Dopamine and other useful Paramedic Drips

My quick and easy way….

400mg in a 250ml bag yields:

• 1600µg per ml
• 26.6µg per gtt (60 gtt set)

So if you need to calculate a drip for a 70kg patient you could do this:

70kg x 5µg (example dose) = 350µg/min . 350/26.6 = 13.15 gtts/min

Works for me…. but some prefer the regular dopamine clock so i have included that below

The clock method

Drug Preparation Rate

Amiodarone (3mg/cc) 150mg in 50cc NS

• 0.5mg/min=10gtts/min

Dopamine (800µg/cc) 200mg in 250cc NS

• 200mcg/min=15gtts/min
• 400mcg/min=30gtts/min
• 600mcg/min=45gtts/min
• 800mcg/min=60gtts/min

Dopamine (1600µg/cc) 400mg in 250cc NS

• 400mcg/min=15gtts/min
• 800mcg/min=30gtts/min
• 1200mcg/min=45gtts/min
• 1600mcg/min=60gtts/min

Epinephrine (4mcg/cc) 1mg in 250cc NS

• 2mcg/min=30gtts/min

Lidocaine (4mg/cc) 1G in 250cc NS

• 1mg/min=15gtts/min
• 2mg/min=30gtts/min
• 3mg/min=45gtts/min
• 4mg/min=60gtts/min

Procainamide (20mg/cc) 1G in a 50cc NS

• 20mg/min=60gtts/min
• 30mg/min=90gtts/min

Procainamide (4mg/cc) 1G in 250cc NS

• 1mg/min=15gtts/min
• 2mg/min=30gtts/min
• 3mg/min=45gtts/min
• 4mg/min=60gtts/min

I always wondered about whether C Collars were really effective at stabilizing the C-spine, now it turns out that it may actually cause more harm than good. I always wondered because of how many times I’ve seen improperly placed c-collars, but this study says that even, or specifically, properly placed c collars actually lift the head off the neck and can cause vertebral separation at C1-C2 of 7.3mm! Do we go back to manual stabilization and then stabilize to backboard with head blocks only? Interesting stuff.

See these the study published in JEMS this month.

‘Distracting’ Injuries Immobilization study presents wake-up call

Also see this discussion about the study.

The other night while on ALS rotations I came across the following patient.

Dispatch info: Elderly Male AMS. Diabetic history.

On arrival find an 84 year old male sitting at table in no apparent distress. Wife states that he been sleeping a lot and just woke up after a 20 hour sleep. Patient is AxOx3 denies any pain or distress and states that his wife was nervous because he wasn’t answering properly. Glucose stick reads 119. Hx of HTN, NIDDM and Asthma.

Airway is patent, breathing is eupneic and color and temp are normal. Lungs reveal an end expiratory wheeze in upper left lobe and nearly absent lung sounds in all other fields. SpO2 is 79% on room air. EKG is NSR as is 12 lead. No edema noted.

Turns out patient is taking a strong narcotic based cough medicine for a persistent productive cough x 4 days, possibly the cause of his lethargy (the narcs that is).

My treatment plan was hi-con O2 and transport. (15 lpm had brought his sat up to 98%). My preceptor wanted to treat the wheeze with albuterol and ipratropium which I thought was unnecessary. She got her way and a treatment did nothing for his slight wheeze and sat was already at 98%.

A while later when I returned to the ER I confirmed that his CXR showed a bilateral pneumonia just as I had suspected.

Question; do we really need to treat every wheeze? If o2 corrected the saturation problem do we need to throw a drug in too?

Copied from Dr. Ex-Medic

I don’t know how much things have improved in more than a decade, but my paramedic text (circa 1997) has exactly 2 references to sepsis or septic shock in its index.  One is a single sentence (not totally correct, though not totally incorrect either, emphasis in original):  ”Septic shock, for example, is caused by the release of an endotoxin from several Gram-negative bacteria.”  The other reference leads to a full page of information, half of it bullet points…in the “Pediatric Medical Emergencies” section.  There is not a single direct reference to adult sepsis in the entire book.  In addition, I’ve not seen any paramedic agencies with sepsis protocols, although they undoubtedly exist. (Current texts have a lot more reference to sepsis and septic shock – ed.)

Recent research might someday change this.  A recent small study looked at just 52 ambulance-delivered patients with severe sepsis; just under half got fluids.  (In case you’re wondering how it took 2 years to get just 52 study patients, the study only looked at patients with severe sepsis–963–then cut out those not brought in by ambulance–down to 216–and further cut out those who didn’t receive “early goal-directed therapy” (EGDT).  Of those final 76, 4 had no EMS tripsheets (!), and 20 were brought in by BLS ambulance, and couldn’t properly be studied for comparison.)

Important bit of information for background purposes:  EGDT is a bundle of treatments intended to be performed early in the patient’s hospital course, with specific treatment goals in mind including blood pressure, central venous pressure, and central venous O2 saturation.

While the numbers were too small to achieve statistical significance, patients receiving prehospital fluid tended to be more likely to achieve these goals within 6 hours of arrival; the data were strongest for the BP goal.  This is despite the fluid group having an average initial SBP 20 points lower, both on-scene and on arrival at the ED.  (Appropriately, then, the apparently sicker fluid group had a higher mortality–but again, not a statistically significant number.)

So is it appropriate for an EMS agency to develop sepsis protocols?  Certainly.  Is it going to help anybody?  Well, this isn’t proof, but a very suggestive hint that it just might.

I’ve been doing my ER internships at a busy ER in NYC and have to agree that nearly every septic patient came in without any sort of fluids running. These are patients that are generally febrile and severely hypotensive. This particular ER has a “Code Sepsis” protocol, but why wait until the ER to start fluids? Some of the patients present with a MAP of 50-60…That can’t be good for long term survival.

Vasopressin, also known as ADH or anti-diuretic hormone stimulates the AVP1A receptors (AVPR1A) which are present in the brain, kidneys, liver and vessels. It causes kidney water retention, peripheral vasoconstriction in higher doses, the release of several clotting factors and gluconeogenesis. Also, per this study it stimulates glycogen breakdown in the liver, similar to the effects of glucagon.

Gluconeogenesis is the second way the body maintains blood sugar levels. (The first is glycogenolysis, the body’s conversion of glycogen stores into glucose) In gluconeogenesis, the body generates glucose from non-carbohydrates such as lactate (lactic acid, milk acid), glycerol (glycerin) and glycogenic amino acids.

I’m not sure how water retention and glucose generation are related but I’m still thinking There are quite a few other seemingly unrelated actions that vasopressin causes on other receptor sites so I’m not sure the actions have to be related.