L6- electrical activity of the heart

Features of cardiac muscle cells (6)

• striated

• Have t tubules

• Have sarcoplasimc reticular

• Have scarmoers

• Are electrically excitable

• Generate action potentials

Features of a sarcomere (4)

• myosin

• Actin

• Tropomyosin

• Troponin

What is the role for the action potential in cardiac muscle

To generation an elevation in cytoplasmic Ca2+ conc

What is the role of elevated ca2+ conc

To generate muscle contration

What is the process of muscle becoming electrically excited and contracting called

Excitation contraction coupling

Steps of Cardiac excitation contraction coupling (10)

• action potential enters from adjacent cell

• Voltage gated ca2+ channels open and ca2+ enter the cell through L type channells

• Ca2+ (trigger ca2+) inducers further ca2+ release from sarcoplasmic reticulum by acting on ryanodine receptor channels

• local release causes a ca2+ spark (each indivual opening of a ranyanide receptor)

• Summed ca2+ sparks create a ca2+ signal (calcium transient)

• Ca2+ ions bind to Troponin to initiate contraction

• Relaxation occurs when ca2+ unbinds from the Troponin

• Ca2+ is pumped back into the sr for storage

• Ca2+ is exchange fr 3 sodium ions by the NCX antiporter

• Na+ gradient is maintained byt eh na+/K+ pump

What does being autorhythmic mean the heart can do

Will continue to beat outside of the body provided it has an oxygen supply and is kept moist

What role does the nerve supply of the heart play in heartbeat

regulates but doesnt initiate heartbeat

What are the 2 groups of myocytes

• conducting cells/systems

• Working myocytes

What are conducting cells/systems used for

For fast spread of activity throughout the heart

What are working myocytes responsible for

Force generation ( are atrial and ventricular cells)

Where is initiation of the heartbeat

Ni the SAN in the right atrium

sinoatrial node

A group of cells that spontaneously fire action potentials which underlies autorhytmicity

What are the 2 ways in which the spread of excitation occurs in

• by specialised conducting fibres called intercalated disks in atria and ventricles

• Cell to cell va gap junctions

What do conducting fibres of the heart ensure

Fast, efficient conduction

Functional syncytium

Working cells that are connected together by the intercalated discs form FS

Partso f the conducting system of the heart (6)

• SAN

• Internodal pathways

• AV node

• AV bundle

• Bundle branches

• Purkinje fibres

What connects the SAN and AVN

The intermodal pathway and muscle cells that are electrically stimulated

How does the atrioventricular bundle split

Into to branches, left and right

What do the left and right branches split into

The purkinje fibres

What is the role of bachmans bundle

Is the intermodal pathway that conducts electrical energy from the SAN in the right side to the left side

What is the important feature of the introventricular septum

Is thick and non conducting

Steps of atrial excitation (5)

• impulses (APs) are spontaneously generates in teh SAN

• Impulses spread from teh SAn through the atrial muscel via cell to cell (intercalated discs) and Fromm teh SAN to the AVN (via internodal tract)

• Reached the AVn ≈70ms later

• Electrical excitiation0→ contration occurs

• Blood is forced nto the ventricles

AVN

The electrical connectciton between the atria and ventricles

What is teh AVN delay and why is it important

Is an ≈100ms delay in excitantes due to slow conduction velocity that allwos for atrial contraction and ventricular filling

Steps of ventricular excitation (4)

• excitation passes from AVVN to AV bundle (bundle of his)

• Bundle of his splits into left and right branches towards apex

• Bundle branches divide into purkinje fibres through the ventriacl

• The apex contract first forcing blod out the correct vessles

Pacemaker potential

The characetiersic of SAN that gives it an undstbale membrane protential that can spontaneously depolarise to threshold at which point an AP is generated

What does the rate of AP generation determine

Heat rate

Average resting heart rate

70bpm

What happens if the SAN becomes dysfunctional due to disease

Other conducting cells such a s AVN take over but these have slower firing rates

Steps of SAN action potential -ionic basis (4)

• slowdepolarization pahse

• Full depolarisation pahse

• Repolarisation pahse

• Minimum potential phase

Slow initial depolarisation phase (2)

• cations enter the cell through non specific cation channels

• Causes membrane to slow depolarise to -40mv threshold

Full depolarisation phase steps (3)

• voltage gated Ca2+ channels open

• Ca2+ enters the cell

• Memrbaen fully depolarises to +10mv with a steep increase

Steps of repolarisation pahse (3)

• Ca2+ channels close

• Voltage gated k+ channels open

• K+ outflow leads to memrbaen repolarisation

Stages of minimum potential phase (3)

• K+ channels remain open

• Memrbaen hyperpolarises

• Open non specific cation channels and cycle repeats

Stages in electrical activtiy of ventricular muscel cells (5)

• 4→ resting potential, controlled by na/k pump at around -80/-90mv

• 0→ some na+ channels open and reach threshold so they all open

• 1→ Na+ channels close

• 2→ ca2+ channels open and fast k+ channels close. Calcium enters activating calcium relase from sr via ryanodine receptors counteracting the depolarising potassium period

• 3→ ca2_channels close and slow k+ channels open

• 4→ resting potential

Comparing to neuronal.skeletalmuscel aps how long are cardiac APs

Much much shorted → ≈5ms vs ≈400ms

stages of ventricular action potentials (4)

• rapid depolarisation pahse → voltage gated na_ channels activate and na enters rapidly depolarising the memrbaen

• Initial repolarisation→ na+ channels are inactivated and some k + channels open causing some k+ to leak out And a small re polisaria atinó

• Plateau pahse→ ca2+ channels open and ca2+ enters as k+ exits prolonging depolarisation

• Repolarisation phase → na+ and ca2+ channels close as k+ continues to to exit causing repolzarizaiton

Trigger calcium

The calcium that enters the muscel cell through voltage gated ca2+ l channels during the plateaus phase of the AP leading to muscel contraction through a process knonw as calcium induced calcium release

What is teh force of muscel contraction proportional to

The number of active cross bridges

What is the umber of active cross bridges determined by

How much calcium is bound o Troponin c which is dependent on the amount fo calcium induced calcium release

Other than number of active cross bridge what affects the force of contration

Sarcomere length

Why does contractile change occur later than the elcrtincal change in muscel cells

It takes time for calcium to diffuse, mind to myofilametn have an effect etc..

Is teh refractory or contraction period longer

Refractory

Why is it important the refractory period is longer than the contractile phase in cardiac

Refractory is needed for the heart to actually pump rather staying in the contracted state

Refractoriness

The property of an excitable medium (myocyte) that stops it from being re excited during a period of recovery from a previous excitation

Absolute refractory period

When cardiac myocytes cannot response to a second stimulus regardless fo strength

Relative refractory period

Cardiac myocytes can respond to a second stimulus despite nt being fully recovered form teh previous excitation if the stimulus is stronger than nomral

What does the refractory period prevent

Tetanic contration of cardiac muscel = sustained state of contraction

What does an ecg do

Records electrical acitivty across tehwholheart during each heartbeat

What does an ecg record

Both the depolarisation and repolarisation of the atrial and ventricular muscel cells

What is an ecg

A measures f the summed electrical activity generated by all working cells of the heart

Parts of teh ECG (3)

• p wave

• QRS compelx

• T wave

Typical duration of the p wave

0.12-0.2s

Typical duration of the QRS complex

0.08-0.12s

Typical duration of the qt interval

0.4s

What is teh qt interval

Time between start of qrs comeplx and end of t wave

P wave (2)

• caused by electro excitation of the atria

• Can observe the delay

QRS complex

Represents fast propagation downt to apex and the contraction that occurs of teh ventricles

T wave

Shows ventricles recovering from excitation

Where on an ecg is atrial repolarisation occurring and why can you not see it

Happens in qrs compelx but is not seen as ventricular contraction is a much bigger singal so repolarisation o atria is not seen

Einthoven’s triangle

Electrode on left arm, right arm and left leg so that heart is on teh middle fro ecg

Which is lead II the most common ecg view

Is from negative end at right arm to positive on left leg but aligns with he normal axis of the heart

What does an upward deflection on an ecg mean

The current flow vector is towards the positive electrode

What does a downward deflection mean

The current flow vector is towards the negative electrode

what ecg does a vecotr that is perpendicular to the axis of the electrode produce

One with no deflection→ the ecg remains at baseline

Arrhythmias

Abnormal or irregular heart rhythms

Wht are the 3 major kinds of arrythmias

• Impulse propagation

• Impulse initiation

Example of impulse propagation And what it causes

heart block → not every p wave leads to a qrs complex

Examples of impulse initiation

• atrial fibrillation

• Ventricular fibrillation

What causes atrial fibrillation

If the SAN goes wrong or other tissues start to generate electrical activity spontaneously it can cause atrial fibrillation meaning there are no p waves

What is teh main effect of ventricular fibrillation

Death :( without quick defibrillation