heart electrical activity

Intrinsic conductance

The hearts ability to spontaneously generate and propagate electrical impulses independently of external nervous system input

What are the two types of myocyte?

1. Conducting cells (pacemaker)

   • nodes

   • Bundles, purkinjie fibres

2. Contractile cells (Non-pacemaker)

   • Contractile proteins

What initiates the heartbeat?

Spontaneous electrical action potentials generated by specialised pacemaker cells in the Sinoatrial node

Pacemaker units vs Contractile cells

Pacemaker cells spontaneously generate action potentials to set the heart rate, while contractile myocytes mechanically pump blood in response to electrical activation

SA node

• is it stable of unstable

• What is its intrinsic rate

• What does it set?

• Depolarisation?

• The main pacemaker cell

• Unstable membrane potential

• Automatically – intrinsic rate of 90–110 BPM: However, this is suppressed by the parasympathetic activity

• Sets the sinus rhythm

• Can generate its own action potential

• Spreads depolarisation to adjacent cells by gap junctions

AV node

• how does the AV node get stimulated

• What is the av node connected too?

• Is there a delay!?

• Gap junction

• What is the AV node role?

• intermodal pathway and action potentials from Bachmann’s Bundle converged to the AV node

• Unstable resting potential

• Connection to the interventricular septum

• 0.05-0.1 S delay from receiving before signals sent on to ensure the atria finish contracting

• Create contraction from Apex to base - This is important because blood is needed to be pushed up (against gravity)

• Allows for atria contraction + ventricular filling

• AV note has fewer gap junctions and smaller diameter

Annulus fibrous

Important structure for atria to contract first, then the ventricles allows for more efficient contraction

Resting membrane potential of cardiac cell

Important ions Na+/K+/Ca2+

Potassium leaves the cell via potassium leaky channels

Sodium and calcium ions leaked into the cell

What is the primary pacemaker and should that fail what happens?

The primary pacemaker is the SA node

However, the AV and purkinjie Fibre also have unstable resting potentials and can act as pacemakers if needed.

The fastest node cell is the pacemaker.

Action potentials In pacemaker vs. Non-pacemaker myocytes

Pacemaker cells feature unstable resting potentials with slow spontaneous depolarisation, where is non-pacemaker cells have stable resting potentials and rapid upstrokes driven by fast sodium channels

How are Myocytes resting membrane potentials maintained?

Leaky Channels

ATP dependent pumps

• Na+/K+ 3 Na+ out, 2K+ in

• Na/Ca pump: 3Na+ in, 1 Ca2+ out

  
  

If the Na+/K+ by a drug, what would happen

The blocking of the Na+/K+ channel would lead to a build up of Na within the cell, which would depolarise the cell

The NCX is bidirectional, so it can cause the Na+ leave in exchange for Ca, which increases intracellular calcium, increasing contractility

Explain the depolarisation in the SA node

• leaking of sodium into the cell which increases the voltage of the cell from -60 to -55

• The increase in voltage causes the T-Type Voltage gated calcium channels to open which increases the voltage from -55 to -40 (this is what meets the threshold potential and Triggers and action potential)

• This increase voltage now opens the voltage gated calcium L type channels. The voltage increases from -40 to +20

What occurs during the repolarisation of the SA node

The closure of all the channels

The voltage gated outward potassium channels open, Which leaves the inside of the cell more negative

What phases occurs at points 1-3

1. PHASE 4: funny sodium channels open = In flux of sodium

2. PHASE 0: funny sodium channels close and Voltage gated L type Ca channels open causing an influx of Ca = depolarisation

3. PHASE 3: El type voltage gated calcium channels close and outward potassium channels open. The leaving of potassium repolarises the cell.

At the yellow dot: This is where the T type calcium channels open the influx of calcium reaches the threshold potential and triggers and action potential

What is the primary ionic mechanism responsible for the Spontaneous slow depolarisation?

The funny sodium channels open up upon hyperpolarisation, allowing the inward leak of sodium that drives slow deep polarisation

Important Of indicated disc

They contain gap junctions that allow direct electrical coupling between adjacent cardiac myocytes enabling the heart to function synchronously

Depolarisation of a contractor non-pacemaker myocyte

• Electrical impulse from the SA node causes the voltage gated fast sodium channels to open.

• Initial repolarisation caused by the fast sodium channels closing and the outward potassium channels opening

• L type calcium channels open this influx of calcium creates a plateau in the action potential - the calcium needed for the RyR

Importance of the plateau/refractory period in cardiac cell

The plateau in phase 2 is maintained by a slow calcium influx which prolongs the refractory period preventing the heart getting locked into a contraction because it’s being stimulated too fast to rest

What is happening at 1-4 in the contractile cells

1. Phase 0 fast sodium channels open causing depolarisation

2. Phase 1 Initial repolarisation the fast sodium channels and outward potassium channels open

3. Phase 2 L type Calcium channels open causing an influx of calcium creating a plateau in the action potential

4. Phase 3 Repolarisation: Closure of the L type Calcium channels. There is a decrease in calcium because there’s an increase in SERCA Activity and potassium is leaving the cell.

Repolarisation in contractile cardiac cells

Occurs when the L type Calcium channels close and potassium channels open allowing potassium to leave the cell and restore a negative resting membrane potential

What does Chronotopy mean

Changing the Heart rate

Regulation of SA nodal pace maker activity

• sympathetic

• Parasympathetic

• controlled by the autonomic nervous system

• sympathetic stimulation increases heart rate via noradrenaline acting on B1 receptors

• While the parasympathetic stimulation decreases the heart rate via acetylcholine acting on the MUS receptor

Sympathetic effect on the SA node

No adrenaline binds to the B1 receptor which is coupled with the GS protein which activates adenyl cyclase Convert ATP to cAMP, This activates PKA

• PKA Can act on the funny sodium channels to increase sodium influx

• CAMP can directly act on the funny sodium channels too

• An increase in sodium leads to an increase in calcium which increases the rate of depolarisation

• PKA Phosphorylates L type calcium channels causing them to open more frequently and for longer, increase in Ca2+

• Increases HR

Parasympathetic effect on SA node

Acetylcholine binds to M2 which is coupled to the Gi protein (inhibitory) Which does not activate AC and therefore the levels of CAMP decrease.

This causes an increase of potassium leaving the cell and a decrease of calcium influx

Causes hyperpolarisation of the cell and decreases the rate of depolarisation

Decrease in HR

Negative Chronotopy