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% Document Info
\author{mallowy}
\pdfinfo{
  /Title (pas-pcrs-initiation-of-heartbeat.pdf)
  /Creator (Cheatography)
  /Author (mallowy)
  /Subject (PAS PCRS Initiation of heartbeat Cheat Sheet)
}

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    \vspace{-2pt}\large{\bf{\textcolor{DarkBackground}{\textrm{PAS PCRS Initiation of heartbeat Cheat Sheet}}}} \\
    \normalsize{by \textcolor{DarkBackground}{mallowy} via \textcolor{DarkBackground}{\uline{cheatography.com/143608/cs/31386/}}}
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  \mymulticolumn{2}{p{5.377cm}}{\bf\textcolor{white}{Cheatographer}}  \\
  \vspace{-2pt}mallowy \\
  \uline{cheatography.com/mallowy} \\
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  \mymulticolumn{1}{p{5.377cm}}{\bf\textcolor{white}{Cheat Sheet}}  \\
   \vspace{-2pt}Not Yet Published.\\
   Updated 28th March, 2022.\\
   Page {\thepage} of \pageref{LastPage}.
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  Measure your website readability!\\
  www.readability-score.com
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\begin{multicols*}{3}

\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Heart rate and basic principles of circulation}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{1}{x{5.377cm}}{Body mass and heart rate} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}Bigger body mass = Larger heart = More cardiac output = Higher stroke volume =Lower heart rate} \tn 
% Row Count 3 (+ 3)
\hhline{>{\arrayrulecolor{DarkBackground}}-}
\end{tabularx}
\par\addvspace{1.3em}

\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Heart rate controlled at cellular level.}}  \tn
% Row 0
\SetRowColor{LightBackground}
\mymulticolumn{1}{x{5.377cm}}{Sympathetic stimulation} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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..} \tn 
% Row Count 11 (+ 11)
% Row 1
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\mymulticolumn{1}{x{5.377cm}}{Parasympathetic stimulation} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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.} \tn 
% Row Count 17 (+ 6)
% Row 2
\SetRowColor{LightBackground}
\mymulticolumn{1}{x{5.377cm}}{Bradycardic agents} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}Non specific: Beta blocks, Non-dihydropyridine L-type Ca channel blockers. Anaesthetics. Anti-arrhythmic agents. Digoxin. Specific bradycardiac agents: Alinidine, Zatebradine and Ivabradine.} \tn 
% Row Count 23 (+ 6)
% Row 3
\SetRowColor{white}
\mymulticolumn{1}{x{5.377cm}}{Ivabradine} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}Only SBA licenced for clinical use. Blocks the funny current.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{If} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}Plotted going down as it's an inward current.} \tn 
% Row Count 28 (+ 2)
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\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{SA node}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{Pace makers} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}Speed: SA node \textgreater{} AV node \textgreater{} His bundle \textgreater{} 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.} \tn 
% Row Count 6 (+ 6)
% Row 1
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\mymulticolumn{1}{x{5.377cm}}{Movement of impulse} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}R.Atrium -{}-\textgreater{} L.Atrium -{}-\textgreater{} Septum -{}-\textgreater{} Ventricular wall} \tn 
% Row Count 9 (+ 3)
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\mymulticolumn{1}{x{5.377cm}}{SA node gross anatomy} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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) -{}-\textgreater{} for normal functioning despite age related changes in heart rate. 50-90\% connective tissue (depending on age).} \tn 
% Row Count 17 (+ 8)
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\mymulticolumn{1}{x{5.377cm}}{SA node microanatomy} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{SA AP} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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} \tn 
% Row Count 39 (+ 11)
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{SA node (cont)}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{Two theories on SA node clock} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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.} \tn 
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\mymulticolumn{1}{x{5.377cm}}{Membrane clock theory} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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.} \tn 
% Row Count 17 (+ 11)
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\mymulticolumn{1}{x{5.377cm}}{Calcium and membrane clock both important} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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.} \tn 
% Row Count 23 (+ 6)
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\begin{tabularx}{5.377cm}{X}
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\mymulticolumn{1}{x{5.377cm}}{\bf\textcolor{white}{Extra lecture info}}  \tn
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\mymulticolumn{1}{x{5.377cm}}{Heart rate and life} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}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)} \tn 
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% Row 1
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\mymulticolumn{1}{x{5.377cm}}{Heart rate and disease prognosis} \tn 
\mymulticolumn{1}{x{5.377cm}}{\hspace*{6 px}\rule{2px}{6px}\hspace*{6 px}1.	Heart rate strongly correlated with CV mortality (risk factor or risk indicator?) -{}-\textgreater{} CHD, Myocardial infarction} \tn 
% Row Count 9 (+ 4)
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% That's all folks
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