L22 - Electrophysiology Flashcards
What is automaticity of the heart?
The heart has the intrinsic ability to spontaneously depolarise itself rhythmically and trigger action potentials to be sent to all other parts of the heart which in turn causes contraction of the myocardium.
What are the two types of specialised myocytic cells present in the myocardium?
- Nodal cells (pacemaker cells) which generate automaticity but do not undergo contraction:
- SA node, AV node, Bundle of His, Bundle branches (right + left), Purkinje fibres
- Contractile cells which undergo contraction but not automaticity:
- Contractile proteins, e.g. actin, myosin, troponin, tropomyosin, etc.
- They contain sarcoplasmic reticulum (intracellular Ca++ storage)
What is the function of the Sinoatrial (SA) node? (aka sinus node)
- Location => in the junction between the upper wall of the right atrium and the opening of the superior vena cava.
- Intrinsic ability to generate 60-80 bpm (aka ‘Sinus Rhythm’)— no sympathetic or parasympathetic input
What is the intrinsic conduction pathways (step by step)?
- SA node sends action potential to the whole atria:
- to left atrium via Bachmans Bundle
- to right atrium via internal pathway - Bachmans Bundle + internal fibres converge at the AV node
- 0.1 sec delay at the AV node — gives time for atria to contract before ventricles contract so all blood emptied into ventricles
- How? => decrease in gap junctions + diameter of fibres, hence slows the conduction speed. - After delay, action potentials travel from AV node to the Bundle of His on the atrioventricular septum
- Bundle of His splits into two Bundle branches - Right & Left - action potentials travels down both.
- Right Bundle branch - right side of myocardium
- Left Bundle branch - left side of myocardium
- Both Bundle branches converge to Purkinje fibres
- Purkinje fibres trigger myocardium to undergo contraction - ventricles contract ti empty blood out of the heart.
Action potential generation in a nodal cell (pacemaker)
- Resting potential = -60 mV
- Leaky Na+ channels allow Na+ ions inside the cell – slow flow, intracellular becomes slightly positive
- Threshold reached at -55 mV – slightly more positive
- T-type Ca++ channels open - surge of Ca++ into cell – slightly positive at -40 mV
- At -40 mV – L-type Ca++ channels open => DEPOLARISATION where it goes up to +40 mV
- At +40 mV – L-type Ca++ channels close AND K+ channels open
- K+ channels open => K+ ions move out of cell – REPOLARISATION
- K+ ions efflux from cell more, causing even more negative membrane potential - HYPERPOLARISATION (below -60 mV)
- Then back to resting potential again at -60 mV
Action potential generation in a contractile cell (myocyte)
- Resting potential = -80 mV
- Leaky Na+ channels allow Na+ ions inside the cell – slow flow, intracellular becomes slightly positive
- Threshold reached really quickly – slightly more positive
- More voltage-gated Na+ channels open (not the leaky ones) - influx of Na+ ions at a steep acceleration - DEPOLARISATION causing generation of action potential
- Plateau (maintained action potential) => opening of slow voltage-gated Ca++ channels and closing of some K+ channels
- Duration of action potential (absolute refractory period) = 250 ms in cardiac muscle
- Ca++ channels close AND K+ channels open
- K+ channels open => K+ ions move out of cell – REPOLARISATION
- K+ ions efflux from cell more, causing even more negative membrane potential - HYPERPOLARISATION (below -80 mV)
- Then back to resting potential again at -80 mV
What is a refractory period during an action potential?
A period of time during which a cell is incapable of repeating an action potential.
The amount of time it takes for an excitable membrane to be ready to respond to a second stimulus once it returns to a resting state.
Why is there a refractory period in the action potential?
Refractory periods give the organ, tissue, or cell time to reset and prevent overstimulation.
What is the difference between the ABSOLUTE refractory period and the RELATIVE refractory period?
ARP => No new action potential can be generated while the current one is ongoing.
- Caused by the voltage gated Na+ channels shutting and not opening for a short period of time.
RRP => The interval of time during which a second action potential can be initiated, but initiation will require a greater stimulus than before as the cell membrane is hyperpolarised.
How does a wave of electrical current propagate through the myocardium?
- Cardiac muscle fibres - branched + connected at their ends by intercalated discs
- Intercalated discs - allow myocytes to contract in a wave-like pattern so heart can work as a pump
- Sarcolemma (excitable membrane) contains:
- Gap junctions => channels between adjacent cardiac muscle fibres, forming electric coupling (quick transmission of action potentials and coordinated contractions) ==> aka SYNCYTIUM
- Desmosomes => a cell structure that anchors the ends of the fibres together - so not pulled apart during stress of individual fibres contracting
- Wave of contraction (syncytium) starts from self-excitable pacemaker cells — exhibits autorhythmicity
- Pacemaker cells - direct control of heart rate
- Pacemaker cells can be influenced by adrenergic stimulation (increases HR) or vagal stimulation (decreases HR)
What is the sympathetic input on the cardiac conduction system? (adrenergic stimulation)
On the pacemaker cells (nodal):
1. Beta1-adrenoceptors stimulated by noradrenaline or adrenaline (catecholamines) from sympathetic nerve
- Increased influx of Ca++ ions into cell via opening of more L-type Ca++ channels
- Speed up of pacemaker current - more frequent depolarisations
- Lowers threshold potential, hence increased depolarisations — increased action potentials
- Increased heart rate = increased cardiac output = increased force of contractions
On the contractile cells:
- Beta1-adrenoceptors stimulated by noradrenaline from sympathetic nerve
- Phosphorylation of Ca++ channels in sarcoplasmic reticulum (SR) – causes Ca++ ions to move back into SR
- Ultimately causes increased activity go myocytic proteins (actin, troponin, etc)
- Leading to increased muscle contractions
- Hence increased HR + increased SV = increased CO —- thus increased BP
- Increased HR = Positive Chronotropic Effect
- Sympathetic input on BOTH nodal cells and contractile cells
- increasing permeability of the nodal cell plasma membrane to Na+ and Ca++.
What is the parasympathetic input on the cardiac conduction system? (vagal stimulation)
- M2-receptor in nodal cells stimulated by acetylcholine from the vagus nerve
- Increased efflux of K+ ions out of cell via opening of more voltage-gated K+ channels
- Cell becomes more negative
- Increased hyperpolarisation
- Decreased depolarisation
- Decrease in action potential firing - slows pacemaker current
- Increased threshold potential
- Decrease in heart rate = Negative Chronotropic Effect
- Parasympathetic input ONLY on nodal cells (not contractile cells)
- increases the permeability to K+ ions, and decreasing the Na+ and Ca++ permeability
- At rest - parasympathetic is predominate
