II. Causes

  1. Pulmonary Arterial Hypertension (e.g. Pulmonary Embolism, ARDS, Pulmonary Hypertension)
    1. Worsened with Hypoxia, hypercarbia and acidosis
  2. Decreased contractility (e.g. right ventricular Myocardial Infarction or Myocarditis)
  3. Volume overload (e.g. Excessive volume Resuscitation as in multisystem Trauma, Sepsis)

III. Pathophysiology: Right Ventricle

  1. Right Ventricle is a "perfusion princess" (Sara Crager)
  2. Right ventricle is normally perfused in systole and diastole
    1. Contrast with the left ventricle which is only perfused in diastole
    2. Right ventricle poorly tolerates hypoperfusion and contractility decreases significantly
  3. Right ventricle systolic perfusion is decreased in progressive Right Heart Failure
    1. High pulmonary artery pressure especially with low systemic pressure (decreased pressure gradient)
    2. Hyperexpansion of the right ventricle results in a precipitous drop in right-sided contractility
      1. Contrast with left ventricle contractility with hyperexpansion which compensates (Starling Curve)
      2. Right Ventricle hyperexpansion also shifts septum left, decreases EF, decreases MAP and perfusion
  4. Left ventricle has an interdependence with the right ventricle
    1. Right ventricular dilates with decreased contractility and tricuspid regurgitation
    2. LV diastolic filling decreases with falling RV ejection fraction
      1. RV dilation also encroaches on the LV via their shared septum
    3. LV can temporarily compensate for reduced Stroke Volume with an increase in Heart Rate (Tachycardia)
    4. Reduced LV Cardiac Output increases pulmonary vascular resistance and right sided Afterload
      1. Other factors increasing pulmonary vascular resistance include hypercapnia, Atelectasis and Hypoxemia
      2. Positive Pressure Ventilation may also increase right sided Afterload

IV. Pathophysiology: Right Ventricular Spiral of Death

  1. Uncompensated Right Ventricular Failure results in hemodynamic collapse
  2. Right Ventricular Afterload (pulmonary artery pressures) increases
  3. Decreases right ventricular coronary pressure (esp. in systole) and results in RV ischemia
  4. Decreases right ventricular ejection fraction
  5. Increases right ventricular volume
  6. Interventricular Septum shifts left (interventricular interpedence), reducing left ventricular volume and cardiac ouput
  7. Decreases mean arterial pressure and further decreases right ventricular pefusion

VI. Resources

  1. Scott Weingart. EMCrit 272 – Right Heart Failure with Sara Crager. EMCrit Blog. Published 4/29/20. Accessed 8/22/20.
    1. https://emcrit.org/emcrit/right-heart-sara-crager/

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