Other Medications Flashcards

1
Q

Calcium Gluconate

(mechanism of action)

A

♦ 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

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2
Q

Calcium Gluconate

(side effects)

A

Hypotension

Bradycardia

Arrhythmia

Cardiac Arrest

Chalky or Metallic Taste

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3
Q

Calcium Gluconate

(indications)

A

♦ Calcium Channel Blocker overdose

♦ Magnesium Sulfate drip toxicity

♦ Hypocalcemia / Hyperkalemia

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4
Q

Calcium Gluconate

(contraindications)

A

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)

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5
Q

Calcium Gluconate

(adult dose - asystole/PEA)

A

Asystole / PEA

1 - 2 GM IO/IV

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6
Q

Calcium Gluconate

(adult dose - bradycardia/CCB overdose

musculoskeletal trauma)

A

Bradycardia / Calcium Channel Blocker Overdose/Musculoskeletal Trauma

1-2 GM Slow IVP

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7
Q

Calcium Gluconate

(adult dose - eclampsia / preeclampsia / preterm labor)

A

Eclampsia / Preeclampsia / Preterm Labor

♦ 1 gram over 2-3 minutes if Mag toxicity is suspected

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8
Q

Calcium Gluconate

(pediatric dose - poisioning/OD/musculoskeletal trauma)

A

Poisoning / Overdose / Musculoskeletal Trauma

60 mg/kg IO/IV slow administration
(max dose 2GM)

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9
Q

Calcium Gluconate

(pregnancy safe)

A

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.

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10
Q

Calcium Chloride

(mechanism of action)

A

♦ 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

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11
Q

Calcium Chloride

(side effects)

A

Hypotension,

bradycardia,

arrhythmia,

cardiac arrest,

chalky or metallic taste

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12
Q

Calcium Chloride

(indications)

A

Calcium Channel Blocker overdose

Magnesium Sulfate drip toxicity

Hypocalcemia / Hyperkalemia

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13
Q

Calcium Chloride

(contraindications)

A

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.

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14
Q

Calcium Chloride

(adult dose)

A

♦ 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

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15
Q

Calcium Chloride

(pediatric dose)

A

♦ Poisoning / Overdose / Musculoskeletal Trauma

20 mg/kg IO/IV slow administration
(max dose 2GM)

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16
Q

Calcium Chloride

(pregnancy safe)

A

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.

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17
Q

Glucagon

(mechanism of action)

A

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.

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18
Q

Glucagon

(onset and duration)

A

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.

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19
Q

Glucagon

(side effects)

A

Allergic reactions may occur and include generalized rash, and in some cases anaphylactic shock, and hypotension, nausea and vomiting

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20
Q

Glucagon

(indications)

A

Hypoglycemia

Beta Blocker overdose

(exhibits chronotrophic and inotropic effects)

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21
Q

Glucagon

(contraindications)

A

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.

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22
Q

Glucagon

(adult dose)

A

♦ Beta Blocker OD / Bradycardia
1 mg IM/IO/IV/IN

♦ Diabetic Emergency
1 mg IM/IN

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23
Q

Glucagon

(pediatric dose)

A

♦ Beta Blocker OD / Bradycardia
→ 0.1mg/kg IV/IO/IM/IN
(max dose 2mg)

♦ Diabetic Emergency
→ 0.1mg/kg IM/IN
(max dose 1mg)

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24
Q

Glucagon

(pregnancy safe)

A

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)

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25
**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
26
**Reglan (Metoclopramide)** **(onset and duration)**
**onset** of action is ***1 to 3 minutes*** after IV injection
27
**Reglan (Metoclopramide)** **(side effects)**
Dystonic Reaction / Seizures / Hallucinations, CHF Hypertension / Hypotension SVT Dizziness / Diarrhea / Rash, Laryngospasm, Hepatic Toxicity
28
**Reglan (Metoclopramide)** **(indications)**
**\>\> Nausea/Vomiting \<\<**
29
**Reglan (Metoclopramide)** **(contraindications)**
Hypersensitivity Phenochromocytoma Seizures GI bleeding GI obstruction
30
**Reglan (Metoclopramide)** **(adult dose)**
**5 - 10 mg** IO/IV/IM **every 6-8 hours**
31
**Reglan (Metoclopramide)** **(pediatric dose)**
**0.1 - 0.2 mg/kg** IO/IV/IM ## Footnote **up to 10 mg every 6-8 hours**
32
**Methylprednisolone** (Solu-Medrol) ## Footnote **(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
33
**Methylprednisolone** (Solu-Medrol) ## Footnote **(onset and duration)**
**Onset IV**: 1 hour excretion is almost complete within 12 hours **Onset IM**: Systemic absorption is rapid following IM administration
34
**Methylprednisolone (Solu-Medrol)** **(side effects)**
**Arrhythmias, bradycardia, headache, depression** Increased ICP (in children only) Anxiety and Tremors
35
**Methylprednisolone** (Solu-Medrol) ## Footnote **(indications)**
♦ Steroid used in **respiratory distress** to _reverse inflammatory and allergic reactions_ ♦ Circulation: Blood Administration ♦ Anaphylactic Shock /Allergic Reaction ♦ Reactive Airway Disease
36
**Methylprednisolone** (Solu-Medrol) ## Footnote **(contraindications)**
Active untreated infections Some forms of meningitis Lactation Cushing's syndrome Uncontrolled hyperglycemia
37
**Methylprednisolone** (Solu-Medrol) ## Footnote **(adult dose)**
## Footnote **125 mg IO/IV**
38
**Methylprednisolone** (Solu-Medrol) ## Footnote **(pediatric dose)**
**2 mg/kg** IO/IV (**Maximum 125 mg)**
39
**Methylprednisolone** (Solu-Medrol) ## Footnote **(pregnancy safe)**
Pregnancy **Class C** ## Footnote 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,
40
**Terbutaline** (Brethine) ## Footnote **(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.
41
**Terbutaline** (Brethine) ## Footnote **(onset and duration)**
**Onset**: 6 - 15 min Half Life: 5.7 hrs **Duration**: 1.5 - 4 hrs
42
**Terbutaline** (Brethine) ## Footnote **(side effects)**
Tremors, Anxiety, Tachycardia, Palpitations, Drowsiness, Nausea/Vomiting, Diaphoresis, Muscle Cramps
43
**Terbutaline** (Brethine) ## Footnote **(indications)**
**Premature Labor**
44
**Terbutaline** (Brethine) ## Footnote **(contraindications)**
## Footnote **Known Hypersensitivity**
45
**Terbutaline** (Brethine) ## Footnote **(dose)**
Pre-term labor **0.25 mg** **subcutaneous q 20 min** **max dose of 1 mg in 4 hrs**.
46
**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.
47
**Thiamine** **(onset and duration)**
**Onset**: 1 hr **Duration**: Unknown
48
**Thiamine** **(side effects)**
None (can't find any)
49
**Thiamine** **(indications)**
Vitamin B1 Deficiency Wernicke-Korsakoff Syndrome Chronic Alcohol Abuse
50
**Thiamine** **(contraindications)**
**Hypersensitivity**
51
**Thiamine** **(adult dose)**
100 mg Intramuscular (**AL CC Protocol - not listed in AC Protocol**)
52
**Thiamine** **(pediatric dose)**
**Not currently indicated**
53
**Tranexamic Acid** (TXA) ## Footnote **(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.
54
**Tranexamic Acid** (TXA) ## Footnote **(onset and duration)**
**Onset**: Immediate Half Life: 3 hrs **Duration**: 24 hrs
55
**Tranexamic Acid** (TXA) ## Footnote **(side effects)**
Increased clot formation Blurred vision Anxiety Nausea/Vomiting DVT PE
56
**Tranexamic Acid** (TXA) ## Footnote **(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.
57
**Tranexamic Acid** (TXA) ## Footnote **(contraindications)**
Time of initial traumatic injury \> 180 min, Patients who have contraindications to antifibrinolytic therapy agents, and medical control discretion.
58
**Tranexamic Acid** (TXA) ## Footnote **(adult dose)**
Mix 1 gram of TXA in 100 ml of normal saline ## Footnote **administer over 10 min**
59
**Tranexamic Acid** (TXA) ## Footnote **(pediatric dose)**
## Footnote **Not indicated for patients less than 18 years of age**
60
**Famotidine** (Pepcid) ## Footnote **(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_.
61
**Famotidine** (Pepcid) ## Footnote **(side effects)**
Fever, Fatigue, Arrhythmia, Urticaria, Depression, Anxiety, Tinnitus
62
**Famotidine** (Pepcid) ## Footnote **(indications)**
H-2 blocker used for allergic reactions
63
**Famotidine** (Pepcid) ## Footnote **(contraindications)**
Known Hypersensitivity
64
**Famotidine** (Pepcid) ## Footnote **(adult dose)**
## Footnote **20 mg IO/IV**
65
**Famotidine** (Pepcid) ## Footnote **(pediatric dose)**
0.25-0.5 mg/kg **Max dose of 20 mg**
66
**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.
67
**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.
68
**Promethazine** **(side effects)**
Dizziness, Drowsiness
69
**Promethazine** **(indications)**
Nausea/vomiting
70
**Promethazine** **(contraindications)**
Lactating females, MAOI use, COPD, HTN, Pregnancy (\*AL Critical Care Protocols)
71
**Promethazine** **(adult dose)**
12.5 mg IV diluted in 10-20 ml of normal saline, administered over 5-10 min (**\*** AL Critical Care Protocols)
72
**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)
73
**Promethazine** **(pregnancy safe)**
Pregnancy **Class C** ## Footnote Promethazine crosses the placenta. Platelet aggregation may be inhibited in newborns following maternal use of promethazine within 2 weeks of delivery.
74
**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**.
75
**Magnesium Sulfate** **(onset and duration)**
**Onset**: Immediate **Duration**: 30 min
76
**Magnesium Sulfate** **(side effects)**
Bradycardia, Hypotension, Hyporeflexia, Diaphoresis and Drowsiness, Decreased Respiratory Rate, Flaccid Paralysis
77
**Magnesium Sulfate** **(indications)**
Torsades de Pointe Digitalis induced ventricular arrhythmias Anticonvulsant in eclampsia Suspected hypomagnesium
78
**Magnesium Sulfate** **(contraindications)**
Hypermagnesium Hypocalcemia Anuria Heart block Active labor
79
**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.
80
**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**
81
**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._**
82
**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
83
**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
84
**Mannitol** **(indications)**
Increased intracranial pressure associated with cerebral edema
85
**Mannitol** **(contraindications)**
Known hypersensitivity Renal Disease Active Intracranial Bleeding Severe Pulmonary Edema/CHF
86
**Mannitol** **(adult dose)**
1g/kg IV administered over 10 minutes. Filter must be used.
87
**Mannitol** **(pediatric dose)**
1g/kg IV administered over 10 minutes. Filter must be used
88
**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_
89
**Lidocaine** (Xylocaine) ## Footnote **(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.
90
**Lidocaine** (Xylocaine) ## Footnote **(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
91
**Lidocaine** (Xylocaine) ## Footnote **(side effects)**
Hypotension, Decreased LOC, Irritability, Muscle Twitching, Eventually Seizures
92
**Lidocaine** (Xylocaine) ## Footnote **(indications)**
Pain Management for IO insertion Cardiac Arrest
93
**Lidocaine** (Xylocaine) ## Footnote **(contraindications)**
Known sensitivity
94
**Lidocaine** (Xylocaine) ## Footnote **(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_
95
**Lidocaine** (Xylocaine) ## Footnote **(pediatric dose)**
♦ 0.5mg/kg (**max dose 40 mg**) for **IO insertion** **♦ Not indicated for pediatric arrest.**
96
**Lidocaine** (Xylocaine) ## Footnote **(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_.
97
**Tranexamic Acid** (TXA) ## Footnote **(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.