test 3: lecture 3 Flashcards
•Properties of cardiac muscle similar to skeletal muscle
- Striated
- Ca2+/troponin/tropomyosin regulation of crossbridge cycling
- Sarcoplasmic reticulum stores and releases Ca2+
- T tubules
how is cardiac and smooth muscle similar
- Gap junctions
- Extracellular Ca2+ required for contraction (Ca<u>2+ </u>induced Ca<u>2+</u> release)
why need ryanodine receptor and Ltype Ca receptor in cardiac muscle
Ltype Ca lets Ca into cell
will bind to ryanodine and ryanodine will let Ca from SR into the cell to trigger power stroke
Ltype and ryanodine not bound together like in the skeletal muscle
3 ways to get calcium out of the cell after power stroke
SERCA → calcium back into sarcoplasmic reticulum
Calcium ATPase: Ca pumped out of cell
sodium calcium exchanger (NCX): 3Na in = 1 Ca out
(3Na out/2K in to even out charges-maintain membrane potential)
why need extracellular Ca in cardiac cells
ryanodine receptor is different from RyR in skeletal (not bound)
needs Ca to trigger it to allow Ca out of the sarcoplasmic reticulum
the long plateau phase of cardiac contractile cells will prevent __
tetanus (summation)
1 AP= 1 beat
contraction same length as AP
how are cardiac and skeletal muscle different?
activity
neural input
gap junctions
cardiac : autorhythmic, autonomic innervation, yes gap junctions
skeletal: no autorhythmic activity needs to be innervated by somatic NS, no gap junctions
compare cardiac and skeletal
Ca source for contraction
Ca release from SR
Ca removal
cardiac: calcium from SR and ECF, Ca released from SR by CICR, Ca removed by SERCA back into SR, CA pump out of cell, NCX (1 Ca out/3Na) in
skeletal: Calcium from SR, Ca release from SR by foot processes, Ca removed by SERCA back into SR
compare cardiac and skeletal
ryanodine receptor
twitch duration
cardiac: RyR2 (needs Ca to trigger its release of Ca), 350 msec
skeletal: RyR1 (linked- will release Ca without binding to its own ECM Ca), 100 msec
systole
contraction of the ventricles (left)
diastole
relaxation of ventricles (left)
valves in heart open ___
passively
___ % of ventricle filling is due to AV contraction
20%
___ prevents signal from going from ventricles to atria
cardiac skeleton
if any conduction cell can initiate its own AP why is SA the hearts pacemaker?
hierarchy of normal automaticity
overdrive suppression
SA fires 70-80 AP a minute, which is faster then all of the other conduction cells
Draw wiggers
draw the pressure part of wiggers graph
draw the volume part of wiggers graph
what happens during mid to late diastole
ventricles filling
atria contracts (atrial depolarization)
aortic valve closed
what happens during systole
both set of valves closed during isovolumetric contraction
ventricles contract, and Aortic valves open
what happens during early diastole?
isovolumetric relaxation- both set of valves closed but no change in amount of blood
then AV valves open and ventricles begin filling
when does isovolumetric relaxation occur?
early diastole
both set of valves closed happens after ventricles contract-
happens when ventricles are relaxing- during repolarization
when does isovolumetric contraction occur?
during systole
atria have contracted and both set of valves closed, ventricles are filled with blood and ventricle contraction has started but it isnt strong enough to open aortic valve yet
EDV
end diastolic volume
•Volume of blood in ventricle at the end of diastole
ESV
End-systolic volume (ESV)
•Volume of blood in ventricle at the end of systole
SV
Stroke volume (SV)
•Volume of blood ejected from ventricle each cycle
SV = EDV – ESV
EF
Ejection fraction (EF) measures heart efficiency
•Fraction of EDV ejected during a heartbeat
EF = SV/EDV
EF= (EDV-ESV)/(EDV)
CO
cardiac output
measures blood output per minute
CO = SV × HR
CO =( EDV=ESV) x HR
____ measures heart efficiency
ejection fraction
EF= SV/EDV
(EDV-ESV)/(ESV)
___ measures blood output per minute
cardiac output
CO= SV x HR
CO= (EDV-ESV) x HR
____ is volume of blood ejected from ventricle each cycle
stroke volume
SV = EDV – ESV
volumes and blood flow rates are similar for the left and right sides of the heart, what differs?
- Systolic pressure on left ventricle: ~120 mm Hg
- Systolic pressure on right ventricle: ~20 mm Hg
(left side has to pump blood to everywhere, there is more resistant therefore left side of the heart is much thicker)
Lub S1
“Lub” S1: backflow hitting AV valves after they close at the start of ventricular systole
hearing turbulence
isovolumic contraction
dub S2
backflow hitting the aortic and pulmonary valves at the start of diastole
•Usually briefer, sharper, and higher pitched•Normally the valves close at the same time
isovolumic relaxation
split S2
Split second heart sound (split S2): the second heart sound (“dub”) is split into two sounds
•Can be normal (during inspiration) really dead breathe= more venous blood into right side of heart → right has more blood then left, takes longer to empty- therefore a second dub sound
•Can be pathological
•Wide splitting •Reverse splitting •Fixed split
C point A marks the beginning of isovolumetric contraction
preload
happens during diastole (heart not actively contracting)
resting/stretched
the tension in the wall of the ventricle produced by the end-diastolic pressure
loosely: the end diastolic pressure
preload is not a measure of volume
___ the tension in the wall produced by the end-diastolic pressure
preload
___ the tension in the wall produced at the time of the opening of the aortic valve (during systole)
afterload
loosely: the pressure at the time of the opening of the aortic valve
afterload
Strictly: the tension in the wall produced at the time of the opening of the aortic valve (during systole)
Loosely: the pressure at the time of the opening of the aortic valve
during ejection, when ventricle is active and shortening
Frank starling relationshi[
In a healthy heart:
- Increased volume (pressure) results in increased force of contraction
- Stroke volumes of the left and right ventricles remain balanced•
Clinical Relevance: If balance were not maintained: blood accumulation in pulmonary or systemic circulation can result (edema)
passive tension
rubber band
the more you stretch it, the more passive tension it supplies
explain passive vs active
cardiac muscle
- Wide dynamic range to take advantage of the increased active tension at longer lengths (greater heart filling produces more force of contraction).
- Significant passive tension at peak active tension lengths
- Passive tension tends to limit the degree of heart filling
skeletal muscle: passive restricted by skeleton
•Relatively short length changes over the dynamic range due to muscle attachment near the joints of bones.
Works over the range of the peak active force
•Very little passive tension at peak active tension lengths
cardiac
- Wide dynamic range to take advantage of the increased active tension at longer lengths (greater heart filling produces more force of contraction).
- Significant passive tension at peak active tension lengths
- Passive tension tends to limit the degree of heart filling
why does cardiac muscle have such a larger working range?
passive tension adds to work range
two ways to increase the force of contraction (tension)
increase length
adjust contractility (Calcium concentration and sensitivity)
what part of the ANS impacts contractility
sympathetic increases contractility (will influence contractile cells in the heart)
Parasympathetic does not effect contractility
what does parasympathetic do to heart
decrease HR
does not impact contractility
what does sympathetic do to heart?
increase HR
increase contractility (only sympathetic will travel to contractile cells in heart)
____ binds to β-adrenergic receptors and causes ___ HR
norephinephrine
Sympathetic response increases HR
norepinephrine released by the ___ nervous system __HR
sympathetic
increases
____ binds to muscarinic cholinergic receptors
- Acetylcholine binds to muscarinic cholinergic receptors
- Parasympathetic response decreases HR
acetylcholine produced by ___ nervous system ___ the heart rate
parasympathetic
decreases
sympathetic innervation of the heart channels
Increased sympathetic activity
(norepinephrine or epinephrine)
β1 receptors in SA node
Increased permeability to sodium and Ca2+ (funny channel and T type calcium channel)
Increased rate of spontaneous depolarization
Increased heart rate and contractility (L type calcium channel and ryanodine Ca receptor)
(norepinephrine or epinephrine)
this binds to Beta1 G protein receptor and causes down stream activity
activates L-type Ca channels and Ryanodine Receptors on the SR to increase intracellular Ca and increase contractility
will increase Calcium sensitivity of troponin
will also increase SERCA (reabsorption of Ca back into the SR) (decreases time it takes for muscle to relax)
sympathetic (norepinephrine or epinephrine) release and bind to Beta 1 g protein receptor in SA node
this causes increased function of the funny channel (Na in) and the T type calcium channel (Ca in)
this increases spontaneous depolarization
parasympathetic activity of the heart
Increased parasympathetic activity
(acetylcholine)
Muscarinic cholinergic receptors in SA node
Increased open state of K+ channels and closed state of Ca2+ channels
Decreased rate of spontaneous depolarization; hyperpolarization
Decreased heart rate
two ways parasympathetic effects heart channels
acetylcholine binds to G protein receptor
increases activity of K channel (K out of cell→ repolarization)
makes it harder for T-type calcium channels to meet threshold
three things EDV is affected by:
venous return
ventricular compliance
diastolic filling time
ESV is affected by ____ and ____
ventricular contractility
afterload
ventricular volume of stiff heart vs normal heart
stiff can’t hold as much (noncompliant)
not stretchy (during diastole → relaxation)
takes more pressure to get the same amount of volume
increased contractility will cause
larger stroke volume
(systole→ ventricle contract)
increase contractility can move more blood then a normal heart
which line is heart disease
decreased contractility (can not pump as much)
what impacts cardiac output
explain pace maker curve
in normal heart→ sympathetic innervation causes the systolic to decrease
the pacemaker did not allow that, it kept systolic the same and only decreased the diastolic (relaxation time)
____ are abnormal disruptions in flow (turbulence) that can be auscultated
murmurs
•Can occur during diastole, systole, or be continuous
____ describes a valve that fails to close completely
Incompetent or insufficient
•Regurgitation describes the backflow across the incompetent valve
___ describes the backflow across the incompetent valve
•Regurgitation
____ occurs when a valve fails to open widely enough
stenosis
when the murmur is so extreme that it can be palpated
thrill
defects that cause a murmur can lead to ___
- Abnormal blood flow to a region of the body
- Abnormal blood pressure in a region of the body
- Cardiac hypertrophy
MR causes
patent ductus causes
mitral stenosis leads to
when would you hear tricuspid or mitral incompetence
lub S1= backflow hitting the AV valves after they close at the start of the ventricular systole
TI and MI do not close all the way and allow back flow, lub would not be as loud??
would hear a continuous murmur as blood leaks back and forth??
