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BRS CVR > Control of Heart Function > Flashcards

Control of Heart Function Flashcards

1
Q

What can the main anatomical components of the heart be broadly categorised as?

A
  1. Muscle cells (cardio-myocytes): can contract and relax in response to electrical stimuli. Essential for pumping blood around the body
  2. Specialised electrical cells create spontaneous currents and those that transmit currents exist within the heart. Essential for regulating contraction of the cardio-myocytes
  3. Vessels:the major blood vessels are responsible for transporting blood in and out of the heart, whilst the coronary blood vessels are responsible for supplying blood to the heart
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2
Q

What is the pacemaker of the heart?

A

Sinoatrial node - usually beats at around 60-100bpm.

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3
Q

Where is the pacemaker of the heart located?

A

Junction of the crista terminalis; upper wall of right atrium and opening of the superior vena cava.

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4
Q

Where is the AV node located?

A

Triangle of Koch at the base of the RA.

(Has pacemaker activity, but it is usually the SAN that controls the heart beat).

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5
Q

What tract connects the SAN and AV nodes?

A

Internodal tracts

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6
Q

What is the pathway of the bundle of His in the heart?

A

From the atria down through the intraventricular septum on to the bundle branches and then through to the actual Purkinje fibres which propagate the electrical current along the ventricles.

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7
Q

How many phases does nodal AP have and name each of them?

A

3

Phase 4 - Pre-potential
Phase 0 - Upstroke
Phase 3 - Re-polarisation

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8
Q

What causes the 2nd phase of a nodal AP?

A

Phase 0 - upstroke; occurs due to calcium influx from outside the nodal cell.

(Phase 3 - repolarisation; due to potassium efflux)

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9
Q

Outline the process of a nodal AP.

A

Pre-potential (phase 4) → Increase in membrane potential from -60 to -40 mV due to Na+ influx through a ‘funny channel’.

Upstroke (phase 0) → Increase in membrane potential -40 to 0 mV due to Ca2+ influx.

Re-polarisation (phase 3) decrease in membrane potential due to K+ efflux.

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10
Q

Is a cardiac muscle AP longer than a nervous AP? How long is a cardiac muscle AP?

A

Yes
Cardiac muscle AP - 200-300 ms
(Nerves - 2-3ms)

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11
Q

What does duration of a cardiac muscle AP control?

A

Duration of contraction of the heart.

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12
Q

How many phases are present in a cardiac muscle AP and name each phase?

A

5

Phase 0 - Upstroke (-90 mV up to ~20-30 mV) → Na+ influx
Phase 1 - Early re-polarisation → Small amount of K+ efflux
Phase 2 - Plateau (maintains cell at a level of depolarisation at value of 0mV) → Due to Ca2+ influx.
Phase 3 - Re-polarisation → Happens at ~270ms after stark of upstroke → More K+ efflux.
Phase 4 - RMP

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13
Q

What is the absolute refractory period of a cardiac muscle AP?

A

Time during which no AP can be initiated regardless of stimulus intensity.

First 200ms

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14
Q

What is the relative refractory period of a cardiac muscle AP?

A

Period after ARP where an AP can be elicited, but only with larger stimulus strength.

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15
Q

What 2 components are important for control of the heart via the CNS via the ANS?

A

Cardio-regulatory centre and vasomotor centres in MO.

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16
Q

What affect do the 2 different components of the ANS have on the heart?

A

Parasympathetic (goes via vagus nerve to the heart) → decrease in HR; done by decreasing the slope of phase 4 (pre-potential nodal AP phase) → reduces HR by affecting the SAN.

Sympathetic → Increased HR (positive chronotropy) → increases the slope of phase 4 (decrease in time of phase 4) + increase in force of contraction (inotropy), increases Ca2+ dynamics.

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17
Q

Where do parasympathetic nerves arise from?

A

Craniosacral outflow

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18
Q

Describe the design of the parasympathetic response in terms of what is released at the pre and post-ganglionic nerve fibres.

A

Pre-ganglionic fibres use ACh as NT. Use nicotinic receptors

Post-ganglionic fibres also use ACh as a NT. Use muscarinic receptors,

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19
Q

Where do sympathetic nerves arise from?

A

Thoracolumbar outflow.

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20
Q

Describe the design of the sympathetic response in terms of what is released at the pre and post-ganglionic nerve fibres.

A

Pre-ganglionic fibres use ACh as their NT; use nicotinic receptors.

Synapse at sympathetic ganglia.

Post-ganglionic fibres use noradrenaline. (In this post-ganglionic fibres are longer than pre-ganglionic fibres).

21
Q

What are the parasympathetic and sympathetic nerve fibres responsible for controlling in the heart?

A

PNS is important for controlling HR

SNS is important for controlling circulation

22
Q

Where is the vasomotor centre located?

A

Bilaterally in reticular substance of medulla and lower third of pons.

23
Q

What is the vasomotor centre composed of?

A

Vasomotor (pressor) area.
Vasodilator (depressor) area.
Cardio-regulatory inhibitory area.

24
Q

Give an example of a part of the brain that can exert powerful excitatory or inhibitory effect on the vasomotor centre.

A

Hypothalamus

25
Q

What do the lateral and medial portions of the VMC control respectively?

A

Lateral - influences HR and contractility.

Medial - Signals via vagus nerve to heart that tend to decrease HR.

26
Q

Outline the process of parasympathetic cardiac innervation.

A

Releases ACh which act on M2 muscarinic receptors; activates G-I (inhibitory), which inhibits adenylyl cyclase activity [reventing cAMP+ATP>Protein kinase A. Negative chronotropy (HR) and ionotrophy (contractility).

HR and contractility decreases.

27
Q

Outline the process of sympathetic cardiac innervation.

A

Released noradrenaline → Increased activity of Beta-1 adrenergic receptors associated with G-S linked proteins, activating adenylyl cyclase, increasing activity of ATP+cAMP > protein kinase A. ^HR and contractility - Positive inotropy and chronotropy. Sympathetic innervation is linked with cAMP intracellular concentrations.

28
Q

What happens if you cut the parasympathetic nerves to the heart?

A

Increase in activity.

29
Q

What affect does sympathetic innervation have on the renal system and how does this affect the heart?

A

Decrease GFR and decrease Na+ excretion therefore increase in blood volume (aldosterone). Change in blood volume as a result of sympathetic activity will be detected by venous volume receptors - Cardiopulmonary circuit (Large pulmonary vessels)

Sympathetic nerves ^ renin secretion > ^angiotensin II > vasoconstriction and increase in BP which is detected by arterial baroreceptors. So the kidneys effect cardiac function by having an impact on blood volume and blood pressure - Arterial circuit (aortic arch, carotid sinus and afferent arterioles of kidneys)

(N.B. Angiotensin-II also causes an increased release of aldosterone which also has an impact of blood volume).

30
Q

What affect does sympathetic innervation on the afferent and efferent arterioles of the glomerulus and nephron tubule cells have on the renal system?

A

The sympathetic activity causes vasoconstriction, which means that they get thinner and this is by activation of alpha-1 adrenoceptors. NA acting on alpha-1, adrenoceptors causing vasoconstriction results in a reduction in GFR and a reduction in the amount of Na+ filtered.

Release of renin from our beta-1 adrenoceptors or the juxtaglomerular cells by beta-1 adrenoceptors, which subsequently increases aldosterone, which increases blood volume.

31
Q

What is the cardiopulmonary circuit?

A

Large pulmonary vessels that are volume sensors (also atria and right ventricle): sending signals via CN 9+10

32
Q

Explain how the cardiopulmonary circuit when there is a decrease in filling in the heart.

A

Decrease filling > decreased baroreceptor firing > increase in SNS activity > increases the HR.

33
Q

What is distention?

A

State of being enlarged due to internal pressure (in terms fo the heart it is when the heart is full - caused by more blood coming back to the heart).

34
Q

Explain how the cardiopulmonary circuit responds to distention.

A

Distention > increase in baroreceptor firing > decrease SNS activity.

35
Q

What is the arterial circuit?

A

Consists of aortic arch, carotid sinus and afferent arterioles of kidneys

Pressure sensors - also send signals through glossopharyngeal and vagus nerves.

36
Q

Explain how the arterial circuit responds to a decrease and increase in pressure.

A

Increase in pressure → Increased baroreceptor firing leading to decreased SNS activity.

Decrease in pressure - Decreased baroreceptor firing leading to increased SNS activity.

37
Q

Describe the relationship between baroreceptor firing and SNS activity.

A

Inversely proportional

38
Q

What is the venous volume distribution affected by?

A

Peripheral venous tone
Skeletal muscle pump
Gravity
Breathing.

39
Q

Which circulation accounts for most of the volume of blood circulating in the human body?

A

Venous volume (systemic blood flow) - 61%

40
Q

What is the central venous pressure?

A

Mean pressure in RA.

41
Q

How does constriction of veins affect compliance and venous return?

A

Constriction reduces compliance and increases venous return.

42
Q

What does arteriole constriction determine?

A

Blood flow to downstream organs
Mean arterial BP
Pattern of blood flow to organs

43
Q

What is difference between the local and systemic mechanisms of regulating blood flow?

A

Local - intrinsic to smooth muscle; important for reflex local blood flow regulation within an organ.

Systemic - extrinsic to smooth muscle; include ANS and circulating hormones.

44
Q

List endothelium-derived vasodilators.

A 
Nitric oxide (NO) - diffuses into vascular smooth muscle cells. 
Prostacyclin - also has antiplatelet and anticoagulant effects.
45
Q

List endothelium-derived vasoconstrictors. (local)

A

Endothelins - generated from nucleus of endothelial cells
TA2 - heavily synthesised in platelets.

ET

46
Q

List non-endothelium-derived vasodilators. (systemic)

A

Kinins - bind to receptors on endothelial cells and stimulate NO synthesis - vasodilator effects.
Atrial natriuretic peptide - secreted from atria in response to stretch.

47
Q

List non-endothelium-derived vasoconstrictors (systemic)

A

Vasopressin - binds V1 receptors on smooth muscle causing vasoconstriction
Angiotensin-II - also stimulates ADH secretion.
NA/Adrenaline - secreted from adrenal glands

48
Q

Outline the control venous return.

A

^SNS + ^Skeletal muscle pump + ^Blood volume + ^Respiratory movements > ^Venous pressure > ^Venous return > ^Atrial pressure

BRS CVR (15 decks)

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