Pressors

Pressing on!

It's important to know these drugs inside out and learn as much as possible about them, so you can use them appropriately. When it comes down to it, if a patient needs a pressor, just pick one and go with it. There are no large scale studies that say that one is better than the other for initial blood pressure management. However, there are a lot of smaller studies that help identify which drug should go where.

Epinephrine:

This is the first agent that needs to be understood. It does everything and is very potent. It is used when patients die (code blue situations) and is quite useful. Epinephrine activates A1, A2, B1, B2 receptors equally and increases cardiac output, systemic vascular resistance and increases heart rate. This drug is rarely used as a pressor unless the others haven't been working. Don't be afraid to use this as a drip medication if nothing else seems to be working. This should not be a first line agent in sepsis (or most other conditions), but don't be afraid to use it if all others are failing.

Norepinephrine:

Slightly weaker than epinephrine, norepinephrine activates the A1 receptors and thereby mainly increase systemic vascular resistance (your arteries constrict). At much higher doses it can activate B1 receptors, but usually not. Norepinephrine does not increase heart rate or cardiac output, don't let anyone fool you into not starting norepinephrine because the "heart rate is too high". There is also evidence that norepinephrine improves perfusion pressure to vital organs, especially splanchnic, renal, and glomerular blood flow and has shown to improve GFR and urine output in septic patients. Also does not raise ICP for head trauma patients, whereas dopamine raises intracranial pressure.

Phenylyephrine:

This is the most targeted one towards A1 that there is. Phenylephrine activates A1 only and very potently. Causes a large increase in systemic vascular resistance and thereby raises blood pressure. The single advantage of phenylephrine is that it has been approved to be given through a peripheral IV and does not have to go through a central line at it's lowest doses. (only if mixed in the correct concentration). But be careful if your dose starts to get higher and higher. You can use this agent as a temporary agent while waiting for a central line. The problem is that this drug also causes constriction of your carotid arteries, your coronary arteries, your splanchnic arteries, your renal arteries. So you end up cutting off circulation to your brain, heart, intestines, kidneys and that is not good. Many hospitals have removed PE from their campii and no one is allowed to use it. It should probably never be used except as a last resort. If someone has bad atherosclerosis (plaques in their arteries), make sure they are never on this drug. Bottomline: Don't ever use!

Dopamine:

Is the precursor to norepinephrine (which is the precursor to epinephrine). It works as a catecholamine in and of itself (like epi and norepi) and by causing release of catecholamines in nerve terminals and acts on it's own dopamine receptors. It's the one that does it all! And that's usually why people use it first line if they aren't sure why someone's blood pressure is not improving. At low doses, dopamine primarily works on dopamine receptors in the renal, mesenteric, and coronary arteries augmenting blood flow to those arteries. But there is no evidence that augmenting this blood flow improves outcomes. At medium doses, you start to see some A1 and a lot of B1 activity. This is usually why you see an increase in heart rate and a lot of ectopy (extra, unusual beats). At higher doses, it basically becomes norepinephrine. It's main effects are by stimulating the A1 receptors. But it still stimulates B1 and the dopamine receptors, so you get an increase in heart rate as well as systemic resistance. Dopamine is usually started because it treats almost everything. No matter what is causing the hypotension, start dopamine and work your way up till it works. Of course, if your heart rate starts to skyrocket or you see a lot of unusual beats (PVCs, etc), you will probably have to change to norepinephrine. Most crash carts have dopamine in them and most ER docs start patients on dopamine if they are unsure. Of course, septic patients (that are really septic) will require much more A1 stimulation than what dopamine can provide, so you will need to switch them eventually if dopamine is not getting the job done.

Dopamine can not be run through a peripheral IV. Don't let anyone fool you! I have heard this misnomer many times. Dopamine is toxic to tissues if it leaks into tissues or the IV site infiltrates. The only one that can be used in a peripheral IV is phenylephrine and ONLY if it is mixed correctly. Otherwise, stop being lazy and start a central line!

Dobutamine:

Dobutamine is the best when it comes to getting the heart to squeeze harder. That's dobutamine's main job. It is the most purely B1 agent we have. However, it can also increase heart rate. This makes it ideal to use in the heart failure setting. If a patient is hypotensive because their heart isn't pumping strong enough, dobutamine should be your agent of choice. Pure B1! Dobutamine does have some A1 effect, but this is minimal and unpredicatble. Sometimes it raises your systemic resistance, sometimes lowers it, sometimes has no effect at all. Dobutamine does not increase heart rate as much as dopamine does. Dopamine is the king of the hill when it comes to increasing heart rate. So if it is heart failure with weak contractility, use dobutamine. If it is heart failure due to mainly a slow rate (rare), think dopamine. If the patients has severe hypotension, dobutamine's effects on blood pressure intially are very unpredictable. If the patient has severe hypotension, use dobutamine with another pressor agent like norepinephrine so they can work together. If a patient has ischemic heart disease or some other reason why their heart may not be receiving as much oxygen as it should, speeding up the heart rate will only make this worse. Try not to use agents that increase heart rate if they have ischemic heart disease.

Vasopressin:

Very few people understand this drug. It has many actions on the body. It is a hormone called anti-diuretic hormone. It acts via the V1 receptors. No one is quite sure how or why vasopressin improves blood pressure but it works. Septic patients usually lose sensitivity to their endogenous vasopressin, and their posteror pituitary can't make it possibly due to hypoperfusion, so they may need exogenous vasopressin. It seems like it only works in patients that have a deficiency in vasopressin (duh!). In normal people, vasopressin does nothing to blood pressure. However, in septic patients, it helps improve their blood pressure and allows us to taper doses of the other agent being used (normally norepinephrine). You normally don't want patients on the highest dose of norepinephrine or phenylephrine for too long as it causes vasoconstriction of their veins and arteries and can lead to fingers, ears, penises, and noses necrosing and falling off. Adding vasopressin allows us to lower the dose of the other agent. Vasopressin has never been shown to improve mortality and morbidity in patients. However, it has been shown to reduce the number of days on a pressor and the length of stay in the ICU. That's good. Vasopressin doesn't work by itself. It has to be administered with norepinephrine to actually do anything. It also seems that only some patients benefit from vasopressin, probably the ones that aren't making it anymore due to their sepsis. Those are probably the same ones that require stress dose steriods (hrydrocortisone IV).

One problem with vasopressin is that it can constrict blood flow to the splanchnic (mesenteric) circulation as well as the myocardium. If a patient has problems with ischemia and or poor circulation to begin with, they may not be a good candidate for vasopressin. If you think a patient has dead gut (ischemic bowel), find another drug to use, vasopressin will exacerbate it. One of the ways to treat a bad GI bleed is with vasopressin, it cuts off mesenteric and splanchnic circulation. Of course, the GI bleed dose is much higher, but you still have to remember this when a patient has ischemic gut issues. The pressor dose of vasopressin is much lower than the GI bleed dose, but don't let that fool you. If you start a patient on vasopressin and their bicarb on their next bmp starts to fall and they have a metabolic acidosis... go feel their belly and stop the vasopressin. Check an arterial lactic acid level to be sure, but the vasopressin isn't helping!