<?xml version="1.0" encoding="UTF-8"?>
<opml version="2.0">
  <head>
    <title>007-01 Foundations</title>
    <ownerName>Integrated Medical Foundations</ownerName>
  </head>
  <body>
    <outline text="Cardiac electrophysiology and the cardiac cycle">
      <outline text="Pacemaker activity">
        <outline text="No stable resting voltage">
          <outline text="Hyperpolarisation-activated inward current"/>
          <outline text="Reduced potassium efflux"/>
          <outline text="Calcium entry toward threshold"/>
        </outline>
        <outline text="Calcium current drives the nodal upstroke"/>
        <outline text="Slope of diastolic depolarisation sets rate"/>
        <outline text="Autonomic control">
          <outline text="Beta one raises cyclic adenosine monophosphate"/>
          <outline text="Steeper pacemaker slope, faster conduction"/>
          <outline text="Muscarinic acetylcholine slows node and conduction"/>
        </outline>
      </outline>
      <outline text="Conduction sequence">
        <outline text="Sinoatrial node to atrial myocardium"/>
        <outline text="Slow atrioventricular node lets atria fill the ventricle"/>
        <outline text="His bundle, bundle branches, Purkinje fibres"/>
        <outline text="Septum and apex before the free wall"/>
      </outline>
      <outline text="Working myocyte action potential">
        <outline text="Fast sodium entry depolarises"/>
        <outline text="Early potassium currents begin repolarisation"/>
        <outline text="Plateau: L-type calcium against potassium efflux"/>
        <outline text="Delayed potassium currents complete repolarisation"/>
        <outline text="Long refractory period prevents tetany"/>
      </outline>
      <outline text="Excitation-contraction coupling">
        <outline text="L-type channels in transverse tubules open"/>
        <outline text="Calcium-induced calcium release through ryanodine receptors"/>
        <outline text="Calcium binds troponin C, tropomyosin moves"/>
        <outline text="Actin-myosin cross-bridge cycling"/>
        <outline text="Relaxation removes calcium">
          <outline text="Sarcoplasmic-reticulum pumps"/>
          <outline text="Sodium-calcium exchange"/>
          <outline text="Membrane calcium pumps"/>
        </outline>
      </outline>
      <outline text="The electrocardiogram">
        <outline text="P wave: atrial depolarisation"/>
        <outline text="P R interval: atrial conduction plus nodal delay"/>
        <outline text="Q R S: ventricular depolarisation"/>
        <outline text="S T segment: ventricular plateau"/>
        <outline text="T wave: ventricular repolarisation"/>
        <outline text="It does not show contraction, output or coronary anatomy"/>
        <outline text="Prolonged corrected Q T">
          <outline text="Early afterdepolarisations"/>
          <outline text="Torsades de pointes"/>
          <outline text="Bradycardia, low potassium, low magnesium, drugs"/>
        </outline>
      </outline>
      <outline text="Mechanical events">
        <outline text="Diastole: atrioventricular valves open, passive filling"/>
        <outline text="End-diastolic volume is maximal"/>
        <outline text="First heart sound closes mitral and tricuspid valves"/>
        <outline text="Isovolumetric contraction: constant volume, rising pressure"/>
        <outline text="Ejection when ventricular pressure exceeds arterial"/>
        <outline text="Stroke volume equals end-diastolic minus end-systolic volume"/>
        <outline text="Ejection fraction is stroke volume over end-diastolic volume"/>
        <outline text="Second heart sound, then isovolumetric relaxation"/>
        <outline text="Tachycardia costs diastolic time first"/>
      </outline>
      <outline text="Mitral regurgitation as a worked route">
        <outline text="Backward flow into the atrium during systole"/>
        <outline text="Ejection fraction can look reassuring"/>
        <outline text="Acute: unadapted atrium transmits pressure to the lungs"/>
        <outline text="Chronic: enlargement and compliance delay symptoms"/>
      </outline>
      <outline text="Preload, afterload, contractility">
        <outline text="Preload is fibre stretch before contraction"/>
        <outline text="Frank-Starling matches output to venous return"/>
        <outline text="Afterload: arterial pressure, obstruction, impedance, geometry"/>
        <outline text="Pressure load gives concentric hypertrophy"/>
        <outline text="Volume load gives dilation and eccentric remodelling"/>
        <outline text="Contractility at fixed load; lusitropy is relaxation"/>
        <outline text="Cardiac output equals rate times stroke volume"/>
      </outline>
      <outline text="Coronary supply and demand">
        <outline text="High oxygen extraction at rest, so flow must rise"/>
        <outline text="Left-ventricular flow is mainly diastolic"/>
        <outline text="Demand: rate, contractility, wall stress, muscle mass"/>
        <outline text="Supply: oxygen content, perfusion pressure, patency, diastolic time"/>
      </outline>
      <outline text="Rhythm disturbance">
        <outline text="Abnormal impulse formation or conduction"/>
        <outline text="Enhanced automaticity and triggered activity"/>
        <outline text="Re-entry needs circuit, unidirectional block, timing"/>
        <outline text="Atrial fibrillation: lost atrial contraction, thrombus risk"/>
        <outline text="Ventricular tachycardia can degenerate to fibrillation"/>
        <outline text="Electrolytes">
          <outline text="Hyperkalaemia slows conduction and widens Q R S"/>
          <outline text="Hypokalaemia increases ectopy and delays repolarisation"/>
          <outline text="Magnesium deficiency and calcium change the plateau and Q T"/>
        </outline>
      </outline>
    </outline>
  </body>
</opml>
