Valsalva Manoeuvre

Valsalva manoeuvre

• Forced expiration against closed glottis
  • Requires airway pressures of 40mmHg for 15 seconds

Phase I

• Onset of manoeuvre
  • Transient increase in blood pressure with a baroreflex bradycardia
    • Intrathoracic pressure transmitted to LV and aorta → Increased ventricular transmural pressure and decreased afterload → Increased cardiac output
    • Increased CO causing hypertension and stretch of aortic and carotid baroreceptors → inhibits sympathetic output and promotes vagal output from the medullary vasomotor centre → Bradycardia

Phase II

• Decreased venous return
  • Decreased blood pressure and baroreflex tachycardia
    • Continual increase in intrathoracic pressure decreases venous return to RV
    • Decreased Venous return → Decreased preload
    • Decreased RV CO secondary to Frank-Starling Mechanism
    • Decreased RV CO → Decreased LV Preload → Decreased LV Cardiac Output
    • Decreased output causes decreased blood pressure → carotid and aortic baroreceptor not stretched → release of sympathetic inhibition and decreased vagal output from medullary vasomotor centre → Tachycardia
  • Reflex tachycardia and sympathetic stimulation tends to restore BP

Phase III

• Release of intrathoracic pressure
  • Transient further decrease in blood pressure and further tachycardia
    • Decreased transmural pressure on LV and aorta leading to increased afterload → Decreased cardiac output → Decreased stretch of baroreceptors → Tachycardia

Phase IV

• Normalization of venous return
  • Venous return to RV promoted by negative intrathoracic pressure on normal respiration → Increased VR → increased RV CO → increased LV VR → Increased LV Cardiac output
  • Increased LV CO → stretch of baroreceptors → Reflex bradycardia

Sakurai 2016

Answer by Sakurai