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CVS > 03b: EKG and CO > Flashcards

03b: EKG and CO Flashcards

1
Q

ECG records changes in (X) versus (Y).

A 
X = electrical potential
Y = time
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2
Q

Upward deflection of ECG is indicative of (X) at (positive/negative) electrode.

A

X = positivity at positive electrode OR negativity at negative electrode

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3
Q

The same size dipole can generate smaller or larger signal, depending on (X).

A

X = orientation with lead axis

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4
Q

Lead I positive and negative electrodes.

A

Neg: RA
Postiive: LA

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5
Q

Lead II positive and negative electrodes.

A

Neg: RA
Positive: LL

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6
Q

Lead III positive and negative electrodes.

A

Neg: LA
Positive: LL

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7
Q

(X) event in cardiac cycle accounts for most of PR interval in ECG.

A

X = AV nodal delay

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8
Q

T wave: (upward/downward) deflection of (de/re)-polarization is due to (endo/epi)cardial fibers repolarizing before (endo/epi)cardial fibers.

A

Upward;
Repolarization (ventricles);
Epicardial;
Endocardial

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9
Q

Resultant vector of T wave points in which direction(s)? This is the same orientation as which other ECG deflection?

A

Down and to the left;

R-wave

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10
Q

T wave lasts (shorter/longer) than QRS complex. This is because (depolarization/repolarization) spreads at slower velocity.

A

Longer;

Repolarization

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11
Q

Sympathetic stimulation of ventricular muscle increases (X) of contraction.

A

X = force and velocity

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12
Q

Since (X) of (veins/arteries) is (Y) times greater than (veins/arteries), to achieve the same change in pressure in vessels of same dimensions, (Y) times the volume would have to be added.

A

X = distensibility;
Veins;
Y = 5-6
Arteries

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13
Q

The volume of blood flowing through

the circulatory system during a given time period.

A

CO

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14
Q

T/F: CO of LV equals CO of RV.

A

True

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15
Q

CO units.

A

L/min

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16
Q

CO is equal to product of (X) and (Y).

A 
X = SV
Y = HR
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17
Q

Cardiac index is based on the fact that (X) is (directly/indirectly) proportional to (Y).

A

X = CO
Directly;
Y = body surface area

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18
Q

The Fick principle is a (direct/indirect) method to measure (X). What’s the equation?

A

Indirect;
X = CO

CO = (O2 uptake by lung)/([O2]a-[O2]v)

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19
Q

Indicator dilution method is one in which (known/unknown) quantity of (X) is injected into (Y).

A

Known;
X = dye
Y = blood stream in central vein or heart

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20
Q

Indicator dilution method: where is the detector?

A

Downstream artery

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21
Q

Increase venous return results in (increase/decrease) in SV. This is due to (increase/decrease) in (X) in (Y) chamber.

A

Increase;
Increase;
X = P and V
Y = RA

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22
Q

Starling stated the Law of the Heart:

A

E of contraction is function of length of muscle fiber

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23
Q

EDV increases. This results in (increase/decrease) preload, aka (X). Explain.

A

Increase;
X = EDP

Increase in length of muscle fibers, leading to increase in passive P in ventricle

24
Q

For given sarcomere length, (cardiac/skeletal) muscle is likely to have more active tension.

A

Skeletal

25
Q

The heart normally functions along (ascending/descending/both) limb(s) of PV curve.

A

Ascending

26
Q

Cardiac Length v Active Tension curve is (more/less/equal) in steepness as Skeletal muscle.

A

More

27
Q

Cardiac Length v Passive Tension curve is (more/less/equal) in steepness as Skeletal muscle.

A

More

28
Q

The shortest sarcomere length at which active tension can be developed is (shorter/longer/equal) in cardiac muscle compared to skeletal muscle.

A

Longer

29
Q

Length-Tension curve: It’s been demonstrated that an increase in (X) of cardiac muscle causes increase in (Y). This accounts for steep curve rise.

A 
X = sarcomere length
Y = myofilament sensitivity to Ca
30
Q

For given sarcomere length, (cardiac/skeletal) muscle is likely to have more passive tension. What’s the reason for this?

A

Cardiac;

Prevents chambers from over-filling

31
Q

Heterometric regulation explains the regulation of (X) in response to changes in (Y). This is considered a(n) (intrinsic/extrinsic) property of the heart.

A

X = SV
Y = venous return
Intrinsic

32
Q

Stimulation of sympathetic nerves or infusion of (X) results in (increased/decreased) contractility. This is simply defined as increased (Y) at a given (Z).

A

X = epi
Increased;
Y = force capability
Z = EDV

33
Q

Regulation of (X) is “homeometric”, because it’s (dependent/independent) of (Y).

A

X = contractility
Independent
Y = change in length

34
Q

T/F: Sympathetic stimulation increases ESV.

A

False - decreases ESV (by increasing SV)

35
Q

T/F: Sympathetic stimulation increases EF.

A

True

36
Q

EF at rest is typically (X)% of (Y). How does that change during exercise?

A 
X = 50-67
Y = EDV;

Can increase to 80% during exercise

37
Q

Maximum rate of rise of ventricular pressure is a measure of (X) of the ventricle.

A

X = contractility

38
Q

Binding of Epi to (X) receptor in heart activates G protein that (increases/decreases) activity of (Y).

A

X = B1
Increases;
Y = AC

39
Q

Epinephrine results in (increase/decrease) of cAMP, resulting in direct (activation/suppression) of (X). What does this then do?

A

Increase;
activation;
X = PKA

Phosphorylates:

  1. Phospholamban
  2. L-type Ca channels
  3. Troponin I
  4. Titin
40
Q

Epi’s effect on (X)-type Ca channels results in (increase/decrease) Ca conductance. This has which effect on Ca release from SR?

A

X = L
Increase;

Also increases Ca release from SR

41
Q

Phospholamban, under normal conditions, has which function?

A

Blocks SR Ca reuptake pump

42
Q

Epi causes (dephosphorylation/phosphorylation) of (X), removing its restraint on (Y) and causing (increase/decrease) in Ca reuptake by SR.

A

Phosphorylation;
X = Phospholamban
Y = SR Ca reuptake pump
Increase

43
Q

Epi causes (increase/decrease) in duration of contractile response and (increase/decrease) rate of relaxation. This is done via (phosphorylation/dephosphorylation) of (X).

A

Decrease;
Increase;
Phosphorylation;
X = Phospholamban

44
Q

What’s Epi’s effect on titin via (X) of titin?

A

X = phosphorylation

Decreases its stiffness (reduced passive wall tension), facilitating ventricular filling

45
Q

T/F: Changes in heart rate affect contractility.

A

True

46
Q

Increase in HR has (positive/negative) ionotropic effect due to (increase/decrease) in (X).

A

Positive;
Increase
X = cytoplasmic Ca availability

47
Q

The (X) is commonly considered the left ventricular muscle’s afterload.

A

X = aortic diastolic P

48
Q

A high afterload affects ejection in which ways?

A
  1. Delayed ejection

2. Reduced rate of ejection

49
Q

Why would high afterload result in ejection delay?

A

Longer time required for ventricular pressure to reach aortic pressure

50
Q

T/F: Afterload for heart is essentially identical during ejection period.

A

False - changing, tracking ventricular chamber pressure

51
Q

Stroke work is product of (X) and (Y).

A 
X = average P
Y = SV
52
Q

Minute work is product of (X) and (Y).

A 
X = average P
Y = CO (HR*SV)
53
Q

Area of PV loop represents:

A

Stroke work

54
Q

The Law of Laplace: the (X) that ventricle must develop to produce given (Y) is influenced by (Z).

A 
X = wall tension
Y = P
Z = radius
55
Q

Wall stress increases proportionally with (X) and is inversely proportional to (Y).

A 
X = radius
Y = wall thickness
56
Q

Wall stress equation: stress increases with increase in (X).

A

X = P and radius

57
Q

Wall stress equation: stress increases with decrease in (X).

A

X = h (thickness of wall)

CVS (11 decks)

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