03b: EKG and CO Flashcards by Nuna H

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

X = electrical potential
Y = time

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

X = positivity at positive electrode OR negativity at negative electrode

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

X = orientation with lead axis

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Lead I positive and negative electrodes.

Neg: RA
Postiive: LA

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Lead II positive and negative electrodes.

Neg: RA
Positive: LL

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Lead III positive and negative electrodes.

Neg: LA
Positive: LL

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

X = AV nodal delay

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

Upward;
Repolarization (ventricles);
Epicardial;
Endocardial

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

Down and to the left;

R-wave

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

Longer;

Repolarization

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

X = force and velocity

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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.

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

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The volume of blood flowing through

the circulatory system during a given time period.

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

True

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CO units.

L/min

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

X = SV
Y = HR

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

X = CO
Directly;
Y = body surface area

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

Indirect;
X = CO

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

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

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

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Indicator dilution method: where is the detector?

Downstream artery

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

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

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Starling stated the Law of the Heart:

E of contraction is function of length of muscle fiber

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

Increase;
X = EDP

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

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

Skeletal

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

Ascending

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

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

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

Longer

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.

``` X = sarcomere length Y = myofilament sensitivity to Ca ```

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

Cardiac; | Prevents chambers from over-filling

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

X = SV Y = venous return Intrinsic

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

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

Regulation of (X) is "homeometric", because it's (dependent/independent) of (Y).

X = contractility Independent Y = change in length

T/F: Sympathetic stimulation increases ESV.

False - decreases ESV (by increasing SV)

T/F: Sympathetic stimulation increases EF.

True

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

``` X = 50-67 Y = EDV; ``` Can increase to 80% during exercise

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

X = contractility

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

X = B1 Increases; Y = AC

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

Increase; activation; X = PKA Phosphorylates: 1. Phospholamban 2. L-type Ca channels 3. Troponin I 4. Titin

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

X = L Increase; Also increases Ca release from SR

Phospholamban, under normal conditions, has which function?

Blocks SR Ca reuptake pump

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

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

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

Decrease; Increase; Phosphorylation; X = Phospholamban

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

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

T/F: Changes in heart rate affect contractility.

True

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

Positive; Increase X = cytoplasmic Ca availability

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

X = aortic diastolic P

A high afterload affects ejection in which ways?

1. Delayed ejection | 2. Reduced rate of ejection

Why would high afterload result in ejection delay?

Longer time required for ventricular pressure to reach aortic pressure

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

False - changing, tracking ventricular chamber pressure

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

``` X = average P Y = SV ```

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

``` X = average P Y = CO (HR*SV) ```

Area of PV loop represents:

Stroke work

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

``` X = wall tension Y = P Z = radius ```

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

``` X = radius Y = wall thickness ```

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

X = P and radius

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

X = h (thickness of wall)