Its about the role an alpha1 agonist plays in treatment of cardiogenic shock. I would like to take Norepinephrine as an example.
NE being alpha1 agonist causes vasoconstriction of arteries and increases blood pressure. But doesn't vasoconstriction actually decrease tissue/organ perfusion and increase the risk of organ failure? Doesn't the vasoconstriction increase the afterload and work that needs to be done by the failing heart? Wouldn'nt it be counterinituitive?
And on the contrary, dopamine is also used in Cardiogenic shock and what it does is cause vasodilation in the coronary, renal, cerebral and other resistance vessels. It increases blood pressure by inotropic and chronotropic action on heart via B1 receptor mediated action. More cardiac output. more perfusion.
I am badly confused
NE being alpha1 agonist causes vasoconstriction of arteries and increases blood pressure. But doesn't vasoconstriction actually decrease tissue/organ perfusion and increase the risk of organ failure? Doesn't the vasoconstriction increase the afterload and work that needs to be done by the failing heart? Wouldn'nt it be counterinituitive?
And on the contrary, dopamine is also used in Cardiogenic shock and what it does is cause vasodilation in the coronary, renal, cerebral and other resistance vessels. It increases blood pressure by inotropic and chronotropic action on heart via B1 receptor mediated action. More cardiac output. more perfusion.
I am badly confused
Last edited:
