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ACP Pharmacology > Drug Monographs > Flashcards

Drug Monographs Flashcards

1
Q

Describe Pharmacodynamics of Adenosine

A
  • Slows conduction time through AV Node
  • Naturally occuring nucleoside
  • Stimulates specific adenosine receptors, causing efflux of potassium and influx of calcium in SAN, atria, and AVN
  • Result is hyperpolarization of nodal tissues, slowing AV conduction and blunting SA discharge
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2
Q

Describe Pharmacokinetics of adenosine

A
  • Intravenous
    • Onset - rapid
    • Duration - very brief
    • Half-life - 6 to 10 seconds
    • Duration - 1 to 2 minutes
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3
Q

Indications for adenosine

A
  • Conversion of supraventricular tachycardia (SVT) / paroxysmal supraventricular tachycardia (PSVT).
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4
Q

Contraindications/precautions for adenosine

2 contraindications, 1 precaution

A

Contraindications

  • Hypersensitivity
  • 2nd or 3rd degree AV block, or sick sinus syndrome (without pacemaker)

Precautions

  • May worsen bronchospasm in asthmatics and some patients with COPD.
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5
Q

Drug to drug interactions of adenosine

3 listed

A
  • Higher than normal doses of Adenosine may be required for patients on xanthines (eg. theophylline).
  • Lower than normal doses (i.e. 3 mg or less) should be used for patients on dipyridamole (Persantine) as this drug potentiates Adenosine.
  • The effects of Adenosine are prolonged in patients taking Carbamazepine (anti-convulsant) and in heart transplant recipients (denervated hearts).
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6
Q

Adverse effects of adenosine

A
  • Dizziness/light headedness/syncope, facial flushing, dyspnea or shortness of breath, gastroninestinal distress (nausea/vomiting), chest pain or discomfort
    • Usually resolves in 1-2 mins
    • Explain to the patient they will likely experience some of the above symptoms and that the symptoms are temporary
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7
Q

Adult dosing for adenosine

A
  • First dose: 6 mg IV direct, given rapidly and immediately followed with 20 mL to 30 mL IV NS or RL flush
    • Run ECG strip as drug is being given
  • If no conversion to sinus rhythm or slowing of rhythm to diagnose underlying rhythm (e.g. atrial flutter or atrial fibrillation) in 1-2 minutes, can give a second dose: 12 mg IV direct, rapid administration followed by 20-30 mL IV NS or RL flush
  • Note: Adenosine must be given very quickly and in the IV site closest to the central circulation (e.g. antecubital, external jugular, central line). It should always be immediately followed by a 20-30 cc flush of NS or RL to make sure that all of the drug is cleared from the IV tubing and delivered to the intended site.
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8
Q

Pediatric dosing for adenosine

A
  • First dose:
    • 0.1 mg/kg IV direct, given rapidly followed by 5-10 mL (depends on weight of child) IV NS or RL
    • maximum 6 mg as a single first dose
  • Second dose:
    • If no conversion to sinus rhythm or slowing of rhythm to diagnose underlying rhythm (e.g. atrial flutter or atrial fibrillation) in 1-2 minutes,0.2 mg/kg IV, administered as above.
    • maximum 12 mg as a single second dose
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9
Q

What is the likelihood of successful conversion with adenosine?

A

Has a > 90% successful conversion of PSVT rate when the full dose is given (Crankin et al, 1989; Garrat et al, 1989; DiMarco et al, 1990).

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10
Q

Describe pharmacodynamics of amiodarone

A
  • Considered a class III anti-arrhythmic.
  • Also possesses electrophysiologic characteristics of all 4 Vaughan Williams classes.
  • Like Class I drugs, amiodarone blocks sodium channels at rapid pacing frequencies.
  • Like class II drugs, it exerts antisympathetic activity through beta-adrenoreceptor (weak) antagonism.
  • Class II type effects: negative chronotropic effect in nodal tissues.
  • Class III effect: lengthens the cardiac action potential.
    • In addition to blocking sodium channels, amiodarone blocks myocardial potassium channels, which contributes to slowing of conduction and prolongation of refractoriness.
    • Antisympathetic action and block of calcium and potassium channels are responsible for the negative dromotropic effects on the sinus node and for the slowing of conduction and prolongation of refractoriness in the atrioventricular (AV) node.
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11
Q

Describe pharmacokinetics of amiodarone

A

Intravenous

  • Onset: Minutes when used as bolus in V.Fib/pulseless VT
  • Peak: 10-15 minutes
  • Duration: Amiodarone has a prolonged duration of action and if used for rhythm control for other than arrest situations has a slow onset of action (1 - 2 hours)
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12
Q

Indications for amiodarone

A
  • Ventricular fibrillation
  • Pulseless ventricular tachycardia
  • Unstable ventricular tachycardia (usually recurrent after cardioversion)
    • NOTE DOSING DIFFERENCES
  • Recurrent unstable VT post cardioversion
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13
Q

Contraindications and precautions for amiodarone

4 contraindications, 1 precaution

A

Contraindications

  • Hypersensitivity
  • Cardiogenic shock
  • Marked sinus bradycardia
  • 2nd or 3rd degree AV block

Precautions

  • Tissue toxic if extravasation
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14
Q

Warnings and drug-to-drug interactions for amiodarone

A

Warning

  • Hypotension of the most common side effect during IV infusion (~39% of patients in one trial). Slow the infusion.
  • May enhance actions of B-Blocker, Ca Channel Blocker or Digoxin.
  • May cause prolongation of the QT interval (>500 ms may lead to Torsade de Pointes)

Drug to drug interactions

  • May enhance action of B-Blocker, Ca Channel blockers, Digoxin.
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15
Q

Adult dosage for amiodarone

A
  • 300 mg IV bolus; may repeat 150 mg bolus in 10 min for ventricular fibrillation/pulseless VT.
  • 150 mg IV over 10 min (150 mg in a 50 mL NS minibag run at 50 gtts/min) for recurrent unstable VT post cardioversion or unstable VT refractory to cardioversion.
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16
Q

Pediatric dosage for amiodarone

A

Trick Question!!

Safety and efficacy in children has not been established.

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17
Q

When should amiodarone be given in unstable VT refractory to cardioversion or recurrent VT requiring multiple cardioversions?

A

For unstable VT refractory to cardioversion or recurrent VT requiring multiple cardioversions, amiodarone should be administered while packaging the patient and initiating transport.

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18
Q

Classification of atropine

A
  • Anticholinergic
  • Antimuscarinic
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19
Q

Pharmacodynamics of atropine

A
  • Parasympatholytic (inhibits stimulation from the parasympathetic nervous system)
  • Vagolytic (inhibits stimulation from the vagus nerve)
  • Inhibits vagal stimulation - allowing the sympathetic nervous system to dominate
  • By allowing the sympathetic nervous system to dominate, impulse generation at the SA node and conduction through the AV node should increase
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20
Q

Pharmacokinetics of atropine

A

Intravenous

  • Onset - 2 to 4 minutes
  • Peak - 2 to 4 minutes
  • Half-life - 13 to 40 hours
  • Duration - 4 to 6 hours
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21
Q

Indications for atropine

A
  • Restoration of cardiac rate in the presence of bradydysrhythmia
  • Sinus bradycardia, less than 50 bpm - accompanied by hemodynamic compromise
  • Acceptable, but controversial, in the setting of bradydysrhythmia secondary to AV blocks
  • Treatment of organophosphate exposure/ingestion (high dose)
  • Antidote for poisoning by certain species of mushrooms (e.g. Amanita muscaria)
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22
Q

Contraindications, precautions, and drug interactions for atropine

A

Contraindications

  • Hypersensitivity to anticholinergics
  • Tachycardia

Precautions

  • Hepatic or renal insufficiency
  • COPD - dries secretions/mucous plugging

Drug to Drug

  • Antimuscurinic effects will be­ increased in patients taking Dysopyramide
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23
Q

Adult dosing for atropine

A
  • 0.6 mg IV push - initial dose
  • 0.04 mg/kg (~3 mg for most adults) = maximum (“full vagolytic”) dose
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24
Q

Pediatric dosing for atropine

A
  • 0.02 mg/kg (give no less than 0.1 mg)
  • Maximum or “full vagolytic” dose is 0.04 mg/kg
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25
Q

When giving atropine, why is it particularly imortant to give the correct dose quickly?

A

given in too low of a dose or too slowly may paradoxically slow the heart rate

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26
Q

Which bradydysrhythmias may not respond appropriately to atropine?

A
  • Considered controversial in the setting of 2nd degree type II AV block. It may paradoxically slow the heart rate if the block is infranodal
  • Not likely to be effective in ventricular escape rhythms as there is minimal parasympathetic innervation in the ventricles
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27
Q

How does prior administration of atropine affect patient assessment in the setting of asystole or PEA?

A

Atropine causes pupil dilation, therefore, assessment of pupils in the setting of asystole or PEA after Atropine has been administered may be unreliable

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28
Q

Pharmacodynamics of epinephrine

A
  • α1 (Alpha 1) Effects: Vasoconstriction
  • β1 (Beta 1) Effects: ­Increased Heartrate, Increased­ force of cardiac contraction
  • β2 (Beta 2) Effects (moderate): Bronchodilation
  • Inhibits histamine release
  • +ve chronotropic, +ve dromotropic and +ve inotropic effects
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29
Q

Pharmacokinetics of epinephrine

A

Intravenous

  • Onset - Immediate if given IV
  • Peak - Unknown
  • Half-life - Unknown
  • Duration - Unknown

Intramuscular

  • Onset - 5 to 15 minutes (variable onset with IM)
  • Peak - Unknown
  • Half-life - Unknown
  • Duration - 1 to 4 hours

Inhalation

  • Onset - 1 to 5 minutes (has a mostly local effect)
  • Peak - Unknown
  • Half-life - Unknown
  • Duration - 1 to 3 hours
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30
Q

Indications for epinephrine

A
  • IV/IO dose - Cardiac arrest: ventricular fibrillation, pulseless ventricular tachycardia, asystole, pulseless electrical activity
  • IM, IV, IO, nebulized: Anaphylaxis
  • IM dose: Bronchospasm (uncommon)
  • Nebulized for severe croup
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31
Q

Contraindications and precautions for epinephrine

2 contraindications, 2 precautions

A

Contraindications

  • Significant tachyarrhythmias
  • See ACLS guidelines re: drug therapy in the setting of hypothermia (< 30 degrees C)

Precautions

  • May cause significant dysrhythmias in patients > 35 y/o and/or cardiovascular disease
  • Reduced dosage may be required for patient on MAO inhibitor as there is an increased sympathomimetic response
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32
Q

Drug to drug interactions and adverse effects of epinephrine

A

Drug to Drug Interactions

  • Epinephrine is neutralized by, and may precipitate with sodium bicarbonate. Therefore, DO NOT administer in the same IV line with Bicarb unless the line has been flushed

Adverse Affects

  • Tachycardia, palpitations, angina, PVC’s
  • Hypertension
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33
Q

Adult dosages for epinephrine (not in the context of peri-arrest cardiogenic shock or bradycarida)

6 possibilities

A
  • 1 mg IV/IO for cardiac arrest. Repeat q 3-5 minutes (current literature suggests maximum dose of 3-4 mg)
  • 2-10 µg/min infusion - generally reserved for patients who are profoundly bradycardic and hemodynamically unstable
  • 0.5 mg 1:1000 IM q 5 min x3 doses for anaphylaxis
  • 0.5 mg IM for asthma with failing respirations - repeat q 5 – 20 min
  • 50-100 µg 1/10000 epinephrine IV or IO repeated as necessary for pre-arrest anaphylaxis or asthma
  • 5 ml nebulized 1/1000 EPINEPHrine in anaphylaxis, if critical angioedema affects airway management
34
Q

Describe dosing and administration of epinephrine for the adult Peri-Cardiac Arrest Cardiogenic Shock or Bradycardia patient

A
  • 10 µg Slow IV/IO Q2 to 3 mins PRN
  • Suggested Method
    • Take a pre-load of Epinephrine (1:10’000 - 1 mg in 10 mL), and empty 9 mL. You will have 100 µg remaining
    • Withdraw 9 mL Normal Saline from the luer lock of an IV line to obtain 100 µg in 10 mL - 10 µg per 1 mL
    • Can now administer 10 µg/1 mL aliquots
35
Q

Pediatric dosages for epinephrine

6 possibilities

A
  • .01 mg/kg IV/IO for cardiac arrest
  • .005 mg/kg IV/IO for pre-arrest anaphylaxis
  • .01 mg/kg IM for respiratory failure /anaphylaxis to a max of 0.5 mg
  • 5 ml nebulized 1/1000 EPINEPHrine in anaphylaxis, if critical angioedema affects airway management
  • 5 mg (5 mL) 1:1000 for croup, by nebulizer mask with an oxygen flow sufficient to aerosolize the medication
    • Patients under 1 year of age receive a weight based dose, 0.5 mg/kg in 5 mL N/S; max 5 mg
  • Peri-intubation resuscitation: 1 µg/kg Slow IV/IO Q2 to 3mins PRN
36
Q

Why should you rarely give an IV bolus of epinephrine to an adult with a pulse?

A

it may be LETHAL. It may be indicated in rare pre-arrest anaphylaxis in adults

37
Q

Usage of what dilution of epinephrine is best practice for cardiac arrest?

A

Best practice for cardiac arrest is to use a 1:10,000 diluted dose of epinephrine (1 mg in 10 mLs)

38
Q

What anatomical location yields the most rapid absorption of IM epinephrine?

A

lateral thigh

39
Q

What is the most beneficial effect of epinephrine in cardiac arrest?

A

It increases systemic vascular resistance thus improving blood flow to vital organs with chest compressions

40
Q

Classification of Ipratropium

A

Anticholinergic

41
Q

Pharmacodynamics of ipratropium (atrovent)

A
  • Parasympatholytic (inhibits stimulation from the parasympathetic nervous system)
  • Vagolytic (inhibits stimulation from the vagus nerve)
  • Inhibits vagal stimulation - allowing the sympathetic nervous system to dominate
  • By allowing the sympathetic nervous system to dominate, impulse generation at the SA node and conduction through the AV node should increase
42
Q

Pharmacokinetics of ipratropium (atrovent)

A

Nebulized

  • Onset - Bronchodilation 1 to 3 min
  • Peak - 1.5 to 2 hours
  • Half-life - ?
  • Duration - ? to 4 hours
43
Q

Indications for ipratropium

A
  • Severe bronchospasm in asthma
  • Severe bronchospasm in COPD
44
Q

Contraindications, precautions, and drug-to-drug interactions for ipratropium

A

Contraindications

  • Hypersensitivity to anticholinergics

Precautions

  • Bronchospasm: Rarely, paradoxical bronchospasm may occur with use of inhaled bronchodilating agents; this should be distinguished from inadequate response
  • Hypersensitivity reactions: Immediate hypersensitivity reactions (urticaria, angioedema, rash, bronchospasm) have been reported

Drug to Drug

  • Anticholinergics: Concurrent use with ipratropium may increase risk of adverse events
45
Q

Adult dosage for ipratropium

A
  • MDI: 8 sprays x 20 mcg = 160 mcg total dose
  • 0.5 mg via nebulizer
    • **DO NOT USE NEBULIZED MEDICATIONS FOR ILI, SUSPECTED OR CONFIRMED CASES OF COVID 19. IF AVAILABLE, USE MDI WITH SPACER OR BLUE CARTRIDGE.
46
Q

Pediatric dosage for ipratropium

A

Trick Question!

not indicated

47
Q

Classification(s) of lidocaine

A
  • Class IB antiarrhythmic
  • Local anaesthetic
48
Q

Pharmacodynamics of lidocaine

A
  • Use-dependant Na channel blocker (i.e. Tends to work fairly specifically on more rapidly depolarizing ectopic foci)
  • Decreases the duration of the action potential by shortening repolarization
49
Q

Pharmacokinetics of lidocaine

A
  • Onset - 2 minutes
  • Peak - Unknown
  • Half-life - Biphasic 8 minutes, 1 to 2 hours
  • Duration - 20minutes
50
Q

Indications for lidocaine

A
  • Pulseless ventricular tachycardia or ventricular fibrillation
  • Topical analgesia
51
Q

Contraindications and relative contraindications for lidocaine

4 absolute, 2 relative

A

Contraindications

  • Allergy or hypersensitivity to lidocaine
  • 3rd degree AV block
  • Ventricular escape rhythms
  • Wolf Parkinson White syndrome
    • Note: Although 2nd degree AV blk is also indicated as a contraindication in several texts, it is essentially a supraventricular rhythm. If it were to appear as a post arrest rhythm, the benefit of administering Lidocaine to prevent recurrence of VF or VT would outweigh the theoretical risks.

Relative Contraindication

  • CHF, cardiogenic shock (consult with the EP)
  • Lidocaine may be used in the setting of ventricular ectopy/VT secondary to cocaine ingestion, however there is an increased risk of seizure due to the synergistic toxic affects of these two agents
52
Q

Precautions, drug-to-drug interactions, and adverse effects of lidocaine

A

Precautions

  • Hepatic or renal failure

Drug to Drug

  • Increased risk of Lidocaine toxicity when given to patients taking cimetidine, ranitidine or beta blockers - Cimetidine inhibits the metabolism of several drugs
  • Giving Lidocaine to patients on Disopyramide may cause bradycardia or cardiac arrest

Adverse Affects

  • Dizziness, light headedness, drowsiness, slurred speech
  • Respiratory arrest – rare
  • Hypotension, cardiac arrhythmias, cardiac arrest
  • Muscle twitching, paraesthesia (tingling in the lips, fingers)
  • “ringing in the ears”
  • Nausea or vomiting, rash, anaphylactoid reaction seizures secondary to lidocaine toxicity.
53
Q

Adult dosing for lidocaine

A
  • 1.0 - 1.5 mg/kg IV bolus or 2.0 mg/kg via ETT if IV not available in the arrested patient
  • Followed by 0.5 - 1.0 mg/kg bolus repeat prn to max of 3 mg/kg
  • Topical spray for analgesia
54
Q

Pediatric dosing for lidocaine

A

Same as for adults!

  • 1.0 - 1.5 mg/kg IV bolus or 2.0 mg/kg via ETT if IV not available in the arrested patient
  • Followed by 0.5 - 1.0 mg/kg bolus repeat prn to max of 3 mg/kg
  • Topical spray for analgesia
55
Q

The priority in treating patients with ventricular ectopy, when considering treatment with lidocaine is:

A

treat the underlying cause of ventricular ectopy first. e.g. cardiac ischemia, electrolyte imbalance, hypoxemia, hypovolemia, etc.

56
Q

Classification(s) of magnesium sulfate

A
  • Antiarrhythmic
  • Airway smooth muscle relaxant
57
Q

Pharmacodynamics of magnesium sulfate

A
  • Used in cardiac care to aid in treatment of VF and pulseless VT and for unstable Torsades de pointes
  • In patients with perfusing rhythms it acts as a smooth muscle relaxant and can induce neuromuscular weakness and heart block therefore must be given slowly
58
Q

Pharmacokinetics of magnesium sulfate

A
  • Onset:
    • IV: Rapid
    • 20-30 minutes when administering as an infusion to asthma patients
  • Peak: <5 minutes
  • Duration: Duration of effect undetermined in cardiac arrest
59
Q

Indications for magnesium sulfate

A
  • VF or pulseless VT
  • Recurrent intermittent episodes of wide complex tachycardia
  • Unstable Torsades de pointes with recurrent periods of loss of perfusing pulse
  • May be administered as an infusion to patients with asthma refractory to bronchodilation
60
Q

Contraindications, precautions, warnings, and drug-to-drug interactions for magnesium sulfate

A

Contraindications

  • Hypersensitivity to Magnesium Sulfate
  • 2nd or 3rd degree AV block

Precautions

  • May prolong effect of non-depolarizing neuromuscular blockers
  • May enhance actions of calcium channel blockers

Warning

  • In patients with perfusing rhythm: hypotension, heart block, nausea, neuromuscular weakness, respiratory depression

Drug to Drug Interactions

  • May enhance action of Calcium channel blockers
61
Q

Adult dosing for magnesium sulfate

A
  • Torsades de points: 2 g IV in 100 mL N/S over 15 min, followed by an infusion.
  • Asthma: 2 g/250 cc N/S infused over 20 min
  • Cardiac Arrest: 4 g IV bolus
62
Q

Pediatric dosing for magnesium sulfate

A
  • See BCEHS Pediatric Dosage (BCEHS Peds Dosages) recommendations for age and weight-appropriate dosing information
  • 50 mg/kg for pediatrics, max 2 g
63
Q

Describe infusion protocols for magnesium sulfate

A
  • 2g over 20 minutes
  • 50ml N/S bag with 10gtts drip set
    • 1gt/2s
  • 250ml N/S bag with 10gtts drip set
    • 2-3gtts/s
64
Q

Classification(s) of midazolam

A
  • Sedative-hypnotic
  • CNS depressant
  • Short-acting benzodiazepine
65
Q

Pharmacodynamics of midazolam

A
  • Short acting benzodiazepine. CNS depressant with sedative, muscle relaxant, anticonvulsant
  • Estimated to be 2 - 4 times more potent than diazepam. Intensifies activity of gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter of the brain. This causes chloride channels to open allowing an influx of chloride (-ve ion) into the cell. This makes the neuronal cells hyperpolarized - i.e. it takes longer for the cells to reach threshold and depolarize. This results in CNS depression.
  • Blocks memory, reduces anxiety, but enables patient to follow commands
  • Strong amnesic effects
66
Q

Pharmacokinetics of midazolam

A
  • Onset: 1 to 5 min (5-15 min IM)
  • Peak: IV route unknown (45 min IM)
  • Half-life: 1.5 to 3 hours
  • Duration: 2 to 6 hours (dose related)
  • Note: All benzodiazepines are metabolized by the liver. Midazolam is converted by the cytochrome P450 enzymes in the liver to a non-active metabolite. This is why Midazolam is shorter acting than diazepam.
67
Q

Indications for midazolam

A
  • Sedation of the agitated patients (provided a correctable underlying cause has been ruled out and the patient is stable)
  • Anti-convulsant
  • Cocaine induced Acute Coronary Syndrome
  • Intubation maintenance, if Ketamine unavailable or contraindicated
68
Q

Contraindications and precautions for midazolam

A

Contraindications

  • Hypersensitivity to midazolam or other benzodiazepines
  • Acute narrow angle glaucoma
  • Shock
  • Coma
  • Alcohol intoxication
  • Depressed vital signs
  • Overdose

Precautions

  • Use cautiously when administration of other CNS depressants / narcotics are being administered (Narcotic + Midazolam = Synergistic effect)
  • Use cautiously in the elderly and those with renal disease
  • Use cautiously in cases of CHF / COPD (respiratory depressant effect)
69
Q

Adverse effects of midazolam

A
  • Over sedation, headache, blurred vision, paradoxical combativeness (rare)
  • Hypotension, variations in pulse rate
  • Nausea, vomiting, hiccoughs
  • Pain and tenderness at injection site
  • Respiratory depression / arrest, cough
70
Q

Drug to drug interactions of midazolam

A
  • Drugs that are known to inhibit the cytochrome P450 enzyme system may increase the potency and duration of midazolam (i.e. some drugs in the drug classes of azole antimycotics, protease inhibitors, calcium channel antagonists, and macrolide antibiotics)
  • Lower doses are necessary for patients receiving concomitant narcotics or other CNS depressants
  • Erythromycin, diltiazem, verapamil, ketoconazole, fluconazole and itraconazole were shown to significantly increase the bioavailability of midazolam and may cause prolonged sedation
  • Ritonavir and nelfinavir may cause intense and prolonged sedation and respiratory depression due to a decrease in plasma clearance of midazolam
  • Rifampin, carbamazepine, and phenytoin may markedly decreased the effectiveness of midazolam
71
Q

Adult dosing for midazolam

A
  • 5 to 10 mg IM
  • 2 to 5 mg IV/IO incrementally to effect
  • May be repeated as required in small increments
72
Q

Pediatric dosing for midazolam

A
  • 0.2 mg/kg IN (Max dose 10 mg)
    • IN administration is the recommended route over IM for MIDAZOLam due to more consistent absorption when given intranasally
    • Administer half dose per nare
  • 0.1 mg/kg IV/IO (Max dose 5 mg) OR
  • 0.2 mg/kg IM (Max dose 10 mg) OR
  • Safety alert: Remember to account for the 0.1 mL dead space in the mucosal atomizer device (MAD) to ensure the accurate dose is administered and documented
73
Q

What is the dose equivalency between midazolam and diazepam?

A

2 mg of Midazolam is approximately equivalent to 5 mg of Diazepam

74
Q

Pharmacodynamics of morphine

A
  • Morphine is an opioid alkaloid that acts on opioid receptors in the CNS to produce analgesia, euphoria and sedation
  • Interacts predominantly with the opioid mu-receptor
  • Interacts with receptors at the spinal cord level, depressing pain impulse transmission
  • Causes venodilation - reduces cardiac preload
75
Q

Pharmacokinetics of morphine

A

Intravenous

  • Onset - Rapid
  • Peak - 20 minutes
  • Half-life - 2 to 3 hours
  • Duration - 4 to 5 hours
76
Q

Indications for morphine

A
  • For symptom relief in palliative/end of life patients presenting with pain and/or shortness of breath
77
Q

Contraindications and precautions for morphine

A

Indications

  • For symptom relief in palliative/end of life patients presenting with pain and/or shortness of breath

Contraindications

  • Allergy or known hypersensitivity to narcotics
  • Use with caution in asthma and COPD
78
Q

Adverse effects and drug to drug interactions of morphine

A

Adverse Effects

  • Lightheadedness, dizziness, sedation, agitation, fear, delirium, hallucinations, drowsiness, disorientation
  • Respiratory depression/apnea.
  • Profound hypotension, reflex tachycardia, bradycardia, palpitations, chest wall rigidity
  • Nausea and vomiting

Drug to Drug Interactions

  • Depressant effects are potentiated by the presence of other CNS depressants such as alcohol, sedatives, antihistaminics, or psychotropic drugs
  • Patients on neuroleptics: Morphine may increase the risk of respiratory depression, hypotension and profound sedation or coma
79
Q

Adult dosing for morphine

A
  • 0.1 mg/kg SC OR 2.5-5 mg SC
  • Repeat q 10-30 min. prn - maintaining blood pressure at > 100 systolic or as per local EP orders
80
Q

Pediatric dosing for morphine

A
  • 0.1 - 0.2 mg/kg (diluted) slow IV (over 5 min.) or SC, IM
  • See BCEHS Pediatric Dosage (BCEHS Peds Dosages) recommendations for age and weight-appropriate dosing information
81
Q
A

ACP Pharmacology (7 decks)

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