Cardiovascular Medicine Book

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Afterload

Aka: Afterload, Ventricular Afterload, Peripheral Vascular Resistance, Systemic Vascular Resistance
  1. See Also
    1. Ventricular Preload
    2. Blood Volume
    3. Cardiac Output (and Stroke Volume)
    4. Blood Pressure Physiology
  2. Definitions
    1. Afterload
      1. Load or resistance (arterial pressure) against which the the ventricle muscle must contract
      2. Ventricular wall stress or peak tension during systolic contraction
  3. Physiology: General
    1. Afterload increases
      1. Requires increased left ventricular tension and increased workload
      2. Contraction becomes less efficient
  4. Physiology: Ventricular wall stress
    1. Laplace Law
      1. Wall tension = (pressure * radius) / (2 * 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
  5. Physiology: Afterload Components
    1. Ventricular Preload (end-diastolic volume)
    2. Pleural pressure
      1. Negative pleural pressure (e.g. inspiration) counteracts ventricular contraction forces
        1. Results in decreased Blood Pressure (e.g. Pulsus Paradoxus)
      2. Positive pleural pressure (e.g. PPV) augments ventricular contraction
        1. Results in transient increased Blood Pressure
        2. However increased pleural pressure (intrathoracic pressure) also can decrease Preload
          1. Decreased venous return lowers Blood Pressure
    3. Vascular impedance
      1. Aorta and pulmonary artery diminish the rate of change of pressure and flow
        1. Dampens fluctuations in pulsatile flow
      2. Key force in ventricular emptying, but is not typically measurable
    4. Peripheral Vascular Resistance or Systemic Vascular Resistance (SVR)
      1. Small terminal vessels (primarily arterioles and capillaries) resist steady flow (non-pulsatile flow)
      2. Vascular resistance increases (and flow decreases)
        1. Increases blood viscosity (increased Hematocrit or Dehydration)
      3. Systemic Vascular Resistance (SVR) Calculation
        1. SVR = (mAoP - mRAP)/CO x 80
        2. Where mAoP = Mean Aortic Pressure (e.g. normal young adult male: 104 mmHg)
        3. Where mRAP= Mean Right Atrial Pressure (e.g. normal young adult male: 5 mmHg)
        4. Where CO = Cardiac Output (e.g. normal young adult male: 5 Liters)
        5. Example = (104-5)/5 * 80 = 1584 dynes/s/cm^-5
      4. Pulmonary Resistance
        1. PR= (mPAP - mPCWP)/CO x 80
        2. Where mPAP = Mean Pulmonary Artery Pressure (e.g. normal young adult male: 16 mmHg)
        3. Where mPCWP = Mean Pulmonary Capillary Wedge Pressure (e.g. normal young adult male: 9 mmHg)
        4. Where CO = Cardiac Output (e.g. normal young adult male: 5 Liters)
        5. Example = (16-9)/5 * 80 = 112 dynes/s/cm^-5
      5. References
        1. Davies (1986) Acute Respiratory Failure, Cyberlog
  6. Physiology: Effectors of Afterload
    1. Decreased Afterload (Vasodilation)
      1. ACE Inhibitors and Angiotensin Receptor Blockers
      2. Hydralizine
      3. Nitroglycerin
      4. Dihydropyridine Calcium Channel Blockers (e.g. Nifedipine, Amlodipine, Nicardipine)
      5. Alpha Adrenergic Central Agonist (e.g. Clonidine)
    2. Increased Afterload
      1. Systemic Hypertension
      2. Aortic Stenosis
      3. Aortic Coarctation
      4. Pulmonary Hypertension (RV Afterload)
  7. Diagnostics
    1. Right Afterload
      1. Mean pulmonary artery pressure or wedge pressure
    2. Left Afterload
      1. Mean arterial pressure
  8. References
    1. Killu and Sarani (2016) Fundamental Critical Care Support, p. 93-114
    2. Marino (2014) ICU Book, 4th Ed Wolters-Kluwer p. 159-66

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