9-18b Cardiac Physiology I Continued

Question 1

What kind of effect does the Sympathetic NS have on heart rate? How is this effect implemented?

Answer 1

Positive Chronotropic effect
Norepinephrine acts on Beta 1 receptors in the sinoatrial node to elevate HR by altering the “funny current” that affects the unstable resting membrane potential

Question 2

What kind of effect does the Parasympathetic NS have on heart rate? How is this effect implemented?

Answer 2

Negative Chronotropic effect

ACh is released from the vagus nerve and acts on muscarinic receptors on the sinoatrial node to lower HR

Question 3

As HR increases, why does CO begin to go down again after HR exceeds 150 bpm?

Answer 3

Increase in HR causes a decreased duration of diastole, which allows less time for ventricular filling
Therefore, at 150 bpm, the filling time is so short that SV is decreased

Question 4

How does the body compensate for lowered SV (stroke volume) when HR exceeds 150 bpm to maintain high CO?

Answer 4

The veins have receptors for Ne and epinephrine (sympathetic neurotransmitters), which can cause vasoconstriction.
This is effective b/c veins typically store pools of blood, but when they’re constricted, there is an increase in venous return.

Question 5

What is preload? How does its size affect SV?

Answer 5

volume of blood in the ventricles at the end of diastole

higher preload, higher SV

Question 6

What is afterload? How does its size affect SV?

Answer 6

the resistance (load must be higher than the pressure in the aorta) the heart has to overcome to eject blood out of the ventricle
Increase in afterload, decrease in SV

Question 7

What is contractility? What is it dependent on? How does its size affect SV?

Answer 7

The strength of the heart’s contraction.
It is dependent on Ca++
Higher contractility, the higher the SV

Question 8

Ventricular end-diastolic volume represents what in comparison to a skeletal m. length-tension relationship?

Answer 8

length

Question 9

AV represents what in comparison to a skeletal m. length-tension relationship?

Answer 9

tension

Question 10

Higher end-diastolic volume results in a higher or lower SV?

Answer 10

higher

Question 11

How does a greater preload cause a higher SV?

Answer 11

Higher preload causes a greater stretch on the myocyte and therefore a stronger contraction and greater SV

Question 12

What affects preload?

Answer 12

venous return and duration of diastole

Question 13

A decrease in afterload causes an increase or decrease in SV?

Answer 13

increase in SV

Question 14

What affects afterload?

Answer 14

hypertension and aortic stenosis increase afterload

hypotension decrease afterload

Question 15

What is a positive inotropic effect? What does it do? What causes it?

Answer 15

It increases intracellular Ca++, leads to a stronger contraction, and a greater SV
greater SNS activation causes NE to act on beta 1 receptors and increase Ca++ during systole to increase the strength of the contraction
Cardiac glycosides (drugs) can also increase Ca++

Question 16

What is a negative inotropic effect? What does it do? What causes it?

Answer 16

It decreases intracellular Ca++, leads to a weaker contraction and lesser SV
It can be caused by drugs that block Ca++ channel blockers

Question 17

Does the parasympathetic NS have an influence on contractility?

Answer 17

No, b/c there are not many muscarinic receptors on ventricular myocites

Question 18

What influence SV?

Answer 18

preload, afterload, and contractility

Question 19

What influence HR?

Answer 19

sympathetic and parasympathetic NS