Unit 2 Flashcards
what band does not change in length during contraction (sarcomere)
A band
what decreases in length during contraction (sarcomere)
- sarcomere
- I-band
- H-zone
S1 region of thick filament
where thin filament binds
where ATP binds
S2 region of thick filament
flexible link between the head and tail region (bends during contraction)
what are the three binding sites on troponin
calcium, actin, tropomyosin
where does most of the calcium come from in skeletal muscle
sarcoplasmic reticulum
is skeletal muscle thin or thick filament regulated
thin filament regulated
smooth muscle characteristics
- not striated, no sarcomeres
- contains thick and think filaments
- use sliding filament mechanism for contraction (think along thick)
mechanism of latch state
- cross-bridge cycling is very slow - so slow that it is more like thin and thick are stuck together
- a protein forms a link between thick and thin filaments - caldesmon
sympathetic releases
NE
parasympathetic releases
ACh
enteric nervous system releases
NE, ACh, and many other NTs
characteristics of cardiac muscle
- heart is a hollow organ (smooth)
- coordinated contractions (smooth)
- fast contractions, short duration (skeletal)
- contains sarcomeres (skeletal)
- controlled by ANS and hormones (smooth)
where does Ca++ come from in cardaic muscle
outside cell and SR
where does Ca++ come from in smooth muscle
SR
which type of muscle involves calcium influx from the extracellular fluid during contractio n
cardiac and smooth muscle
which type of muscle involves calcium induced caclium release from the SR during contraction
cardiac and smooth muscle
re-entry arrythmias
due to slow or blocked conduction
atrial premature complexes (APCs)
area of atria other than SA node causes contraction
venctriuclar premature complexes (VPCs)
contraction starts in the ventricles
atrial flutter
fast but organized contraction rate of atria
atrial fibrilation
no organized contraction of the atria
* ventricles fast and irregular
ventricular fibrilation
no organized contraction of the ventricles
* no blood is being pumped - death
AV block
problems with spread of depolarization getting through the AV node
first degree AV block
long PR interval
second degree, type I AV block
PR interval lengthens until conduction faisl - P wave with no QRS complex
second degree, type II AV block
PR interval is long but constant
third degree AV block
no conduction gets through AV node
no connection between the P wave and QRS complex
determinants of resistance
viscosity
tube length
tube radius
MAP =
CO x TPR
CO =
HR x SV
angiotensin II
general vasoconstriction
increased BP
vasopressin (ADH)
general vasoconstriction
increase BP
atrial natriuretic peptide (ANP)
general vasodilation
* decrease blood pressure
what hapens when ventrciles contract
ventricular pressure increase - AV valves close - SL valves open - blood flows into arteries (ejection)
what happens when ventricles relax
ventricular pressure decreases - SL valves close - AV valves open - blood flows into ventricles (filling)
which way does ventricular depolarization spread
endocardium -> myocardium -> epidcardium
which way does repolarization spread
epicardium -> myocardium -> endocardium
ventricular systole
ventricles contracted (systolic pressure)
ventricular diastole
ventricle relaxed (diastolic pressure)
atrial systole
atria contracted
atrial diastole
atria relaxed
what happens during isovolumetric contraction
ventricular pressure is increased
all valves are closed, no change in volume
ejection
SL valves open
AV valves closed
stroke volume
amount of blood ejected each heart beat
ejection fraction
fraction of blood ejected each heart beat
isvolumetric relaxtion
SL valves close
AV valves closed
ventricular filling
AV valves open
SL valves closed
rapid filling
when ventricular pressure first falls below atrial pressure (AV valves open)
slow filling
after rapid filling, filling continues but only at the rate of venous return
atrial contraction
atrial systole - after slow filling - atria contract
*extra push of blood into the ventricles
atrial contraction
atrial systole - after slow filling - atria contract
*extra push of blood into the ventricles
first heart sound
AV valves close
second heart sound
SL valves open
third heart sound
when AV valves open
third heart sound
when AV valves open
fourth heart sound
atrial contraction (AV valves still open)
phase 0 of cardiac action potential
rapid depol
* opening of voltage gated Na+ channels
* required delp to threshold by spread through gap junction
phase 1 of cardiac action potential
slight repolarization
* voltage gated Na+ channels close (inactivate)
* transient outward rectifier K+ channels open
phase 2 of cardiac action potential
plateau phase
* balance of Ca++ and K+ channels keep Vm=0
* voltage gated Ca++ channels open (L-Type)
* delayed outward rectifier K+ channels open
*
phase 3 of cardiac action potential
repolarization
* L-type Ca++ channels close (inactivate)
* delayed outward rectifier K+ channel dominates
phase 4 of cardiac action potential
resting membrane potential
* inward rectifier K+ channel open- but carries outward K+ current
* keeps Vm at about -85 mM
phase 0 of pacemaker cell
rising phase
* open voltage gated Ca++ channels (l-type)
* no voltage gated Na+ channels - slower rising phase
phase 3 of pacemaker cells
repolarization
* voltage gated Ca++ close
* delayed outward rectifier K+ channels open
phase 4 of pacemaker cells
spontaneous depolarization
* increased Na+ perm - funny Na+ channels open
* decreased K+ perm - delayed outward rectifier K+ channels close
* increased Ca++ perm - t-type Ca++ channels open
SV is determined by 3 factors:
- preload: how much blood goes in
- contractility: actual beating of heart
- afterload: blood pressure
