EMS Pharmacology Reference Guide | RI Department of Health, Study notes of Pharmacology

Download EMS Pharmacology Reference Guide | RI Department of Health and more Study notes Pharmacology in PDF only on Docsity!

Rhode Island Department of Health - Center for Emergency Medical Services

EMS Pharmacology

Reference Guide

A companion to the 2017 Statewide Emergency Medical Services Protocols

1

3

6

Acetaminophen (Tylenol, APAP)

Classification: Analgesic, antipyretic

General:

Acetaminophen has analgesic and antipyretic properties with effects equivalent to those of aspirin. Its analgesic and antipyretics effects are likely the result from the inhibition of prostaglandin E2 (PGE 2 ). It does not fall into the non-steroidal anti-inflammatory class of medications as it has no anti-inflammatory effects. Acetaminophen acts on a variant of cycloxygenase (COX3) that is only expressed in the central nervous system. Unlike aspirin, it has no effect on COX1 or COX2 and therefore, it has no effect on platelets. Acetaminophen elevates the pain threshold and readjusts the hypothalamic temperature regulatory center.

Protocol Indication(s):

1. Mild to moderate pain
2. Fever

Contraindications:

1. Known hypersensitivity
2. Environmental hyperthermia

Precautions:

1. Acetaminophen should be used with caution in patients with liver disease/failure.
2. The maximum adult daily dose of acetaminophen is 4,000 mg.

Significant adverse/side effects:

1. Nausea/vomiting
2. Stevens-Johnson Syndrome (rare)
3. Toxic epidermal necrolysis (rare)

Dosage per protocol(s): 2.07 Patient Comfort - Adult 2.07 Patient Comfort - Pediatric 2.15 Fever - Adult 2.15 Fever - Adult

7

Activated Charcoal

Classification: Gastric decontaminant

General:

Activated charcoal (AC) is charcoal which has been treated with oxygen, which results in the opening up of millions of pores between the charcoal’s carbon atoms. These pores directly absorb (bind) the molecules of a multitude of substances. In the EMS setting, AC is utilized as a single dose gastrointestinal decontaminant following the oral ingestion of a toxin (in the hospital, multiple doses are sometimes administered to enhance elimination of a toxin). There are a number of substances that are not chemically attracted to AC and are absorbed poorly if at all by AC. These include electrolytes, iron, lithium, heavy metals, acids or bases, alcohols, cyanide, most common solvents, and most water insoluble compounds such as hydrocarbons (petroleum distillates).

Protocol Indication(s):

1. Oral toxic ingestion within 1 hour of EMS contact

Contraindications:

1. Known hypersensitivity
2. Patient with altered mental status without a protected airway (i.e. not intubated)
3. Due to the increased risk of aspiration without out benefit, AC should not be administered following the ingestion of a substance known not to be absorbed by AC
4. Corrosive ingestion (AC obscures endoscopy, which is performed in such ingestions) unless there are life threatening co-ingestants which are adsorbed by AC

Precautions:

1. Administration of AC increases the risk for aspiration.

Significant adverse/side effects:

1. Nausea/vomiting
2. Intestinal obstruction (associated with the administration of multiple doses)

Dosage per protocol(s): 4.18 Toxicological Emergencies - Adult 4.18 Toxicological Emergencies - Pediatric

9

Precautions:

3. Patients that are status post cardiac transplant may demonstrate increased sensitivity to

Adenosine

4. Patients who receive adenosine via central line should receive half the normal dose.

Significant adverse/side effects:

1. Headache
2. Chest pain
3. Flushing
4. Dyspnea/bronchoconstriction
5. Bradycardia
6. AV block
7. Sinus pause/asystole

Dosage per protocol(s): 3.06 Narrow Complex Tachycardia - Adult 3.06 Narrow Complex Tachycardia - Pediatric 3.07 Wide Complex Tachycardia - Adult

10

Albuterol (Ventolin, Proventil)

Classification: Beta adrenergic agonist (β2 selective)

General:

Albuterol is a short acting β2 selective adrenergic receptor agonist used in the management of bronchospasm. Albuterol stimulates β2 receptors resulting in an increase in cyclic adenosine monophosphate (cAMP), which leads to the activation of protein kinase A inhibiting phosphorylation of myosin and lowering intracellular ionic calcium concentrations, resulting in relaxation of bronchial smooth muscle (bronchodilation) and relaxation of uterine and vascular smooth muscle. Increasing cAMP concentrations also inhibits the release of mediators from mast cells in the airway. Because it relaxes vascular smooth muscle, some peripheral vasodilation may also occur, which may be reflected by a decrease in the diastolic blood pressure. As a result of sympathomimetic stimulation, an intracellular shift of potassium may occur. This may result in a small (approximately 0.5 mEq/L) decrease in the serum potassium concentration. This is generally not of clinical concern, unless large doses of beta agonist are being administered. However, this effect may be useful in the management of hyperkalemia. Due to its effect on uterine smooth muscle, it may be used to arrest premature labor. When administered via inhalation, significant bronchodilation occurs within 15 minutes, and this effect is demonstrated for 3-4 hours.

Protocol Indication(s):

1. Bronchospasm (asthma/reactive airway)
2. Premature labor
3. Hyperkalemia

Contraindications:

1. Known hypersensitivity

Precautions:

1. Use with caution in patients with myocardial ischemia.
2. Paradoxical bronchospasm may occur in a small percentage of patients who receive albuterol. A proposed etiology is attributed to other compounds in the albuterol preparation. If paradoxical bronchospasm (evidenced by significantly increased and severe bronchospasm following administration) is suspected, discontinue use (avoid levalbuterol as well).

12

Amiodarone (Cordarone, Nexterone)

Classification: Antiarrhythmic

General:

Amiodarone is primarily a class III antiarrhythmic, but it also demonstrates electrophysiological effects of class I, II, and IV antiarrythmics. As a class III antiarrhythmic, it binds to and blocks the potassium channels that are responsible for phase 3 repolarization. By blocking potassium channels, it delays repolarization, which leads to an increase in action potential duration and an increase in the effective refractory period (ERP) of all cardiac fibers. This prolongs the period of time that the cell is unexcitable (refractory) and therefore makes the cell less excitable. Amiodarone depresses the slope of phase 0 by inhibiting the transmembrane influx of extracellular sodium ions (class 1 effect), antagonizes beta receptors (class II effect) and displays weak calcium channel blocking effects (class IV). Amiodarone also has α adrenergic blocking properties, which in combination with its beta antagonistic properties, are likely to be partly responsible for its hypotensive effects. Amiodarone decreases the rate of SA node firing, suppresses automaticity, and interrupts reentrant pathways. On the ECG, it prolongs the PR, QRS and QT intervals. Amiodarone is useful in the management of atrial (atrial fibrillation) and ventricular tachyarrhythmias, particularly those resulting from a reentrant mechanism. In ventricular fibrillation or ventricular fibrillation, evidence demonstrating the superiority of amiodarone over lidocaine is lacking.

Protocol Indication(s):

1. Ventricular tachycardia
2. Ventricular fibrillation
3. Wide complex tachycardia
4. Pediatric narrow complex tachycardia

Contraindications:

1. Known hypersensitivity
2. Iodine hypersensitivity
3. Bradycardia
4. AV block >1 degree in the absence of a pacemaker
5. Hypotension (SBP <100 mmHg)

Precautions:

1. Due to its vasodilatory properties, the administration of amiodarone in cardiac arrest should be preceded by the administration of a vasopressor (i.e. epinephrine).

13

Precautions:

2. Amiodarone should not be used in individuals with polymorphic VT associated with a prolonged QT interval.
3. Amiodarone for infusion should only be diluted with D5W and given with an in-line filter.
4. Use with beta or calcium blocking agents may increase risk of hypotension and bradycardia.

Significant adverse/side effects:

1. Hypotension
2. Bradycardia
3. AV block
4. Torsades de pointes
5. Congestive heart failure
6. Phlebitis

Dosage per protocol(s): 3.03 Cardiac Arrest - Adult 3.03 Cardiac Arrest - Pediatric 3.06 Narrow Complex Tachycardia - Pediatric 3.07 Wide Complex Tachycardia - Adult 3.07 Wide Complex Tachycardia - Pediatric Notes:

1. The conventional IV preparation of IV amiodarone contains polysorbate 80 and benzyl alcohol. These preservatives are believed to be partly responsible for bradycardia and hypotension associated with the administration of amiodarone. A newer formulation (Nexterone) that does not contain polysorbate 80 or benzyl alcohol is available.
2. Infusions of amiodarone should be mixed in D5W. In cardiac arrest, the bolus dose may be diluted in 20-50 ml normal saline or D5W.
3. The total maximum cumulative 24 hour dose of amiodarone is 2.2 gm.

15

Precautions:

1. ASA is contraindicated in pediatric or adolescents due to concern for Reye’s syndrome (Reye’s syndrome is characterized by CNS damage, liver injury, and hypoglycemia).

Significant adverse/side effects:

1. Gastritis
2. Nausea
3. Vomiting
4. Upper GI bleeding
5. Increased bleeding

Dosage per protocol(s): 2.07 Patient Comfort - Adult 3.01 Acute Decompensated Heart Failure - Pulmonary Edema 3.02 Chest Pain - Acute Coronary Syndrome - STEMI

16

Atropine Sulfate

Classification: Anticholinergic (more specifically, antimuscarinic)

General:

Atropine sulfate competitively antagonizes acetylcholine (Ach) at muscarinic cholinergic receptors found predominantly in the heart, lungs, GI tract, GU tract, and glands. Atropine sulfate does not antagonize Ach at nicotinic cholinergic receptors (nicotinic receptors are cholinergic receptors found at the neuromuscular junction). Ach is constantly released from parasympathetic nerve endings and stimulates muscarinic receptors. In the heart (SA/AV nodes) stimulation of muscarinic receptors by Ach decreases heart rate and conduction velocity. Atropine sulfate increases heart rate and conduction velocity by removing the influence of Ach. As noted above, muscarinic receptors are located in other areas of the body and are affected by the antagonism of Ach. In the respiratory tract, antagonism of Ach results in decreased airway secretions and bronchodilation (this is the mechanism of action of ipratropium bromide). This includes the effect of decreased salivation (antisialagogue effect) and this is why atropine is sometimes administered to manage increased salivation associated with ketamine administration. In the GI tract it decreases secretions and motility. Ocular effects include mydriasis (pupillary dilation), unresponsiveness to light, and cycloplegia (inability to focus for near vision). In the genitourinary tract, it results in decreased bladder motility and urinary retention. While not an actual antidote for organophosphate toxicity, atropine is used in its management by antagonizing the action of acetylcholine at muscarinic receptors. Organophosphates inhibit acetylcholinesterase (the enzyme responsible for the breakdown of Ach) resulting in increased levels of Ach at the muscarinic receptor sites.

Protocol Indication(s):

1. Bradycardia associated with inadequate perfusion
2. Organophosphate/nerve agent toxicity
3. Hypersalivation associated with ketamine administration

Contraindications:

1. Known hypersensitivity
2. Glaucoma (relative contraindication to atropine administration in the setting of life threatening bradycardia)

Precautions:

1. Atropine should be used cautiously in the presence of myocardial ischemia and hypoxia since it increases oxygen demand of heart and can worsen ischemia.

18

Calcium Chloride

Classification: Electrolyte

General:

Calcium is a positively charged ion involved in multiple physiologic functions. Calcium is required for muscle contraction, nerve impulse transmission, hormone secretion, blood coagulation, cell division, cell motility and wound healing. In vascular smooth muscle, calcium is involved in the maintenance of vascular tone. Calcium is also required for cardiac muscle contraction. The entry of calcium into cardiac cells during depolarization triggers additional intracellular calcium release from the sarcoplasmic reticulum, leading to myocardial contraction. The cardiac pacemaker cells of the SA and AV nodes depend on an inward calcium current for depolarization. Calcium antagonizes the effects of both potassium and magnesium at the cell membrane. Calcium chloride contains three times more elemental calcium than calcium gluconate (1 gm of calcium chloride is equivalent to 3 gm of calcium gluconate).

Protocol Indication(s):

1. Hyperkalemia
2. Hydrofluoric acid (HF) exposure
3. Calcium channel blocker toxicity
4. Beta blocker toxicity
5. Muscle spasm following marine envenomation
6. Pretreatment prior to the administration of a calcium channel blockers in a patient with a tenuous blood pressure

Contraindications:

1. Known hypersensitivity
2. Digitalis toxicity

Precautions:

1. Administer slowly if not in cardiac arrest.

Significant adverse/side effects:

1. Bradycardia
2. Ventricular fibrillation
3. Extravasation necrosis
4. Abdominal pain
5. Nausea/vomiting

19

Dosage per protocol(s): 3.06 Narrow Complex Tachycardia 4.18 Toxicological Emergencies - Adult 4.18 Toxicological Emergencies - Pediatric 4.09 Crush Injury 2.11 Dialysis Emergencies and Renal Failure 4.08 Chemical and Electrical Burn Injury 4.16 Marine Envenomation Notes:

 Calcium was routinely administered in cardiac arrest (asystole, PEA). It is now known that calcium is a prime mediator in ischemic neuronal damage and should be reserved for cardiac arrest related to hyperkalemia, calcium channel or beta blocker overdose.

 Fluoride ions bind calcium and magnesium and may result in hypocalcemia following exposure to HF.  In hyperkalemia, calcium antagonizes cardiac membrane excitability. It has no effect on the serum potassium level. The effect of cardiac membrane stabilization is temporary (20- min) and some patients may require a repeat dose.

 Calcium chloride and calcium gluconate are two commonly used parenteral formations of calcium. In the EMS setting, the two preparation may be used interchangeably, but it should be noted that calcium chloride contains three time more elemental calcium than does calcium gluconate (1 gm of calcium chloride is equivalent to 3 gm of calcium gluconate).

 Calcium chloride has greater bioavailability, but is more likely to cause tissue damage if extravasation occurs.  Sodium bicarbonate and calcium preparations are not compatible and should be given through separate IV lines if possible. If they must be administered via the same IV line, the line should be flushed in between the administration of each.  Calcium channel blockers of the dihydropyridine class [nifedipine, nicardipine] reduce vascular tone by blocking calcium entry through voltage gated channels.