Frank Starling Mechanism Flashcards

1
Q

Frank-starling mechanism

A

-the relationship between length and tension at the level of the cardiac muscle fiber and the left ventricle

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2
Q

Sarcomere

A
  • contractile unit of the cardiomyocyte
  • when you increase stretch then force of contraction also increases

**there is an optimal length to produce maximal force (too much or too little stretch decrease force production)

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3
Q

Operating point

A

-the point in which the length and force of contraction are at during cardiac muscle contraction

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4
Q

Diastole

A

-filling of ventricle

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5
Q

Left ventricle during diastole

A

-fills during diastole (preload)
-an increase in venous return will increase the preload (filling), which increases the stretch, and therefore the stroke volume

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6
Q

Way to increase venous return

A

exercise

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7
Q

Ways to decrease venous return

A

-hemorrhage

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8
Q

Left ventricle end diastolic pressure (LVEDP)

A

-can be a surrogate for filling meaning it is the pressure/fill of the left ventricle during diastole (before systole)

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9
Q

Afterloads effect on LVEDP

A

-afterload is the amount of pressure that the heart needs to exert to eject blood during ventricular contraction
-if increased, then a decrease in stroke volume will occur, and therefore an increase in LVEDP
-if decreased, then an increase in stroke volume, and decrease in LVEDP

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10
Q

Inotropys effect on LVEDP

A

-Inotropy is the force/strength of muscular contractions
-if increased then an increase in stroke volume will occur, and therefore a decrease in LVEDP
-if decreased then a decrease in stroke volume will occur, and an increase in LVEDP

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11
Q

Left ventricle pressure and volume

A

Phase A: diastole, LV filling
- increasing/high volume, low pressure
- mitral valve closes at end of this phase

Phase B: Systole, isovolumetric contraction
- High volume, increasing/high pressure
- aortic valve opens at end of this phase

Phase C: Systole, Ejection period
- low volume, high pressure
- aortic valve closes at end of this phase

Phase D: diastole, isovolumetric relaxation
- decreasing/low pressure, low volume
- mitral valve opens at end of this phase

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12
Q

Stroke volume equation

A

End diastolic volume (EDV)-end systolic volume (ESV) = stroke volume

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13
Q

Effects of increase preload

A

-increase preload (venous return/filling prior to contraction)
-results in increased end diastolic volume, increased stroke volume and increased contractility

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14
Q

Effects of decreased preload

A

-decreased preload (venous return/filling prior to contraction)
-results in decreased end diastolic volume, stroke volume and contractility

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15
Q

Effects of removed pericardium

A

-pericardium restricts ventricular filling (preload)
-when removed, dogs had better cardiac outputs during exercise because the ventricles are able to fill more

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16
Q

Modulators of preload

A

-blood volume
-ventricular filling

17
Q

Modulators of blood volume

A

-RAAS
-blood loss
-fluid therapy

-muscle/respiratory pump
-venous compliance
-venous resistance
-right atrial pressure

18
Q

Modulators of ventricular filling

A

-tricuspid valve
-pulmonary valve/circulation
-pericardium (tamponade)

19
Q

Effects of increased afterload

A

-increased afterload (pressure LV must overcome to pump blood)
-results in increased end systolic volume (blood left after contraction), decreased stroke volume.

20
Q

Effects of decreased afterload

A

-decreased afterload (pressure LF must overcome to pump blood)
-results in decreased end systolic volume (ESV) and an increased stroke volume

21
Q

Modulators of afterload

A

-blood pressure
-ventricular ejection

22
Q

Ways that blood pressure is effected

A

CO X SVR
-affected by blood volume and sympathetic activity
- constriction/dilation of arteries (affected by sympathetic activation or deactivation, RAAS, local dilation vs hypertension)

23
Q

Ways that ventricular ejection is affected

A

-aortic or pulmonic valves

24
Q

Remodelling of heart and the next beat

A

-next beat will be higher or lower depending on the previous beat.
-an increase in afterload will result in an increased preload on the next beat = Self-correcting

25
Q

Effects of increased inotropy

A
  • increased inotropy (contractility)
  • results in decreased end systolic volume, and increased stroke volume
26
Q

Effects of decreased inotropy

A

-decreased inotropy (contractility)
-results in increased end systolic volume, and decreased stroke volume

27
Q

Modulators of inotropy

A

-state of arousal
-sympathetic activity (local norepinephrine, circulating factors epinephrine)
-parasympathetic activity (local acetylcholine)
-Calcium handling
-drug targets