19 Regulation Of The Heart

Question 1

what is the frank starling mechanism?

Answer 1

it states: an increase in preload will lead to increased force of contraction and stroke volume.

Question 2

What causes the increase in force of contraction with increased preload?

Answer 2

The stretch of the muscle fibers themselves result in a more forceful contraction.

Question 3

what is the staircase phenomenon?

Answer 3

contractility increases with increases in heart rate.

This is caused by 1) increased numbers of action potentials 2) more Ca+ per action potential.

Question 4

what is extrasystole?

Answer 4

aka PVC (pre ventricular contraction)

Question 5

T/F a PVC results in an immediate large contraction?

Answer 5

False, it results in a premature weak contraction followed by a large strong contraction.

Question 6

Why is the beat that follows the PVC (contraction A) so large?

Answer 6

more time to fill (preload)
more calcium is ready for contraction B
(It is also important to note that contraction C is also a little larger)

Question 7

How do the sympathetics work on the heart?

Answer 7

1) stellate ganglia (periphery)

2) release norepi which targets the B1 receptors of the SA node, AV node, and atria.

Question 8

How do the parasympathetics work on the heart?

Answer 8

1) vegus nerve
2) release acetylcholine which activates the muscarinic (M2) receptor on the AV node, SA node, atria, and very little on ventricles.

Question 9

Once the B1 receptor is stimulated, what is the pathway?

Answer 9

B1 are coupled to G-proteins, activation of adenylate cyclase, ATP to cAMP, activation of PKA, phosphorylation of proteins.

Question 10

Once the M2 receptor is stimulated, what is the pathway?

Answer 10

M2 (muscarinic receptors) are coupled to a G-protein. The G-protein inhibits PKA activation through cAMP.

Question 11

what is the nodose ganglia? where signals synapse?

Answer 11

cell bodies of afferent neuronal fibers from the heart that sense discomfort. Remember that the cell bodies are in the nodose gangia but that they synapse in the nucleus tractus solitari (NTS) that follow.

Question 12

where are the cell bodies located for the afferent fibers picking up chemical irritation (pain) form the heart?

Answer 12

Dorsal root ganglia

Question 13

what is the net effect with stimulation of the B1 receptor on the heart?

Answer 13

increased contractility

decrease the duration of contraction

Question 14

Once PKA has become activated from the sympathetics, what does it do?

Answer 14

phosphorylates phospholamban
phosphorylates troponin 1
phosphorylates Ca+ channel

Question 15

What effect does phosphorylation of the Ca+ channel have?

Answer 15

increased Ca+ influx and increased contractility.

Question 16

what effect does phosphorylation have on troponin 1?

Answer 16

troponin 1 increases the off-rate of calcium from troponin C which allows for a more speedy relaxation and a decreased duration of contraction.

Question 17

what is the effect of phosphorylating phospholamban?

Answer 17

(Phospholamban normally inhibits SERCA.) By phosphorylating it, SERCA can work faster allowing for quicker reuptake of Ca+ into the SR resulting in increased speed of relaxation, and decreased duration of contraction.

Question 18

What is inotropy?

Answer 18

Increased contractility

Question 19

T/F Sympathetic stimulation causes shortening of diastole and lengthening of systole?

Answer 19

False, just the opposite

Question 20

what does increased contractility do to your diastolic ventricular pressure?

Answer 20

reduces it.

Question 21

Increased contractility causes?

Answer 21

1) increased peak pressure
2) increased velocity of contraction
3) shortening of systole and lengthening of diastole
4) decreased ventricular diastolic pressure
5) decreased end systolic ventricular volume because of a higher ejection fraction.

Question 22

T/F the parasympathetics work of the ventricles directly?

Answer 22

True, but only very little. Most of the effects of the parasympathetics are on the AV and SA nodes.

Question 23

If all of the autonomics are blocked, what would be the new heart rate?

Answer 23

about 100 beats per minute

Question 24

what is atropine?

Answer 24

a muscarinic (M2) receptor antagonist. Therefore it will cause blockage of the parasympathetics and speed the heart up.

Question 25

what is propranolol?

Answer 25

a beta adrenergic receptor antagonist. Therefore it will cause blockage of the sympathetics and slow down the heart. (AKA beta blocker)

Question 26

Are the parasympathetics fast or slow?

Answer 26

very fast, they can regulate the heart on a beat to beat basis.

Question 27

T/F At rest, the sympathetics are active?

Answer 27

True, but just a little bit. The majority of innervation is from the parasympathetics. This was shown by giving propranolol which blocks beta receptors and seeing a slight drop in heart rate.

Question 28

Which of the two, sympathetics or parasympathetics, affect the heart more quickly?

Answer 28

parasympathetics. Sympathetics are still relatively fast.

Question 29

T/F Hypocalcemia and hyperkalemia both cause muscles to twitch easily?

Answer 29

True.
Ca+ = threshold
K+ = resting membrane potential

Question 30

how do the parasympathetics control the Nodal cells? 4 ways

Answer 30

1) The acetylcholine activates a G protein that releases a heterodimer that opens the inward rectifier K+ channels (GIRK). This causes phase 4 to be more negative which takes longer to reach threshold.
2) decreasing the steepness of phase 4
3) moving threshold to a more positive value.
4) slowing conduction through AV node

Question 31

T/F during exercise, the sympathetic nervous system takes over the majority of the bodily functions?

Answer 31

True, so it increases heart rate.

Question 32

What would cause an increase in the slope of phase 4 nodal cells?

Answer 32

Increasing permeability of funny channels (cations)
increasing permeability of Ca+ channels.
Decreasing permeability of K+ channels

Question 33

What activates the renin-angiotensin pathway?

Answer 33

1) decreased blood flow to kidneys (due to decreased C.O. or increased peripheral resistance)
2) juxtaglomerular cells release renin
3) renin converts angiotensin 1 to angiotensin 2
4) Angiotensin 2 causes the release of aldosterone, ADH, and increases sympathetic activity.

Question 34

How is it possible that cardiac transplant patients can increase their heart rates without the sympathetic innervation?

Answer 34

By the release of Epinephrine from the adrenal medulla.