Page 586 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Shock Syndromes 573

TABLE 23-7 Dosages and Receptor Activity of Vasopressor and Inotropic Drugs

Dosage
Drug a Activity b Activity (mg/kg/min) Comments

Dobutamine þ B 1 þþþ,B 2 þþ 2-20 May cause seizures in cats
Dopamine 0-þ 0-þ 1-4 Vasodilatory dose
(low dose)
Dopamine þ-þþ þ-þþþ 5-10 Inconsistent plasma levels
(medium dose)
Dopamine þ-þþþ þ-þþþ 10-20 Inconsistent plasma levels
(high dose)
Epinephrine þþþ þþ-þþþ 0.05-1.0 Significant side effects
Norepinephrine þþþ þ-þþ 0.05-1.0 Primarily a- adrenergic activity
Phenylephrine þþþ 0-þ 0.1-1.0 Significant vasoconstriction and
potential side effects
Vasopressin 0 0 0.5-5 mU/kg/min Nonadrenergic vasopressor
activity at vasopressin
receptors

Modified with permission from Simmons JP, Wohl JS. Vasoactive catecholamines. In: Silverstein DC, Hopper K, editors. Small animal critical care. St Louis:
Saunders Elsevier, 2009.

patient because it is dependent on individual variability although it can be used as a sole first-line agent in
in enzymatic dopamine inactivation, receptor down- vasodilated, hypotensive animals. Since phenylephrine
regulation, and the degree of autonomic derangement. has no b-agonist activity, it is the least arrhythmogenic
Dopamine can be used as a single agent therapy to pro­ of the sympathomimetic pressor drugs and is therefore
vide both inotropic and pressor support in animals with desirable in animals that develop tachyarrhythmias in
vasodilatation and decreased cardiac contractility. Despite response to other pressor agents. The intravenous dose
dopamine’s beneficial effects on cardiac output and blood range is 0.5 to 3 mg/kg/min.
pressure, it may have deleterious effects on renal, Dobutamine is a b-agonist with minimal a effects.
mesenteric, and skeletal blood flow. It increases cardiac output, oxygen delivery, and oxygen
Norepinephrine (NE) has mixed a- and b-adrenergic consumption without causing vasoconstriction. 133 It is
receptor agonism with preferential a-receptor activity. 133 therefore useful in animals with cardiac insufficiency.
Therefore the effects on heart rate and contractility are Dobutamine may worsen or precipitate tachyarrhythmias
mild, and NE is commonly used as a pressor agent in and may precipitate seizure activity in cats. The intrave­
animals with normal or increased cardiac output states. nous dose range is 1 to 5 mg/kg/min in cats and 2.5 to
The vasopressor dose of NE in humans (and extrapolated 20 mg/kg/min in dogs.
to dogs) is 0.05 to 3.3 mg/kg/min intravenously. Vasopressin is a nonadrenergic vasopressor agent.
Epinephrine is a potent pressor with mixed a-and It has both direct and indirect effects on the vascular
b-agonist activity. 133 Although epinephrine is thought to smooth muscle via the V 1 receptors and induces vasocon­
have more potent b-agonist effects than NE, individual striction in most vascular beds. 132 In vitro, vasopressin is a
response is quite variable in patients with systemic inflam­ more potent vasoconstrictor than phenylephrine or NE.
matory diseases and hypotension. Epinephrine may At low doses, this drug causes vasodilatation in renal,
significantly impair splanchnic blood flow compared to pulmonary, mesenteric, and cerebral vasculature in an
other vasopressor drugs. The vasopressor dose of intrave­ attempt to maintain perfusion to these vital organs.
nous epinephrine is 0.01 to 0.1 m/kg/min and for primar­ Low flow states secondary to hypovolemia or septic shock
ily b-agonist effects is 0.005 to 0.02 mg/kg/min. are associated with a biphasic response in endogenous
Epinephrine is rarely used as a sole first-line vasopressor serum vasopressin levels. There is an early increase in
agent due to its potential side effects, but may be the release of vasopressin from the neurohypophysis in
necessary in critically ill animals. Phenylephrine is a pure response to hypoxia, hypotension, and/or acidosis,
a-agonist drug that causes profound vasoconstriction. which leads to high levels of serum vasopressin. This plays
It has been shown to cause an increase in cardiac output a role in the stabilization of arterial pressure and organ
and blood pressure, presumably due to increased venous perfusion in the initial stages of shock. There appears to
return to the heart and activation of a-1 receptors in be a subsequent decrease in circulating vasopressin levels,
the myocardium. Phenylephrine is typically used in most likely due to a depletion of hypothalamic stores. The
patients that are unresponsive to other sympathomimetics, use of vasopressin in animals in the later stages of shock,