B1W3: Cardiac Muscle

Question 1

AV Valves

Answer 1

LAB RAT bicuspid/mitral tricupid Chordae tendae pull back Between atria and ventricles

Question 2

Aortic/pulmonary valves

Answer 2

Prevent backflow from aorta/pulmonary artery into ventricles

Question 3

Prolapsed valve

Answer 3

Mitral valve that accidently lets blood leak through backwards

Question 4

Rheumatic fever

Answer 4

Causes high instance of valvular stinosis (interferes with transfer of blood)

Question 5

Mitral regurgitation

Answer 5

Elevates arterial pressure because blood is not moving forward, staying put

This elevates the atrial pressue a little more each cycle, messing up end diastolic volume and diastolic pressure

Question 6

S1 heart sound

Answer 6

the “lub”

• marks beginning of systole/end of diastole
• closure of mitral/tricuspid valves

Question 7

S2 heart sound

Answer 7

The “dub”

End of systole/beginning of diastole

Closure of aortic/pulmonary valves

Question 8

Additional heart sounds

Answer 8

• swishing means there’s a problem with laminar flow
• 3rd sound=increased atrial pressur
• 4th sound=stiffened left ventricles

It is important to listen to the nature and timing of the sound

Question 9

Three different types of cells in myocardium

Answer 9

• Myocardial muscle: in atria and ventricles, generates force
• Conducting: bundle of His, purkinje fibers; coordinates contraction
• Pacemaker: SA node and AV node; initiates heart-beat, and control of heart beat

Question 10

Cardiac muscle ccomponents

Answer 10

• actin/myosin
• intercalated disks, i.e. gap junctions

Question 11

Major conducting pathways

Answer 11

1. Atrial syncytium
2. AV node
3. Bundle of His
4. Ventricular syncytium

Question 12

• Action potential in cardiac muscle

Answer 12

• due to influx of Na+ and Ca2+
• Calcium causes plateau phase, where calcium enters and binds to troponin
• Abslutely refractory period and relative refractory period

Question 13

Cardiac excitation-contraction coupling

Answer 13

Needs external calcium to contract–DEPENDENT ON IT

• Ca2+ enters cell via L type Ca2+ channels during plateau for calcium-induced-calcium released
• T tubule helps Ca2+ released from SR using RyR receptors
• Ca2+ also stays in T tubules!

Question 14

End diastolic volume

Answer 14

Volume of blood filling the ventricle during rapid filling

Question 15

Stroke volume

Answer 15

Volume of blood ejected as the ventricles contract during systole

Question 16

End-Systolic Volume

Answer 16

Volume remaining in each ventricle after contraction

Question 17

Ejection fraction

Answer 17

Fraction of the end-diastolic volume that is ejected; will be reduced in people at end stage of heart disease

Question 18

Equation for Stroke Volume

Answer 18

Stroke Volume=EDV - ESV

Question 19

Calcium’s role in contraction

Answer 19

Binds to Troponin C once released from SR, T-tubules or extracellular fluid

Troponin C does conformation chainge on tropomyosin

Active sites on actin are uncovered for myosin to bind

Question 20

Ejection fraction equation

Answer 20

EF=SV/EDV

Question 21

Volume-Pressure Relationship

Answer 21

As you fill heart, pressure increases

Just adding volume generates pressure

This works to a point until you pass the Frank-Starling relationship

Question 22

Stroke work

Answer 22

Output of heart

(work=force x distance)

Question 23

Chronotropic action

Answer 23

effecting the heart rate

Question 24

inotropic

Answer 24

effecting the strength of cardiac contraction

Question 25

lusitropic action

Answer 25

effect on rate of relaxation

Question 26

preload

Answer 26

The load in heart before systole (i.e. EDV)

Question 27

afterload effects ESV

Answer 27

resistance in aorta against ventricular pumping

Question 28

determinants of stroke volume

Answer 28

preload contractility afterload

Question 29

length tension relationship in cardiac muscle

Answer 29

Tension of heart increases, length will increase too

Question 30

What affects EDV

Answer 30

Ventricular performance increases as we increase EDV * venous tone * total blood volume * body position * pumping of skeleatl muscle * atrial contribution to ventricular filing * intrathoracic pressure * intrapericardial pressure, ventricular compliance

Question 31

Effect on preload of compliance

Answer 31

Compliance of ventricles If they're stiff, more pressure at less volume If too compliant, more volume out with little pressure * extrinsic compression (pleural pressure, tumor), thickness of LV wall (edema, muscle) and elasticity due to cross-bridges will all affect

Question 32

How is contraction measured?

Answer 32

Using isovolumic pressure-volume curve Clamp aorta, fill ventricle with varying amounts, can see the max amount of tension heart can have at any volume

Question 33

factors affecting myocardial contractility

Answer 33

* sympathetic/parasympathetic impulses/hormones circulating

Question 34

Role of sympathetic on heart

Answer 34

Chronotrophic and inotrophic (increases heart rate and stroke volume) SA node discharge rate increased

Question 35

Role of parasympathetic on heart

Answer 35

Innervates only nodes, not ventricles (unlike sympathetic) Slows heart rate SA discharge rate decreased

Question 36

Catecholamines on heart contractility

Answer 36

increases

Question 37

B blockers on contractility

Answer 37

block stimulation of Ca2+ channels and Na+/Ca2+ exchangers Constant depolarization

Question 38

Ca2+ channel blockers

Answer 38

Block L-type Ca2+ channels

Question 39

Digitalis glycosides

Answer 39

Inhibit Na/K pump and Ca channels; increases cytosolic Ca2+

Question 40

Cardiac output and arterial pressure

Answer 40

Cardiac output not affected by increases in afterload until over 160 (hypertension) --CO is determined almost entirely by ease of blood flow

Question 41

Increase in afterload on volume/pressure curve

Answer 41

Narrows and moves upward

Question 42

Volume/pressure curve under increase of volume

Answer 42

widens

Question 43

Increase in contractile state on volume/perssure curve

Answer 43

Widens; pushes up isovolumetric-volume curve (makes line steeper)

Question 44

Sinus nodal fiber compared to ventricular muscle fiber

Answer 44

* no plateau * looks like "normal" action potential

Question 45

Purpose of AV node

Answer 45

Delays transmission from SA node to ventricles Allows time for atria to empty

Question 46

Pacemaker Node Contraction

Answer 46

No plateau Unstable resting potential--Funny Na+ channels (IF) slowly open until threshold, then Ca2+ channels open

Question 47

Pulmonary system

Answer 47

low resistance/pressure

Question 48

Systemic system

Answer 48

high resistance/pressure

Question 49

increase in preload causes...

Answer 49

increase in stroke volume thick and thin filaments stretch, overlap, more cross bridges

Question 50

positive inotropic effect

Answer 50

increase contractility

Question 51

negative inotropic effect

Answer 51

decrease contractility

Question 52

increasing contractility means...

Answer 52

greater stroke volume Frank Starling curve becomes near vertical...for that given EDV, more blood will be pumped out

Question 53

Cardiac output equation

Answer 53

CO=HR x SV

Question 54

if afterload increases:

Answer 54

higher pressure needed to open aortic valve ejection phase shortened stroke volume decreases

Question 55

if preload increases

Answer 55

stroke volume increases end systolic volume does not change

Question 56

Accumulation of what solute is responsible for tetanus?

Answer 56

Ca2+