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PAS PCRS Initiation of heartbeat Cheat Sheet (DRAFT) by

Principles of circulation & what determines heart rate SA node as primary pacemaker Heart rate controlled at cellular level Autonomic control of the heart Spread of excitation through the heart Features of ECG & how it's recorded

This is a draft cheat sheet. It is a work in progress and is not finished yet.

Heart rate and basic principles of circul­ation

Body mass and heart rate
Bigger body mass = Larger heart = More cardiac output = Higher stroke volume =Lower heart rate

Heart rate controlled at cellular level.

Sympat­hetic stimul­ation
Speeds up heart rate. Raising cAMP: Noradre or adre bind to beta receptors to raise cAMP. raised cAMP binds to channel for If and increases its current. cAMP activates protein KA which phosph­ory­lates the L type calcium channel, phosph­olamban and the ryanodine receptor in the sarcop­lasmic reticulum (this affects membrane clock as it is affected by Ca2+). Phosph­ory­lation + activating If = increase rate of diastolic depola­ris­ation = increase heart rate..
Parasy­mpa­thetic stimul­ation
Slows down heart rate. Lowering cAMP. Ach binds to muscarinic receptors & directly activates a receptor coupled K channel (Ik(Ach)). Muscarinic receptors also lower the cAMP conc in the cell.
Bradyc­ardic agents
Non specific: Beta blocks, Non-di­hyd­rop­yridine L-type Ca channel blockers. Anaest­hetics. Anti-a­rrh­ythmic agents. Digoxin. Specific bradyc­ardiac agents: Alinidine, Zatebr­adine and Ivabra­dine.
Ivabradine
Only SBA licenced for clinical use. Blocks the funny current.
If
Plotted going down as it's an inward current.
 

SA node

Pace makers
Speed: SA node > AV node > His bundle > purknje fibres. Each have intrinisic rate which is conducted by the SA node (primary pacema­ker). Cardiac arrythmias can occur if others fire faster than SA or at randomly.
Movement of impulse
R.Atrium --> L.Atrium --> Septum --> Ventri­cular wall
SA node gross anatomy
Tear drop shape, top of R.Atrium. At junction of SVC & IVC. On one side bounded by Crista terminalis (thick ridge atrial muscle). Hetero­genous mix (speci­alised nodal cells, atrial cells & connective tissue) --> for normal functi­oning despite age related changes in heart rate. 50-90% connective tissue (depending on age).
SA node microa­natomy
From centre to periphery: Spindle cells, Elongated spindle cell and spinder cell. Gradual + smooth transition from centre to periphery. All have nucleus, lots of membrane and little cytoplasm as needed for AP generation not as muscle cells. P cells in centre: small, poorly differ­ent­iated, sparse mitoch­ondria, numerous caveolae (membrane invagi­nat­ions). Towards periphery: larger, more organised, more muscle filaments and well-d­efined structure.
SA AP
1) Diasto­lic­/pa­cemaker depola­ris­ati­on/­Phase 4 of AP: sloping baseline between action potent­ials. 2) Pacemaker potential generated by combo of increasing inward currents & decreasing outward currents. 3) Membrane potential hits threshold & Na+ and/or Ca2+ channels open generating AP. 4) Na+ and Ca2+ channels quickly shut & K+ channels open repola­rising membrane down to its min diastolic level. 5) Repeat with regular rhythm
Two theories on SA node clock
Membrane Clock theory: Cyclic changes in ion currents drive membrane potential to threshold. Calcium clock: Cyclic release of Ca from intrac­ellular store drives membrane potential up and down.
Membrane clock theory
Funny current (inward current bringing +ve ions into cell) so activates when membrane hyperp­ola­rises. Channel closed during AP. Membrane repola­rises and channel slowly opens being +ve into cell. Membrane depola­rises till AP can fire. Funny current switches off as channels are inacti­vated. During diastolic interval some other ionic currents switch on and off. Time & voltage dependent activation of ion currents drives the repetitive clock.
Calcium and membrane clock both important
Modulate each other. Both stimulated & inhibited by neurot­ran­smi­tters (NA & Ach). Membrane clock dominate mechanism (as generation of AP needed for pacemaker activity) & Calcium clock fine tunes.
 

Extra lecture info

Heart rate and life
1. Negative linear relati­onship between heart rate and life expectancy in animals as higher heart rate means more metabolism so more free radicals (except humans due to chronic diseases)
Heart rate and disease prognosis
1. Heart rate strongly correlated with CV mortality (risk factor or risk indica­tor?) --> CHD, Myocardial infarction