Other Medications Flashcards
Calcium Gluconate
(mechanism of action)
♦ Intravenous administration of calcium gluconate increases serum ionized calcium level
♦ essential for the functional integrity of the nervous, muscular, and skeletal systems
♦ plays a role in normal cardiac function, renal function, respiration, blood coagulation, and cell membrane and capillary permeability
Calcium Gluconate
(side effects)
Hypotension
Bradycardia
Arrhythmia
Cardiac Arrest
Chalky or Metallic Taste
Calcium Gluconate
(indications)
♦ Calcium Channel Blocker overdose
♦ Magnesium Sulfate drip toxicity
♦ Hypocalcemia / Hyperkalemia
Calcium Gluconate
(contraindications)
♦ Cardiac arrhythmias may occur if calcium and cardiac glycosides are administered together.
♦ Hypercalcemia increases the risk of digoxin toxicity
♦ Administration of Calcium Gluconate in Sodium Chloride Injection should be avoided in patients receiving cardiac glycosides (Digoxin / Lanoxicaps, Lanoxin, Digibind)
Calcium Gluconate
(adult dose - asystole/PEA)
Asystole / PEA
1 - 2 GM IO/IV
Calcium Gluconate
(adult dose - bradycardia/CCB overdose
musculoskeletal trauma)
Bradycardia / Calcium Channel Blocker Overdose/Musculoskeletal Trauma
♦ 1-2 GM Slow IVP
Calcium Gluconate
(adult dose - eclampsia / preeclampsia / preterm labor)
Eclampsia / Preeclampsia / Preterm Labor
♦ 1 gram over 2-3 minutes if Mag toxicity is suspected
Calcium Gluconate
(pediatric dose - poisioning/OD/musculoskeletal trauma)
Poisoning / Overdose / Musculoskeletal Trauma
♦ 60 mg/kg IO/IV slow administration
(max dose 2GM)
Calcium Gluconate
(pregnancy safe)
Pregnancy Class C
It is unknown if calcium gluconate can cause fetal harm when administered during pregnancy or can affect reproductive capacity.
Calcium gluconate should be given to a pregnant woman only if clearly needed.
Calcium Chloride
(mechanism of action)
♦ Calcium is the primary component of skeletal tissue
♦ The fifth most abundant element in the body
♦ Essential for the functional integrity of the nervous and muscular systems
♦ For hyperkalemia, the influx of calcium helps restore the normal gradient between threshold potential and resting membrane potential
Calcium Chloride
(side effects)
Hypotension,
bradycardia,
arrhythmia,
cardiac arrest,
chalky or metallic taste
Calcium Chloride
(indications)
Calcium Channel Blocker overdose
Magnesium Sulfate drip toxicity
Hypocalcemia / Hyperkalemia
Calcium Chloride
(contraindications)
Calcium gluconate is contraindicated in patients with hypercalcemia.
Use with extreme caution in patients taking digitalis or digitalis toxicity because of an increased risk of developing arrhythmias.
Cardiac glycosides and calcium gluconate both increase intracellular calcium, so calcium gluconate can worsen digitalis toxicity.
Calcium Chloride
(adult dose)
♦ Asystole / PEA
→ 1 GM IO/IV
♦ Bradycardia / Calcium Channel Blocker
Overdose/Musculoskeletal Trauma
→ 1 GM IV slow administration
♦ Eclampsia / Preeclampsia / Preterm Labor
→ 1 GM over 2-3 minutes if toxicity of Magnesium is suspected
Calcium Chloride
(pediatric dose)
♦ Poisoning / Overdose / Musculoskeletal Trauma
→ 20 mg/kg IO/IV slow administration
(max dose 2GM)
Calcium Chloride
(pregnancy safe)
Pregnancy Class C
It is unknown if calcium gluconate can cause fetal harm when administered during pregnancy or can affect reproductive capacity. Calcium gluconate should be given to a pregnant woman only if clearly needed.
Glucagon
(mechanism of action)
Native human glucagon is a hormone synthesized by the alpha-2 cells of the pancreatic islets of Langerhans and acts to increase blood glucose.
♦ Glucagon induces glycogenolysis to increase blood glucose. (causes liver to convert stored glycogen into glucose and release into blood stream)
♦ Also exhibits chronotrophic and inotropic effects.
Glucagon
(onset and duration)
♦ IM - The maximal glucose concentrations occur 30 minutes Blood glucose concentrations return to normal or hypoglycemic levels within 1 to 2 hours.
♦ IV - The maximal glucose concentrations occur 5 to 20 minutes Blood glucose concentrations return to normal or hypoglycemic levels within 1 to 2 hours.
Glucagon
(side effects)
Allergic reactions may occur and include generalized rash, and in some cases anaphylactic shock, and hypotension, nausea and vomiting
Glucagon
(indications)
Hypoglycemia
Beta Blocker overdose
(exhibits chronotrophic and inotropic effects)
Glucagon
(contraindications)
Insulinoma, glucagon may produce an initial increase in blood glucose; however, glucagon administration may directly or indirectly (through an initial rise in blood glucose) stimulate exaggerated insulin release from the insulinoma.
Pheochromocytoma, because the drug may stimulate the release of catecholamines from the tumor. Stimulation of catecholamine release by exogenous glucagon can cause a substantial increase in blood pressure.
Glucagon
(adult dose)
♦ Beta Blocker OD / Bradycardia
→ 1 mg IM/IO/IV/IN
♦ Diabetic Emergency
→ 1 mg IM/IN
Glucagon
(pediatric dose)
♦ Beta Blocker OD / Bradycardia
→ 0.1mg/kg IV/IO/IM/IN
(max dose 2mg)
♦ Diabetic Emergency
→ 0.1mg/kg IM/IN
(max dose 1mg)
Glucagon
(pregnancy safe)
Pregnancy Class B
limited clinical data in humans have revealed that there is very low or even negligible embryo and/or fetal risk from glucagon administered during pregnancy.
(there appears to be little risk to the nursing infant if the drug is clinically necessary for treatment of the lactating woman)
Reglan (Metoclopramide)
(mechanism of action)
♦ Metoclopramide enhances gastric motility without stimulating gastric secretions.
♦ High doses of metoclopramide depress the mechanical activity of GI smooth muscle, while low doses stimulate it.
♦ Antiemetic effects of metoclopramide are mainly the result of central dopamine antagonism and increased gastric motility
Reglan (Metoclopramide)
(onset and duration)
onset of action is 1 to 3 minutes after IV injection
Reglan (Metoclopramide)
(side effects)
Dystonic Reaction / Seizures / Hallucinations,
CHF
Hypertension / Hypotension
SVT
Dizziness / Diarrhea / Rash,
Laryngospasm,
Hepatic Toxicity
Reglan (Metoclopramide)
(indications)
>> Nausea/Vomiting <<
Reglan (Metoclopramide)
(contraindications)
Hypersensitivity
Phenochromocytoma
Seizures
GI bleeding
GI obstruction
Reglan (Metoclopramide)
(adult dose)
5 - 10 mg IO/IV/IM every 6-8 hours
Reglan (Metoclopramide)
(pediatric dose)
0.1 - 0.2 mg/kg IO/IV/IM
up to 10 mg every 6-8 hours
Methylprednisolone (Solu-Medrol)
(mechanism of action)
♦ Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals
♦ The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation
♦ Decreases inflammation by suppression of migration of polymorphonuclear leukocytes and reversal of increased capillary permeability
Methylprednisolone (Solu-Medrol)
(onset and duration)
Onset IV: 1 hour
excretion is almost complete within 12 hours
Onset IM: Systemic absorption is rapid following IM administration
Methylprednisolone (Solu-Medrol)
(side effects)
Arrhythmias, bradycardia, headache, depression
Increased ICP (in children only)
Anxiety and Tremors
Methylprednisolone (Solu-Medrol)
(indications)
♦ Steroid used in respiratory distress to reverse inflammatory and allergic reactions
♦ Circulation: Blood Administration
♦ Anaphylactic Shock /Allergic Reaction
♦ Reactive Airway Disease
Methylprednisolone (Solu-Medrol)
(contraindications)
Active untreated infections
Some forms of meningitis
Lactation
Cushing’s syndrome
Uncontrolled hyperglycemia
Methylprednisolone (Solu-Medrol)
(adult dose)
125 mg IO/IV
Methylprednisolone (Solu-Medrol)
(pediatric dose)
2 mg/kg IO/IV
(Maximum 125 mg)
Methylprednisolone (Solu-Medrol)
(pregnancy safe)
Pregnancy Class C
There are no adequate and well-controlled studies in humans, but potential benefits may warrant use of the drug in pregnant women despite potential risks.
Complications, including cleft palate, stillbirth, and premature abortion, have been reported when corticosteroids were administered during pregnancy in animals.
Corticosteroids distribute into breast milk, and the manufacturer states that because of the potential for serious adverse reactions in nursing babies,
Terbutaline (Brethine)
(mechanism of action)
Relaxes bronchial and uterine smooth muscles by selectively binding to the Beta2 receptors causing bronchodilation, inhibiting the release of mediators of immediate hypersensitivity reactions from mast cells and relaxing the uterus.
Terbutaline (Brethine)
(onset and duration)
Onset: 6 - 15 min
Half Life: 5.7 hrs
Duration: 1.5 - 4 hrs
Terbutaline (Brethine)
(side effects)
Tremors,
Anxiety,
Tachycardia, Palpitations,
Drowsiness,
Nausea/Vomiting,
Diaphoresis,
Muscle Cramps
Terbutaline (Brethine)
(indications)
Premature Labor
Terbutaline (Brethine)
(contraindications)
Known Hypersensitivity
Terbutaline (Brethine)
(dose)
Pre-term labor 0.25 mg subcutaneous q 20 min
max dose of 1 mg in 4 hrs.
Thiamine
(mechanism of action)
Thiamine combines with adenosine triphosphate (ATP) in the liver, kidneys, and leukocytes to produce thiamine diphosphate.
Thiamine diphosphate acts as a coenzyme in carbohydrate metabolism, in transketolation reactions, and in the utilization of hexose in the hexose-monophosphate shunt.
Without adequate thiamine, pyruvic acid does not undergo conversion to acetyl-CoA and cannot enter the Krebs cycle. Pyruvic acid accumulates in the blood and is subsequently converted to lactic acid, with the potential development of lactic acidosis.
Diminished production of NADH in the Krebs cycle also results in lactic acid production through facilitation of anaerobic glycolysis.
Thiamine
(onset and duration)
Onset: 1 hr
Duration: Unknown
Thiamine
(side effects)
None
(can’t find any)
Thiamine
(indications)
Vitamin B1 Deficiency
Wernicke-Korsakoff
Syndrome
Chronic Alcohol Abuse
Thiamine
(contraindications)
Hypersensitivity
Thiamine
(adult dose)
100 mg Intramuscular
(AL CC Protocol - not listed in AC Protocol)
Thiamine
(pediatric dose)
Not currently indicated
Tranexamic Acid (TXA)
(mechanism of action)
TXA is a synthetic lysine amino acid derivative that inhibits the activation of plasminogen to plasmin to prevent the breakdown of fibrin clots.
With the reduction of plasmin activity, it also reduces complement and C1 activation associated with the hereditary angioedema.
Tranexamic Acid (TXA)
(onset and duration)
Onset: Immediate
Half Life: 3 hrs
Duration: 24 hrs
Tranexamic Acid (TXA)
(side effects)
Increased clot formation
Blurred vision
Anxiety
Nausea/Vomiting
DVT
PE
Tranexamic Acid (TXA)
(indications)
♦ Patient > 18years signs and symptoms of severe hemorrhage (internal or external)
♦ Hemodynamic Instability: SBP < 90, Pulse rate > 110 bpm, Respiratory rate > 24 breaths per minute, evidence of peripheral vasoconstriction.
Duration from initial injury is less than 180 min.
Tranexamic Acid (TXA)
(contraindications)
Time of initial traumatic injury > 180 min,
Patients who have contraindications to antifibrinolytic therapy agents,
and medical control discretion.
Tranexamic Acid (TXA)
(adult dose)
Mix 1 gram of TXA in 100 ml of normal saline
administer over 10 min
Tranexamic Acid (TXA)
(pediatric dose)
Not indicated for patients less than 18 years of age
Famotidine (Pepcid)
(mechanism of action)
Famotidine competitively inhibits the binding of histamine to H2-receptors on the gastric basolateral membrane of parietal cells, reducing basal and nocturnal gastric acid secretions. The drug also decreases the gastric acid response to stimuli such as food, caffeine, insulin, betazole, or pentagastrin.
Famotidine reduces the total volume of gastric juice, thus indirectly decreasing pepsin secretion. The drug does not appear to alter gastric motility, gastric emptying, esophageal pressures, biliary secretions, or pancreatic secretions.
Famotidine (Pepcid)
(side effects)
Fever,
Fatigue,
Arrhythmia,
Urticaria,
Depression,
Anxiety,
Tinnitus
Famotidine (Pepcid)
(indications)
H-2 blocker used for allergic reactions
Famotidine (Pepcid)
(contraindications)
Known Hypersensitivity
Famotidine (Pepcid)
(adult dose)
20 mg IO/IV
Famotidine (Pepcid)
(pediatric dose)
0.25-0.5 mg/kg
Max dose of 20 mg
Promethazine
(mechanism of action)
The predominant action of promethazine is antagonism of H1-receptors. Although promethazine is classified as a phenothiazine, its ability to antagonize dopamine is approximately one-tenth that of chlorpromazine.
Like other H1-antagonists, promethazine does not prevent the release of histamine, but competes with free histamine for binding at H1-receptor sites.
The relief of motion sickness and nausea/vomiting appear to be related to central anticholinergic actions and may implicate activity on the medullary chemoreceptor trigger zone.
Promethazine
(onset and duration)
Onset IV: 3 - 5 min
Antihistaminic and sedative effects are sustained for 4—6 hours and 2—8 hours, respectively.
Onset IM: within 20 minutes
Antihistaminic and sedative effects are sustained for 4—6 hours and 2—8 hours, respectively.
Promethazine
(side effects)
Dizziness,
Drowsiness
Promethazine
(indications)
Nausea/vomiting
Promethazine
(contraindications)
Lactating females,
MAOI use,
COPD,
HTN,
Pregnancy
(*AL Critical Care Protocols)
Promethazine
(adult dose)
12.5 mg IV diluted in 10-20 ml of normal saline, administered over 5-10 min
(* AL Critical Care Protocols)
Promethazine
(pediatric dose)
0.5mg/kg IV diluted in 10-20 ml of normal saline, administered over 10-15 min
*Max dose 12.5 mg
*Do not administer less than 2 years of age
(* AL Critical Care Protocols)
Promethazine
(pregnancy safe)
Pregnancy Class C
Promethazine crosses the placenta. Platelet aggregation may be inhibited in newborns following maternal use of promethazine within 2 weeks of delivery.
Magnesium Sulfate
(mechanism of action)
Effects the myocardium, bronchial tree, skeletal and smooth muscle by reducing the release of acetylcholine at the neuromuscular junction reducing muscle contractions and promoting relaxation.
Magnesium Sulfate
(onset and duration)
Onset: Immediate
Duration: 30 min
Magnesium Sulfate
(side effects)
Bradycardia,
Hypotension,
Hyporeflexia,
Diaphoresis and Drowsiness,
Decreased Respiratory Rate,
Flaccid Paralysis
Magnesium Sulfate
(indications)
Torsades de Pointe
Digitalis induced ventricular arrhythmias
Anticonvulsant in eclampsia
Suspected hypomagnesium
Magnesium Sulfate
(contraindications)
Hypermagnesium
Hypocalcemia
Anuria
Heart block
Active labor
Magnesium Sulfate
(adult dose)
Eclampsia / Pre-Eclampsia
4 grams IO/IV over 20 minutes
Pulseless V-Tach / V-Fib
If patient is in refractory V-Tach unresponsive to Amiodarone or in Torsades de Pointes, administer 2 grams slow IO/IV push over 20 minutes.
Reactive Airway Disease
2 grams IO/IV over 10 minutes.
If patient is being transferred with Magnesium Sulfate administering, continue at current rate. If rate is > 4 grams/hr, contact receiving MD.
Magnesium Sulfate
(pediatric dose)
Pulseless V-Tach / V-Fib
If patient is in refractory V-Tach unresponsive to Amiodarone or in Torsades de Pointes, administer 50 mg/kg slow IO/IV over 20 minutes
Maximum 2 grams
Mannitol
(mechanism of action)
Intravenous mannitol exerts its osmotic diuretic effect as a solute of relatively small molecular size being largely confined to the extracellular space.
Mannitol hinders tubular reabsorption of water and enhances excretion of sodium and chloride by elevating the osmolarity of the glomerular filtrate.
The increase in extracellular osmolarity induces the movement of intracellular water to the extracellular and vascular spaces.
This action underlies the role of mannitol in in reducing intracranial pressure, intracranial edema, and intraocular pressure.
Mannitol
(onset and duration)
distributes into the extracellular space within 20 to 40 minutes
Diuresis generally occurs in 1 to 3 hours
Decrease in the cerebrospinal fluid pressure will occur in approximately 15 minutes
Will persist for 3 to 8 hours after the infusion is stopped
Mannitol
(side effects)
Dizziness,
Fever,
Headache, Seizures,
Angina,
Edema - with vascular congestion or pulmonary edema - manitol administration may result in hypervolemia leading to or exacerbating existing congestive heart failure
Hypotension - mannitol acutely raises plasma and extracellular osmolality, which leads to an increase in circulating blood volume. This leads to increase in stroke volume, cardiac output, and blood pressure. Following diuresis, patients may be slightly hypovolemic with associated decreases cardiac output and blood pressure.
Tachycardia,
Blurred Vision,
Dehydration - Too rapid infusion of large amounts of mannitol will cause a shift of intracellular water into the extracellular compartment resulting in cellular dehydration
Urticarial,
Chills,
Thrombophlebitis,
Fluid and electrolyte imbalance - Excessive loss of water and electrolytes may lead to serious imbalances. (hyponatremia, hypernatremia, hyperkalemia, hypokalemia; metabolic acidosis)
CHF - mannitol administration may result in hypervolemia leading to or exacerbating existing congestive heart failure. Accumulation of mannitol due to insufficient renal excretion increases the risk of hypervolemia.
GI distress
Mannitol
(indications)
Increased intracranial pressure associated with cerebral edema
Mannitol
(contraindications)
Known hypersensitivity
Renal Disease
Active Intracranial Bleeding
Severe Pulmonary Edema/CHF
Mannitol
(adult dose)
1g/kg IV administered over 10 minutes.
Filter must be used.
Mannitol
(pediatric dose)
1g/kg IV administered over 10 minutes.
Filter must be used
Mannitol
(pregnancy safe)
Pregnancy Class C
Mannitol crosses the placenta and may cause fluid shifts that could potentially result in adverse effects in the fetus
No adequate and well-controlled studies in humans, but potential benifits may warrant use
Lidocaine (Xylocaine)
(mechanism of action)
Lidocaine stabilizes neuronal membranes by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action.
Lidocaine produces its analgesics effects through a reversible nerve conduction blockade by diminishing nerve membrane permeability to sodium, just as it affects sodium permeability in myocardial cells.
Lidocaine’s antiarrhythmic effects result from its ability to inhibit the influx of sodium through the “fast” channels of the myocardial cell membrane, thereby increasing the recovery period after repolarization. Lidocaine suppresses automaticity and decreases the effective refractory period and the action potential duration in the His-Purkinje system at concentrations that do not suppress automaticity at the SA node.
Lidocaine (Xylocaine)
(onset and duration)
After intravenous injection, lidocaine distributes in 2 phases
early phase represents distribution into the most highly perfused tissues
the second, slower phase, the drug distributes into adipose and skeletal muscle tissues
Onset: Immediate
Duration: 10 to 20 minutes
Lidocaine (Xylocaine)
(side effects)
Hypotension,
Decreased LOC,
Irritability,
Muscle Twitching,
Eventually Seizures
Lidocaine (Xylocaine)
(indications)
Pain Management for IO insertion
Cardiac Arrest
Lidocaine (Xylocaine)
(contraindications)
Known sensitivity
Lidocaine (Xylocaine)
(adult dose)
♦ 40 mg 2% for IO insertion
♦ 1.5mg/kg IV/IO followed by 0.75 mg/kg,
up to max dose of 3mg/kg for pulseless V-fib/V-Tach.
Followed by a maintenance infusion of 2-4 mg/min
Lidocaine (Xylocaine)
(pediatric dose)
♦ 0.5mg/kg (max dose 40 mg) for IO insertion
♦ Not indicated for pediatric arrest.
Lidocaine (Xylocaine)
(pregnancy safe)
Pregnancy Calss B
Local anesthetics are known to cross the placenta rapidly and, when administered for epidural, paracervical, pudendal, or caudal block anesthesia, and to cause fetal toxicity.
There are, however, no adequate and well-controlled studies in pregnant women.
Tranexamic Acid (TXA)
(pregnancy safe)
Pregnancy Class B
Animal reproduction studies have failed to demonstrate a risk to the fetus, and there are no adequate and well-controlled studies in pregnant women.
