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Get Rid of Dopamine in EMS!, What about Levophed?



In this podcast, we take a look at the ever changing world of EMS and how the critical care arena is playing into the decision to carry specific medications. Dopamine has always been the staple inopressor medication for all EMS ambulances.  We’ve always had access to this medication, but limited access to other excellent vasopressor and inopressor agents.  However, the decision to use the medication, and the paramedic’s understanding of its mechanism of action, weighed heavily on how and when it was utilized.  Obviously, it was used on different levels based on the EMS system, the medical directors preference, and the clinicians comfort level. 

I can say that I’ve used Dopamine more times than I can remember in severe shock states related to cardiogenic shock and associated bradycardia.  I’ve always seen good improvement hemodynamically, and coupled with pacing, Dopamine has allowed me to get most patients to the definitive facility for further cardiac care.  If you notice however, that was in a specific setting; cardiogenic shock secondary to a diseased left ventricle and associated bradycardia.  It’s a good medication for this type of patient. However, most other patient subsets we treat do not have the positive response to Dopamine. 

This podcast lays out a brief overview of how our body responds to the stressors of an acute disease process related to hemodynamic shock states.  With that being said, understanding the basic aspects of volume resuscitation and our venous systems role in compensation, is essential to providing good care. 

Our venous system is essentially a big reservoir that holds nearly 80% of our circulating blood volume, with three-fourths of that volume stored in the venules and small vessels.  This is called our unstressed volume.  It’s important to understand that this unstressed volume is our lifeline.  When our bodies enter into an acute stress situation, the unstressed volume becomes stressed volume. This volume needs to be moving toward the heart in a way that optimizes our overall stroke volume (SV) and cardiac output (CO). 

Understanding fluid resuscitation and how our body responds to fluid makes it much easier in your decision making process.  Fluid resuscitation needs to be provided in moderation.  Gone are the days of dumping 6-10L of fluid in a patient.  Studies have shown that volume replacement greatly affects overall morbidity and mortality.  Fluid volumes should be targeted to 2-3L during the resuscitation process in both trauma and medical patients. 

What does fluid do?  High amounts of NS will increase the patients serum Na+ and Cl-.  Both of these are strong acids and play a big role in overall acid-base balance.  In addition, NS is very acidotic in nature.  With a pH of 6.0, large amounts of NS can lead to other issues.  Studies have shown that NS can increase the incidence of inflammatory cascades, thus starting a vicious cycle that leads to DIC and ARDS.  In addition, large amounts of volume that increase overall right atrial pressures and cause stretching of the right atrium, causes a release of both ANP and BNP.  These two peptides have been associated with destroying the glycocalyx.  The glycocalyx are finger like hair projections that line the blood vessels and aid in keeping osmotic pressure normal and preventing capillary leakage. This breakdown will cause the glycocalyx to fail, thus causing capillary leakage seen in our severe sepsis patients and massive third spacing of volume.

What’s our goal? 

Brain requirement: >60-65mmHg (CPP = 70mmHg)

Kidney:  >65mmHg

The goal in a decompensated patient suffering from hemodynamic collapse is to increase the MAP >60-65mmHg.  We do this by providing hemodynamic support that optimizes flow, not BP.  What do I mean by that?  If we give a medication, like phenylephrine, that has very potent alpha 1 properties, you’ll see a great BP, but is the squeeze so much that it inhibits actual flow?  Yes.  We need to provide just enough squeeze to optimize flow, increase MAP, increase SV and overall CO.  Remember, we need to circulate oxygen rich hemoglobin to our body systems that need that extra oxygen stores.   Patients exhibiting these presentations are in a hyperdynamic state, meaning their oxygen demand is far exceeding what they have available in their dissolved plasma.  We need to understand that in a normal homeostasis, we take in and process 1000mL of oxygen each minute.  However, we only use the plasma stores (2%) for normal, everyday function.  The other 98% is stored on our Hgb for times of high-required oxygenation.   With that being said, patients in a hyperdynamic state need blood flow optimized for all those oxygen rich Hgb to be used for oxygenation and overall ATP production.

Vasopressor selection needs:


1. Increased flow

2. MAP >60-65mmHg

3. Increased SV

4. Increased CO

5. Optimized diastolic filling & clearing





    1.    Great chronotropic effects that will aid in a bradycardic hemodynamically unstable patient that needs the rate help.


    1. Increases urine output on patients that shouldn’t be producing urine         due to their shock state and low MAP

    2.    Gives the clinician a false sense that the patient is perfusing, when they’re actually in profound shock.

    3.    Very narrow therapeutic window – 5-10mcg/kg/min

    4.    Doses greater than 10mcg/kg/min will start reducing CO

    5.    Massive chronotropic effects and increased HR inhibits diastolic filling and clearing.

    6.    High incidence of A-Fib

Norepinephrine (Levophed)


    1.    Excellent venous and arterial effects that will increase preload and afterload.

    2.    Limited HR effects

    3.    Alpha 1 & 2 receptor stimulation

    4.    Optimizes venous return (venous stress volume flow)

In the end, studies have not shown a huge difference in morbidity and mortality associated with the use of Dopamine vs. Levophed.  However, the upside to Levophed is evident and its broad range of positive effects makes it the go-to Inopressor for most clinical presentations needing hemodynamic support.

Check out the studies and decide for yourself. 






Collins. The Endothelial Glycocalyx: Emerging Concepts in Pulmonary Edema and Acute Lung Injury. Anesth Analg 2013;117(3):664-674

Collins. The Endothelial Glycocalyx: Emerging Concepts in Pulmonary Edema and Acute Lung Injury. Anesth Analg 2013;117(3):664-674

Full Text:  Seymour. Prehospital intravenous access and fluid resuscitation in severe sepsis: an observational cohort study. Critical Care 2014;18:533

Marik. The Physiology of Volume Resuscitation. Curr Anesthesiol Rep 2014;epublished September 10th

Full Text:  Bai. Early versus delayed administration of norepinephrine in patients with septic shock. Critical Care 2014;18:532

Abstract: Oba. Mortality benefit of vasopressor and inotropic agents in septic shock: A Bayesian network meta-analysis of randomized controlled trials. J Crit Care 2014;epublished April 28th

Bangash. Use of inotropes and vasopressor agents in critically ill patients. Br J Pharmacol 2012;165(7):2015–2033

Senz. Review article: inotrope and vasopressor use in the emergency department. Emerg Med Australas 2009;21(5):342-51

Overgaard. Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease. Circulation 2008;118(10):1047-56

Debaveye. Is There Still a Place for Dopamine in the Modern Intensive Care Unit? Anesth Analg 2004;98:461–8

Patel. Choice of vasopressor in septic shock: does it matter? Crit Care 2007;11(6):174.

Vincent. Dopamine versus norepinephrine: is one better? Minerva Anestesiol. 2009 May;75(5):333-7

De Backer. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl 2010;362:779-89 



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