II. Definition

  1. Load or resistance (arterial pressure) against which the the left ventricle muscle must contract
  2. Ventricular wall stress or peak tension during systole

III. Physiology: Ventricular wall stress

  1. Laplace Law
    1. Wall tension = (pressure x radius) / (2 x wallThickness)
  2. Causes of increased ventricular wall stress
    1. Increased peak ventricular transmural pressure
    2. Increased ventricular chamber size
  3. Causes of decreased ventricular wall stress
    1. Increased ventricular hypertrophy

IV. Physiology: Afterload Components

  1. Ventricular Preload (end-diastolic volume)
  2. Pleural pressure
    1. Negative pleural pressure (e.g. inspiration) counteracts ventricular contraction forces resulting in decreased Blood Pressure (e.g. Pulsus Paradoxus)
    2. Positive pleural pressure (e.g. PPV) augments ventricular contraction resulting in transient increased Blood Pressure
      1. However increased pleural pressure (intrathoracic pressure) also can decrease Preload (venous return) which lowers Blood Pressure
  3. Vascular impedance
    1. Aorta and pulmonary artery diminish the rate of change of pressure and flow (dampen fluctuations in pulsatile flow)
    2. Key force in ventricular emptying, but is not typically measurable
  4. Peripheral vascular resistance
    1. Small terminal vessels (primarily arterioles and capillaries) resist steady flow (non-pulsatile flow)
    2. Vascular resistance increases (and flow decreases) with increasing blood viscosity (increased Hematocrit or dehydration)

V. References

  1. Marino (2014) ICU Book, 4th Ed Wolters-Kluwer p. 159-66

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