Electrical Properties of the Heart Flashcards
We can predict what a potential will be across a semi-permeable membrane using the ……………. What is the name of this equation?
We can predict what a potential will be across a semi-permeable membrane using the Nernst equation
Resting Membrane Potential
This can be predicted using the NERNST EQUATION
Potassium Concentrations:
Inside = 120 mM
Outside = 5 mM
If you plug these values into the Nerst equation then you get an equilibrium potential of around -80 mV
-80 mV is very near the resting membrane potential of a ventricular myocyte
K+ concentration is maintained by the sodium-potassium pump
REMEMBER: Resting membrane potential is established by the movement of potassium through channels and does NOT have anything to do with the Sodium-Potassium Pump
The Potassium Hypothesis
The membrane is more permeable to potassium ions than anything else
The potassium ions can move down their concentration gradient carrying positive charge with it
As it moves down the concentration gradient, there is a build up of positive charge in the right chamber and the left chamber becomes increasingly negative (relative to the right chamber)
ELECTRICAL GRADIENT OPPOSES THE CONCENTRATION GRADIENT
Eventually you get to a point where the electrical gradient is EQUAL to the concentration gradient
At this point the ion is in EQUILIBRIUM
Ions can move back and forth randomly through the channel but there is NO net movement of ions
Look at the first few slides of this lecture
If the membrane is only permeable to K at rest (diastole) then the potential across it will ……….. the K equilibrium potential, EK
If the membrane is only permeable to K at rest (diastole) then the potential across it will equal the K equilibrium potential, EK
In the heart, the membrane potential depends on the flow of ………………… out of cells
In the heart, the membrane potential depends on the flow of K out of cells
If the membrane is only permeable to Na (during the upstroke of the action potential) then the potential across it will equal the ………………. ……………… ………………….
If the membrane is only permeable to Na (during the upstroke of the action potential) then the potential across it will equal the Na equilibrium potential, ENa
What is the equilibrium potential?
What is the name of the equation that can calculate it?
Equilibrium (or reversal) potentials. For each ion, theequilibrium (or reversal) potential is the membranepotential where the net flow through any open channels is 0. In other words, at Erev, the chemical and electrical forces are in balance. Erev can be calculated using the Nernst equation
- In reality membrane potential better described by ………………….-…………….-……………… equation
- Takes into account relative permeabilities of ions
- In reality membrane potential better described by Goldman-Hodgkin-Katz equation
- Takes into account relative permeabilities of ions
Nerve action potentials last about 2 ms but this is NOT appropriate for the heart
Action potentials in the heart last 200 - 400 ms
TMP= Transmembrane Potential
- Compared with nerve the cardiac action potential is long (several hundred milliseconds vs 2 – 3 msec)
- Duration of action potential controls the duration of ……………… of the heart
- Long, slow ……………. is required to produce an effective pump
- Compared with nerve the cardiac action potential is long (several hundred milliseconds vs 2 – 3 msec)
- Duration of action potential controls the duration of contraction of the heart
- Long, slow contraction is required to produce an effective pump
What is the Absolute refractory period?
What is the Relative refractory period?
- Like nerve cells, cardiac cells have refractory periods
- Absolute refractory period (ARP) = time during which no action potential can be initiated regardless of stimulus intensity
- Relative refractory period = period after ARP where an AP can be elicited but only with stimulus strength larger than normal.
Refractory Periods
Occur as a result of ……………. …………….. …………………. Na channels recover from inactivation when the membrane is ………………..
Refractory Periods
Occur as a result of Na channel inactivation. Na channels recover from inactivation when the membrane is repolarized
Why can’t the cardiac muscle be tetanized?
Tetany- Action potential being delivered in rapid succession- thus maintaining a sustained skeletal muscle contraction
Pathophysiology of tetany-
Pathophysiology[edit]
Hypocalcemia is the primary cause of tetany. Low ionized calcium levels in the extracellular fluid increase the permeability of neuronal membranes to sodium ion, causing a progressive depolarization, which increases the possibility of action potentials. This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells. When calcium ions are absent the voltage level required to open voltage gated sodium channels is significantly altered (less excitation is required).[1] If the plasma Ca2+ decreases to less than 50% of the normal value of 9.4 mg/dl, action potentials may be spontaneously generated, causing contraction of peripheral skeletal muscles. Hypocalcemia is not a term for tetany but is rather a cause of tetany.
In cardiac muscle it is not possible to re-excite the muscle until the process of contraction is well underway hence cardiac muscle cannot be tetanized.
UPSTROKE - exactly the same as in a nerve - caused by the opening of …………… ……………… (the cells drive towards the equilibrium potential of ……………)
…………… channels then INACTIVATE so the membrane potential starts to recover and repolarise slightly
As the sodium channels inactivate, there is a brief increase in the permeability to …………… (due to the opening of TRANSIENT OUTWARD channels)
This brief increase in …………… permeability (and subsequent efflux of ……………) repolarises the membrane giving rise to this characteristic notch
The …………… channels inactivate quickly and can NOT be opened for a long period of time
This is the …………… …………… ……………
Cardiac muscle has a …………… absolute refractory period meaning that you can’t re-stimulate the muscle for a long time so the cardiac muscle WILL NOT ……………
KEY FEATURE: there is an increase in Permeability to…………… and these …………… channels remain open for a long time which is why they are called L-type …………… Channels (L = long lasting)
This influx of …………… just about balances the efflux of potassium thus keeping the membrane depolarised at the plateau value (around 0 mV)
Repolarisation does eventually occur due to the eventual inactivation of the L-type …………… channels and the opening of a another subtype of potassium channel
UPSTROKE - exactly the same as in a nerve - caused by the opening of sodium channels (the cells drive towards the equilibrium potential of sodium)
Sodium channels then INACTIVATE so the membrane potential starts to recover and repolarise slightly
As the sodium channels inactivate, there is a brief increase in the permeability to potassium (due to the opening of TRANSIENT OUTWARD channels)
This brief increase in potassium permeability (and subsequent efflux of potassium) repolarises the membrane giving rise to this characteristic notch
The sodium channels inactivate quickly and can NOT be opened for a long period of time
This is the ASBOLUTE REFRACTORY PERIOD
Cardiac muscle has a LONG absolute refractory period meaning that you can’t re-stimulate the muscle for a long time so the cardiac muscle WILL NOT TETANISE
KEY FEATURE: there is an increase in Permeability to CALCIUM and these calcium channels remain open for a long time which is why they are called L-type Calcium Channels (L = long lasting)
This influx of calcium just about balances the efflux of potassium thus keeping the membrane depolarised at the plateau value (around 0 mV)
Repolarisation does eventually occur due to the eventual inactivation of the L-type calcium channels and the opening of a another subtype of potassium channel
General Notes on Cardiac Action Potential
Cardiac action potential is LONG (several hundred milliseconds)
Duration of action potential determines the duration of the contraction of the heart
Long, slow contraction is necessary to produce an effective pump
At REST, membrane potential is determined by potassium
Absolute Refractory Period = time during which no action potential can be initiated regardless of stimulus intensity
Relative Refractory Period = period after absolute refractory period where an action potential can only be elicited with stimulus strength that is larger than normal
Full Recovery Time = the time at which a normal action potential can be elicited with normal stimulus
In a few words dscribe what phase0, 1 , 2 ,3 ,4 are?
What happens during phase 4 and 0 in the cardiac cycle?
Phase 0-Rapid Na+ Influx through open fast Na+ channels -UPSTROKE
Phase 4- Na+, Ca2+ channels close, open K+ rectifer channels keep TMP stable at -90 mV
Why is phase 2 roughly a flat line?
Why is an Ca2+ required?
Influx of Ca2+ through L-type Ca2+ channels is electrically balanced by K+ efflux through delayed rectifier K+ channels
Increase in calcium permeability takes place rapidly but not as rapidly as the influx of sodium
Calcium permeability can be inhibited by a variety of drugs used for anti-hypertensive therapy
Name 3 examples of these drugs and state how they work?
Calcium permeability can be inhibited by a variety of drugs used for anti-hypertensive therapy - calcium channel antagonists are used such as:
Nifedipine
Nitrendipine
Nisoldipine
These work by blocking calcium entry by binding to the L-type calcium channels
These drugs also work in smooth muscle (which governs vessel pressure) - smooth muscle also has L-type calcium channels
Phase 3
A small (normal) ……………. current starts to activate towards the end of the plateau and this begin repolarisation
This is only a slight increase in permeability to …………….
There is a weird ……………. current in cardiac tissue called ……………. which switches off during depolarisation but as the membrane gets gradually more and more repolarised (due to the efflux of ……………. via the normal channel) the ……………. channel switches on
This ……………. current is large and flows during DIASTOLE
……………. stabilises the resting membrane potential and reduces the risk of …………..
A small (normal) potassium current starts to activate towards the end of the plateau and this begin repolarisation
This is only a slight increase in permeability to potassium
There is a weird potassium current in cardiac tissue called IK1 which switches off during depolarisation but as the membrane gets gradually more and more repolarised (due to the efflux of potassium via the normal channel) the IK1 channel switches on
This IK1 current is large and flows during DIASTOLE
IK1 stabilises the resting membrane potential and reduces the risk of arrhythmia
•Different parts of the heart have different action potential shapes
Why is this?
•Different parts of the heart have different action potential shapes
This is because of different ionic currents flowing
Which, in turn, is due to different expression of ion channels
The electrical properties of the heart are intrinsic (ie belong to the heart itself)
- Specialised conduction system
- The heart can beat independently even after being separated from its nerve supply
Where does the heart’s extrinsic nerve supply come from?
•The extrinsic nerve supply coming from the Autonomic Nervous System serves to modify and control the intrinsic beating established by the heart
The SA node cell have no resting membrane potential, constant activity.
What are the reasons for this?
What causes the Upstroke in a SA node action potential?
Image below of SA node cell depolarisation
The membrane potential isn’t very stable because the is no IK1 current, the very large one, that allow stability.
Also very little Na+ influx, the upstroke takes place much slowly compared to the ventricular cell. There are hardly any sodium channels present in a SA node cell.
The upstroke is produced by Ca influx
SA Node
When you have sympathetic stimulation of the heart (e.g. adrenaline or noradrenaline) it makes the pacemaker potential STEEPER
It moves from the green trace to the orange trace
By making the pacemaker potential steeper, threshold potential is reached MORE QUICKLY
With parasympathetic stimulation (e.g. acetylcholine) there is a DECREASE in the gradient of the pacemaker potential
It moves from the green line to the purple line
It takes longer for the membrane potential to reach threshold thus decreasing heart rate
This is how the autonomic nervous system modulates heart rate
Increased parasympathetic stimulation of the SA node ……………… the heart rate.
Increased sympathetic stimulation of the SA node …………… the heart rate and strength of contraction.
.
SA node lies lies just below the ……………. ………………. at the boundary between the right atrium and the ………………… ……………… …………….
The specialized cells that comprise the node mark the start of the …………………… ……………….
SA node lies lies just below the epicardial surface at the boundary between the right atrium and the superior vena cava.
The specialized cells that comprise the node mark the start of the conduction pathway
epi=outside
There are four basic components to the heart’s conduction system
Name them
What two features help the propagation of a cardiac action potential?
……………… ………… resistance determines extent of spread of excitatory current.
Where do gap juntions form at in cardiac tissue?
The propagation of the cardiac action potential is due to a combination of passive spread of current and the existence of a threshold. The passive spread of current excites the neighbouring cells easily because the membrane resistance between cells is low due to gap junctions.
Gap junction resistance determines extent of spread of excitatory current.
Intercelated discs
How are the effects of a wave depolarisation detected between two electrodes?
What type of deflection occurs when a wave of depolarisation is moving towards the posistive electrode?
What type of deflection occurs when a wave of depolarisation is moving away from the posistive electrode?
What type of deflection occurs when a wave of depolarisation is moving away from the posistive electrode?
The Basis of the ECG
The effects of a wave of depolarisation are detected as the potential difference between two electrodes
When a wave of depolarisation is moving TOWARDS the positive electrode - this causes an UPWARD deflection
When it is moving AWAY from the positive electrode you get a DOWNWARD deflection
IMPORTANT NOTE: when a wave of REPOLARISATION current is moving AWAY from the positive electrode it causes an UPWARD deflection
Repolarising waves have the opposite effect on the trace
In the image below, what causes the bump in the ECG for the picture which has SA node exciting the atrium?
Talk about the position of the electrode
Do this for all 4 images and the ECG image shown below it.
Image 1- When the SA node is activated the wave of depolarisation moves towards the Electrode hence causing an upstroke-Half of the p wave
Image 2- The wave of depolarising moves towards to excite the left atrium so the wave of depolarisation doesn’t really move towards the electrode- so wave front you see is a decrease- the downward part of the p wave
Image 3- The wave of depolarisation passes the at AV node and the bundle of his and starts its journey down the bundle branches on the left and right side. Because you are exciting a lot of muscle you get a large deflection on the ECG. Becuase it is moving towards the electrode you get a large upward deflcetion on the ECG. This upward deflection indicates the beginning of ventricular activation and depolarisation.
Image 4- The impulse now travels upwards and away from the electrode causing a decrease in the waveform in the ECG. You get a QRS complex signifing ventricular excitation.
What causes a T wave?
Talk about the electrode
T wave- ventricular repolarisation- the cells repolarise from the epicardium to the endocardium- hence repolarisation moving away from the electrode.
You can’t see the repolarising of the atrium because it is very small.
