3.1.4. Heart Mechanics Flashcards
Describe a cardiac cell. What kind of cell membrane does it have?
Striated; centrally-located nuclei
Cell membrane: sarcolemma
What are the vertical lines in cardiac tissue called and what are they for?
Intercalated Discs: location of gap junctions
What is a T-tubule?
T-tubule: large invagination (at Z-disks) in sarcolemma rich with Ca++ channels (much less prominent in skeletal muscles
How is the sarcoplasmic reticulum related to Ca?
sarcoplasmic reticulum: storage for Ca++; complexes with T-tubule
What is a RyR- ryanodine receptor?
calcium release channel (RyR- ryanodine receptor): release of Ca++ into the cytoplasm during contraction
What is a SERCA?
SR Ca++-ATPase pump (SERCA): removing Ca++ from the cytoplasm during relaxation
Where do we find SERCAs?
SERCA primarily found in the parts of the SR that form a junction with the T tubules, while the calcium pump is present throughout the SR
actively transports Ca (“sequesters” it) from the cytosol into the SR (hydrolyzes ATP to maintain a favorable Ca diffusion gradient)
Describe the functional unit of the cardiac cell.
Cardiac myocyte contain several sarcomeres and are separated by intercalated discs that both attach two cells in a fiber and provide diffusional connections through gap jxns
What is the fundamental contractile unit? What are its parts?
sarcomere = fundamental contractile unit; thick (myosin) and thin (actin) filaments
A band (dark staining)
I band (light staining)
Z-line: thin filaments anchored here (define the borders of individual sarcomeres)
How are myocytes arranged?
myocytes are arranged in end to end in a branching pattern, connected by intercalated discs containing gap jxns
communicate electrically and chemically via the gap jxns
When does the heart begin to develop? What is the first thing to develop?
NORMAL embryonic cardiac development begins in wk 4 of gestation and establishes the primary heart tube’s typical left-right polarity.
When does the heart begin to beat? What organs develop before the heart?
the heart is the FIRST functional organ in vertebrate embryos and beats spontaneously by the fourth week of gestation
What is kartagener syndrome and what causes it? When does this defect happen?
at the molecular level, a defect in left-right dynein (which is responsible for the normal asymmetric development) can lead to dextrocardia
heart orientation is reversed: right-to-left, instead of other way around
classically seen in Kartagener syndrome
What is Kartagener syndrome also called?
(AKA “primary ciliary dyskinesia”)
During excitation Contraction coupling, where does depolarization begin?
Waves of depolarization originating at the SA node; autonomic nervous input regulates the rate of SA node depolarization
After waves of depolarization begin at the SA node, what happens in the cardiac cells?
AP voltage activates voltage-gated calcium channel in t-tubule
AP plateau opens L-type Ca++ channel
What happens once the influx of Ca++ results in a sudden increase in local calcium concentration in the neighborhood of the SR?
Ca++ triggers release of Ca++ from SR (RyR) by CICR- calcium-induced calcium release
100 fold increase in cytosolic [Ca++]
For cross bridge formation, what else is required? What happens when they are both present?
Arrival of Ca++ and binding by troponin C changes the conformation of tropomyosin and reveals the binding site on the actin; cross-bridge formation occurs
What does the myosin head do?
Arrival of Ca++ and binding by troponin C changes the conformation of tropomyosin and reveals the binding site on the actin; cross-bridge formation occurs
prior to this, ATP is hydrolyzed by myosin head (this hydrolysis forms the cross-bridge)
What happens when the head binds to the active site?
Head binds active site
conformational change in head protein
tilts towards the middle of the cell (M line) [ADP & Pi released]
pulls the thin filament towards the center
cell shortens
ATP bound to myosin releases the active site on actin
optimal sarcomere length is one that what?
maximizes the number of actin-myosin cross-bridges
What is preload?
Preload: myocardial wall tension PRIOR (“pre”) to contraction
What determines preload?
depends on
1) venous tone, and
2) the circulating blood volume
effectively, this sets the sarcomeres’ lengths
vEnodilators DEcrease prEload (eg nitroglycerin)
What is EDV and what does it do?
end diastolic volume (EDV) stretches the myocytes and sets the sarcomere length
What is La Place’s Law and what do we use it for?
end diastolic pressure calculation
[La Place’s law: T= (Pxr)/2h]
Tension, pressure, chamber radius
h = wall thickness
What is afterload
Afterload: tension in the chamber wall during contraction. Can be approximated clinically by the Mean Arterial Pressure (MAP)
How does contraction affect afterload? Why does it have this effect?
during systole (ventricular contraction), chamber radius falls, so afterload decreases during ejection
How does the left ventricle adapt to an increased afterload?
over time, the LV wall compensates for an increased afterload by hypertrophying in order to decrease wall tension
Vasodilators do what to afterload?
vAsodilators DECREASE Afterload (eg hydralazine)
What do Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) do to both preload and afterload
Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) decrease both preload and afterload
If afterload is constant, what does an increase in preload do?
increasing preload increases the velocity and extent of shortening if afterload is constant
What happens when you increase AFTERLOAD?
increasing afterload reduces velocity and extent of shortening for any given preload
What does the Frank-Starling curve show us?
the Frank-Starling curve demonstrates the preload vs CO during different physiological states
The force of contraction is proportional to what?
the force of contraction is proportional to the end-diastolic length of cardiac muscle fibers (preload)
What do we do to increase contractility?
INCREASE contractility with
1) catecholamines
2) digoxin
3) Norepinephrine
What do we do to decrease contractility?
DECREASE contractility with
1) loss of myocardium (seen in MI),
2) beta-blockers,
3) Ca channel blockers, and
4) dilated cardiomyopathy
What is contractility?
Contractility: power developed by the muscle for any given sarcomere length
How do we estimate contractility?
estimated by ejection fraction
EF = (EDV - ESV) / EDV
What does the body do to increase contractility?
Increase HR or give sympathetic input
