Cardiovascular control 1 Flashcards
What is the potassium hypothesis?
If you have an impermeable membrane, with solutions either side with different potassium concentrations, there will be a chemical concentration gradeint but no potential difference between the chambers.
The membrane has to be permeable to both ions (cation and anion) for a pd to form.
Eventually, when there are the right channels in the membrane, a potential difference can be set up. Take a membrane that is permeable to K+ and CL-
K+ will diffuse down it’s concentration gradient, taking its large amounts of positive charge. The electrical gradient builds up opposing the movement of K+. When the electrical gradeint exactly balances the chemical gradient, equilibrium is achieved and there is no further net movement of ions.
What do we mean by equilibrium?
When electro-chemical gradient is established, the ions will move randomly backwards and forwards between the compartments. There will not be any net movement of ions though
The driving force- ie the difference between the concentration and the electrical gradient, is 0 at equilibrium.
What does the resting membrane potential depend on?
The flow of K+ out of cells
How can you predict what the potential across a semi-permeable membrane?
Use the nerst equation!
If the membrane is only permeable to K+ at rest (diastole) then the potential across it will be equal to the K+ equilibrium potential (EK)
Sodium and potassium pump pumps potassium against gradient into cell and sodium out of cell. Needs energy for active transport
The resting membrane potential changes- what does this depend on?
It depends on the relative permeabilities of the membrane to various ions.
Using the Na+ values, you can calculate the RMP using the nerst equation.
If the membrane is only permeable to na+, then the potential across it will be equal to the Na+ equilibrium potential (ENa)
Why would you use the GHK equation instead to describe the RMP?
Because it takes into account the relative permeabilities of several ions simultaneously
What is the difference in time for nerve AP vs cardiac AP
Nerve AP- 2ms
Cardiac AP- 200-400ms
The duration of the AP controls the duration of contraction of the heartbeat. This is needed for efficient pumping (slow long pumping)
Describe the absolute refractory and relative refractory period in the cardiac AP
Absolute refractory period (ARP)- time during which no AP can be initiated regardless of the stimulus intensity
Relative refractory period (RRP)- period after ARP where an AP can be elicited but only with a stronger stimulus than normal
Having a refractory period is useful because it allows the heart to fill up before the next contraction.
Describe the phases of the cardiac AP
AP causes Na channels to open- drives the cells to the equilibrium potential of sodium (very positive)- this is the upstroke
Phase 0- upstroke. Influx of sodium, depolarising cell to Na equilibrium.
Phase 1- early repolarisation phase due to Na channel inactivation
Phase 2- plateau of AP caused by L type Ca channels opening
Phase 3- main repolarisation event causes by K channels opening
Phase 4- diastole, resting membrane potential
Nb the Ca channels opening balances the efflux of K+
Cardiac cells have a longer refractory period vs skeletal muscle- what is the consequence of this?
In skeletal muscle, repolarisation occurs very early on in the contraction phase making restimulation and summation of contraction possible
In cardiac muscle, the long refractory period means that it is not possible to re-excite the muscleuntil the process of contraction owell underway hence the cardiac muscle cannot be tetanised.
Tetanus- sustained muscle contraction- at a high rate
Left is skeletal and right is cardiac
Phases of the action potential in cardiac cell- detail
- RMP is determined by the flow of K+ out of cells
- Upstroke is determined by a large increase in membrane Na+ permeability
- Small repolarisation- Ca2+ influx is required to trigger Ca2+ release from intracellular stores- essential for contraction so there is an increase in permeability of Ca2+ in the membrane.
- After this event, there is a gradual activation of K+ channels- K+ effluxes balancing out the influx of Ca2+
- The large K+ current that is inactive during the plateau starts to flow once the cells have partially repolarised. Specialised K channel gives rise to this current- IK1. Large conductance pulls the RMP back to normal- efflux the cell and bring it back to normal. Plateau is a long phase- Ca in and K out. This allows AP to be long.
Different parts of the heart will have different AP shapes
This is because there are different ion currents flowing and different ion (na and K) channel expression in cell membranes.
Try to learn the following patterns
Intrisic electrical properties of the heart
The heart is capable of independent, spontaneous generation and coordination propagation of electrical activity.
There is a specialised conduction system so that the heart can beat independently of nerve supply.
There is an extrinsic nerve supply coming from the autonomic system that can change the rate of the heart beat and modify it for the bodies needs.
What is the SAN?
The sinoatrial node= pacemaker cells.
They can be found in where the superior and inferior vena cava join to the RA.
Pacemaker does not have RMP, it is always oscillating. Most channels exist in the SAN to some extent but does not have IK1 current- therefore very little Na influx and upstroke produced by Ca influx. Repolarisation is broight about by an increase in K activity. Main upstroke is caused by L-type calcium channels (which also exist in smooth channels). Calcium channel blockers are used to combat hypertension, allowing smooth muscles to relax reducing the pressure.
Bascially, they are the start of the conduction pathway and they spontaneously depolarise which allows the heart to generate its own rhythm.
How does the nervous system affect HR?
Increased sympathetic stimulation, depolarisation and AP firing will occur at a greater rate- more quickly. So the HR increases- uses noradrenaline hormone
Increased parasympathetic stimulation (acetylcholine) will decrease HR as diastolic depolarisation will slow down.
How is the intrinsic heart rate modulated?
There is a cardioregulatory centre and vasomotor centre in the medulla.
PNS innervation slows HR by the parasympathetic (vagus) nerve
SNS innervation (sympathetic nervous system) increases HR (chronotropy) and contractility (inotropy)
Describe the Cardiac conduction system
Initiation in the SAN- a specialised cluster of autorhythmic cells
Rapid conduction across the atria on RHS and LHS by internodal fibres.
Conduction is slowed at the Atrioventricular node, allowing atrial contraction to be separated from ventricular contraction.
Bundle of His- rapid conduction cells to transport an insulated wave of excitation
Spread from the apex to the base of the heart, upwards. Causes ventricular excitation.
what is impulse propagation?
The AP generates threshold in neighbouring cell in order for AP to propagate. Will eventually dwindle away.
There is a passive spread of current and existence of threshold which, if high enough, will cause the cell to generate its own AP.
Gap junctions greatly reduce membrane resistance allowing current to leak from one cell to another. Gap junction have a lower resistance.
Location of gap junctions
They form at intercalated discs.
Intercellular communication and impulse conduction relies on gap junction.
