Phys:t3– Turla (Set 1)

Front 1

What causes cardiac valves to open or close?

Back 1

Changes in pressure

Front 2

If pressure in the atria is higher than that of the ventricles, which valves are open? (Names and corresponding sides)

Back 2

Atrioventricular (AV) valves;

Tricuspid on the right side, Mitral(/bicuspid) on the left side.

Front 3

In this moment in time, the semilunar valves are open. What does this tell you about pressure in the different parts of the heart?

Back 3

Pressure is higher in the ventricles than in the aorta.

Front 4

What are the names of the two semilunar valves? What do they lead to?

Back 4

Pulmonary (R side); leads to pulmonary trunk.

Aortic (L side); leads to aorta.

Front 5

Chordae tendinae are associated with these types of heart valves:

Back 5

Atrioventricular (tricuspid, mitral) valves

Front 6

The "first heart sound" is associated with this action:

Back 6

Closing of the atrioventricular valves

Front 7

"Insufficiency, prolapse, or regurgitation" in the heart can result in this condition and is associated with these valves:

Back 7

Heart murmur; atrioventricular

Front 8

What is stenosis in reference to heart valves?

Back 8

Failure for valves to open completely

Front 9

What are the two primarily contractile muscle types in the heart?

Back 9

Atrial and ventricular myocytes

Front 10

What feature connects cardiocytes?

Back 10

Intercalated discs

Front 11

What are the three components of intercalated discs?

Back 11

Desmosomes, gap junctions, and interlocking plasma membrane.

Front 12

What is responsible for allowing the atria and ventricles to operate as separate "synctiums"?

Back 12

Thick fibrous tissue separation

Front 13

What are the two reasons why it's important that the atria and ventricles are separate synctiums?

Back 13

- Inappropriate communication via conductive cells is somewhat blocked

- Promotes a brief lapse in time for blood from atria to flow into ventricles before electrical signal for ventricular contraction is processed

Front 14

In regards to length, how do action potentials in cardiac muscle cells compare to that of skeletal muscle cells?

Back 14

Their action potentials last around 15x longer.

Front 15

Describe the ion channel system responsible for the "plateau phase" of a cardiac muscle AP:

Back 15

- Fast voltage-gated K channels (K out) close

- Slow voltage-gated K channels open

- Voltage gated "L-type" Ca channels open (slow Ca2+ in)

- Balance between slow K out and slow Ca in causes a membrane potential "plateau effect"

Front 16

In cardiac muscle, what causes repolarization after the plateau effect? (2 actions)

Back 16

- L-type Ca channels close,

- More slow-voltage K channels open

Front 17

Where is the absolute refractory period occurring? What about the relative refractory period?

Back 17

Front 18

Why is the long absolute refractory period of cardiomyocytes essential?

Back 18

Temporal summation of AP's is prevented, meaning that cardiomyocytes are not susceptible to tetany

Front 19

What are T-tubules used for in myocytes? Where are they most common?

Back 19

Excitation contraction coupling; ventricles

Front 20

Where is extracellular calcium stored for use by cardiomyocytes?

Back 20

On mucopolysaccharides bound to the T-tubules

Front 21

How does Ca storage in cardiomyocyte SR's compare to that in skeletal muscle SR's?

(SR= sarcoplasmic reticulum)

Back 21

Cardiomyocytes store much less Ca in their SR's.

Front 22

To initiate contraction, what protein does Ca bind in the muscle? What is the effect of this binding?

Back 22

Ca binds troponin, which causes movement of tropomyosin, which exposes the "active sites" for binding on actin fibers.

Front 23

When is the Na/Ca exchanger in cardiomyocytes most active? What kind of transporter is this?

Back 23

In cardiomyocyte relaxation; it's a secondary active antiporter.

Front 24

In response to a single AP, how do cardiomyocytes differ from skeletal myocytes?

Back 24

Cardiac response is graded; strength of contraction is dependent on amount of intracellular calcium. The amount of intracellular calcium is regulated in order to tightly control saturation of troponin with calcium.

Front 25

Systole and diastole– which is contraction and which is relaxation?

Back 25

Systole is contraction, diastole is relaxation.

Front 26

When does isovolumetric contraction occur in the cardiac cycle?

Back 26

Atrial diastole/ early ventricular systole

Front 27

What is going on during the "ejection phase" of the cardiac cycle?

Back 27

Late ventricular systole

Front 28

What is happening with the atria/ventricles when "active filling" of the heart is occurring?

Back 28

Atrial systole, ventricular diastole.

Front 29

Isovolumetric relaxation is experienced during what phase of the cardiac cycle?

Back 29

Early ventricular diastole

Front 30

When does passive filling of the heart occur?

Back 30

Between heartbeats.

Front 31

What amount of blood for contraction is loaded into the heart during the "passive filling" phase between beats?

Back 31

80%

Front 32

Between beats, the pressure of the atria compared to the pressure in the veins is described as what?

Back 32

Pressure in atria is lower than the pressure in the veins.

Front 33

There is only one phase where pressure in the atria is greater than the pressure in the veins. What is it?

Back 33

Atrial systole.

Front 34

How does the pressure in the ventricles compare to the pressure in the arteries during atrial systole?

Back 34

Pressure in the ventricles is lower than the pressure in the arteries during atrial systole.

Front 35

There is only one phase in which pressure in the ventricles is greater than pressure in the arteries. Which phase is this?

Back 35

Late ventricular systole.

Front 36

In atrial diastole and early ventricular systole, how does the pressure in the atria compare to that in the ventricles?

Back 36

The atria are lower in pressure than the ventricles.

Front 37

During late ventricular diastole, how does the pressure in the atria compare to the pressure in the ventricles?

Back 37

The pressure in the atria is greater than that in the ventricles.

Front 38

What is the stroke volume?

Back 38

Volume of blood ejected per heartbeat

Front 39

How do we find stroke volume?

Back 39

End diastolic volume (EDV)- End systolic volume (ESV)

Front 40

What part of the heart do we make volume pressure diagrams for?

Back 40

The left ventricle

Front 41

Describe what the "ejection fraction" refers to:

Back 41

The amount of end diastolic volume ejected per beat

Front 42

Is "end systolic volume" or "end diastolic volume" a higher value for the left ventricle?

Back 42

End diastolic volume.

Front 43

In this condition, a murmur is heard when heart valves are open.

In what condition is a murmur heard when heart valves are closed?

Back 43

Open: stenosis (abnormally narrow opening).

Closed: Regurgitation/prolapse (incomplete closing)

Front 44

What's the formula for cardiac output?

Back 44

CO=HR (heart rate) x SV (stroke volume)

Front 45

What's normal resting cardiac output?

Back 45

5L/min

Front 46

What effects will blood loss and heart disease have on cardiac output?

Back 46

Decrease

Front 47

What three factors change stroke volume?

Back 47

- Change in preload (end diastolic volume)

-Change in afterload (end systolic volume)

-Change in contractility (this is force of contraction, would affect end systolic volume (ESV))

Front 48

What does "VR" stand for?

Back 48

Venous return; the rate at which blood is returned to the heart by veins

Front 49

How much total blood volume can be held in veins?

Back 49

Up to 60%

Front 50

What three things can increase the venous return?

Back 50

- Increasing the effect of the skeletal muscle pumps

- Increasing the effect of the thoracic pump

- Venoconstriction via sympathetic activation of alpha receptors

Front 51

What has a greater effect on cardiac output– stroke volume or heart rate?

Back 51

Heart rate

Front 52

Greater maximal atrial pressure will result in a greater value for this measured volume of the left ventricle:

Back 52

End diastolic volume (EDV)

Front 53

What's the relationship between EDV and CO?

Back 53

Greater EDV, greater CO

(EDV = end diastolic volume, CO = cardiac output)

Front 54

Which ventricle requires a greater increase in atrial pressure to generate a greater output?

Back 54

Left ventricle. The right ventricle is more sensitive to pressure increase in the right atrium, and will increase output more quickly.

Front 55

Define "afterload"

Back 55

The pressure that ventricles must overcome to force open aortic and pulmonary valves.

Front 56

Hypertension would increase this element that affects stroke volume:

Back 56

Afterload

Front 57

What is the effect of increased afterload on stroke volume?

Back 57

Increased afterload (ESV) decreases stroke volume

Front 58

Relationship between stroke volume, end diastolic and end systolic volumes?

Back 58

SV= EDV-ESV

Front 59

What's the effect of hypertension on the equation SV = EDV-ESV?

Back 59

Hypertension increases afterload; a factor affecting ESV. This increases ESV, thereby decreases SV.

Front 60

Define "contractility"

Back 60

Ability of the heart to contract at any given resting fiber length.

Front 61

How is contractility changed by the heart?

Back 61

Modifying the amount of Ca that enters contractile cells via manipulation of L-type voltage-gated Ca channels

Front 62

What nervous system has no direct effects on contractility?

Back 62

Parasympathetic

Front 63

What's the primary molecular mechanism by which beta-1 receptors modify contractility?

Back 63

Phosphorylation

Front 64

What five molecules in the cardiomyocyte are phosphorylated in response to beta-1 receptor activation?

Back 64

1) L-type Ca channels

2) Ryanodine receptors

3) Troponin

4) Myosin head ATPase

5) Ca ATPase in sarcoplasm

Front 65

What's the difference between a positive and negative inotropic agent? Examples of each?

Back 65

Positive: Increases heart contractility. Epi/Norepi are examples.

Negative: Decreases heart contractility. Beta-blockers, Ca channel blockers

Front 66

What is digitalis?

Back 66

A positive inotropic agent (increases contractility)

Front 67

The dashed lines represent changes in stroke volume brought on by what effect?

Back 67

Increased preload

Front 68

The dashed lines represent changes in stroke volume brought on by what effect? (Left vent. pressure on Y axis)

Back 68

Increased afterload

Front 69

The dashed lines represent changes in stroke volume brought on by what effect? (Left vent. pressure on Y axis)

Back 69

Increased contractility

Front 70

At what age does cardiac output peak (on average)

Back 70

10 years

Front 71

Effects of hyper- and hypo- calcemia on cardiac output?

Back 71

Hyper- increases contractility, thus increases output

Hypo- opposite

Front 72

What's the effect of hyperkalemia on conduction speed of AP's through cardiac tissue?

Back 72

It decreases conduction speed.

Front 73

What's the effect of hyperkalemia on rate of potassium movement through potassium channels (conductance)?

Back 73

It increases this rate of movement

Front 74

What's the overall effect of hyperkalemia on tissue excitability?

Back 74

Decrease

Front 75

What's the effect of extreme tachycardia (HR) on cardia output?

Back 75

Decrease in CO

Front 76

Describe what causes cardiac tamponade and what its effect is on SV = EDV-ESV?

Back 76

Card. tamponade occurs when blood or fluid accumulates in the pericardial sac; it increases interpericardial pressure, and decreases end diastolic volume because it decreases ventricular filling. Thus, SV (stroke volume) goes down.

Front 77

What are the effects of high temperature or pregnancy on cardiac output?

Back 77

They increase cardiac output

Front 78

What's the effect of rapid arrythmias on cardiac output?

Back 78

They decrease cardiac output

Front 79

What element of stroke volume is affected by physiological cardiac remodeling?

Back 79

Hypertrophy increases force of contraction which serves to decrease ESV, which in turn increases SV

Front 80

What's the effect of physiological cardiac remodeling on heart rate?

Back 80

Decrease (heart is more efficient, doesn't need to work as hard)

Front 81

What are hallmarks of "pathological" cardiac remodeling?

Back 81

Irreversible changes to heart proportions and function often brought on by pathology

Front 82

Describe "concentric hypertrophy"

Back 82

Increased wall thickness of the heart results in decreased compliance of ventricles and increased contractility. Overall effect is increased afterload (hypertension).

Front 83

Describe "eccentric hypertrophy"

Back 83

The lumen of ventricles increases. Also, speed of contraction increases. This decreases mechanical efficiency and also ejection fraction. Overall effect is increased preload.

Front 84

Ventricular hypertrophy is often a side-effect of ____ and has this effect on cardiac output:

Back 84

Exercise; increase

Front 85

Concentric and eccentric hypertrophies often result in a heart described using this term:

Back 85

"Hypoeffective"