Cardiac Muscle Flashcards
how is cardiac muscle similar to skeletal
-striated
-same mechanics of skeletal muscle
however, there is a simultaneous contraction of all fibers
intercolated junctions
mechanically and electrically connected at these spots
-connected by gap junctions and desmosomes
types of contractions
- twitches
- variable force (not all or nothing)
- no fatigue
excitation contraction coupling in cardiac muscle
cardiac action potential
- voltage gated Na+, Ca++, K+ channels
- calcium plateau, causes ca++-stimulated Ca++ release from SR through ryanodine receptors
- very long refractory period-no tetanus
cardiac output equation
CO (liters/min)=Heart Rate (beats/min)X Stroke Volume (liters/beat)
average CO
5L/min (resting)
average HR
93 bpm
average stroke volume
.07L/b
calculating max heart rate
220-age
Heart rate: pacemaker potential
a different type of voltage-gated Na+ channels: pacemaker channels (If channels)
- open by hyperpolarization
- cause slow depolarization when cell returns to resting potential
- AP shuts If channels
- gets closer to ENa+ when open
- open slowly
- controlling how fast channels open back up controls HR
pacemaker potential
-controls heart rate
-changes in rate are called chronotropic effects
-sympathetic response: epinephrine/norepinephrine
B-adrenergic receptors->increased cAMP->increased rate of pacemaker channel opening
-parasympathetic response: acetocholine
muscarin Ach receptors-> Gk protein-> opens K+ channel-> slows pacemaker potential
Stroke volume
force development depends on cytoplasmic [Ca++] and on preload of the muscle
- changes in force of contraction are known as inotropic effects
- increased force of contraction results in an increased stroke volume (volume of blood pumped per beat)
chronotropic effects
changes in heart rate
inotropic effects
changes in force of contraction
Frank starling law of the heart
change in force development as a function of preload
- really the length-tension relationship of cardiac muscle
- resting length of cardiac muscle is such that increases in preload (filling) cause increased force and therefore increased ejection of blood
change in contractility
change in contraction strength by control of Ca++
- changes are usually caused by increasing th eamount of Ca++ loaded into the sarcoplasmic reticulum
- changes in contractility change the ejection fraction
ejection fraction
fraction of the blood in the ventricle that is ejected into the artery
control of contractility
- troponin/tropmoyosin controls activity of the myosin ATPase (like skeletal muscle)
- Ca++ enters cell through plasma membrane during action potential and also comes from SR, as a result of calcium induced calcium release from the SR through RyR
how does Ca++ leave the cytoplasm
leaves between beats
- Ca-ATPase pumps it back into the SR
- A Na?Ca-exchanger (countertransport) system moves calcium out of the cell by secondary active mechanism
staircase effect
change in contractility
- at high heart rates, the Na/Ca-exchanger cannot extrude all of the calcium that enters during the AP
- the excess calcium that builds up in the cell is taken up the SR, since the Ca-ATPase is not as limited as the Na/CA exchanger
- known as calcium loading of the SR
- calcium loading leads to increased contractility, which is an increase in the force produced at any given preload
how do catecholamines cause in increase in contractility
- they interact with B-adrenergic receptors
- increased [cAMP] activates protein kinase A which phosphorylates multiple target proteins
1. voltage gated calcium channels of the plasma membrane
2. Ca-atpase of sarcoplasmic reticulum
3. troponin
voltage gated calcium channels of the plasma membrane
- increased inward calcium flow during the action potential leads to increased [calcium] and also to calcium loading of the SR
- the channels then close more quickly, leading to a shorter action potential, shorter contraction, and increased filling time
Ca-ATPase of sarcoplasmic reticulum
increased rate of this pump causes SR loading
-it also decreases the time needed to relax between beats. this increases filling time
troponin
causes troponin to release its calcium more quickly, again leading to increased filling time
digitalis
a drug that increases contractility
-causes the Na/Ca-exchanger to work more slowly, thus promoting Ca++-loading of the SR
control of HR through sympathetic
nor/epinephrine
- B-adrenergic
- Gs increases cAMP
- phosphorylates If channels, open faster, less time to get back to threshold
control through parasympathetic
slow HR
- acetylcholine (muscarinic receptors
- alpha subunit: GI protein decreases cAMP, fewer phosphorylated If channels
- B subunit: Gk open K+ channels, extra hyperpolarization
pacemaker of the heart
SA node
what happens to smooth muscle tension when HR increase
it decreases in the blood vessels, allows greater ouput
what connects the para/sympathetic to the heart
the vagus nerve
stroke volume
higher pressure=higher stroke volume
- contract more forcefully, increase pressure, increase stroke volume
- need each cell to contract more strongly (already have 100% recruitment)
- frank starling law (increased filling increases SV)
preload
fill heart more, increase volume, stretches chamber more
- more blood, stronger contraction
- heart only ejects half of whats in it
ejection fraction
EF=SV (what leaves heart)/EDV (end diastolic volume, filling of heart)
ex= 70/135=.52
2 ways to increase contractility
- staircase effect
- epinephrine (B receptor increases cAMP, phosphorylates SR ca++atpase, loads up SR with ca++, increases contractility)
- also phosphorylates ca++ channel of plasma membrane (AP channel, lets more ca++ in, plateau gets taller)
ways that epinephrine effects contractility
- If channels increase rate
- phosphorylate SR ca++ atpase (makes it faster)
- phosphorylates ca++ channel of plasma membrane (AP channel)
- troponin
first 3 affect contractility
-3+4 make relaxation faster
what makes the SA node different from the hearts other myocytes
it contains specialized autorhythmic cells that control the overall cardiac rhythm
from the SA node, where do the AP go
conducted from cell to cell through the gap juncitons thorugh the atrial contractile cells and also through an internodal pathway to the AV node
-depolarization occurs slowly across atria, conduction slows through AVn ode
from the AV node, where do the AP go
the AV node delays the AP, then conducts it through the bundle of His, bundle branches, and purkinje fibers to the ventricular contractile cells`
- moves rapidly through ventricular conducting system to the apex of the heart
- spread upward from apex, FAST
what does the AV node do
controls the rate of AP and sends signal out after receiving it
ECG/EKG
a recording of the spread of the action potential across the heart. The recording shows an upward deflection if the action potential is moving toward the positive electrode
P wave
result of atrial depolarization
PR interval
result of the delay of the action potential by the AV node
QRS wave
result of depolarization of the ventricles
QRS interval
tells us how long it takes for the AP to spread across the the ventricles
QT interval
recorded while the ventricles are depolarized
-calcium plateau, all contracting
T wave
result of repolarization of the ventricles
flat lines
all contracting, no movement
atrial systole
atria contract, completing ventricular filling
-correlates with the P wave of the ECG
diastole
atria and ventricles are at rest, ventricles are filling
ventricular systole
ventricles contract, ejecting blood into aorta and pulmonary arteries
steps of ventricular systole
- AV valves (bicuspid/tricuspid) close producing first heart sound. correlates with QRS wave of ECG. ventricles are done filling and contain the end diastolic volume
- isovolumic contraction: both AV valves and both semilunar valves (aortic and pulmonary) are closed, so the ventricle builds up pressure without any change in volume. the semilunar valves will not open until ventricular pressure exceeds arterial pressure. this is analogous to the isometric phase of a skeletal muscle mixed contraction
- ejection phase: (ventricular systole) begins when semilunar valves open. during this phase, the ventricular pressure is approximately equal to arterial pressure. the pressure increases as more blood is forced into the elastic arteries. ventricular volume decreases to end systolic volume as the cardiac muscle fibers shorten. this is analogous to the isotonic phase of a skeletal muscle mixed contraction
- semilunar valves close when the cardiac contraction begins its isovolumic relaxation phase. this produces the second heart sound. it correlates with the T wave of the ECG
- AV valves open when the pressure in the ventricle drops below the atrial pressure. this marks the beginning of diastole, and the ventricles begin to fill again
what is the afterload
pressure preventing valves from opening (diastolic arterial pressure)
arteriole pressure determined by?
the volume of blood contained in the arteries
arterial pressure (ejection phase)
- arterires are elastic, so more blood they contain the more their walls are stretched, and greater the pressure on the blood
- during the ejection phase, more blood is being forced into the arteries by the heart. during this phase the arterial pressure is approximately the same as ventricular pressure. the highest pressure attained during this time period is systolic pressure
arteriole pressure (diastole)
the pressure in the arteries is driving the blood through the arterioles and into the capillaries and veins
- as blood leaves the arteries, the arterial pressure falls
- this occurs until the semilunar valves open to begin the next ejection phase.
- the lowest pressure attained, just before the SL valves open is diastolic pressure
diastolic pressure
- says what the arteries are doing
- easy blood flow=open arteries and lower diastolic pressure
- constricted=higher diastolic pressure
- also tells time between heart beats
cardiac output equation
CO=HRXSV
stroke volume calculation
end diastolic volume-end systolic volume
what happens as end diastolic volume increases
the preload on the cardiac muscles increase. the frank-starling law tells us that as preload increases, contraction force increases and therefore stroke volume increases
-EDV increases if venous return to the heart increases
how does contractility affect SV
it changes the ejection fraction (EF=SV/EDV)
-affected by staircase effect, B-adrenergic receptors, and digitalis
