Session 4- heart contraction Flashcards
What does automaticity mean in the heart?
Which channels are responsible for automaticity?
Ability of nodal cells/ pacemaker cells to spontaneously depolarise and generate an action potential; thus setting the heart rate
HCN channels (Hyperpolarisation-activated Cyclic Nucleotide-gated channels)
How do the pacemaker cells depolarise?
- In diastole the membrane is repolarised (-60 mV). This potential activates the HCN channels
- Funny current flows into the cells and potential rises
- VOCC’s open which depolarises the cells (+30mV)
- VOCC’s close and voltage gated potassium channels open allowing K+ efflux from the cell
- Cell repolarises
What causes the pacemaker cells to depolarise?
What potential do they rise to?
The resting membrane potential in diastole (-60 mV) activates the HCN channels which open to allow cation influx
+30 mV
The action potential of pacemaker cells is mediated by which cation?
Calcium ions
Why is the HCN mediated ion influx called, the ‘funny current’?
How does the funny current determine heart rate?
mix of Na+ and Ca+ ions
influx is very slow (poor kinetics) which means depolarisation is slow
Why does the depolarisation rate of the SAN determine the heart rate when other cells have automaticity too?
bc the SAN rate is quickest and overrides others
Cardiac myocytes depolarise from ____ mV to ____ mV?
-90 mV to + 30 mV
Which channels mediate the early repolarisation phase of the cardiac action potential?
What is their current called?
Voltage gated potassium channels which open in response to depolarisation
Transient outward current (Ito)
Which calcium channels are involved in the cardiac myocyte action potential?
T-type
L-type
T-type contribute to the rapid upstroke (phase 0) and (Transiently) open as the membrane potential rises
L-type channels open at a higher voltage and remain open longer. They allow a sustained calcium influx which creates the calcium plateau
How many phases are there in the cardiac myocyte action potential?
4
Which channels cause the rapid upstroke in cardiac myocyte depolarisation?
How are they activated?
When do they inactivate and what does this create?
Fast sodium channels
Activated by depolarisation of the membrane near the gap junction (adjacent cell)
Inactivate as potential rises (almost simultaneously with their activation)
- Creates the absolute refractory period- cannot generate another action potential bc no more Na+ ions can enter
What generates the relative refractory period?
As membrane potential begins to fall, the fast Na+ channels (inactivated by high membrane potential) begin to recover
If the stimulus is large enough an action potential can be generated
Which ion largely determines the RMP of the cardiac myocyte? Why?
Through which channels does the ion move?
Potassium ions
Myocytes are most permeable to K+ ions at rest
Kir channels (inwardly rectifying K+ channels)
3 major actions of the Kir channels?
How?
- Generate RMP of ventricular myocytes
- Initiate depolarisation
- Initiate repolarisation
- Presence of Kir channels in the myocyte increases its permeability to K+ above permeability to any other ion at rest (Goldman Hodgkin Katz equation)
- K+ flows easily into the cell when the potential is repolarised (negative)
- When the cell is depolarised (positive) , K+ effluxes (via Kir) down its electric gradient
What does ‘Kir channel’ stand for and how does it relate to their function?
inwardly rectifying potassium (K+) channel
channels favour inward movement of potassium ions
What is the RMP of a cardiac myocyte?
Which ion determines the RMP and what is its equilibrium potential?
-90 mV
K+
-95 mV
Normal potassium concentration?
3.5-5.5 mmol/ L
What effect does hyperkalemia have on the cardiac myocyte?
Explain why
How can hyperkalemia become life threatening?
Makes it less excitable
Hyperkalemia raises the resting membrane potential because it’s proportional to the extracellular concentration of K+. This inactivates fast Na+ channels (inactivate at higher potentials) which slows the upstroke of depolarisation
If the heart can’t depolarises due to closed Na+ channels it cannot contract- asystole
How do you treat hyperkalemia?
calcium gluconate / glucose and insulin
(insulin and K+ have the same transporter into the cell).
What life threatening condition can hypokalemia cause?
ventricular fibrillation (no cardiac output)
What’s the problem with extending the length of a ventricular action potential?
More likely for EAD’s to occur (early after depolarisations) which cause the membrane potential to oscillate and can cause arrythmias (VF)
What effect does hypokalemia have on the ventricular action potential?
Why?
lengthens it
membrane repolarises slower because some potassium channels don’t work as well with low extracellular potassium
ECG appearance in hyperkalemia?
ECG appearance in hypokalemia?
Peaked T waves
Small/ no p waves
Broad QRS
sine wave pattern if very high K+ levels
Low T waves
High U wave
Low ST segment
Where is the U wave on an ECG?
What does it indicate?
after the T wave
delayed repolarisation
which causes EAD’s like the U wave
* early after depolarisations
