This Sunday, we bring to you an old article from our archives section. Prof. Dr. Sundeep Mishra provides a quick prescription guide for the selection and dosage of vasopressors (adrenalin, nor-adrenalin, dopamine or others) used in the treatment of different types of shocks.

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Various agents increase blood pressure acting on the sympathetic nervous system, either increasing cardiac output (β1 receptors) or increasing peripheral vascular resistance (α receptors). Thus, different agents are useful depending upon the type of shock.

In general, when blood pressure is markedly reduced in the presence of near-normal heart function, a predominant vasopressor (agent active on α receptor) is better; nor-adrenalin. On the other hand, when inability to generate blood pressure is related to reduction in cardiac output, an agent acting predominantly on β1 receptor may be beneficial; dobutamine, adrenalin.

Dopamine acts predominantly on dopamine receptors (DA receptors) and only in high doses on α or β receptors as such (although widely used in practice because of easy availability), conceptually it is not very useful in case of shocks as a primary agent. Indeed SOAP II trial has shown that compared to nor-adrenalin, dopamine was less useful in all types of shock; rather it increased the risks of arrhythmias.

Table 1: Action of vasopressor adrenalin/ ionotropic agents on various receptors

Agents	Receptors
Adrenalin	β1>β2>α
Noradrenalin	α=β1>β2
Dopamine	DA Receptors → release of endogenous noradrenalin +  with high dose →α>—β1>β2
Dobutamine	β1>>α & β2
Vasopressin	V1 receptors → ↓portal blood flow, portal systemic collateral blood flow & variceal pressure but ↑PVR ↓CO & CBF

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Hypovolumic shock

Since this shock involves fluid depletion; fluid replacement is the best strategy. However, till adequate fluid can be given, the blood pressure may be temporarily maintained by using nor-adrenalin (α receptors) which increases total peripheral resistance.

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Septic (warm) shock

Since this shock involves peripheral vasodilation and peripheral pooling of blood, an agent which increases peripheral vascular resistance (PVR) with minimal stimulation of heart like nor-adrenalin would be more useful (Table 1).

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Cardiogenic (warm) shock

On the other hand, when the shock is due to ineffective cardiac pumping, an ionotropic agent which increases contractility (β1 receptors) would be more useful. Among the agents, dobutamine has a predominant activity against β1 receptors with minimal activity against α or β2 receptors and is therefore the agent of choice in this situation. However, dobutamine has a relatively longer onset of action and therefore with severe hypotension, in emergency situations, due to its quick onset of action adrenalin may be more useful (β1≥β2>α). However, adrenalin should be used with caution because it may worsen myocardial dysfunction and could lead to increase in arrhythmias.

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Shock associated with cardiac arrest

In this situation we may require a balanced vasopressor ionotrope (both β1 & α activity) with quick onset of action. Here adrenalin (β1≥β2>α) nicely fits the bill but again its usefulness in long run may be limited by its arrhythmogenoicity and ability to increase myocardial dysfunction. Another factor working against adrenalin is a relative acidotic milieu which may limit its effectivity; in hypoxaemic, acidotic conditions vasopressin (anti-diuretic hormone) may work better than epinephrine but it is limited by its action on reducing cardiac output and coronary blood flow (which is generally the cause of cardiac arrest). Thus on the balance of things adrenalin is still the drug of first choice, use of vasopressin restricted to those cases refractory to use of adrenalin.

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Shock associated with anaphylaxis

Here adrenalin is the ideal choice because it not only possesses both β1 & α activity but it also causes broncho-dilation vide its action on β2 receptors.

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Shock associated with variceal bleed

In chronic liver disease, fibrosis of the liver → ↑portal venous pressure (as mesenteric blood requires ↑g pressure to flow through the scarred liver) → opening up of collateral circulation (to allow the return of blood to the systemic circulation through shunts); intrinsic and extrinsic gastro-oesophageal veins dilate forming varices → ↑variceal pressure → rupture of varices.

Vasopressin (acting via V1 receptors) → ↓portal blood flow, portal systemic collateral blood flow & variceal pressure→ decreasing bleeding. However, its side-effects include ↑PVR, ↓ cardiac output & ↓coronary blood flow. The combined use of glyceryl trinitrate with vasopressin has been shown to reduce these side-effects.

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This article was originally published on November 17, 2020.

Disclaimer- The views and opinions expressed in this article are those of the author's and do not necessarily reflect the official policy or position of M3 India.

The author, Dr. Sundeep Mishra is a Professor of Cardiology.