Cardioviscular Physiology 3 Flashcards

1
Q

Explain the Diastole period!

A

After blood got pushed out of the ventricles: more blood in the aorta and pulmonary trunk than in the ventricles, and more blood in the ventricles than in the atria

aorta > Left ventricle > Left atrial
Pulm. trunk > right ventricle > right atrial

Isovolumetric ventricular relaxation

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2
Q

What is the Isovolumetric ventricular relaxation?

A

no change of the volume in the ventricular, all valves are closed,
ventricular is relaxing after pushing out the blood to the aorta/pulmonary trunk

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3
Q

What is the quiescent period?

A

atria is relaxed, ventricle is relaxed –> passive flow blood from atria to ventricle

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4
Q

State of pressure when ventricles are filling?

A

aorta still has the highest pressure, semilunar valves are closed

aorta > left atrial > left ventricle

pulmonary trunk > right atrial > right ventricle

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5
Q

Explain the Systole process!

A

After atrial contraction, all blood is pushed to the ventricle -> AV closes, and semilunar valves are closed too because the ventricles are about to contract and build up to pressure (which will open semilunar valves)

–> Isovolumetric ventricular contraction - no change of volume, all valves closed

pressure same as Isov. ventr. relaxation
aorta > Left ventricle > Left atrial
Pulm. trunk > right ventricle > right atrial

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6
Q

State of pressure when blood gets pushed out?

A

Left ventricular > aortic > Left atrial

Right ventricular > pulmonary trunk > right atrial

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7
Q

What is the cardiac output (CO)?

A

amount of blood pumped out by each ventricle per minute
so, how often does the heart pump - heart rate
how much does it pump per beat - stroke volume

CO = HR * SV

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8
Q

How is stroke volume (SV) calculated?

A

How much blood comes into the heart after diastole? EDV
How much blood remains in the heart after it pumps? ESV

SV = EDV - ESV -> it will tell us how strong the stroke volume is -> how much we pump out per contraction

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9
Q

What factors will affect heart rate?

A

Sympathetic will increase slope to reach AP quicker -> increase of HR
Parasympathetic vice versa -> decrease of HR

Epinephrine secreted by the adrenal medulla -> increase of heart rate

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10
Q

What factors will affect stroke volume?

A

Preload: amount ventricles are stretched by contained blood, how much blood comes back (EDV) - increased SV with increased venous return - Frank Starlin law
-> increase stroke volume

Contractility: cardiac cell contractile force by factors other than EDV (ESV is decreased!!, more contractile force) - comes from Ca2+ by increasing sympathetic input!! -> more contracting cross bridging in sarcomeres
-> increase stroke volume

Afterload: back pressure exerted by blood in the large arteries leaving the heart (ESV) - it is harder to overcome the pressure of arteries when there is much blood there -> if it is hard to overcome the pressure, there will be less blood pumped out -> more ESV ->
DECREASE stroke volume

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11
Q

How can Contractillity be increased?
What is its effect?

A

By Ca2+ -> by an increase of sympathetic or epinephrine input to the heart or drugs

Decrease of ESV and thus increase of stroke volume

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12
Q

What is the consequence of afterload?

A

more force is needed to overcome pressure in ventricles to pump blood -> so increase of ESV
-> high blood pressure increase afterload

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13
Q

What is the consequence of increased venous return?

A

Increase of preload (EDV) -> the heart’s ability to stretch more, when EDV is increased -> increase of stroke volume

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14
Q

When do we see a big increase of SV?

A

Increased EDV and increased Contractility by sympathetic NS or epinephrine (ESV down)
up to 5x increase of CO

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15
Q

Frank-Starlin law of the heart

A

The heart can adapt to EDV -> the more blood flows into the ventricle (EDV), the harder it can pumps (SV) -> also makes sense with SV = EDV - ESV

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16
Q

PRELOAD
How can cardiac muscle adapt to the increase in EDV?

A

at normal EDV flow, there is an overlap in the sarcomere

when EDV increases sarcomere length reaches the optimal length

venous return determines how well cardiac muscle will stretch -> and thereby pump

17
Q

What is the stimulus of Contractility

A

Ca2+

Contractility is independent of EDV and stretch, it has to do with how well the heart contracts
also has to do with how much blood is left over after contraction = ESV

18
Q

Where do we get Ca from in cardiac muscles

A

L-type Ca channels and from ryanodine receptors in Sarcoplasmic reticulum

19
Q

Describe the role of myosin heads during a contraction!

A

Normal contractility: there is not as much Ca present -> not all myosin heads are involved in filament binding

Increased contractility: more Ca released -> more myosin involved in binding filaments -> optimal length reached -> more contraction

20
Q

What is the function of beta blockers?

A

they can reduce blood pressure, by reducing the heart rate and force of contraction of the heart

21
Q

How can Cardiac output be increased efficiently

A

By increasing SV rather than heart rate, because with every heart rate we consume blood

22
Q

What happens in case of high blood pressure?

A

increased afterload -> increase of O2 consumption -> the heart has to work more -> weighs on vascular system

23
Q

What does the P-wave represent?

A

Atrial depolarization -> SA node firing

24
Q

What does the QRS-wave represent?

A

-Ventricular depolarization -> Perkunjie fibers firing

-at the same time atrial repolarization but masked by ventricular depolarization

25
Q

What does the T-wave represent?

A

Ventricular repolarization