In our protocols we have two beta blockers to choose from depending on the patient’s problem. The two are Metoprolol and Labetalol and they are actually quite different in their actions and therefore, their use.

Metoprolol is a selective beta 1 blocker which will specifically block the effects of epinephrine and norepinephrine on the heart. For our purposes this will blunt their chronotropic and inotropic effects thereby reducing CO and blood pressure. Additionally Metoprolol also has been shown to reduce the incidence of post MI arrhythmias.

Labetalol on the other hand is a non-specific beta blocker and also has alpha 1 blocking effects. This alpha blocking effect would make it specifically useful for lowering a high DIASTOLIC pressure as that number is driven primarily by peripheral vascular resistance.

Our protocols allow for Metoprolol is cases of ACS/MI and allow for either one in cases of hypertensive crisis and CVA with associated hypertension. We also can use nitroglycerin in the latter two but NTG has more of an effect on the veins (preload) than the arteries (afterload). I imagine that the choice would be based on whether its the systolic or diastolic that is really high.

(Hat tip Medic 122)

An explanation I found….

Because the aortic valve is tight/stenosed, it restricts the amount of blood being ejected from the ventricle. With nitro (and most other drugs that effect peripheral resistance) the peripheral vessels will dilate. A normal ventricle would be able to ‘relax’ a bit because peripheral resistance is lowered and the heart’s work-load is lessened. However, in aortic stenosis, the afterload (pressure the heart beats against) isnt being dictated by peripheral resistance, but rather the stenosed valve. This stenosed valve is unaffected by nitro (or any other drug) and so the hearts work-load (and amount of ejected blood) stays the same…regardless of nitro/drugs/less peripheral resistance. Giving this patient nitro/drugs can become a big problem because if you dilate out the vessels, and the the restriced cardiac output does not change, you drop your ability to perfuse even more…(you take a hose and turn it on to ‘perfuse’…but when you suddenly dilate/widen the hose while keeping the water supply constant, your pressure will drop…as well as your ability to perfuse…)

This is why people become syncopal and (with pre-existing coronary disease) will experience angina…

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

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.

Many times throughout the Paramedic Program I have come across a drug that has an unexpected use listed in the profile. Not very often are we given a comprehensive explanation as to why this drug works for this other use and it is left to us to try and figure this out. One example that I have seen recently is the use of Glucagon for beta blocker overdose. Glucagon is a hormone used in diabetic emergencies; its use for beta blocker overdose is actually pretty simple once it is explained.

This pharmacology booklet was handed out the other night, it is very useful and comprehensive. This was originally prepared for the St Vincent’s class and any references to protocols refer to NYC REMAC (as of 2006).

Sample page:

_________

También encontré un gran recurso si usted está buscando para comprar en línea de equipos médicos. Ellos llevan las máquinas de EKG, máquinas de ultrasonido, así como desfibriladores

1-5 mcg – Renal Vasoconstriction

5-15 mcg – Peripheral Vasoconstriction

15-20 mcg – Mesenteric Vasoconstriction

Mix: 200mg or 400mg into 250cc of NS

When using a 60gtts drip set each gtt = 13.3mcg/ml for the 200/250 concentration or 26.6mcg/ml for the 400/250 concentration.

Contraindicated in Hypovolemia and exsanguination

Indicated: Cardiogenic Shock, shock secondary to bradycardia, septic shock

1/25/09

Some notes on Neuromuscular-blocking drugs: -most taken from Wikipedia

These drugs fall into two groups:

• Depolarizing blocking agents: (succinylcholine) These agents act by depolarizing the plasma membrane (cell membrane) of the skeletal muscle fiber. This persistent depolarization makes the muscle fiber resistant to further stimulation by ACh.
  • Depolarizing blocking agents work by depolarizing the plasma membrane of the muscle fiber, similar to acetylcholine. However, these agents are more resistant to degradation by acetylcholinesterase (AChE), the enzyme responsible for degrading acetylcholine, and can thus more persistently depolarize the muscle fibers. This differs from acetylcholine, which is rapidly degraded and only transiently depolarizes the muscle.
  • There are two phases to the depolarizing block. During phase I (depolarizing phase), they cause muscular fasciculations (muscle twitches) while they are depolarizing the muscle fibers. Eventually, after sufficient depolarization has occurred, phase II (desensitizing phase) sets in and the muscle is no longer responsive to acetylcholine released by the motoneurons. At this point, full neuromuscular block has been achieved

     

• Non-depolarizing blocking agents: (e.g. Vecuronium )These agents constitute the majority of the clinically-relevant neuromuscular blockers. They act by blocking the binding of ACh to its receptors, and in some cases, they also directly block the ionotropic activity of the ACh receptors.

Class:

Depolarizing Neuromuscular Blocker

Description:

Succinylcholine is a short acting, depolarizing skeletal muscle relaxant used to facilitate endotracheal intubation.

Mechanism of Action:

Like acetylcholine, Succinylcholine combines with cholinergic receptors in the motor nerves to cause depolarization. Neuromuscular transmission is thus inhibited, which renders the muscles unable to be stimulated by acetylcholine. Complete paralysis is obtained within 60 to 90 seconds, and persists for approximately 4 to 5 minutes. Effects then begin to fade, and a return to normal is seen within 6 minutes. Muscle relaxation begins in the eyelids and the jaw, and then progresses to the limbs, abdomen, diaphragm, and intercostals. Succinylcholine has no effect on consciousness.

Indications:

Succinylcholine is used to achieve temporary paralysis when endotracheal intubation is indicated, and muscle tone or seizure activity prevents it.

Contraindications:

Known hypersensitivity, penetrating eye injuries, and narrow-angle-glaucoma.

Precautions:

Succinylcholine should not be administered unless personnel skilled in endotracheal intubation are present and ready to perform the procedure. Oxygen and emergency resuscitative drugs should be readily available. Cardiac arrest and ventricular arrhythmias have been reported when Succinylcholine was administered to patients with severe burns and severe crush injuries.

Side Effects:

Succinylcholine can cause wheezing, respiratory depression, apnea, aspiration, arrhythmias, bradycardia, sinus arrest, hypertension, hypotension, increased intraocular pressure, increased intracranial pressure.

Interactions:

Lidocaine, Procainamide, beta-blockers, magnesium sulfate, and other neuromuscular blockers enhance the effects of Succinylcholine.

Dosing: 1.5mg/kg IVP

Class:

General anesthetic and adjunct to general anesthesia

Description:

Etomidate is a short-acting, intravenously administered sedative hypnotic. Etomidate has a rapid onset of action and recovery. It has minimal cardiac and respiratory-depressive effects and causes no histamine release, so it is useful in patients with compromised cardiopulmonary function.

Mechanism of Action:

Etomidate appears to facilitate GABAminergic neurotransmission by increasing the number of available GABA receptors, possibly by displacing endogenous inhibitors of GABA binding. Etomidate produces clinical responses such as hypnosis, elevations in arterial carbon dioxide tension, reduced cortisol plasma levels, and a transient 20—30% decrease in cerebral blood flow. Its effects are at least partially due to depression of the brainstem reticular formation.

Indications:

Induction of general anesthesia.

Contraindications:

Use with caution in the elderly and in patients with hepatic disease because they are more likely to develop etomidate-related adverse reactions.

Precautions:

Use with caution during lactation.

Side Effects:

Skeletal muscle: Myoclonic skeletal muscle movements, tonic movements. Respiratory: Apnea of short duration, hyperventilation or hypoventilation, laryngospasm. CV: Either hypertension or hypotension; tachycardia or bradycardia; arrhythmias. GI: Postoperative N&V. Miscellaneous: Eye movements, averting movements, hiccoughs, snoring.

Interactions:

Etomidate potentiates the effects of CNS depressants such as ethanol, general anesthetics, local anesthetics, antidepressants, H1-blockers, opiate agonists, skeletal muscle relaxants, phenothiazines, barbiturates, and benzodiazepines. Concurrent use of antihypertensive agents and etomidate can result in hypotension. This is particularly true if any of the following agents are used with etomidate: calcium-channel blockers, diazoxide, mecamylamine.

Dosing: 0.3mg/kg IVP