pressors and sepsis

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I was just wondering if anyone out there can tell me why Levophed is the pressor-of-choice over Dopamine for Septic Shock pts? :specs:

Thanks

Specializes in CTICU.
Wow thanks guys! I have been in ICU for 9 mos now, and i always knew that Dopamine wasnt used as much because of the higher HR, but i never realized it had anything to do with O2..not sure if i just missed this information while working with these patients, or if it wasnt presented to me at all..but i know now! eh..i learned something after all :)

In ICU, especially when learning, it's always good to ask why you're doing certain things. They wanted to avoid tachycardia.. why?? Because that will increase oxygen consumption and reduce supply.

Specializes in CCRN, MICU, CCU.

According to the fellow on my unit, the literature shows greater survival using levo for sepsis and SIRS. From what I could find, it does in fact. Dopa, at lower levels, has almost purely beta stim whereas at higher levels has almost purely alpha. Due to hypotensive compensation, hr is usually elevated and more beta will not help CO (even despite its ino/chronotropic effects). Levo, is almost purely alpha 1 and 2 but at higher levels will stim. beta. In most cases, septic shock/ SIRS is a peripheral vascualr resistance issue because of leaky vessels. We need to "squeeze" those vessels first to increase preload: Levo will increase preload.

Dopa will increase cardiac 02 consumption. However, this is not as much concern in septic pt with no s/s of myocardial infarct.

Specializes in ICU/ER.

Same as the others on the Levo and Dopamine-however while there may not be much data on Vasopressin I have seen it work when high dose Levo, Neo, and Dopamine have failed.

Dopa will increase cardiac 02 consumption. However, this is not as much concern in septic pt with no s/s of myocardial infarct.

Yes, it is as much of a concern in the non-cardiac patient as those with a cardiac history. Septic shock is not just an issue of periph. vascular problems. It also involves oxygen demand vs oxygen delivery to the tissues.

Specializes in SICU/CVICU.
Hypotensive septic pts usually have a high HR already. Dopamine increases the HR. Levophed doesn't, making it the drug of choice most of the time, there is always an exception to the rule though.

Levophed does increase heart rate some as it's a potent alpha AND beta adrenergic inotropic-vasopressor. Every patient will respond differently, but there is a breaking point where the chronotropic beta effect will kick in and you'll start to see an increase in their heart rate. Maybe that will happen at only 5mcg or maybe it's 50mcg. But none the less, it's important to recognize that some patient's heart rates will not tolerate levophed at higher doses.

Yes, it is as much of a concern in the non-cardiac patient as those with a cardiac history. Septic shock is not just an issue of periph. vascular problems. It also involves oxygen demand vs oxygen delivery to the tissues.

I think the critical issue is that the SIRS-sepsis-septic shock cascade involves significant myocardial depression; whatever it is in the inflammatory process that causes vasodilation (cytokines etc), myocardial contractility is impaired as well.

The O2 extraction defect at the peripheral tissue level is one thing. The relative myocardial stunning is another. Cardiac and noncardiac pts suffer the same process, but those w/ underlying heart dz will become impaired sooner.

Norepi will give you a much more potent chronotropic and pressor response than Dopa, which will cause the above mentioned tachyarhythmias etc when given at the doses needed for alpha effects (15-20 mcg +.....)

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