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Cardio/Pulm Final > Lecture 6 (DSA): Cardiac Electomechanical Coupling > Flashcards

Lecture 6 (DSA): Cardiac Electomechanical Coupling Flashcards

1
Q

What 3 criteria must be met to qualify as normal sinus rhythm?

A

1) AP must originate in SA node
2) SA nodal impulses must occur regularly at a rate of 60-100 impulses/min
3) Activation of myocardium occurs in the correct sequence with the correct timing and delays

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2
Q

The RMP of cardiac cells is determined primarily by?

A

K+ ions

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3
Q

How does the duration of the AP in cardiac tissues compare to that of skeletal muscle?

A

The AP in cardiac tissues is of long durartion, compared to the very brief duration in nerve and skeletal muscle

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4
Q

How does the duration of an AP affect refractory periods?

A

The longer the AP, the longer the cell is refractory to firing another AP

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5
Q

The transverse tubules of cardiac cells form _______ with the SR?

A

Dyads

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6
Q

How are the T tubules of cardiac muscle different than that of skeletal muscle?

A

Much larger in diameter, and contain a much greater amount of Ca2+

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7
Q

What 2 components are found within myocardial cells that are not found within skeletal muscle?

A

Intercalated discs and Gap Junctions

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8
Q

What leads to the plateau phase seen in cardiac AP; via what channel?

A

Inward Ca2+ current via dihydropyridine receptors

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9
Q

What does entry of Ca2+ into the myocardial cell cause?

A

Triggers the release of more Ca2+ from the SR (Ca2+-induced Ca2+ release)

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10
Q

What are the receptors for Ca2+ on the SR

A

Ryanodine receptors

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11
Q

What 2 factors determine how much Ca2+ is released from the SR?

A

1) Amount of Ca2+ previously stored in the SR
2) Size of the inward Ca2+ current during the plateua of the AP

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12
Q

What does the Ca2+ bind to after being released from the SR; leads to?

A

Troponin C - moves tropomyosin out of way - actin and myosin can now interact

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13
Q

The magnitude of tension developed by myocardial cells is proportional to?

A

The intracellular Ca2+ concentration

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14
Q

What helps reaccumulate Ca2+ back into the SR; causes?

A

Ca2+-ATPase; causes relaxation

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15
Q

What helps get the rest of the intracellular Ca2+ out of the cell?

A

Ca2+-ATPase and Ca2+-Na+ exchange in the sarcolemmal membrane

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16
Q

How does the Ca2+-Na exchanger pump out Ca2+ against its electrochemical gradient?

A

Using the energy from the inward Na+ gradient.

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17
Q

What is a positive inotropic effect; increase what 2 things?

A

Agents that produce an increase in contractility. Increase both the rate of tension development and the peak tension

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18
Q

What are the 3 important features of the positive inotropic effect on the myocardium produced by the sympathetic nervous system?

A

1) Increased peak tension
2) Increased rate of tension development
3) Faster rate of relaxation

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19
Q

The positive inotropic effect by the sympathetic nervous system is mediated by activation of what receptor?

A

β1 receptors

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20
Q

Phosphorylation of what 2 proteins produc the increase in contractility?

A

1) Sarcolemmal Ca2+ channels that carry inward Ca2+ current during the AP
2) Phospholamban, results in greater upatake and storage of Ca2+ by SR

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21
Q

Stimulation of the parasympathetic nervous system and ACh have a _________ on the _____.

A

Negative inotropic effect on the atria

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22
Q

Which receptors mediate the negative inotropic effect produced by the parasympathetic nervous system?

A

Muscarinic receptors

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23
Q

What 2 ways does the parasympathetic nervous system decrease atrial contractility?

A

1) ACh decreases inward Ca2+ current during plateua of AP
2) ACh increases K+ leaving the cell, shorteining the duration of the AP

24
Q

What 2 ways does an increased HR increase contractility?

A

1) More AP per unit time and increase in total amount of Ca2+ entering during plateau phase
2) SR accumulates this increased Ca2+ for subsequent release

25
Q

When an extrasystole beat occurs what happens to the tension of the next beat?

A

Tension will be greater than normal due to unexpected increase in amount of Ca2+ that was accumulated by SR

26
Q

How do cardiac glycosides (digitoxin and ourabain) inhibiting Na+-K+ have a positive inotropic effect?

A

Increases the intracellular Na+ concentration, which alters the function of the Ca2+-Na+ exchanger. Less Ca2+ will be pumped of the cell producing an increase in tension

27
Q

The major use of cardiac glycosides is in the treatment of?

A

Congestive heart failure

28
Q

Increasing the cardiac muscl length increases Ca2+ sensitivity to; increases Ca2+ release from?

A

Troponin C; release from the SR

29
Q

The length of a single left ventricular muscle
fiber just prior to contraction corresponds to?

A

Left ventricular end-diastolic volume

30
Q

What is preload?

A

End-diastolic volume, tension of blood pushing out against the walls of the chamber just before it contracts

31
Q

What is afterload?

A

Pressure which must be generated in order for the ejection of blood to occur. In the left ventricle this = aortic pressure.

32
Q

What is stroke volume; how is it calculated?

A

Volume of blood ejected on one ventricular contraction, or the difference between the volume of blood in the ventricle before ejection (end-diastolic volume) and the volume remaining in the ventricle after ejection (end-systolic volume)

End-diastolic volume - End-systolic volume

33
Q

What is ejection fraction; how is it calculated?

A

The effectivness of the ventricles in ejecting blood

Ejection fraction = Stroke volume/End-diastolic volume

34
Q

Ejection fraction is an indicator of?

A

Contractility

35
Q

What is cardiac output; how is it calculated?

A

Total volume of blood ejected per unit time

Cardiac output = Stroke Volume x Heart Rate

36
Q

What does the Frank-Starling relationship (Law of the heart) state?

A

Volume of blood ejected by the ventricle depends on the volume present in the ventricles at the end of diastole

37
Q

How does the Frank-Starling Law of the heart ensure output of left and right ventricles are equal?

A

In the steady state, cardiac output equals venous return. This relationship governs normal ventricular function and ensures the volume the heart ejects in systole equals the volume it receives in venous return

38
Q

As venous return to the heart increases, end-diastolic volume increases, and because of the length-tension relationship in the ventricles, what happens to stroke volume?

A

Stroke volume will increase accordingly

39
Q

How do positive inotropic effects change stroke volume, cardiac output, and ejection fraction?

A

Increase the stroke volume and cardiac output. The result is that a larger fraction of end-diastolic volume is ejected per beat and there is an increase in ejection fraction.

40
Q

What are the effects of increased afterload?

A

Decreases stroke volume (SV) and at the same time increases left ventricular end-diastolic pressure (LVEDP).

41
Q

What are the effects of decreased afterload?

A

Increases SV and at the same time reduces LVEDP.

42
Q

What is occuring at point 1—->2

A

End of diastole (point 1) and beginnging of isovolumetric contraction

43
Q

What is occuring at point 2—->3?

A

Left ventricular pressure becomes higher than aortic pressure, causing the aortic valve to open. Blood is rapidly ejected from the left ventricle into the aorta

44
Q

What does the width of the pressure-volume loop represent?

A

Stroke Volume

45
Q

What is occuring at point 3—>4?

A

Systole ends and isovolumetric relaxation begins as soon as the aortic valve closes.

46
Q

What is occuring at point 4—->1?

A

Ventricular pressure has become less than atrial pressure, the AV valve opens, ventricle begins to rapidly fill with blood

47
Q

What occurs to stroke volume with an increased pre-load?

A

Stroke volume will increase

48
Q

What occurs to stroke volume and end-systolic volume with increased afterload?

A

Less blood is ejected from ventricle during systole; thus stroke volume decreases, more blood remains in the ventricle at the end of systole, and end-systolic volume increases

49
Q

What are the affects of increased contractility on stroke volume and end-systolic volume?

A

Stroke volume increases, as does ejection fraction; less blood remains in the ventricle at the end of systole, and, consequently, end-systolic volume decreases

50
Q

What does the area inside the pressure-volume loop represent?

A

Work of the left ventricle (cardiac work)

51
Q

How is stroke work different than stroke volume?

A

Stroke work = Stroke volume x Aortic Pressure

52
Q

What does the Fick principle state in regards to O2 utilization?

A
  • States there is a conservation of mass
  • In the steady state, the rate of O2 consumption by the body must equal the amount of O2 leaving the lungs in the pulmonary vein minus the amount of O2 returning to the lungs in the pulmonary artery
53
Q

What does the Fick principle say about cardiac output?

A

In the steady state, the cardiac output of the left and right ventricles is equal

54
Q

Why can the O2 content of pulmonary venous blood be measured by sampling peripheral arterial blood?

A

Because none of the O2 added to the blood in the lungs has been consumed by the tissues yet

55
Q

The O2 content of pulmonry arterial blood is equal to that of; can be sampled where?

A

Mixed venous blood and can be sampled in the pulmonary artery itself or in the right ventricle

Cardio/Pulm Final (18 decks)

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