Heart Pump Flashcards

1
Q

Isovolumetric Contraction –

A

all valves are close, no change in volume but heart is contracting

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2
Q

Isovolumetric Relaxation –

A

all valves are close but heart is relaxing

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3
Q

Cardiac Cycle – Right Heart is different than left heart: pressure difference

A

Magnitude of the peak systolic pressure is lower in RIGHT because less resistance to flow from lungs vs. systemic organs
Systolic Pressure: 24 mm Hg
Diastolic Pressure: 8 mm Hg

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4
Q

S3: presence may indicate

A

left ventricular failure (but can also sometimes be detected in normal children!)

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5
Q

S4: presence may indicate

A

ventricular diastolic stiffness

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6
Q

Preload: is

A

end-diastolic pressure/vol. that stretches the ventricle to its greatest dimensions under physiologic demand

The passive/resting tension placed on cardiac muscle cells before contraction. (A function of the volume and pressure at the end of diastole)

EDV or atrial pressure are used as surrogates

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7
Q

Starling’s Law of the Heart:

A

stroke volume increases as cardiac filling increases

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8
Q

Increased preload will:

A

Increase initial muscle fiber length, thus increase the extent of shortening during contraction
Increase end-diastolic volume and stroke volume

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9
Q

Afterload: is the

A

tension or stress that develops in the cardiomyocytes of the left ventricle during ejection/contraction

The active tension placed on cardiac muscle cells during contraction. (A function of the resistance the left ventricle must overcome to circulate blood)

Abnormal: increased afterload will decrease SV –ex. hypertension, aortic valve obstruction

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10
Q

As afterload increases, cardiac output

A

decreases.

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11
Q

5 effects That are initiated by norepi interaction with BETA-1 ADRENERGIC RECEPTORS:

A

An increase in heart rate (positive chronotropic effect)-Activates funny–current in SA node

An increase in rate of action potential conduction, particularly evident in the AV node (positive dromotropic effect)–Alters conductivity of gap junctions

An increase in cardiac contractility (positive inotropic effect), which increases the contractile ability of cardiac muscle at any given preload–Activates the Ca2+ current and increases Ca2+ release from SR

An increase in the rate of cardiac relaxation (positive lusitropic effect) which minimizes the detrimental effects of high heart rates on diastolic filling time–Increase Ca2+ uptake by SR

A decrease in cardiac action potential duration, which promotes early relaxation and contributes to the positive lusitropic effect–Early activation of delayed K+ current

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12
Q

chronotropic effect

A

changes the SA node rate

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13
Q

dromotropic effect

A

changes the AV node rate

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14
Q

lusitropic effect

A

changes the relaxation of the cardiac muscle cells

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15
Q

main source of cardiac muscle energy

A

60 – 90% of fuel is ATP from oxidative phosphorylation
fatty acids in adults
Fetal and newborn is glucose and lactate
Severe heart failure there is an observable shift back to glucose metabolism

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16
Q

Strategies to Reduce O2 Consumption

A

decrease heart rate-More efficient to achieve CO with low HR and high SV than vice versa.
Reduce cardiac preload (end-diastolic volume)
Reduce cardiac afterload (systemic arterial pressure)
Reduce cardiac contractility (sympathetic drive)