Happy Pharmacology Phriday! We’ve been talking about sympathomimetics, which are drugs which either imitate the actions of the sympathetic nervous system or cause effects in the sympathetic nervous system. Earlier we took a moment to get a “down and dirty” intro to the sympathetic nervous system and sympathomimetics in general. Now, we’re going to go into more detail with one of the most widely used sympathomimetic drugs in EMS, dopamine.
The “Dope” on Dopamine (Get It? Yes?)
So how does it work? Dopamine is a sympathetic agonist. In plain speech, this means that it affects the sympathetic nervous system. Agonist is just a big word for a chemical which binds to a receptor, and causes the receptor to cause a biological response. Dopamine occurs naturally in the body, and is turned into norepinephrine. If you want to get technical, it’s the norepinephrine which then binds to receptors, and causes a biological response.
One of the many cool things about dopamine is that depending on dose, it can cause alpha, beta1, or dopaminergic effects. Does that sound complicated? Let’s break that down.
Alpha 1 receptors cause peripheral vasoconstriction. In other words, when dopamine binds with an alpha 1 receptor, the blood vessels in the extremities will get smaller. When Beta 1 receptors are stimulated, they cause the heart to beat with increased force, without causing the rate to increase too much. If you want to put that in medical terms, you could say that beta 1 receptors cause an increased inotropic effect, without causing an increased chronotropic effect. Finally, dopaminergic receptors, when stimulated, cause dilation of the renal, coronary, and cerebral arteries. So in high doses, dopamine increases blood flow to the kidneys, the heart, and the brain.
What Does Dopamine Treat?
One of the most common uses of dopamine is treating cardiogenic shock. Recall that cardiogenic shock is hypoperfusion caused by an underperforming heart. Dopamine can be used to treat cardiogenic shock by causing vasoconstriction in peripheral blood vessels via alpha 1 receptors, which subsequently raises blood pressure. Dopamine can also work directly on the heart by acting on beta 1 receptors, which causes the heart to squeeze harder. In my system, one of the times we break out dopamine post-cardiac arrest/post-ROSC if we need to increase a patient’s blood pressure.
We can also use dopamine to treat septic shock. Septic shock is also hypoperfusion. However, instead of being caused by a balky heart, septic shock is caused by toxic bacterial byproducts making the blood vessels become dilated. We can use those beta 1 properties to make the heart beat stronger, and therefore compensate for the larger container size. Or, we can use the alpha 1 properties to make the peripheral veins shrink.
Dopamine is also used to treat prolonged anaphylactic reactions. An anaphylactic reaction is a massive, overblown immune response which results in distributive and hypovolemic shock. Recall that hypovolemic shock is hypoperfusion caused by lack of blood or fluid volume, and that distributive shock is hypoperfusion caused by abnormal distribution of blood. Anaphylaxis causes capillaries to become “leaky,” which allows fluid to move out of the capillaries (which causes hypovolemia and low blood pressure) into the third space (which is “abnormal distribution”). Again, just like in septic and cardiogenic shock, dopamine’s beta 1 properties to make the heart beat stronger, and therefore compensate for the loss of volume. Or, we can use the alpha 1 properties to make the peripheral veins shrink, which also compensates for the loss of volume.
Dopamine as several other “odd-ball” uses. Dopimine can be used as a second method of treatment in patients with symptomatic bradycardia who do not respond to atropine. Dopamine can also be used to treat hypotension associated with calcium channel overdoses. Calcium channel overdose causes distributive shock by causing vasodilation, which then causes hypoperfusion.
Some Basics
The dosing for dopamine is 2-10 mcg/kg/minute, increased for effect to maximum of 20 mcg/kg/minute. The effect you’re looking for is increased blood pressure. Dopamine is given as an IV drip. Lower doses (in the 5-10 mcg/kg/minute range) cause beta 1 effects/positive inotropic effects. Higher doses (10-20 mcg/kg/minute range) cause alpha 1 effects/peripheral vasoconstriction.
When should you reach for the dopamine? Indications are: 1) Hypotension, with a systolic blood pressure between 70 and 100 mmHg not resulting from hypovolemia. 2) Cardiogenic shock. 3) Symptomatic bradycardia that does not respond to atropine.
Perhaps more importantly, when should you NOT reach for the dopamine? 1) Dopamine should not be used by its self to manage patients in hypovolemic shock without fluids running. 2) Don’t use dopamine if the patient is allergic to it (duh). 3) Dopamine should not be given to patients with tumors of the adrenal gland, which is called pheochromocytoma.
Some things to keep in mind: dopamine can increase heart rate. It can also induce or make supraventricular and ventricular arrhythmias worse, so it should not be given to patients in SVT, or to patients in ventricular fibrillation. When dopamine is given in doses over 20 mcg/kg/minute, alpha 1 effects dominate and its effects become very much like norepinephrine (also called levophed). Common side effects are nervousness, headache, arrhythmias, palpitations, chest pain, shortness of breath, nausea, and vomitting.
Dopamine can be deactivated by alkalotic compounds, such as sodium bicarbonate. If a patient is taking MAOI’s (monoamine-oxidase inhibitors; a type of antidepressant), they should get a reduced dose of dopamine. Dopamine can cause hypotension if given with dilantin (used to treat seizures).
As always, if you have edits or questions please don't hesitate to share. I write this blog for its educational value, both for those who may be able to use the information, as well as for the re-education I get when i research. As always, follow your local protocols and directives from your medical director.
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