14-09-22 - Physiological Properties of the Heart Flashcards
Learning outcomes
• To describe the ionic basis for the different stages of the membrane potential changes in atrial/ventricular muscle, nodal and conducting tissue throughout the heart.
• To describe how the sympathetic and parasympathetic nerves modify the spontaneous electrical activity of the heart.
• To explain how the spread of electrical activity throughout the heart can be measured non-invasively by means of the ECG, and how the shape and features of the ECG relate to the cellular action potentials.
What normally starts the electrical depolarisation in the heart?
How does the depolarisation spread?
What is functional syncytium?
What does it allow cells in the heart to do?
What does this then allow the heart to do?
• The pacemaker activity of the SA node normally starts the process of depolarisation
• The depolarisation then spreads due to the functional syncytium
• The striated muscle in the heart works as a functional syncytium.
• This means that the individual cells work with adjacent cells for coordinated action.
• Rapid transmission of electrical impulses between cells triggers simultaneous contraction of the heart muscle.
What does membrane potential mean?
What is the resting membrane potential in the cells of the atrium and ventricles?
What are the 5 phases of the atrial/ventricular action potential?
• Membrane potential is the potential gradient that forces ions to passively move in 1 direction
• The resting membrane potential in the cells of the atria is typically -65 to -80millivolts (mV)
• The resting membrane potential in the cells of the ventricles is typically -80 to -90mV
• This means the inside of the cells are more negative, so positive ions will want to flow inside
• 5 phases of the atrial/ventricular action potential:
1) Phase 0
• Rapid depolarisation due to increase in Na+ permeability (gNa+) as fast voltage-gated Na+ channels open
2) Phase 1
• Start of repolarisation as fast Na+ channels close
3) Phase 2
• Effect of Ca2+ entry via L-type Dihydropyridine channels
• Calcium coming in from L-type channels can allow channels on the Sarcoplasmic Reticulum to release calcium in a process called calcium induced calcium release
4) Phase 3
• Rapid repolarisation as the intracellular calcium stimulates K+ channels to open, causing K+ permeability to increase and K+ to move out of the cell
• Ca2+ L-type channels close
5) Phase 4
• Stable resting membrane potential where gK+ exceeds gNa+ by 50:1
What is the threshold potential of the SA node pacemaker cells?
What are the phases of SA node cell action potential?
• The threshold potential of the SA node pacemaker cells is around -40mV
• Phases of SA node cell action potential:
1) Phase 1
• Gradual drift increases in resting membrane potential due to an increase in gNa+ as F-type (funny type) Na+ channels open (opposite to how regular voltage gated sodium channel’s function)
• This is known as the pacemaker potential, which is the slow, positive increase in voltage across the cell’s membrane that occurs between the end of one action potential and the beginning of the next action potential
• As the we get closer to the threshold frequency of the SA node (-40mV), the more likely the F-type Na+ channels are to close
• Transient (T) Ca2+ channels help with the final push towards the threshold potential
• There is also a decrease in gK+ as K+ channels slowly close
• As the potassium tries to repolarise the cell after an action potential, this increases the permeability of the F-type Na+ channels
2) Phase 2
• Moderately rapid depolarisation due to Ca2+ entry via slow (L) channels
3) Phase 3
• Rapid repolarisation as elevated internal Ca2+ stimulates the opening of K+ channels, which leads to an increase in gK+
• We have heart cells that never have a stable resting membrane potential and are constantly oscillating, triggering action potentials, and resetting
• The rate of this is the intrinsic heart rate
What does chronotropic effect mean?
What chronotropic effect does the ANS have on heart rate?
Where can autonomics (sympathetic and parasympathetic) be found on the heart?
What stimulation does the ANS have on pacemaker activity?
Through what processes do they achieve this?
• Chronotropic effects are those that change the heart rate
• How the ANS affects the nervous system stimulation on pacemaker activity
• Sympathetic innervation
• Positive chronotropic effect
• Capable of modifying the intrinsic pacemaker potential in the SA node and conduction through the AV node
* Sympathetic innervation is found throughout the heart
• Only sympathetic innervation can control contractile forces of the heart
• Noradrenaline (neurotransmitter in the sympathetic nervous system) acts on β1 receptors to increase cAMP production
• Beta-1 receptors, along with beta-2, alpha-1, and alpha-2 receptors, are adrenergic receptors primarily responsible for signalling in the sympathetic nervous system.
• This increases the rate of SAN phase 1 depolarisation through increasing gCa2+ and gNa+ via F-type channels (funny channels)
• These changes increase the heart rate
• Parasympathetic
• Negative chronotropic effect
• Capable of modifying the intrinsic pacemaker potential in the SA node and conduction through the AV node
• Vagi (parasympathetic control) innervates only nodal tissue
• Acetylcholine (neurotransmitter in paraysmpathetic nervous system) actson M2 receptors, which decrease Camp production
• The M2 muscarinic receptors are located in the heart, where they act to slow the heart
• Parasympathetic innervation reduces the rate of phase 1 depolarisation
• It does this by hyperpolarising the membrane potential to a lower starting potential
• This is done by increasing the extent and duration of opening of K+ channels, therefore increasing the gK+
Describe the 6 steps in the electrical conduction pathway of the heart
• Steps of the electrical conduction pathway of the heart:
1) SA node depolarises
2) Depolarisation spreads down the functional syncytium of the left and right atria
3) Electrical conduction goes down the internodal pathways
4) Coalesces round the AV node (only point of electrical conductivity between the atria and the ventricles) and slows down. This slowing down allows the atria to contract a fraction of a second before the ventricles, as this will allow the blood from the atria to enter into the ventricles before they contract.
5) Depolarisation gets into the AV bundle (bundle of His) branches at the midline of the heart and gets transmitted down them
6) Depolarisation comes up from the base of the heart through the purkinje fibres, which results in depolarisation of the deep ventricle tissue
What are the rates of depolarisation of:
• The sinoatrial node (SA node)
• Atrioventricular node (AV node)
• Bundle of His (AV bundle)
• Purkinje fibres
• Ventricles
Why is the SAN the intrinsic pacemaker?
Why is it important that other structures also depolarise?
• Rates of depolarisation of:
• The sinoatrial node (SA node) – 90bpm (beats per minute)
• Atrioventricular node (AV node) – 60bpm
• Bundle of His (AV bundle) – 50bpm
• Purkinje fibres – 40bpm
• Ventricles – 30 bpm
• The SAN has the fastest rate so it is the intrinsic pacemaker
• The depolarisation spreads from SAN throughout the heart before other regions spontaneously depolarise
• It is important that other structures depolarise as if conduction is blocked, downstream tissues can assume their intrinsic rate i.e if the SAN stops working, the heart can still beat
What is the length of conduction in different areas of the electrical conduction pathway?
What is the signal delay in the AV node?
Why is the signal delay in the AV node clinically important?
• The signal delay in the AV node (0.09s) is clinically important as the timing can be represented on an ECG
• This means we can see if the AV node is functioning properly or not
What does the electrocardiogram (ECG) measure?
How does it measure this?
• The electrocardiogram (ECG) measures the electrical activity of the heart over time
• The ECG uses 10 electrodes:
• 4 electrodes on the limbs:
• 1 electrode is an earth, used to remove background noise (placed on right leg)
• 3 electrodes used to create virtual leads between each pair of electrodes
• The 3 electrodes on the limbs form the Einthoven triangle
• The limb leads measure the sum of the electrical activity of the heart and the direction that electrical activity is moving in
• One end of each lead is designated positive
• Depolarisation moving towards the positive causes the trace to go up
• Depolarisation moving away from the positive causes the trace to go down
• 6 electrodes across the chest to give more specific localised information about areas of the heart
What 2 things is the size of the electrical signals from the heart determined by?
What makes the ECG trace stronger?
What is the formula for observed signal?
• Size of the electrical signals from the heart determined by:
1) Current (proportional to tissues mass)
2) Direction of signal
• The more in line the lead is with the electrical axis of the heart where the majority of the electrical activity is going, the stronger the shape of the ECG trace
• If the lead is perpendicular to this axis, there will be no ECG trace
Describe the 3 different waves in the electrocardiogram.
Describe the 3 different important timing intervals and how long they each last for
• 3 different waves of the electrocardiogram:
1) P wave – atrial depolarisation
2) QRS wave – ventricular depolarisation
3) T wave – ventricular repolarisation
• 3 different important timing intervals:
1) P-R interval – (0.12-0.2s)
2) QRS complex width (0.06-0.12s)
3) Q-T interval (0.25-0.35s)
