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Cardiovascular Biology 311 > Lecture 7b: Regulation of the heart > Flashcards

Lecture 7b: Regulation of the heart Flashcards

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1
Q

Describe heart regulation

A

Extrinsic; Neural and hormonal

Intrinsic; preload (frank starling, LT LD), afterload

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2
Q

What branches of the nervous system innervate the heart?

A

Sympathetic and parasympathetic

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3
Q

Where in the heart is sympathetically innervated?

A
  • Sympathetic innervation of the heart is relatively homogenous (its alls somehwat innervated)
  • Dense innervation of the SAN, AVN, atrial and ventricular myocardium
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4
Q

Describe specifically the fibres that innervate the AVN and SAN

A
  • SAN is innervated the right sympathetic fibres

- AVN is innervated by left sympathetic fibres(left side of spinal cord origin)

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5
Q

How do left and right sympathetic fibres differ probably in humans?

A
  • Left symp have more affect on contracility while right have more affect on HR

Relative to each other.

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6
Q

Describe parasympathetic innervation of the heart

A

Parasympathetic innervation of the AVN and SAN is extremely dense, atrial myocardium is also richly innervated

  • Some innervation of the ventricles
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7
Q

What do the SAN and AVN receive innervation from in terms of the vagus?

A

Right vagus affects SAN

Left vagus affects AVN

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8
Q

Describe the location of parasympathetic nerve terminals

A

Parasympathetic nerve terminals often lie close to sympathetic adernergic terminals in the heart

NA inhibits Ach release and vice versa from each terminals

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9
Q

What receptors does noradrenalin bind to in the heart?

A

Alpha and beta adrenergic receptors

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10
Q

What does activation of the alpha and beta adrenergic receptors result in?

A

A number of changes in cellular function mediated through the g protein coupled pathway

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11
Q

What is the net result of sympathetic stimulation on the heart?

A

Net result is the elevation of cAMP-dependant PKA which increases cytosolic Ca concentration and contractility during systole and accelerates contraction and relaxation

i.e increased contractility and HR

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12
Q

How does sympathetic stimulation increase HR?

A

Sympathetic stimulation increases HR.

  • Due to accelerated rate of diastolic self depolarisation in the SAN because of increases in pacemaker currents.
  • HR response to sympathetic stimulation is slow and has a latency of 1-3 seconds and can take 30 seconds to reach steady state
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13
Q

How does sympathetic stimulation affect heart rhythm?

A
  • AP duration decreases

- Accelerated propogation of impulse through the AV node.

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14
Q

How can sympathetic stimulation cause arrhythmia?

A

Sympathetic stimulation may also facilitate pacemaker activity of cells in the AVN

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15
Q

How does sympathetic activity influence cardiac contractility?

A
  • Symp stim increases the inotropic state of both the atria and the ventricels
  • This can be observed on a LV function curve
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16
Q

What does sympathetic stimulation markedly alter?

A

The dynamics of the cardiac cycle

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17
Q

Describe how sympathetic stimulation alters the cardiac cycle?

A
  • Increased systolic atrial pressure
  • Increased rate and peak LV systolic pressure
  • Increased rate of ventricular ejection and max aortic flow
  • Reduced LVEDV but SV maintained or increased
  • increased rapid filling rate
  • Reduced diastolic and systolic interval
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18
Q

How does Ach effect HR?

A

Reduced HR as SAN cells become hyperpolarized and reduced rate of diastolic depolarisation.

HR response to steep change in vagal activity is rapid in comparison to effects of SNS.

19
Q

How does Ach effect rhythm?

A
  • Reduced AP length in atrial myocardium
  • Deceleration of impulse through AV node

Complete AV block with too much vagal stimulation.

20
Q

How does Ach affect contractility?

A
  • Decreased inotropic state of the atria.
  • Ventricular inotropic state may be reduced, but this is limited and represents the sparse PSN innovation of the ventricles.
21
Q

Are the effects of PNS and SNS additive? i.e equal one another so could cancel.

A

No they are not.

i.e

HR is more sensitive to PNS stimulation

22
Q

Describe the SNS and PNS basal activity

A

SNS and PNS are tonically active.

23
Q

What happens of the SNS and PNS were blocked?

A

HR increase to ~105
Inotropic state would decrease

Indicating at rest there is SNS maintenance of contractile state and vagal restraint on HR

24
Q

Describe the interaction of both SNS and PNS co-activation of HR

A
  • HR is incredibly more sensitive to vagal stimulation than SNS
  • Vagal stimulation can even over ride the effects of sns even at high levels
  • Despite acting in concert, PNS is thought to dominate HR
  • SNS controls inotropic state
25
Q

Why do SNS and PNS take different lengths of time to function?

A

PNS acts directly on ion channels

SNS acts via the g proteins pathway

PNS also terminates faster than SNS which is more prolonged`

26
Q

Why does PNS stimulation terminate faster?

A

SAN and AVN are rich in choline esterase, thus Ach is hydrolysed quickly and PNS stimulation decays quickly and nerve activity ceases.

27
Q

How can Ach exhibit beat to beat control?

A

Ach release is rapid and binds to M2 receptors which leads to G beta and gamma subunits binding to the ion channels to elicit activation

28
Q

Describe the release and action of NA?

A

NA is released at a slow rate and is mediated by a g protein that uses cAMP (slow) secondary messenger systems

29
Q

Describe NA termination

A

Terminatino of SNS response is slow as re-uptake of NA is slow as is its removal from the blood

Thus SNS cannot exhibit beat to beat control

30
Q

What are the types of humoral regulation of cardiac function?

A
  • Catecholamines
  • Thyroid Hormones
  • Insulin and Glucagon
31
Q

What do catecholamines binds to?

A

B1 receptors

32
Q

What are the effects of thyroid hormones?

A
  • Enhance myocardial contractility

- Increase density of B1 receptors

33
Q

What are the effects of insulin and glucagon?

A

Both have positive inotropic effects on the heart

34
Q

Describe the origins of the ANS innervation?

A

ANS output to the heart originates from;

  • Higher centers
  • Emotional excitement
  • Anticipation of exercise
35
Q

What reflexes have an affect on cardiac regulation?

A
  • Baroreceptor reflex
  • Bainbridge reflex
  • Respiratory sinus arrhythmia
  • Chemoreceptor reflex
  • Ventricular receptor reflex
36
Q

What is the baroreceptor reflex?

A

Low BP, results in increased Sympathetic drive to the heart

37
Q

What is the bainbridge reflex?

A

When blood volume increases, there is increased atrial receptor stimulation and thus increased heart rate.

When blood volume decreases this evokes the baroreflex.

38
Q

What is the respiratory sinus arrhythmia?

A

Rhythmic variations in HR occuring at the frequency of respiration.

i.e HR increases with inspiration and decreases with expiration.

This is generated by changes in vagal activity. As is the increased venous return caused by inspiration drawing blood up.

39
Q

What is the chemoreceptor reflex?

A

when peripheral chemoreceptors are activated it can result in changes in heart rate but to a limited extent.

These chemoreceptors also change respiration rates too.

40
Q

What is the ventricular response reflex?

A

These receptors exhibit similar properties to baroreceptors and their activation diminishes HR, TPR.

41
Q

How do xanthines work?

A

I.e coffee

Inhibits PDE fucntion. prevents cAMP breakdown

Increased inotropic state

42
Q

How doe cardiac glycosides function?

A

i.e digoxin

Inhibits Na/K ATPase
Deminishes NA gradint
NCX function slows
Ca accumulates

Increased inotropic state

43
Q

How does Ca channel blockers work?

A

I.e verapamil

Reduced Ca entry across the sarcolemma

Decreased inotropic state

Cardiovascular Biology 311 (18 decks)

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