3.1.4. Heart Mechanics

Question 1

Describe a cardiac cell. What kind of cell membrane does it have?

Answer 1

Striated; centrally-located nuclei

Cell membrane: sarcolemma

Question 2

What are the vertical lines in cardiac tissue called and what are they for?

Answer 2

Intercalated Discs: location of gap junctions

Question 3

What is a T-tubule?

Answer 3

T-tubule: large invagination (at Z-disks) in sarcolemma rich with Ca++ channels (much less prominent in skeletal muscles

Question 4

How is the sarcoplasmic reticulum related to Ca?

Answer 4

sarcoplasmic reticulum: storage for Ca++; complexes with T-tubule

Question 5

What is a RyR- ryanodine receptor?

Answer 5

calcium release channel (RyR- ryanodine receptor): release of Ca++ into the cytoplasm during contraction

Question 6

What is a SERCA?

Answer 6

SR Ca++-ATPase pump (SERCA): removing Ca++ from the cytoplasm during relaxation

Question 7

Where do we find SERCAs?

Answer 7

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)

Question 8

Describe the functional unit of the cardiac cell.

Answer 8

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

Question 9

What is the fundamental contractile unit? What are its parts?

Answer 9

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)

Question 10

How are myocytes arranged?

Answer 10

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

Question 11

When does the heart begin to develop? What is the first thing to develop?

Answer 11

NORMAL embryonic cardiac development begins in wk 4 of gestation and establishes the primary heart tube’s typical left-right polarity.

Question 12

When does the heart begin to beat? What organs develop before the heart?

Answer 12

the heart is the FIRST functional organ in vertebrate embryos and beats spontaneously by the fourth week of gestation

Question 13

What is kartagener syndrome and what causes it? When does this defect happen?

Answer 13

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

Question 14

What is Kartagener syndrome also called?

Answer 14

(AKA “primary ciliary dyskinesia”)

Question 15

During excitation Contraction coupling, where does depolarization begin?

Answer 15

Waves of depolarization originating at the SA node; autonomic nervous input regulates the rate of SA node depolarization

Question 16

After waves of depolarization begin at the SA node, what happens in the cardiac cells?

Answer 16

AP voltage activates voltage-gated calcium channel in t-tubule

AP plateau opens L-type Ca++ channel

Question 17

What happens once the influx of Ca++ results in a sudden increase in local calcium concentration in the neighborhood of the SR?

Answer 17

Ca++ triggers release of Ca++ from SR (RyR) by CICR- calcium-induced calcium release

100 fold increase in cytosolic [Ca++]

Question 18

For cross bridge formation, what else is required? What happens when they are both present?

Answer 18

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

Question 19

What does the myosin head do?

Answer 19

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)

Question 20

What happens when the head binds to the active site?

Answer 20

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

Question 21

optimal sarcomere length is one that what?

Answer 21

maximizes the number of actin-myosin cross-bridges

Question 22

What is preload?

Answer 22

Preload: myocardial wall tension PRIOR (“pre”) to contraction

Question 23

What determines preload?

Answer 23

depends on

1) venous tone, and
2) the circulating blood volume

effectively, this sets the sarcomeres’ lengths

vEnodilators DEcrease prEload (eg nitroglycerin)

Question 24

What is EDV and what does it do?

Answer 24

end diastolic volume (EDV) stretches the myocytes and sets the sarcomere length

Question 25

What is La Place’s Law and what do we use it for?

Answer 25

end diastolic pressure calculation

[La Place’s law: T= (Pxr)/2h]

Tension, pressure, chamber radius
h = wall thickness

Question 26

What is afterload

Answer 26

Afterload: tension in the chamber wall during contraction. Can be approximated clinically by the Mean Arterial Pressure (MAP)

Question 27

How does contraction affect afterload? Why does it have this effect?

Answer 27

during systole (ventricular contraction), chamber radius falls, so afterload decreases during ejection

Question 28

How does the left ventricle adapt to an increased afterload?

Answer 28

over time, the LV wall compensates for an increased afterload by hypertrophying in order to decrease wall tension

Question 29

Vasodilators do what to afterload?

Answer 29

vAsodilators DECREASE Afterload (eg hydralazine)

Question 30

What do Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) do to both preload and afterload

Answer 30

Angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) decrease both preload and afterload

Question 31

If afterload is constant, what does an increase in preload do?

Answer 31

increasing preload increases the velocity and extent of shortening if afterload is constant

Question 32

What happens when you increase AFTERLOAD?

Answer 32

increasing afterload reduces velocity and extent of shortening for any given preload

Question 33

What does the Frank-Starling curve show us?

Answer 33

the Frank-Starling curve demonstrates the preload vs CO during different physiological states

Question 34

The force of contraction is proportional to what?

Answer 34

the force of contraction is proportional to the end-diastolic length of cardiac muscle fibers (preload)

Question 35

What do we do to increase contractility?

Answer 35

INCREASE contractility with

1) catecholamines
2) digoxin
3) Norepinephrine

Question 36

What do we do to decrease contractility?

Answer 36

DECREASE contractility with

1) loss of myocardium (seen in MI),
2) beta-blockers,
3) Ca channel blockers, and
4) dilated cardiomyopathy

Question 37

What is contractility?

Answer 37

Contractility: power developed by the muscle for any given sarcomere length

Question 38

How do we estimate contractility?

Answer 38

estimated by ejection fraction

EF = (EDV - ESV) / EDV

Question 39

What does the body do to increase contractility?

Answer 39

Increase HR or give sympathetic input