Control of Heart Function Flashcards

1
Q

What are the three main anatomical components of the heart

A

Muscle cells (Cardio-myocytes) - contract and relax

Specialised eletrical cells - create spontaneous currents, essential for regulating contraction

Vessels - major blood vessels responsible for transporting blood in and out

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2
Q

Where is the sinoatrial node located

A

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

60-100bpm

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3
Q

Where is the atrioventricular node

A

Located at the triangle of koch at base of right atrium

Has pacemaker activity: slow calcium mediated action potential - normally SA node

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4
Q

What are the tracts of the heart

A

Internodal tracts

Bundle of HIS - bundle brunches - purkinje fibres - apex

Specialised conducting fibres

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5
Q

What is the nodal cell action potential

A

3 phases - 0,3,4

Phase 0 - Uptake calcium influx

Phase 3 - repolarisation due to K efflux

Phase 4 - Nodal cells don’t have a resting membrane potential - due to Na influx through a funny channel

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6
Q

Why do the action potential profiles have differen action potential shapes

A

Caused by different ion current flowing and differen ion channel expression

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7
Q

What is the time difference between cardiac muscle and nerve muscle

A

Cardiac AP is long

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8
Q

Why does cardiac muscle AP have a long slow contraction

A

Required to produce an effective pump

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9
Q

What is the cardiac muscle action potential

A

Phase 0 - upstroke

Phase 1 - early repolarisation

Phase 2 - plateau phase

Phase 3 - repolrisation

Phase 4 - membrane potential

Absolute refractory period - heart cannot start another action potential

Relative refractory period - can be elicitied if stimulus strength is high enough

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10
Q

What is the diagram of ventricular cell

A
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11
Q

What part fo the CNS controls the heart

A

Autonomic nervous system (cardio-regulatory centre & vasomotor centres in medulla)

parasymthatetic nervous system - vagus nerve

decrease slope of phase 4 - reduce activity of SAN

sympathetic nervous system

increase in heart rate (chronotropy) - increase slope of phase 4

increase force of contraction (inotropy) - increases Ca dynamics

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12
Q

Where is the vasomotor centre located

A

Bilaterally in reticular substance of medulla and lower third of pons

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13
Q

What are facts of the vasomotor centre

A

Composed of vasoconstrictor area

Composed of vasodilator area

Cardio-regulatory inhibitory area

Transmits impulses distally through spinal cord to almost all blood vessels

Higher centres of the brain can exert powerful excitatory or inhibitory effects on VMC

Lateral VMC - influencing heart rate and contractility

Medial VMC - trasmits signals via vagus nerve to heart that decreases heart rate

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14
Q

Parasympathetic action at the SAN

A

Ach act on M2 receptor of SAN

Gi protein causes inhibition fo adenylyl cyclase which converts ATP to protein kinase A

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15
Q

Sympathetic action at the SAN

A

Noradrenaline acts on B1-receptors

Stimulate increase in andenylyl cyclase

Increase in protein kinase A

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16
Q

Why does the heart rate dip when sympathetic nerves are cut

A

Already some level of sympathetic activity, occurs all the time

17
Q

What do sympathetic nerves do to the kidney

A

Decrease glomerular filtration - decrease Na excretion - increase in blood volume

Blood bolume detected by venous volume receptors

Increase in renin secretion - increase angiotensin-11- increase in vasoconstriction and increased blood pressure

blood pressure detected by arterial baroreceptors

18
Q

What happens in the glomerulus during sympathetic stimulation

A

Sympathetic nerve fibres innervate afferent and efferent arterioles

noradrenaline acts on a1-adrenoceptor causes vasoconstriction

decrease in glomerular filtration rate and amount of sodium filtered

b1-adrenoceptor causes renin secretion, this increases aldosterone which raises blood volume

19
Q

Cardiopulmonary cicurti

A

Pulmonary vessels - volume sensors - send signals trhough glossopharyngeal and vagus nerves

Decrease in filling (less blood coming to the heart) - decrease in baroreceptor firing - increase in sympathetic nerve (SNS) activity

Distention (heart is full) - increase baroreceptor - decrease SNS

20
Q

Arterial circuit - aortic arch, carotid sinus and afferent arterioles of kidneys

A

Pressure sensors: signals through glossopharyngeal and vagus nerves

Decrease in pressure - decrease in baroreceptor firing - increase SNS activity

Increase in pressure - increase baroreceptor firing - decrease SNS activity

21
Q

How is venous pressure and volume affected

A

Venous volume distribution - peripheral venous tone, gravity, skeletal muscle pump and breathing

Central venous pressure - determines amount of blood flowing back to heart

Amount of blood flowing back to the heart determines stroke volume

Veins - constriction reduces compliance and increases venous return

Arterioles - constriction determines blood flow to downstream organs, mean arterial blood pressure, the pattern of blood flow to organs

22
Q

Local mechanisms that affect blood vessels

A

Nitric oxide: vasodilator

Prostacylin: vasodilator - antiplatelet and anticoagulant effects

Thromboxane A2 (TXA2): vasoconstrictor that is heavily synthesised in platelets

Endotehlins: vasoconstrictors generated from nucleus of endothelial cells

Local blood flow regulation within an organ

23
Q

Systemic mechanisms that affect blood vessels

A

Extrinsic to the smooth muscle

Autonomic nervous system and circulating hormones

Kinins: bind to receptors on endothelial cells and stimulate NO synthesis

Atrial natriuretic peptide: ANP - secreted from atria in response to stretch - vasodilator to reduce BP

Vasopressin (ADH) - binds to V1 receptors to cause vasoconstriction

Noradrenaline/adrenaline: secreted from adrenal gland - causes vasoconstriction

Angiotensin 2 - vasoconstrictor from renin-angiotensin-aldosterone axis, stimulates ADH secretion

24
Q
A