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.

Glucagon – Profile

Glucagon is a hormone produced by the alpha cells in the pancreas, it is opposed by insulin, a hormone produced by the beta cells in the pancreas. During periods of low blood sugar, for example, between meals, glucagon is secreted into the bloodstream which then begins the process of breaking down glycogen stores in the liver and muscle (glycogenolysis) to increase available blood glucose. After meals and at time of increased blood sugar, insulin is secreted to allow the cells to take up circulating glucose and stimulate the formation of glycogen (glycogenesis). Glucagon is also released during periods of stress to increase available energy during the fight or flight response. Additionally, glucagon possesses an inotropic quality, increasing the contractility of the myocardium thereby increasing stroke volume and cardiac output.

Glucagon – Use in Emergency Medicine

As an emergency drug, glucagon is administered to patients in severe hypoglycemia/insulin shock where IV access is unavailable. The expected response takes around 10 minutes to start and will only work if the patient has adequate glycogen stores available. This will not work for starving patients and alcoholics. The dose is 1mg IM.

Its use for beta blocker and calcium channel blocker overdose relies on its inotropic properties. Being that the beta adrenergic receptors are being blocked, epinephrine cannot exert its inotropic effect on the heart. Glucagon, in high doses (initial dose of 3-5mg IV) may have enough of an inotropic effect to increase cardiac output and blood pressure. For CCB overdoses it works the same way, just this time it the calcium channels that are blocked which also cause reduced contractility.

Glucagon is also used in cases of anaphylactic shock when epinephrine is not working (usually due to beta blocker use). The dose in this case would be 1-2mg IV over 5 minutes.

Hope it’s clear now, worked for me

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

(Versed)

Class:

Sedative and Hypnotic

Description:

Midazolam is a benzodiazepine with strong hypnotic and amnestic properties.

Mechanism of Action:

Midazolam is a potent but short-acting benzodiazepine used as a sedative and hypnotic. It is three to four times more potent than Diazepam. Its onset of action is approximately 1.5 minutes when administered IV. Midazolam has impressive amnestic properties, and like other benzodiazepines, it has no effect on pain.

Indications:

Midazolam is used as a premedication before cardioversion and other painful procedures.

Contraindications:

Known hypersensitivity, narrow angle glaucoma, shock, depressed vital signs, and alcoholic coma.

Precautions:

Emergency resuscitative equipment must be available prior to the administration of Midazolam. Midazolam has more potential than the other benzodiazepines to cause respiratory depression and respiratory arrest.

Side Effects:

Laryngospasm, bronchospasm, dyspnea, respiratory depression and arrest, drowsiness, altered mental status, amnesia, bradycardia, tachycardia, premature ventricular contractions, and retching.

Interactions:

The effects of Midazolam can be accentuated by CNS depressants such as narcotics and alcohol.

Dosage and administration

• Adults:
  • For sedation – 2.0-2.5 mg slow IV over 2-3 minutes. May be repeated to max of 0.1mg/kg
• Peds: Not recommended

1/7/09 (UPDATED 1/11/08

RSI (Rapid sequence intubation)

Indications:

• Trauma with GCS of <9, with gag reflex or significant facial trauma
• Closed head injury – major stroke
• Burn patients
• Any patient who can’t maintain an airway, still has gag reflex,- with possibility of successful intubation

6 ps

• Prep
  
• Preoxygenate, sat at 100% (do not bag while patient is under, all sphincters are relaxed)
• Pretreat (medicating)
  • LOAD
    • Lidocaine – 1-1.5 mg/kg (suppress gag reflex – gag can increase ICP)
    • (Opiods – Fentanyl 3mcg/kg IV – decrease sympathetic response – also for AA or ICP)
      
    • Atropine –0.02 mg/kg – decreases parasympathetic response (also decreases brady affect of Succinylcholine- especially peds)
    • (Defasiculating dose – 10% of normal dose (non-depolarizing) – 2-5 minutes before Succinylcholine)(
      Vecuronium 0.1mg/kg) -
      

       

• Induction (sedation)
  
  • Etomidate – 0.3 mg/kg
    • Rapid onset – 15-45 sec
    • Short duration – 3-12 min
  • Midazolam (Versed) – 0.1-0.3 mg/kg – usual dose is 2 mg because causes hypotension
    • 30-60 sec onset
    • 15-30 minute duration
    • Amnesic effects
• Paralysis (not performed in NYS by paramedics)
  
  • Bind to ACH nicotinic receptors
  • Depolarizing
    • Succinylcholine (sux) – binds to Ach receptors blocking contraction of muscle
    • 1-2mg/kg – max 150mg
    • Peds 1-1.5mg/kg
      • Hyperkalemia (renal problems, significant muscle damage, burn patients, )
      • Bradycardia
      • Dysrythmias
      • hypertension
  • Non-depolarizing
    • Do not cause fasciculations
    • Longer onset
    • Longer action
  • Paralyzed patient has no definitive airway
  • Must be ventilated manually throughout duration of paralysis
  • No affect on mental status – MUST sedate
• Placement of tube
  
• Post intubation management

12/1/08 (Also see previous post)

Drugs. Used to reverse, prevent or control disease

• History/allergies
• Physical findings
• Formulate a plan

   

Sources

• Plants , opiates, atropine, digitalis (purple foxglove)
• Animals
• Minerals
• Laboratory

Drug Standards and legislation

• Pure Food and Drug act of 1906 – first legislation in US
• Harrison narcotic act of 1914 – regulated import of narcotics
• Federal food drug and cosmetic act – 1938 – required labeling, side effects, habit forming, etc
• Narcotic control act 1956 – increased penalties for breaking Harrison act
• Controlled substance act 1970 – categorized drugs , storage and record keeping rules, supersedes Harrison act, created drug schedules based on abuse potential, etc
  • Schedule I – high abuse, no accepted medical use – LSD, Cocaine, heroin, Marijuana
  • Schedule II – high abuse , accepted medical use – may lead to severe addiction – opiates, amphetamines, barbiturates,
  • Schedule III – lower abuse potential, some physical or psychological dependence –
  • Schedule IV – lower abuse potential, some physical or psychological dependence –Phenobarbital, valium
  • Schedule V – lowest potential for abuse. Cough meds with codeine
• Drug Names
  • Chemical name: describes drug’s chemical makeup
  • Generic name: general name for drug, usually named by company that originally manufactured the drug, many times a shortened version of chemical name
  • Trade name: Unique name given by original manufacturer and registered with the FDA (Capitlaized)
  • Official name: after generic name is approved and drug is approved by the FDA it is listed in the USP and call generic name USP

Black box warnings

PNS > Autonomic NS

Nerve fibers

• Visceral afferent (sensory) organs to CNS
• Visceral efferent (motor) from CNS to internal organs , glands, smooth and cardiac muscle

Double set of nerve fibers

• Sympathetic (adrenergic) exits from thoracic and lumbar regions
  • Norepinephrine
  • Epinephrine
  • Receptors (produce when stimulated)
    • Alpha 1 – peripheral vasoconstriction, mild bronchoconstriction, speed metabolism (Smooth Muscle, blood vessels etc)
    • Alpha 2 – release of Norepinephrine (bladder, prostate)
    • Beta 1 – increase heart rate, cause cardiac muscle to contract, produce automaticity, triggers cardiac electrical conduction
    • Beta 2 – vasodilatation, bronchodilation

   

• Parasympathetic (cholinergic) exits from cranial and sacral regions
  • Acetylcholine (Ach) –Neurotransmitter
  • Receptors (produce when stimulated)
    • Muscarinic – SLUDGEM if over stimulated – The specific antidote is atropine – also give 2-Pam (Pralidoxime Chloride)
    • Nicotinic – excitatory response, dilated pupils (mydriasis) MTWT(h)FS – mydriasis, tachycardia, weakness, hypertension, fasciculations, sweating

Both function continuously, occasionally reciprocally, most organs dominated by one system

Path of a nerve impulse: Preganglionic neuron > Ganglia> postganglionic neuron >neuroeffector transmitter > organ

Classes

• Cholinergic – parasympathomimetic
• Anticholinergic – parasympatholytic
• Adrenergic – sypathomimetic
• Adrenergic blocking – sympatholytic

Terms

• Dissolution
• Pharmacokinetics
• Pharmacodynamics
• Drug absorption
• Solubility
• PH 7.35 – 7.45
• Concentration
• Therapeutic Level
• Dosage forms (Drug Forms – AAOS page 7.15)
• Blood brain barrier
• Placental barrier
• Biotransformation
• Potentiation – To enhance or increase the effect of (a drug). To promote or strengthen (a biochemical or physiological action or effect).
• Agonist – triggers an action (provoke physiological response)
• Antagonist – blocks action (prevent physiological response)
• Affinity
• Efficacy
• Peak level
• Therapeutic level
• Half life
• Onset of action

Therapeutic index

11/5/2008 (basic info) (notes added on 12/1/08)

What do you need to know about a drug before you administer it? EVERYTHING

Gather Information (Get to know your patient, avoid potentially dangerous interactions)

• Family
• Go looking (Fridge, medicine cabinet)
• Medic alert tags

Pt Rights

• Right to refuse
• Right to be fully informed of effects, side effects etc

Different meds target different areas of the body

• CNS (control Center, interprets stimulus)
• PNS (All nerves outside brain & spinal cord) (The main function of the PNS is to connect the CNS to the limbs and organs)
  • Somatic nervous system – Voluntary control of body movements
  • Autonomic nervous system – Mostly involuntary, maintains homeostasis
    • Sympathetic Nervous System (SNS) – Fight or Flight, Dominant during stress (hypoglycemia, hypothermia, shock, etc.) or activity, produces adrenaline.
    • Parasympathetic Nervous System (PSNS) Rest and repose, Limited control
  • ganglia – Ganglia provide relay points and intermediary connections between different neurological structures in the body, such as the peripheral and central nervous systems.

Drug Forms

• Liquids
  • Solutions – dissolved in water
  • Suspensions – finely divided drug suspended in liquid (eg. Oil & water)
  • Extract
  • Elixir – syrup with alcohol
  • Tincture – dilute alcoholic extract of a drug
  • Spirits
• Solids
  • Capsules
  • Pills
  • Powders
  • Suppository
  • etc
• Gas

Routes of admin (and rates)

• Enteral (slower)
  • Oral (30-90 min)
  • Rectal (5-30 min – unpredictable)
• Paraenteral (any route other than the GI tract, skin and mucous membranes) (fastest, more immediate results)
  • IV (30-60 sec)
  • IO (60 sec)
  • IM (10-20 min) (1 -5 ml , usually 3ml, 1″ to 3″ needle, 21 gauge)
  • SQ (15-30 min) (1ml or less syringe w/ ½” to 1″ needle 24-26 gauge)
• Percutaneous (skin and mucous membranes)
  • Transdermal (min to hrs)
  • SL (3-5 min)
  • buccal
  • nasal
  • occular

Medication administration

• Pt hx
• Make sure its theirs
• Compliant? Date of rx and exp date

6 Rights

1. Right patient
2. Right Drug
3. Right dose
4. Right route
5. Right time
6. Right documentation

Vitals – before and two minutes after and med admin