Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Cardiac Muscle
Organisation of the Body
| Question | Answer |
|---|---|
| What is the heart | A muscular pump that alternated between contraction (systole) and relaxation (diastole) Depending on activity will give around 3 billion beats in 80 years |
| What is cardiac output and how is it regulated | 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 |
| Gross structure of the heart | 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 |
| Cardiac myocytes | Ventricular - brick like appearance with striations, mono-nucleated to provide the contraction force Atrial - smaller as less force is needed, still striated SAN - very thin, no sarcomeric structures, key cells in the pacemaker |
| Ultrastructure of myocardium | 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 |
| Gap junctions | 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 |
| Organisation of contractile filaments | Similar to that of skeletal muscle Thick filaments - myosin Thin filaments - actin, tropomyosin, troponins Mechanism of contraction is also highly similar |
| Starling's law of the heart | 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 |
| Spread of impulse in the heart | Generated in the SAN, cannot go directly to the ventricles so must pass through the AVN. This ensures the atria contract before the ventricles Action potential is prolonged, so the muscle fully relaxes before another AP can be generated |
| Different Action Potential shapes | 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 |
| Functions of different action potentials | Pacemaker function - myogenic rhythm Fast/slow conduction to synchronise contraction Long plateau to maintain refractoriness and avoid high frequency activation |
| Phases of the Action potential in the SAN | Phase 0 - slow upstroke due to Ca2+ (L-type channels) Phase 3 - repolarisation due to closing of Ca2+ and opening of K+ Phase 4 - electrical diastolic phase. Changes in K+, Ca2+ and HCN channels produce pacemaker activity - degrades resting potential |
| What are HCN channels | Funny current carried by hyperpolarisation-activated cyclic nucleotide channel Opens on hyperpolarisation at around -65 mV Allows inwards flow of Na+ to depolarise the membrane until Ca2+ channels open |
| What sets the pacemaker current | Inwards Ca2+ current De activation of outwards K+ current Inwards cation current (HCN at negative voltage) Sodium Calcium exchanger Background inwards Na+ leak |
| Phases of the action potential in ventricular myocytes | 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 |
| Excitation contraction coupling | T-tubules run parallel to the z-lines in dyads with one SR cisternae Influx of Ca through voltage gated channels bind to the RyR, triggering it to open The Ca triggers contraction before being taken back up into the SR via SERCA proteins or out the cell |
| The sodium calcium exchanger | This is used to exclude calcium from myocytes following contraction This is an electrogenic pump as per Ca extruded 3 Na move in leading to a positive inwards flow The Na/K pump helps to maintain the Na gradient and offset this |
| Action of Ouabain | Inhibits the Na/K pump Na gradient lost Ability to remove Ca2+ reduced Drugs that generate a Ca2+ gradient can help ad it allows passive removal of calcium |
| Evidence for the role of Ca2+ | Adding a Ca2+ dye to a cardiac myocyte reveals a Ca2+ wave on excitation, which moves through the cell allowing for synchronous contraction |
| Relationship between active tension and systolic Ca2+ conc | 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 |
| Modulation of cardiac output | Cardiac output = stroke volume x heart rate Can change frequency of contraction - chronotropy Can change force of contraction - inotropy |
| Regulation of Chronotropy - Increased heart rate | Noradrenaline binds to beta adrenergic receptors, activating adenylyl cyclase and producing cAMP. This binds to HCN channels to increase open probability and accelerate pacemaker potential decay Phosphorylation of LTCC and K+ channels also does this |
| Regulation of Chronotropy - Decreased heart rate | 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 |
| Regulation of inotropy - hormones | 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 |
| Regulation of inotropy - cell length | 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 |
Created by:
12345678987654321000000
Popular Medical sets