Cardiovascular Medicine Book





Aka: Preload, Ventricular Preload, Frank-Starling Curve
  1. See Also
    1. Ventricular Afterload
    2. Blood Volume
    3. Cardiac Output (and Stroke Volume)
  2. Definitions
    1. Preload (right atrium Preload)
      1. Determined by venous return and right ventricular compliance
      2. End-diastolic wall tension (and end-diastolic volume) of the right ventricle
        1. Ventricular Muscle stretches in response to increased pressure during diastole
  3. Images
    1. Cardiac Cycle Volumes and Pressures (Wiggers Diagram)
      1. cvCardiacCycleWiggers.png
  4. Physiology: Frank-Starling Curve
    1. Normal heart
      1. Diastolic volume is the key determinent of ventricular contraction strength in the normal heart
      2. As end-diastolic volume (and pressure) increases, peak systolic pressure (contraction strength) increases
        1. Systole starts with isometric contraction (constant Muscle length)
          1. Contraction against increased ventricular volume with closed aortic valve and pulmonic valve
          2. Preload is the ventricular wall tension that increases with chamber filling
        2. Systole transitions into isotonic contraction (constant Muscle tension)
          1. Aortic valve and pulmonic valve open, allowing ventricular emptying
          2. Afterload is the constant tension in ventricular Muscle as it contracts and shortens
    2. Augmented contractility (e.g. inotrope infusion)
      1. Frank-Starling Curve shifts up and to the left
      2. For any given end-diastolic volume, the ventricular contraction (Stroke Volume) is increased
    3. Congestive Heart Failure
      1. Frank-Starling Curve shifts downward and flattens
      2. For any given end-diastolic volume in CHF
        1. Ventricular contraction (Stroke Volume) is less than in a normal patient
      3. Increasing end-diastolic volume in CHF has adverse effects
        1. Stroke Volume increases minimally (flat part of Frank-Starling Curve)
        2. Peak systolic pressure increases significantly and results in vascular congestion
        3. Maladaptive long-term compensatory mechanisms develop to maintain Stroke Volume
          1. Ventricle dilates (Cardiomyopathy) to allow for increased filling
          2. Ventricle becomes stiff (Diastolic Dysfunction)
  5. Physiology: Effectors of Preload
    1. Decreased Preload
      1. Nitroglycerin (vasodilation)
      2. Diuretics (decreased intravascular volume)
      3. ACE Inhibitors and Angiotensin Receptor Blockers (vasodilation via suppression of Renin-Angiotensin System)
      4. Dihydropyridine Calcium Channel Blockers (vasodilation)
      5. Dehydration
      6. Increased intrathoracic pressure (e.g. Non-Invasive Positive Pressure Ventilation, Tension Pneumothorax)
    2. Increased Preload
      1. Volume Overload (e.g. Congestive Heart Failure, Renal Failure, excessive Intravenous Fluid or transfusion)
      2. Excessive salt ingestion
      3. Pregnancy
  6. Diagnostics
    1. Right Preload
      1. Central Venous Pressure (see precaution below)
      2. IVC Ultrasound for Volume Status (Caval Aorta Index)
    2. Left Preload
      1. Pulmonary Artery Occlusion pressure or wedge pressure (see precaution below)
      2. Symptoms (Orthopnea or Dyspnea on exertion)
      3. Signs (Pulmonary Edema, rales)
      4. Imaging (Lung Ultrasound)
  7. Precautions
    1. End diastolic pressure (e.g. CVP and Wedge Pressure) correlates poorly with end diastolic volume even in healthy patients
      1. Hence CVP and Wedge Pressure are unreliable markers of ventricular filling and volume status
  8. References
    1. Killu and Sarani (2016) Fundamental Critical Care Support, p. 93-114
    2. Marino (2014) ICU Book, 4th Ed Wolters-Kluwer p. 151-7

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