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  <head>
    <title>007-02 Pressure-volume loops, arrhythmia mechanisms, and pump efficiency</title>
    <ownerName>Integrated Medical Foundations</ownerName>
  </head>
  <body>
    <outline text="Pressure-volume loops and arrhythmia mechanisms">
      <outline text="Reading the pressure-volume loop">
        <outline text="Filling adds volume at low pressure"/>
        <outline text="Isovolumetric contraction raises pressure alone"/>
        <outline text="Ejection reduces volume"/>
        <outline text="Isovolumetric relaxation at constant end-systolic volume"/>
        <outline text="Width is stroke volume"/>
        <outline text="Enclosed area approximates stroke work"/>
        <outline text="End-diastolic relation reflects passive compliance"/>
        <outline text="End-systolic relation reflects contractile state"/>
      </outline>
      <outline text="Loading changes the loop">
        <outline text="More preload widens it through Frank-Starling"/>
        <outline text="More afterload raises end-systolic volume"/>
        <outline text="More contractility lowers end-systolic volume"/>
        <outline text="Mitral regurgitation: volume escapes to a low-pressure atrium"/>
        <outline text="Aortic stenosis: pressure work and wall stress rise"/>
      </outline>
      <outline text="Wall stress and remodelling">
        <outline text="Rises with pressure and radius, falls with thickness"/>
        <outline text="Pressure overload thickens the wall"/>
        <outline text="Volume overload adds sarcomeres in series"/>
        <outline text="Adaptation fails with fibrosis and capillary mismatch"/>
        <outline text="Hypertrophy is not stronger effective pumping"/>
        <outline text="Preserved ejection fraction with high filling pressure"/>
      </outline>
      <outline text="Oxygen demand without occlusion">
        <outline text="Demand tracks wall stress, rate, contractile activity"/>
        <outline text="Dilated ventricle faces greater wall stress"/>
        <outline text="Hypertrophied ventricle has lower capillary density per mass"/>
        <outline text="Tachycardia adds demand and shortens diastole"/>
      </outline>
      <outline text="Diastole and ventricular interaction">
        <outline text="Relaxation is energy-dependent"/>
        <outline text="Ischaemia impairs diastole before systole"/>
        <outline text="A stiff ventricle depends on atrial contraction"/>
        <outline text="Shared septum inside the pericardium">
          <outline text="Right dilation shifts the septum leftward"/>
          <outline text="Tamponade and high airway pressure limit both chambers"/>
        </outline>
        <outline text="Positive-pressure ventilation">
          <outline text="Reduces venous return when volume is low"/>
          <outline text="Reduces left transmural afterload"/>
        </outline>
      </outline>
      <outline text="Arrhythmia initiation">
        <outline text="Abnormal automaticity outside the sinoatrial node"/>
        <outline text="Triggered activity depends on a preceding beat">
          <outline text="Early afterdepolarisations during prolonged repolarisation"/>
          <outline text="Delayed afterdepolarisations after calcium overload"/>
        </outline>
        <outline text="Re-entry needs substrate and trigger">
          <outline text="Scar, fibrosis, unequal refractoriness, accessory pathway"/>
          <outline text="A premature impulse supplies the trigger"/>
        </outline>
        <outline text="Antiarrhythmics can be proarrhythmic">
          <outline text="Sodium block promotes another circuit"/>
          <outline text="Potassium block permits early afterdepolarisations"/>
          <outline text="Nodal blockers can worsen accessory-pathway rhythms"/>
        </outline>
      </outline>
      <outline text="Electrocardiography as spatial sampling">
        <outline text="Each lead projects the cardiac vector onto an axis"/>
        <outline text="Biphasic signal when the vector is perpendicular"/>
        <outline text="Axis deviation is a clue, not a diagnosis"/>
        <outline text="Broad Q R S: block, ventricular origin, pre-excitation, pacing, drugs"/>
        <outline text="S T and T changes are not specific to occlusion"/>
        <outline text="Corrected Q T formulae fail at rate extremes"/>
      </outline>
      <outline text="Haemodynamic consequence and priorities">
        <outline text="Danger comes from rate, lost synchrony, or degeneration"/>
        <outline text="Adverse features">
          <outline text="Hypotension or shock"/>
          <outline text="Ongoing ischaemic chest discomfort"/>
          <outline text="Acute pulmonary oedema or altered consciousness"/>
        </outline>
        <outline text="Then find substrate and trigger">
          <outline text="Ischaemia, infection, electrolytes, endocrine, drugs"/>
          <outline text="A transient trigger does not exclude a substrate"/>
        </outline>
        <outline text="Serial assessment, because loading and tone change fast"/>
      </outline>
    </outline>
  </body>
</opml>
