"giving fluids is an inferior way of treating a vasodilated circulation which is a leaky one. giving colloids makes a little more sense." - anaesami
I wonder why do you think that a otherwise normal system vasodilated by sympathetic blocakde of SAB is leaky.
Physiology is not so fragile. I wonder if there is any reference to support that arguement.
Hypotension in CNB is primarily due to a decrease in preload , due to decreased venous return to the right side of the heart. This occurs due to the relative hypovolumia due to the sympathetic blockade. The venous capacitance vessels in the lower limbs retain a large amount of blood in them. When preload decreases the CO is also decreased. Decreases in CO produce decrease in Diastolic BP and hence possibly decreases in coronary blood flow. Hence theorotically the myocardial O2 supply can be decreased.
Management must include fluids ( crystalloids or colloids) and vasopressors that produce alpha stimulation and hence increase SVR and BP.
Vasopressors of choice would be phenylephrine, mephentramine, ephedrine, metraminol and nor-adrenaline
Now there is a slight difference between vasopresoors and inotropes.
Vasopresssors increase the SVR without increasing myocardial contractility too much and hence are not arrythmogenic and do not increase myocardial oxygen demand very much.
Inotropes like Dopamine actually increase rate and myocardial contractility and hence increase myocardial O2 consumption
So in a CNB scenario where myocardial O2 supply is low , using dopamine increases myocardial O2 demand and hence worsens the imbalance
Also in sympathetic block of CNB, the myocardial contractility in largely unaffected. So why do we need to increase contractility, we only need a vasoconstrictor like an alpha agonist.
Dopamine can produce alpha stimulation, but in high doses of > 15mcg/ kg/min. Such high doses can produce severe tachycardia. I wonder if you really used Dopamine in such high doses.
Using dopamine in lower doses primarily acts through
DA2 receptors(< 3 mcg/kg/min) where it will produce splanchnic vasodilatation and hence decrease in MAP
BETA recetors ( 15mcg/kg/min) where it will produce tachycardia and vasodilatation and hence decrease in MAP
If you so want an inotrope with alpha action I think adrenaline makes a better choice than dopamine
Dopamine is NOT A PANACEA for hypotension of any cause.
You should google the side effects of Dopamine and see the results
with this arguement i rest my case aganst the routine use of adrenaline to manage hypotension produced by extensive CNB blocks
I think if after a CNB block a patient needs Inotrope to maintain his BP then the choice of CNB in such a patient itself may be questionable.
Regional anaesthesia has no parallels if used on the right patient for the right indication
But i think we are guilty of abusing RA in certain situations