5 - Cardiovascular control 1 Flashcards

1
Q

The potassium hypothesis - 2 chambers, left has high [K+], right has low [K+]. The membrane is impermeable. What happens?

A

No movement even though concentration gradient exists.

Potential = 0mV

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2
Q

The potassium hypothesis - 2 chambers, left has high [Cl-], right has low [Cl-]. The membrane is permeable to K+. What happens?

A

No movement as membrane isn’t permeable to Cl-.

Potential = 0mV

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3
Q

The potassium hypothesis - 2 chambers, left has high [K+], right has low [K+].
The membrane is permeable to K+. What happens?

A

K+ moves from left to right down conc. gradient.
+e charge builds up on right side - electrical gradient stops further entry of K+.
Potential = -58mV

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4
Q

When is equilibrium achieved in a membrane?

A

When the concentration gradient matches the electrical gradient. No net movement of ions.

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5
Q

What does membrane potential depend on?

A

Potassium moving OUT of the cells.

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6
Q

What equation do you use to work out the potential across a membrane, if it is ONLY permeable to 1 thing?

A

Nernst equation

E(K)= RT/zF x ln([K] outside / [K] inside)

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7
Q

At rest, if the membrane is only permeable to K+, what is the membrane potential?

A

Membrane potential equals equilibrium potential for K+ (-80mV)

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8
Q

What maintains [K+]?

A

Na+/K+ ATPase

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9
Q

If the membrane is ONLY permeable to Na+, what is the membrane potential?

A

+66mV

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10
Q

What equation is used to calculate resting membrane potential?

A

Goldman-Hodgkin-Katz equation. Takes into account permeability to different ions.
E = -61log (inside added together)/(outside added together)

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11
Q

Are cardiac action potentials longer or shorter in time than nerve action potentials? Why?

A

Longer. IT controls duration of contraction of the heart. Long, slow contractions makes the heart more effective.

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12
Q

What is the absolute refractory period? (ARP)

A

Time when no action potential can be generated regardless of stimulus intensity. Due to sodium channel inactivation.

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13
Q

What is the relative refractory peroid? (RRP)

A

Time after ARP where an AP can be generated IF the stimulus strength is larger than normal.
Due to sodium channel inactivation

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14
Q

Draw a cardiac action potential. What are the phases?

A
Drawing.
Phase 0 - Upstroke
Phase 1 - Early repolarisation
Phase 2 - Plateau
Phase 3 - Repolarisation
Phase 4 - Resting membrane potential
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15
Q

Why can APs be generated during the RRP? (At the end)

A

During repolarisation, gradually more sodium channels become available.

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16
Q

Why are ARPs and RRPs necessary in the heart?

A

So the heart can fill/empty with blood before the next contraction occurs.
The muscle cannot be re-exicited too soon so cardiac muscle cannot become tetanised.

17
Q

When do different ion channels open during cardiac action potential?

A

Na+ open. Na+ enters cell.
Ca+ open. Ca+ enters
Various K+ open. Ka+ leaves cell.
I(K1) responsible for repolarising cell.

18
Q

Why do different parts of the heart have different action potential shapes?

A

Different parts have different ion channel expression in their cell membranes.

19
Q

Can the heart beat without a nervous stimulation?

A

Yes - it can beat independently. The nervous supply from the autonomic nervous system is there only to modify the intrinsic heart beat.

20
Q

Draw the membrane potential graph for the SA node cells. Why is there no resting potential?

A

Drawing
Upstroke is caused by Ca2+ influx - NOT sodium as there is litte Na+ influx.
There is no I(K1) channel so no resting membrane established.

21
Q

L-type and T-type calcium channels - which activate at more negative potentials?

22
Q

What transmitters are released from the sympathetic and parasympathetic nervous system that influences heart rate?

A

Parasympathetic: acetylcholine
Sympathetic: noradrenaline

23
Q

What does increased sympathetic stimulation to the SAN do?

A

More noradrenaline = depolarisation is quicker.

HR increases

24
Q

What does increased parasympathetic stimulation to the SAN do?

A

More acetylcholine = depolarisation is slower.

HR decreases

25
What part of the brain regulates heart rate?
Cardioregulatory centre in the medulla
26
How do nervous impulses travel from the brain to the SAN in the parasympathetic system? What is the effect?
Via vagus nerve. SLOWS HR
27
How do nervous impulses travel from the brain to the heart in the sympathetic system? What is the effect?
``` Via sympathetic nerves. INCREASES HR (chronotropy) INCREASES CONTRACTILITY (inotropy) ```
28
Where is the SAN located?
Just below epicardial surface at boundary between right atrium and the superior vena cava.
29
What does autorhythmicity mean?
SAN cells depolarise spontaneously so the heart generates its own rhythm.
30
Describe the cardiac conduction system
1. SAN (autorhythmic cells) 2. Internodal fibres carry rapid impluse. Stimulates atria to contract. 3. AV node - cells delay electrical excitation (allows blood to leave atria) 4. Bundle of His - rapid conduction cells to carry wave of excitation down septum to apex. 5. Ventricular (purkinje) fibres - propagate impulse across ventricular myocardium. From bottom to top.
31
How are impulses propagated in cardiac cells?
Depolarisation in pacemaker cell. Passive spread of current into next cell. Depolarisation of next cell - if threshold is overcome then cell generates its own AP. Current flows through gap junctions.
32
What is the purpose of gap junctions?
Reduce membrane resistance. Allow current to easily travel from one cell to the next. *** LOW RESISTANCE CONDUCTION PATHWAY from one myocyte to the next***
33
How are gap junctions formed?
Each cell has many connexons (made of connexins) in the membrane at the end. These butt up to the connexon in the next cell. The connexins open so there is a continous gap from one cell to the next through the connexon. They form at intercalated discs (the end of the membrane)