous system mediated by
vagus nerve
what is the conduction velocity through the nodal pathways
1 m/s
function of the SA node
automatic depolarization triggers action potential in cardiac muscle cells through gap junctions
what is the conduction velocity through the AV node
.05 m/s
-has the SLOWEST conduction velocity
3 reasons why conduction is slow in the AV node
- fewer funny current
- fewer gap junctions
- lots of vagal innervation with Ach
why is slow conduction through the AV node a good thing?
allows atria to fully contract before ventricles contract
where is the only place conduction signal can cross through the conduction system
bundle of HIS
- everywhere else is insulated
conduction velocity through the perkinjie fibers
- 5-4 m/s
- has the FASTEST conduction velocity
conduction velocity through the muscle fibers
0.3-0.5 m/s
total time it takes the impulse to travel through the heart
1/3 of a second= 0.22
common cardiac agents used for short term treatment of heart failure
inotropic agents
mechanism of digoxin/ digitalis
- cardiac glycoside/ inotropic agent
- inhibits the Na+/ K+ pump
- Ca++ builds inside the cell and increases contraction
- depresses SA node and slows conduction through the AV node
effects of digoxin/ digitalis
- proper dose will increase cardiac contractility
- decrease HR and prevents arrythmias
- too high of dose can lead to arrythmias from increased Ca++
mechanism of dobutamine
inotropic agent- increases contractility
- B1 adrenergic agonist
- increases Ca++
effects of dobutamine
- increases HR
- arrhythmias
mechanism of milrinone
- inotropic agent- increases contractility
- phosphodiesterase 3 inhibitor
- increases cAMP (prevents breakdown)
- increases Ca++
effects of milrinone
- increases the HR
- arrhythmias
mechanism of levosimenden
- inotropic agent- increases cardiac contractility
- increases calcium sensitization of troponin C
- does NOT increase HR
what does the QT interval represent
depolarization and depolarization
what is the normal time of the QT interval?
0.35-0.42 s
what does hypocalcemia do to the QT interval
long QT interval
-less Ca++ takes more time for Ca++ to move in to the cell
what does hypercalcemia do to the QT interval
short QT interval
-increased Ca++ outside the cell increases the drive of Ca++ to want to move into the cell more quickly
what do changes to the QT interval do to the contractility of the heart
susceptible to arrhythmias because you are changing the absolute refractory period
what is the most likely ion channel that is involved in prolonged QT intervals due to genetic mutations
K+ channels because you are changing the repolarization rate
ST segment depression refers to
myocardial ischemia
ST segment elevation refers to
myocardial infarction ( heart attack)
what does the ECG measure as far as membrane potential
- measures the potential outside of the cardiomyocytes with is positive (why the ECG is positive waves)
- measures the potential difference between 2 leads
which directions does the heart repolarize
from epicardium to endocardium
-epicardium action potential and absolute refractory period is shorter
“first area to depolarize is the last area to repolarize”
in which direction does the heart depolarize
from endocardium to epicardium
why is the t-wave positive?
you are repolarizing the heart in the opposite direction
when would you get an inverted t-wave?
- when the first area to depolarize is the first area to repolarize
- endocardium repolarizes first
3 causes of an inverted t-wave
- coronary ischemia
- hypertrophy- more heart muscle so endocardium action potential will actually be quicker
- bundle branch block
