CVS Control Flashcards
What is the potassium hypothesis?
Potassium ions can move over the semi-permeable cell membranes, while chloride ions cannot, diffusing out the cell down their concentration gradient and reaching equilibrium when the positive charge outside the cell begins to repel the efflux of ions, so there is no net movement over the membrane
What is the Goldman–Hodgkin–Katz equation?
Takes into account the relative permeabilities of K+, Na+ and Cl- in order to calculate a membrane potential
What is the resting membrane potential dependent on?
Depends on the flow of K+ out of the cells, and the [K+] is maintained by the Na+/K+-ATPase pumps
Describe a graph of Membrane potential against time showing changes in permeability:
- Sodium permeability increases, allowing an Na+ influx
- Transient outward current due to brief K+ efflux
- Calcium permeability increases, allowing a Ca2+ influx to prolong the AP (CICR)
- Potassium permeability slowly increases to partially depolarise, and when potential becomes low enough, IK1 opens significantly to efflux a large amount of K+ and returning cell to RMP
- IK1 open to allow flow in diastole to stabilise RMP
Draw an action potential for the ventricle
Draw an action potential for an SA node cell
What are the differences between action potentials for ventricular and SAN cells?
- SA node is always oscillating
- SA node has no IK1 current and so no RMP
- Sodium channels open in SA node diastole to produce small depolarisation, but upstroke provided by calcium influx
Where is the SAN located?
Below the epicardial surface at the RA/SVC boundary
What is the role of the SAN?
To spontaneously depolarise to allow autorhythmic contraction (start conduction pathway)
What happens to the SAN upon increased sympathetic stimulation?
Decreases the length of an SA node AP - Noradrenaline; depolarise and reach threshold more quickly to increase HR
What is the effect of Increased parasympathetic stimulation on the SAN?
Increases length of an SA node AP - Acetylcholine; depolarise and reach threshold more slowly to decrease HR
What modulates the intrinsic heart rate?
- Parasympathetic vagus nerve from cardioregulatory/vasomotor centres in the Medulla to slow heart rate
- Sympathetic innervation increases heart rate (chronotropy) and contractility (inotropy)
Compare cardiac action potentail and nervous action potential:
Cardiac much longer than nervous (200-300ms v 2-3ms); duration of AP controls duration of contraction, so longer + slower contraction needed for effective pumping
What is the absolute refractory period?
NO action potentials can be initiated regardless of stimulus intensity
What is the relative refractory period?
A larger than normal stimulus can produce an action potential
What are refractory periods?
Caused by Na+ channel inactivation; recovery in repolarisation (more negative membrane potential = more channels reactivated - allow heart filling
What is the AV node?
Specialised cells delay wave of excitation and insulate from superior ventricular myocardium, allowing ventricular filling through separation of atrial/ventricular contraction
What are internodal fibres?
Rapid conduction tracts to stimulate atrial myocardium
What is the bundle of His?
Rapid conducting fibres that are slightly insulated - allowing conduction to apex
What are ventricular fibres?
Allow upward spread from apex, producing ventricular excitation for increased pressure
How does a wave of depolarisation carry to other cells?
Wave of depolarisation carried to neighbouring cell, and if exceeds threshold will cause an AP, but keeps spreading and diminishing
What reduces resistance to APs between cells?
Gap junctions reduce resistance between cells to allow current to leak
What are connexons?
Connexons in the gap junctions join to form tube between cells
What is Flow autoregulation?
Intrinsic capacity to compensate for changes in perfusion pressure by changing vascular resistance; decreased perfusion pressure would decrease flow, but autoregulation decreases resistance to increase flow
