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Cardiovascular health &Health Promotion HH2602

& HH5607

Lecture 2: MicroscopicStructure and Function of

the Heart

2pm 28-02-17 ESGW

Teaching Aims

To introduce you to the micro-structure of heart muscle.

To highlight the link between cardiacstructure and cardiac function

Learning Out-comes:

At the end of the session you will beable to:

Outline the structure of cardiac muscle

Identify the unique functions andproperties of heart cells, and linkstructure to function.

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The Myocardium:

Consists of 3 types of excitable cells

1. myocardial cells +++

2. pace-maker cells

3. cells of the intrinsic cardiacconducting system

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Figure 18.8 a, b

Cardiac cytoskeleton :

Function of cardiac cytoskeleton:

1. Orientates muscle fibres

2. Acts as a tendon

2. Re-enforces vessel entry / exit points

3. Re-enforces valves

4. Forms a non- excitable zone between atria& ventricles – to safe-guard the independentelectrical and mechanical activity of the 2“hemispheres”

Cardiac cytoskeleton :

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The innervation of the heart:

SNS – muscle fibres generally espVentricular fibres, PM cells, cells of theintrinsic conducting system – all via β1

receptors (+ coronary arteries via αreceptors)

Paraympathetic n.s. – predominantlyPM cells, few atrial fibres – virtually NOventricular fibres

Myocardial Cells:

Cardiac muscle is structurally similarto skeletal muscle. However …

there are some important anatomical

and physiological distinctions

that account for…

the different behaviour of cardiac &skeletal muscle

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Fibre structure:

Intercalated Discs:

Intercalated discs contain:

Desmosomes

Gap junctions / nexi

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Desmosomes:

provide cell to cell cohesion (rivets)

optimise force transmission

Provide attachment site for actin

Gap Junctions: (nexi)Gap junctions form:

Low resistance - high conductancechannels thro’ which ions can flow fromfibre to fibre to …

i.e. AP propagation - in an All or nonemanner.

Mass excitation of a hemisphere masscontraction of each “hemisphere” in turn

Mitochondria: What does the table

suggest?

Cell type % cell volume

Type II Skeletal mm 2%

Type I Skeletal mm 12 – 15%

Cardiac mm 25 – 35%

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What is the sarcoplasmic reticulum?

What function does it serve?

How is this function slightly different incardiac muscle?

And what is the significance of thedifference?

SR in skeletal mm

Arrival of an AP in the t-tubule causesthe terminal cisternae of the SR torelease Ca2+ into mm cytoplasm.

This Ca2+ binds to troponin…

This sequence of events also happensin cardiac mm But its also a little bitdifferent… massive functionalsignificance

Cardiac Sarcoplasmic Reticulum:

Arrival of an AP at the sarcolemma

opening of sarcolemmal Ca2+ channels

influx of a small amt Ca2+ from the ECF

causing the SR to release larger amts ofCa2+ - amplifying effect

binding with troponin contraction

Calcuim induced calcium release - CICR

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Ca2+ induced Ca2+ release; (CICR)

ECFsarcolemma

Ca++ Ca++Ca++Ca++

Ca++Ca++

Ca++ Ca++

CICR happens when?

All the time / every time an APdepolarises the sarcolemma.

Its just how cardiac muscle works – dayin day out!

BUT CICR can be enhanced to ouradvantage when necessary

A couple of thoughts.

What would happen if the ECF Ca2+influx was increased?

How might the ECF influx beincreased?

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CICR is a useful means of increasingthe FORCE of contraction.

When activated sympathetic nerves &sympathetic hormones (catecholamines)

can cause more sarcolemmal Ca2+channels to open than usual.

What is the consequence of sympathetic n.s action?

So how does that work??

Significance of CICR – SNS openingof more SL Ca2+ channels than normal

ECF

Ca++ Ca++

Ca++

Ca++Ca++

Ca++

Ca++Ca++

Ca++

Ca++

Ca++

Ca++

Ca++Ca++

Ca++

Ca++

Ca++

SNS opening more Ca2+ channels in cellmembrane than usual

•Means more Ca2+ enters the cell

•Causes the release of more Ca2+ from SR

• Ca2+ availability to troponin

more XB than usual

more force larger volume ofblood ejected

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An increased force ofcontraction caused by a

sympathetically increasedCa2+ influx is known as ..

Inotropy or ↑contractility

Drugs to manipulate inotropy:

e.g blockers: Atenol, Propanol, Sotalol,

Nadolol, Metrolol – effect is to …

Used in those in whom cardiac work inexcess of blood supply capacitymyocardial ischaemia i.e those with …

e.g inotropic support – critically ill e.g acuteheart failure, septicaemia, AMI etc.. effectis to….

Pacemaker Cells

PM cells

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Myogenicity:

Skeletal mm = neurogenic

Cardiac mm = myogenic

auto-rhythmicity = inherent ability tospontaneously depolarise and createAPs contraction

Figure 18.14

SAN inherent rate of depolarisation

= ~ 100 bpm

What is your resting HR now?

Is it close to 100bpm?

If not – why not?

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Myogenic rates of depolarisationare modulated by the ANS

i.e by both the sympathetic & the

parasympathetic n.s.

Sympathetic n.s speeds up HR

Parasympathetic n.s slows down HR

The ANS & HRs: Parasympathetic n.s (vagus nerve) slows

rate of SAN depolarisation HR / HRrest

(negative chronotropy)

Sympathetic n.s. - speeds up SANdepolarisation HR e.g. exercise(positive chronotropy)

Both PNS & SNS nerves must synapsedirectly with the PM cells

Also - SNS hormones esp. epinephrine mustalso make contact with β1 PM cells.

Where does SNS or PNS activationcome from?

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Sympathetic n.s also force ofcontraction by increasing CICR

Inotropy or increasedcontractility

To cause inotropy the sympatheticnerves together with epinephrine mustmake direct contact / synapse withthe myocardial muscle cells

Note epinephrine – adrenal medulla

Can cardiac contractions besummated?

Sk mm twitches can be summatedbecause APs are v. short cf to the

twitch. Twitch summation but

Cardiac APs are as long as the twitch

Refractory periods are long

Twitch summation

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Summation & tetanisation

At high stimulation frequencies Sk mmcan tetanise force

But the heart can’t.

What would happen to cardiac output ifthe heart were capable of summation /tetanisation?

Conclusion:

Highlighted the main physiologicaldifferences between cardiac muscleand skeletal muscle namely:

Branching structure of cardiac fibres

Presence of intercalated discs, gapjunctions and desmosomes

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Interconnectivity:

Branching & desmosomes = physicalinterconnectivity between all fibres astructural entity

Gap junctions / nexi = electricalinterconnectivity between all fibres in ahemisphere electrical coupling afunctional entity

High aerobic capacity, poor anaerobiccapacity of cardiac muscle

Dependence on external sources ofCa2+ in addition to SR supplies

Myogenic properties particularly of thepace-maker zones

Role of the ANS in modulating pace-maker activity & therefore HR

the role of the sympathetic n.s inmodulating force

Long cardiac refractory periodsprevent summation

Next session ICS & cardiac cycle.

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Knowledge check:

What would happen to your HR rest if theANS supply to your PM cells was cut now?

What would happen to your HR if the SAN –gave up now?

When SNS activity is increased whatchanges HR (& how) ? Or force ofcontraction (& how)?

Possible Viva Qs?

Describe how the Autonomic nervoussystem (ANS) influences

i) pace-maker cell function (5 marks) and

ii) force production ( 5 marks)

Describe how the microscopic structure ofheart muscle facilitates the unique functionof the heart