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Organ Systems Anatomy and Physiology > Organ Systems Brons MT3 Heart 3 Lecture 10/22/13 (2 of 2) > Flashcards

Organ Systems Brons MT3 Heart 3 Lecture 10/22/13 (2 of 2) Flashcards

1
Q

Preload or EDV (end diastolic volume) depends on

A

Venous filling pressure, duration of diastole, ventricular compliance

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2
Q

Does increased venous pressure (preload) increase or decrease stroke volume?

A

Increase

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3
Q

Does ventricular hypertrophy reduce or increase compliance? Does it reduce or increase stroke volume?

A

Reduces compliance

Diminishes stroke volume

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4
Q

Afterload

A

The systolic pressure needed to overcome the blood pressure within the aorta in order to eject blood. End systolic volume, ESV

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5
Q

Does afterload include isometric contraction? Isotonic contraction?

A

Isometric contraction to reach afterload pressure levels.

Isotonic contraction during ejection

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6
Q

Increased aortic pressure (afterload) __________the velocity of ventricular contraction (increases or reduces)?

A

Reduces. This in turn reduces how much blood is ejected during a cycle.

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7
Q

Does greater contractility increase or decrease velocity?

A

Increase.

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8
Q

How does the body compensate for decreased velocity?

A

By increasing contractility which increases the velocity of blood flow during ejection.

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9
Q

Does increased aortic pressure (afterload) increase or decrease stroke volume?

A

Decrease

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10
Q

Does increased ESV reduce or increase stroke volume?

A

Reduce

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11
Q

Contractility or Inotropism

A

The intrinsic ability of myocardial cells to develop force at a given preload and afterload

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12
Q

Increases in contractility (positive inotropy) are caused by any mechanisms that _________ Ca++ and its binding to ___________.

A

increase; troponin

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13
Q

What is/are involved in the regulation of myocardial contractility by the sympathetic nervous system? What is their effect?

A

Catecholamines (along with cardiac glycosides) increase contractility. Sympathetic = fight or flight

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14
Q

What is/are involved in the regulation of myocardial contractility by the parasympathetic nervous system? What is their effect?

A

Ach muscarinic receptors decrease contractility. Parasympathetic = Rest and Digest

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15
Q

Changes in contractility involve changes in

A

Contraction force

Latency of contraction and relaxation

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16
Q

Increased contractility by NE and EPI does what pressure and time of ventricular contraction?

A

Early onset, enhanced force, and early relaxation (start early, go higher, finish early)

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17
Q

What is an advantage of finishing contraction early?

A

Gives more time for refilling

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18
Q

Decreased contractility from Ach results in what?

A

Late onset, less force, late to normal finish.

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19
Q

What is the sequence of events in the excitation-contraction of cardiac muscle?

A
  1. AP opens L-type Ca++ channel. 2. This triggers release of Ca++ from the SR via the RyR channel. 3. Ca++ from the SR (not extracellular) binds to troponin complex and activates contractile apparatus.
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20
Q

How reliable is this cycle of events in producing contractions?

A

There are many places in the system that could have a mutation in one or multiple genes that could produce arrhythmias. Impact how faithfully the communication with Ca++ operates.

21
Q

What is the mechanism by which NE and EPI accelerate onset and increase the magnitude of contraction (start early and go higher)?

A

cAMP activates protein kinase PK. cAMP-PK enhances Ca++ channel opening and subsequent release of Ca++ from SR.

22
Q

What is the mechanism by which NE and EPI stop contraction sooner (finish early)?

A

cAMP-PK activates phospholamban to increase SR uptake of Ca++ (pumps Ca++ back into SR). Reduces Ca++ binding to troponin C, relaxing the myofibrils.

23
Q

Stroke Volume (SV) = ?

A

SV = EDV - ESV

24
Q

Does increased contractility expand or diminish stroke volume?

A

Expand

25
Q

EDV=?

A

End diastolic volume.(preload)

26
Q

Does increased ESV reduce or increase stroke volume?

A

Reduce. SV = EDV - ESV. Larger ESV will reduce SV.

27
Q

Congestive heart failure (CHF) leads to a/an ________ in contractility, but is compensated for by __________ the preload.

A

Decrease in contractility; increasing the preload

28
Q

Cardiomyopathy

A

Weak myocardial contraction

29
Q

Effects of cardiomyopathy

A

Blood backs up and expands ventricular spaces. Overstretch the myocardium, hence high EDV.

30
Q

Stretching muscles results in _____________ contractility?

A

Increased. Increase cross bridges, increase force, up to a point.

31
Q

Overstretching muscles results in ______________ contractility?

A

Decreased

32
Q

Heart function in early stage CHF?

A

Increased stretching compensates for the weak myocardium and low cardiac output with enhanced contractility, improving heart function.

33
Q

Heart function in late stage CHF?

A

Further stretching reduces actin-myosin cross bridging and lowers contractility.

34
Q

Four effects of cardiac glycosides (eg Digitalis, Digoxin) on cardiac function?

A
  1. increase vagal tone. 2. Sensitization of baroreceptors. 3. central vagal stimulation, 4. facilitation of muscarinic transmission to heart.
35
Q

What is the effect of Digitalis on the Na+ K+ pump?

A

Slows it down

36
Q

In the Na+ Ca++ exchanger, what comes in the cell and what goes out?

A

Na+ always goes into cell. Facilitates Ca++ going out.

37
Q

What is the effect of Digoxin on Na-K ATPase? What does this do to contractility?

A

Digoxin increases contractility by inhibiting Na+ K+ ATPase

38
Q

Inhibition of Na+K+ ATPase causes what?

A

Cell gains sodium, decreasing Na+ conc. gradient. Ca/Na exchange is reduced. Ca++ accumulates within cell to initiate contraction.

39
Q

Cardiac work = ?

A

work (contractility) = force X distance

40
Q

External work = ?

A

External work = ventricular pressure X stroke volume (muscle length)

41
Q

External work is isotonic or isometric?

A

Isotonic

42
Q

External work has high or low O2 requirement?

A

Low

43
Q

Internal work has high or low O2 requirement?

A

High

44
Q

Internal work is isotonic or isometric?

A

Isometric

45
Q

Describe internal work

A

Isometrically builds ventricular pressure during isovolumic contraction and is released as heat. Increases to overcome aortic pressure. Not calculated, graphically estimated.

46
Q

Aortic stenosis

A

Aortic valve calcified (fixed diameter). Only partially opens. Backflow. Takes more (isometric) work. Must build pressure to higher level than afterload. Increased aortic pressure.

47
Q

Would the increased internal work involved in aortic stenosis require more O2 or less?

A

More

48
Q

Increase in contractility _________ internal work and thus __________ O2 consumption

A

decreases: reduces

Organ Systems Anatomy and Physiology (6 decks)

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