Regulation of stroke volume and heart rate Flashcards

1
Q

What is stroke volume?

A

Volume of blood pumped per ventricle per contraction

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2
Q

What is End diastole volume?

A

Volume of blood in the ventricles at the beginning of contraction.

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3
Q

What does End Diastole volume determine?

A

The length of the muscle

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4
Q

What is stroke volume directly related to?

A

The force generated by cardiac muscle during contraction

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5
Q

What is force of ventricular contraction affected by?

A
  1. Length of muscle fibres at the beginning of contraction

2. Contractility of the heart

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6
Q

What determines the length of cardiac muscle fibres at the beginning of contraction?

A

End diastole volume- how full the ventricle is of blood at the beginning of contraction

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7
Q

What is contractilty of the heart determined by?

A

Function of Ca interaction with the contractile filaments.

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8
Q

As contraction force increases, _______ increases

A

stroke volume

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9
Q

What is the force created by a muscle fibre directly related to?

A

The sarcomere length, AS INDICATED BY THE INITial length of the muscle fibre

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10
Q

Relate the sarcomere length and how the initial length of a muscle fibre creates a bigger force to the HEART.

A

As stretch of the ventricle wall increases it increases the stroke volume.

-If additional blood flows into the ventricle, the muscle fibres stretches and contracts more forcefully, ejecting more blood.

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11
Q

What is preload?

A

The degree of myocardial stretch before contraction begins

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12
Q

What is End diastole volume a measure of?

A

Measure of stretch in the ventricles

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13
Q

What does the measure of stretch in the ventricles determine?

A

Sarcomere length

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14
Q

What does the X axis of the Starling curve show?

A

End diastolic volume which is a measure of stretch of the ventricles which in turn determines sarcomere length.

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15
Q

What does the Y axis of the Starling curve show?

A

Stroke volume, which indicates the force of contraction

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16
Q

What does the Starling curve show?

A

Stroke volume is proportional to End Diastolic Volume ie stroke volume increases as end diastolic volume increases.

17
Q

What is venous return affected by?

A
  1. Sympathetic innervation of veins
  2. Skeletal muscle pump (its contractions compress/contract the veins, particularly in the legs, to squeeze more blood out of them and towards theheart)
  3. Respiratory pump (pressure changes in the abdomen and thorax during breathing)
18
Q

How can you affect contractility?

A

Via the nervous and endocrine system.

  • As the amount of calcium svailable for contraction increases, contractility increases.
  • Norepinephrine and epinephine bind to B1 receptors.
  • This phosphoryltes voltage gated Ca channels, and opens them for longer, increasing Ca entry from ECF.
  • Increases Ca stores in Sarcoplasmic reticulum, increases the amount of Ca being released, giving a stronger strength of contraction.
  • Ca is removed from cytosol faster, shortening the Ca-troponin binding time, shorter duration of contraction
19
Q

If left ventricle is damaged, what effect does this have on cardiac output?

A

Ventricular myocardium has weakened therefore decreased sstroke volume, in turn decreased cardiac outut

20
Q

CO = ?

A

HR * SV

21
Q

What is afterload?

A

Combined EDV and arteriolar resistance during ventricular contraction.

Load placed on the ventricle as it contracts

22
Q

What determines afterload?

A

End diastolic volume + Arterial blood pressure

23
Q

When do we see afterload and what is its effect over a long period of time?

A
  • High arteriolar blood pressure and loss of stretchability (compliance) in the Aorta
  • Myocardial hypertrophy because to maintain constant stroke volume the heart muscle has to work harder and ventricle increases its force of contraction, increases the uscles need for oxygen and ATP production
24
Q

What is heart rate affected by? What does heart rate determine?

A
  • Autonomic divisions of the nervous system i.e. parasympathetic (acetylcholine acting on muscarinic receptors, increases K efflux and decreases Ca release, hyperpolarising the cell) and sympathetic nervous system (norepinephrine on B1 receptors, increases K and Ca influx, depolarising the cell)
  • Epinephrine
25
Q

What does afterload reflect?

A
  • The preload and the effort required to push the blood out into the arterial system.
26
Q

What is a clinical indicator of Afterload?

A

Mean arterial pressure

27
Q

What does a)Norepinephrine and epinephrine act on and b)Acetylcholine act on?

A

a) Norepinephrine and epinephrine acts on B1 receptors to speed up the rate of pacemaker depolrisation.
b) Acetylcholine acts on muscarinic receptors to hyperpolaise the pacemaker cells.

28
Q

What does echocardiography allow?

A

Ejection fraction (stroke volume/end diastole volume) to be calcualted. Indicates ventricualr function