Organisation of the Body
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| show | A muscular pump that alternated between contraction (systole) and relaxation (diastole)
Depending on activity will give around 3 billion beats in 80 years
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| show | Pump rate in regulated from 5 l/min (resting) to around 30 l/min (intense exercise)
Regulated by modulation of the strength of contraction and rate of contraction
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| show | Sinoatrial node - pacemaker allowing for myogenic activity
Atrioventricular node
Atrioventricular bundle - Bundle of His
Bundle branches
Purkinje fibres
These create a conduction system to allow depolarisation to propagate and the heart to contract
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| Cardiac myocytes | show 🗑
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| show | The myocardium works as a mechanical and electrical syncytium
Gap junctions allow for electrical coupling
Desmosomes allow for mechanical coupling - made of proteins embedded in plasmalemma that connect in the extracellular space
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| show | Make of connexin 43, 6 monomers form a connexon tunnel which spans the membrane projecting into the extracellular space where it connects to connexons of adjacent cells
This allows movement of ions and hormones between myocytes
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| Organisation of contractile filaments | show 🗑
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| show | The greater the filling of the cardiac chamber the greater individual myocardial fibres are stretched, hence the greater the subsequent force of contraction
Small changes in size of a myocyte will therefor produce large changes in force generated
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| Spread of impulse in the heart | show 🗑
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| show | Different myocytes have different Vrest so have different excitability
Shape of the AP is different in different regions
Longest AP is the bundle branches to ensure ventricles relax before another contraction
Extended plateau phase prevents summation
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| show | Pacemaker function - myogenic rhythm
Fast/slow conduction to synchronise contraction
Long plateau to maintain refractoriness and avoid high frequency activation
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| Phases of the Action potential in the SAN | show 🗑
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| What are HCN channels | show 🗑
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| show | Inwards Ca2+ current
De activation of outwards K+ current
Inwards cation current (HCN at negative voltage)
Sodium Calcium exchanger
Background inwards Na+ leak
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| show | Phase 0-fast upstroke due to Ca and Na
Phase 1-rapid repolarisation due to inactivation of Ca and Na
Phase 2-plateau. Continued entry of Ca or Na ions through channels and exchanger
Phase 3-repolarisation due to K+
Phase 4-electrical diastolic phase
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| Excitation contraction coupling | show 🗑
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| The sodium calcium exchanger | show 🗑
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| Action of Ouabain | show 🗑
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| Evidence for the role of Ca2+ | show 🗑
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| show | The rise in [Ca2+] in normal cardiomyocytes during a beat is only large enough to produce a fraction of the intrinsically available strength (50%)
The strength of contraction can be increased by increments of [Ca2+] attained via ionotropic interventions
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| show | Cardiac output = stroke volume x heart rate
Can change frequency of contraction - chronotropy
Can change force of contraction - inotropy
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| Regulation of Chronotropy - Increased heart rate | show 🗑
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| show | Rate decreased by vagus nerve. Ach binds to M2 type receptors which are coupled with Gi proteins. These inhibit activity of adenylyl cyclase so reduces cAMP
This increases time for Vrest decay, repolarisation and depolarisation
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| show | Sympathetic nerves innervate ventricular myocytes. Noradrenaline activates adenylyl cyclase
PKa phosphorylates Ca channels to increase Ca release.
Phosphorylates PLB to increase Ca reuptake for effective relaxation before next contraction
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| show | Starling's law states that as length of the myocyte increases, force generated increases
Steep change in tension depends on: change in double actin overlap and length dependant change in TpnC Ca affinity
More blood in chambers more forceful contraction
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