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            Dopamine works in the body by binding to alpha 1 and beta 1 receptors to increase peripheral arterial and venous constriction and increase cardiac contractility and heart rate. Alpha 1 receptors are found in smooth muscle vasculature and control vasoconstriction and Beta 1 receptors are typically found in the heart and control inotropy and chronotropy. In lower doses from 1-5 mcg/kg/min it mostly affects the renal arteries and in doses from 5-20 mcg/kg/min, it increases its inotropic and chronotropic effects on the heart and systemic vasoconstriction. This is important because in lower doses it does not affect cardiac contractility and may not increase blood pressure; it may, however, increase urinary output and also may improve pulmonary edema due to increased fluid excretion from the body. Dopamine is used to increase blood pressure in patients that are hypotensive due to cardiac or septic shock. It is contraindicated in hypovolemic shock as the patient needs fluid replacement and blood and not to increase vasoconstriction which can lead to tissue ischemia.

            How do you know when to use Dopamine? Dopamine is useful in cases where the patient is hypotensive and likely vasodilated due to cardiac arrest, anaphylaxis, or sepsis, or when the heart is not contracting hard or fast enough. This is especially useful after a cardiac arrest in which fluids have been given but the patient is still hypotensive and you do not want to fluid overload them and cause pulmonary edema. It can also be used in patients with a heart block and bradycardia in order to help maintain blood pressure and increase the heart rate. In short, Dopamine can be considered if hypovolemia has already been addressed and the patient is still hypotensive and the reason is bradycardia or diffuse vasodilation. That being said, Dopamine is not considered a first-line medication in sepsis or anaphylaxis as Epinephrine would be used to treat this first, but if not available or per medical direction, Dopamine can also be used in these cases.

            Why is Dopamine not a first choice for treating patients with bradycardia or vasodilation? Dopamine also has a long list of side effects and negative effects and a narrow therapeutic window. Some of the adverse effects of Dopamine include Ventricular arrhythmias, atrial fibrillation, ectopic beats, hypertension, increase in anginal pain, palpitations, widened QRS complex, abdominal pain, nausea, vomiting, headache, anxiety, and sodium/potassium imbalances. Why is this? The ionotropic effects cause increased oxygen demand by the heart and the increased contractility of the heart can cause hypertension. The chronotropic effects can cause dysrhythmias due to causing more than once pacemaker cell to fire or causing disorganized firing in the heart. The increased anginal pain can come from the increased load on the heart as it is forced to work harder and also from the vasoconstriction. The abdominal pain and nausea/vomiting come from vasoconstriction in the gastrointestinal system and the headache can be from vasoconstriction as well. Sodium and potassium imbalances can come from increased urine excretion. And the anxiety and many other effects come from the effects that mimic the sympathetic nervous system as Dopamine is a sympathomimetic. Why is this important to know? We often have patients with multiple co-morbidities and when considering administering a strong sympathomimetic we need to consider how it will affect other systems in the body, not just the blood pressure. We do not want to solve the blood pressure but cause another problem instead. Therefore, if the bradycardia can be effectively managed with Atropine that is preferable as it has less of a systemic effect and is not going to cause diffuse vasoconstriction and possible tissue ischemia.

            So you have decided to give Dopamine to our patient, but how do you do it? Dopamine can be given intravenously and intraosseously. Depending on your agency and what you carry you may need to mix up an infusion or you may already have premixed bags. The starting concentration will vary based on your department but Dopamine is commonly carried in 40, 80, or 160mg/ml vials or in 80, 160, or 320 mg/100ml bags. So become familiar with what your agency carries. If you have the vials you will need to mix it into a bag to create an infusion. It is important to remember to use a microdrip or (60gtt/ml) set as you will need to titrate the drops to give the proper dose to your patient. Say you have a 160mg/100ml solution and you have an 80 kg patient and you are going to start at 5 mcg/kg/min. You know that means you need 400 mcg/min. Your solution is 1.6mg/ml or 1600 mcg/ml. How many drops per minute should you administer? Well you know you have 1600 mcg/ml and you need 400 mcg/min so you need 0.25 ml/min. And your drip set is 60 gtt/ml so you need 15 gtt/min, or 1 drop every 4 seconds.

            Now that you have your drip running what do you do next? It is important to constantly monitor your patient to determine if the drip is having the intended effect. Is the blood pressure rising, is the heart rate increasing? Are they appearing to improve or do they appear to be worsening? Are they developing any adverse effects such as widening QRS, dysrhythmias they did not have before if they are conscious are they complaining of chest pain, abdominal pain or nausea? Another thing to remember is to frequently check the patency of the IV or IO as Dopamine can cause tissue ischemia if it extravasates due to being a vasoconstrictor. Use the minimum dose necessary to achieve your desired results. Another thing to remember with Dopamine is it is not compatible with sodium bicarbonate. So if you are administering sodium bicarbonate and Dopamine you will need two separate IVs and lines.

            In summary, in patients that are bradycardic and not responding to Atropine, or patients that are hypotensive due to vasodilation such as cardiac arrest, sepsis, or anaphylaxis and are not hypovolemic, Dopamine may be used to improve their outcomes. It is a potent sympathomimetic and can be effective at increasing vasoconstriction, and the chronotropic and inotropic actions of the heart.

View Sources

Girardeau, R. P. (2014, September 15). Use of Antihypotensive Medications in Shock Patients. Retrieved from https://www.jems.com/articles/print/volume-39/issue-9/features/use-antihypotensive-medications-shock-pa.html


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