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22 Cards in this Set
- Front
- Back
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Name different types of cells in the heart...
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Pacemaker cells
(SA node, AV node, bundle of his, Purkinjie fibres) Non pacemaker cells (Atrial and ventricular myocytes) Non pacemaker cells |
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What are the function of pace maker cells?
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- They generate spontaneous action potentials
- SA node has the highest rate of firing, and sets the pace as its has the highest firing rate - They display automaticity (have the ability to depolarize above threshold volate in a rhytmic fashion) |
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What are the function of Non pace maker cells?
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- Do not normally generate spontaneous APs
- Stimulated by a wave of depolarization initiated from nearby PM cells - Contract in repsonse to depolarization waves |
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Describe how AP is generated in SA node...
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Phase 0 - Once hit a particular voltage volt gated ca++ channels open resulting ion rapid depolarisation
Phase 3- Ca++ channel close and K+ channel opens, K+ exit the cells, loss of +ve charge causes membrane repolarisation, membrane drops to -60mV Phase 4 - Slow spontaneous depolarisation caused by an inward current mainly Na+ though non specific cation channels, membrane channel starts to rise INFLUX OF CA IS IMPORTANT FOR DEPOLARISATION IN SA NODE |
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Describe how AP is generated in contractile cells...
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Phase 0 - AP reaches ventricular myocite, Na+ channels open and get transient increase in inward Na+ current (very rapid depolarisation).
Phase 1 - K+ chennl opens briefly. Partoal repolarisation due to transient outward flow of K+ ions Phase 2 - Plateau phase (unique to cardiac cells) Ca++ chennel opens and gets influc of Ca++. Na+/K+ pump pushes Na+ out and K+ in (the net effect is to pump excess of +ve chage out of the cell) Phase 3 - repolarisation of the membrane due to K+ outward movement dominating and Ca++ inward current decreasing Phase 4 - Pacemaker depolarisation. Achieving a resting membrane potential |
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What is the main role of Ca++ in ventricular myocyte?
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In contraction of muscle cells
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What causes arrhythmias?
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Defects in impulse formation and/or conduction can lead to disturbances in cardiac rhythm
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How are arrhythmias classified?
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Site - sinus, supraventricular, ventricular
Rate - increase HR - tachycardias, decrease HR - Bradycardias |
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What are the causes of electrical dysfunction?
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Ischaemia
MI Electrolyte imbalance Drug toxicity Surgery Congenital defects |
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What are the mechanisms of defects in impulse formation?
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Altered automaticity
Triggered Activity |
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Describe altered automaticity mechanism of defects in impulse formation...
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Escape beat - SA node becomes pathologically slow/impaired and latent pace maker cells initiate impulse
Ectopic Beats - Latent pacemaker cells develope a rate of firing that is faster than the SA node |
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In the triggered activity mechanism of defects in impulse formation what is after depolarization and when does it occur?
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Afterdepolarization occur when a normal AP triggers extra abnormal depolarisations. There are 2 types
- Early afterdepolarisations - Delayed afterdepolarisations |
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Describe Early afterpolarisation...
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Caused by anything that increase duration of AP. Eg. Anti-arrhythmic drugs. That is because some Na+ chennls by this stage recover from initial AP and from inactivated states and ready to be activated again and therefore result in inward Na+ movement and upstroke.
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Explain Delayed afterdepolarisations...
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This is triggered by high intracellular ca++ which leads to activation of Na++/Ca++ exchanger -> inward Na++ movement and Ca++ moves out.
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How does Digoxin work?
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It increase intracellular Ca++ and increase duration of AP. Used in conditions like Heart Failure (due to compensatory sympathetic activation)
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What causes defects in impulse conduction?
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- Re-entry
- Conduction block - Accessory tract pathway |
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Describe how Re-entry affects impulse formation
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- Normally an impulse travels via two pathways
- In re-entry, the impulse travels down pathway 1 only, as pathway 2 is blocked in one direction due to damage. - Impulse gets to point B and continues backwards to point A but this conduction is slowed due to damage in the area. - When impulse reaches A the cells in pathway 1 have repolarised and non longer refactory. |
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Describe how a conduction block affects impulse conduction..
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Impulse fails to propogate due to an excitable area of tissue
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Describe how an accessory tract pathway affects impulse conduction...
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An additional pathway. Conduction occurs in normal and accessory pathways
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Describe a paroxsymal supraventricular tachycard (re-entry situation)
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Mainly occurs during exercise. Normal impulse happens just before premature impulse, the cells in the accessory pathway are refractory and dont conduct. Therefore, premature impulse generated can't go down accessory pathway. However they can do down normal pathway and by the time they get to accessory part the cells are NOT refractory anymore and can conduct.
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Describe Atrial fibrillation (re-entry situation)
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- Atria beats too fast and ineffectively
- Atrial contribution to ventricular filling is low (normally ~ 40% of ventricular filling) - Blood pools in the atria and gets stasis of blood in atria - Patients at risk of thrombosus formation in atria it can result in pulmonary embolism if in the right atrium - If thrombosus forms in left atrium it will enter systemic circulation and cause a stroke |
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Describe ventricular tachycardia and MI (re-entry situation)
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- Usually associated with ischaemic heart disease, MI in particular
- Ventricles beating too fast - Ventricular fibrillation is a very serious type of arrhythmia - Cardiac output is almost ZERO - Can occur during and 24 hrs after heart attack as a result of sympathetic activity and release of catecholamines |
