8 Electrical Activity of the Heart Flashcards
Q: Set the scene for the potassium hypothesis. What’s the chemical concentration gradient? potential difference?
A: 2 chambers separated by impermeable membrane
2 different concentrations of KCl added to each compartment (high conc. on one side & low conc. on the other)
Add measuring device-> can measure potential across membrane
Chemical concentration gradient but since barrier is impermeable there is no potential difference between the chambers
Q: What happens when you take the potassium hypothesis set up and make the membrane permeable to potassium only? (3) What happens if this is left for longer?
A: 1. K ions diffuse down their concentration gradient carrying positive charge with them
- Cl ions are still separated by impermeable barrier so there is a concentration gradient for Cl ions but no movement of Cl from one chamber to another
- net result- small electrical gradient forms in opp direction to potassium movement
Q: What happens when you take the potassium hypothesis set up and make the membrane permeable to potassium only and the system is left for a long time? (4) What happens when things stop changing? (2)
A: K ions diffuse down their concentration gradient carrying positive charge with them
Positive charge accumulates in the right hand compartment and an electrical gradient builds up
Electrical gradient opposes the movement of K
When the electrical gradient exactly balances the chemical gradient, equilibrium is achieved and there is no further net movement of ions
- At equilibrium, K ions more randomly back and forth
- The driving force, the difference between the concentration and the electrical gradient, is zero at equilibrium
Q: What does the resting membrane depend on? How can we predict what a potential will be across a semi-permeable membrane? What will the membrane potential change depending on?
A: flow of K out of cells
Nernst equation
………..RT……..[K+]o
E(k)= —- x ln——-
………..zF………[K+]i
relative permeabilities of the membrane to various ions
Q: What happens if a membrane is only permeable to K at rest? Calculation? What maintains the K concentration?
What would the membrane potential value be in this situation?
A: (diastole)
the potential across it will equal the K equilibrium potential, E(K)
Equilibrium potential is calculated by solving the Nernst equation for K
Na/K ATPase
-80mV
Q: Membrane permability switches from K to Na only. What will the membrane potential equal? Value? How was this calculated?
A: (during the upstroke of the action potential)
then the potential across it will equal the Na equilibrium potential, E(Na)
+66mV
We can predict what a potential will be across a semi-permeable membrane when the membrane is permeable to Na also using the Nernst equation.
Q: When is a cell permeable to K+? to Na+?
A: diastole
during the upstroke of the action potential
Q: In reality, membrane potential is better described by? why?
A: Goldman-Hodgkin-Katz equation (not nernst)
Takes into account relative permeabilities of ions
Q: What causes an upstroke in the membrane potential in an action potential? goes towards? What’s this followed by?
How long does an AP last in a nerve cell? how long is a cardiac one? Why is there a difference?
A: permeability to Na+ (goes towards Na eqm potential)
increase in K permeability -> cell repolarises
1-2 miliseconds
several hundred milliseconds (much longer)
Duration of action potential controls the duration of contraction of the heart
Long, slow contraction is required to produce an effective pump
Q: How are nerve and cardiac cells action potential similar? 2 subtypes.
A: 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.
Q: Why do refractory periods exist? When does it end?
A: Occur as a result of Na channel inactivation
Na channels recover from inactivation when the membrane is repolarised (more negative the membrane gets, the more Na channels that are available for activation)
Q: What’s the benefit of the refractory period in cardiac cells? (2) How does this compare to skeletal muscle? (3)
A: 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
heart muscle takes a while to be restimulated
In skeletal muscle repolarization occurs very early in the contraction phase making re-stimulation and summation of contraction possible
=> allow the production an unfused tetanus (raises membrane potential reached)
=> if in even faster succession get a fused tetanus (no relaxation)
Q: What are the 5 phases of a cardiac muscle cell action potential? Draw graph.
A: Phase 0 = upstroke Phase 1 = early repolarisation Phase 2 = plateau Phase 3 = repolarization Phase 4 = resting membrane potential (diastole)
Q: Phases 4 and 0 of the cardiac action potential. What determines each one?
A: Phase 4 = resting membrane potential (diastole)
Phase 0 = upstroke
Resting membrane potential determined by K flowing out of cells
Upstroke determined by large increase in permeability of membrane to Na
Q: Phase 2 of the cardiac action potential. What causes it? Why does this happen?
Explain the shape.
A: Phase 2 = plateau
Ca influx through L type channel= required to trigger Ca release from intracellular stores = essential for contraction
get plateau because gradual activation of K currents (K moving outward) that balance, then overcome, inward flow of Ca
Q: What can block Ca influx? 3 examples. Where are they used?
A: L type calcium channel blockers
Inhibited by dihydropyridine Ca channel antagonists e.g.:
Nifedipine
Nitrendipine
Nisoldipine
blood pressure control
Q: Phase 3 of the cardiac action potential. What happens? What is responsible? What else does it do?
A: Phase 3 = repolarization
Large K current (IK1) that is inactive during the plateau starts to flow once the cells have partially repolarised
I(K1) is responsible for fully repolarising the cell (is a voltage gated channel)
I(K1) is large and flows during diastole. It stabilises the resting membrane potential reducing the risk of arrhythmias by requiring a large stimulus to excite the cells
Q: How do action potentials vary across the heart? why? (2)
A: Different parts of the heart have different action potential shapes
Due to different ionic currents flowing
(^ is due to) Different degrees of expression of ionic channels
Q: What are the electrical properties of the heart described as? What does it have? (2) Nerve supply?
A: intrinsic (ie belong to the heart itself)
= Independent generation and propagation of electrical activity (intrinsic activity starts at SAN)
Specialised conduction system
The heart can beat independently even after being separated from its nerve supply
The extrinsic nerve supply coming from the Autonomic Nervous System serves to modify and control the intrinsic beating established by the heart (can affect pacemaker potential)
Q: What is the SAN described as? What channels does it have? What are the main differences to other cardiac cells? (3) What is present? affected by? (2)
A: pacemaker
Most channels exist in SA node – to some extent
Exception is IK1 – no IK1 in SA node (hence lack of membrane stability= constantly oscillating)
- Very little Na influx – upstroke produced by Ca influx
- Also T-type Ca channels that activate at more negative potentials than L-type
- doesn’t rest
Pacemaker current (If) present - para slows and sympa speeds up-> change how long it takes to reach threshold potential
Q: Modulating intrinsic heart rate. What controls it? 2 methods?
A: Cardioregulatory and vasomotor centres in the medulla oblongata
Increased parasympathetic stimulation of the SA node decreases the heart rate via vagus nerve
Increased sympathetic stimulation of the SA node increases the heart rate and strength of contraction.
Q: Where is the SAN? What makes it up? start of?
A: 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
Q: There are four basic components to the heart’s conduction system. They are…
Which part slows it down?
A: (1) SA node
(2) inter-nodal fibre bundles (stimulate the atria) (and bachmanns bundle to innervate LA)
(3) atrioventricular node (AV node) and His bundle ***
(4) ventricular bundles (left and right bundle branches-> apex and Purkinje fibres)
Q: What causes the propagation of the cardiac action potential? (2) Describe. Intercellular communication and impulse conduction from one cell to the next relies on?
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.
gap junctions
Q: ECG. What creates the image? How do the movements reflect this?
A: 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 it causes an UPWARD deflection.
When it is moving AWAY from the positive electrode it causes a DOWNWARD deflection.
When a wave of repolarising current is moving AWAY the positive electrode it causes an UPWARD deflection.
Q: Explain the T wave.
A: repolarisation (ventricular, not really atrial because it just blends in)
occurs in the direction of epicardium to endocardiam (from apex)
