Control of heart function Flashcards

1
Q

What is the sinoatrial node?

A

Pacemaker of the heart: 600-100bpm

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

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2
Q

What is the atrioventricular node?

A

Has pacemaker activity: slow calcium mediated AP

Triangle of koch at base of right atrium

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3
Q

What is the bundle of his and bundle branches?

A

Specialised myocytes

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4
Q

What are purkinje fibres?

A

Specialised conducting fibres

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5
Q

What are the different phases of SA node AP?

A

Nodal AP has 3 phases (0,3,4):
Phase 4: pre-potential- Na+ influx through funny channel. Theres no resting membrane potential
Phase 0: Upstroke due to Ca2+ influx
Phase 3: Repolarisation due to K+ efflux

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6
Q

How does AP profiles change across the heart?

A

Different parts of the heart have different AP shapes

This is caused by different ion currents flowing and different ion channel expression in cell membranes

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7
Q

What are the different phases of cardiac muscle AP?

A
Compared to nerves, cardiac AP is long
Duration of AP controls duration of contraction of heart
Long, slow contraction is requires to produce effective pump 
AP has 5 phases (0-4)
Phase 0: upstroke 
Phase 1: early repolarisation
Phase 2: Plateau
Phase 3: Repolarisation
Phase 4: Resting membrane potential 

There’s an absolute refractory period where no AP can be initiated
There’s also a relative refractory period where AP can be initiated but needs a larger stimulus strength

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8
Q

How does the parasympathetic nervous system affect cardiac function?

A

Decreases heart rate - decreases slope of phase 4
Long pre-ganglionic fibre from spinal cord synapses with post-ganglionic fibre via nicotinic receptor that uses ACh
Short post-ganglionic fibre will synapse with target organs using ACh but on muscarinic receptors

M2 receptor are Gi protein linked- ACh acts on M2 receptor to cause inhibition of adenyl cyclase and prevent conversion of ATP to protein kinase A

This leads to decreased cAMP so decreases the opening of LTCCs so less Ca2+ influx and less forceful contractions so decreased heart rate

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9
Q

How does the sympathetic nervous affect cardiac function?

A

Increases heart rate- increases slope of phase 4
Short pre-ganlionic fibre from spinal cord synapses with long post-ganglionic fibre via nicotinic receptor that uses ACh
Long post-ganglionic fibre synapses at target organ and uses noradrenaline and alpha or beta receptor depending on organ (at adrenal medulla direct noradrenaline is received)
Noradrenaline acts at beta-1 receptors (Gs protein linked) and stimulates adenyl cyclase production. This increases levels of pKA and cAMP

This increases LTCC opening so theres increases Ca2+ influx and increased force of contraction (inotropy) so increased heart rate

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10
Q

Where is the vasomotor centre?

A

The vasomotor centre is located bilaterally in reticular substance of medulla and lower third of pons

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11
Q

What is the vasomotor centre?

A

Composed of:

  • vasoconstrictor (pressor) area
  • vasodilator (depressor) area
  • cardio-regulatory inhibitory area

Transmits impulses distally through spinal cord to almost all blood vessels
Many higher areas such as the hypothalamus can exert powerful excitatory or inhibitory effects on the VMC
Lateral portions of the VMC control heart activity and influence heart rate and contractility
Medial portion of VMC transmits signals via vagus nerve to heart that tend to decrease heart rate

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12
Q

How do the kidneys affect blood volume and pressure at afferent arterioles ?

A

The kidneys have sympathetic innervation to afferent and efferent arterioles of glomerulus
Sympathetic nerves act on alpha-1 receptors in afferent arterial causing vasoconstriction
Vasoconstriction causes less blood flow so lower glomerular filtration rate (GFR) so less Na+ enters filtrate therefor less water is lost
This increases water remaining in the blood so increased blood volume and blood pressure

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13
Q

How do the kidneys affect blood pressure and volume at juxtaglomeluar cells?

A

Sympathetic fibres act on beta-1 receptors in juxtaglomerular cells and cause the release of renin.
Renin is also released due to lower pressure in afferent arteriole detected by baroreceptors and low sodium in afferent arteriol detected by macula densa
Renin activates renin-angiotensin-aldosterone system which creates angiotensin II. Angiotensin II is a vasoconstrictor of blood vessels.
Angiotensin II also causes release of aldosterone which increases Na+ retention so increases water retention

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14
Q

What is the role of the cardiopulmonary circuit in cardiac control?

A

Cardiopulmonary circuit involves large blood vessels
Volume sensors send signals through glossopharyngeal and vagus nerves
When theres decrease in filling theres decreased cardiac output
This leads to decreased baroreceptor firing so increased SNS activity
This leads to increased HR and vasoconstriction and increased blood volume/ pressure
When there is dissension (heart is full), theres increased baroreceptor firing so decreased SNS activity
This leads to vasodilation, decreased HR, and decreased blood pressure/ volume

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15
Q

What is the role of the arteriole circuits in cardiac control?

A

Arteriol circuit includes aortic arch, carotid sinus, and afferent arterioles of kidneys)
Pressure sensors send signals through glossopharyngeal and vagus nerve
A decrease in pressure causes decrease in baroreceptor firing which increases SNS activity
This leads to vasoconstriction so increases in blood pressure and blood volume

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16
Q

How is the circulatory system designed?

A

There are two circulations: pulmonary and systemic

17
Q

What is the importance of venous circulation?

A

Venous volume and distribution is affected by peripheral venous tone, gravity, skeletal muscle pump and breathing
Central venous pressure determines the amount of blood flowing back to the heart
Amount of blood flowing to the heart determines stroke volume
In veins constriction reduces compliance and increases venous return

18
Q

What does constriction determine in arterioles?

A
  1. Blood flow to downstream organs
  2. Mean arteriole blood pressure
  3. Pattern of blood flow to organs
19
Q

What are local mechanisms to regulate blood flow?

A

Intrinsic to the smooth muscle
Important for reflex local blood flow regulation within an organ
Endothelium derived mediators include:
Nitric oxide- potent vasodilator which diffuses into vascular smooth muscle cells
Prostacyclin- vasodilator that also has anti-platelet and anticoagulant effects
Thromboxane A2- vasoconstrictor that is heavily synthesised in platelets
Endothelins- vasoconstrictors generated from nucleus of endothelial cells

20
Q

What are systemic mechanisms to regulate blood flow?

A

Extrinsic to the smooth muscle
Includes ANS and circulating hormones
Non- endothelial derived mediators include:
Kinins- bind to receptors on endothelial cells and stimulate NO synthesis- vasodilator effects
Atrial natriuretic peptide (ANP)- secreted from atria in response to stretch- vasodilator effects
Vasopressin: secreted from pituitary gland. Binds to V1 receptors on smooth muscle to cause vasoconstriction
Angiotensin II- potent vasoconstrictor from the renin-angiotensin-aldosterone axis. Also stimulates ADH secretion