Intravenous Medications and Adjuncts

Question 1

What is the treatment of malignant hyperthermia?

Answer 1

Dantrolene- developed as a muscle relaxant initially for the treatment of chronic spasticity.

Dantrolene blocks muscle spasm and thus heat production by preventing calcium release from the sarcoplasmic reticulum.

Question 2

T or F: dantrolene must be reconstituted in 60 mL of normal saline.

Answer 2

True

Question 3

T or F: pH of dantrolene is high (it is basic)

Answer 3

true

Question 4

T or F: reconstituted dantrolene contains 3 gm of mannitol and brisk diuresis is likely to occur.

Answer 4

True

Question 5

What is the half-life of dantrolene?

Answer 5

12 hours

Question 6

T or F: once pt stabilized, dantrolene infusion must continue for 24 hours in ICU

Answer 6

true

Question 7

T or F: dantrolene is metabolized in the liver.

Answer 7

True

Question 8

T or F: alcohol-dependent patients will show cross-tolerance to barbiturates and benzos but not to opioids.

Answer 8

True

Question 9

T of R: droperidol is a dopamine antagonist neuroleptic agent with antipsychotic and antiemetic action.

Answer 9

True- used for the treatment of PONV, duration of action does not correspond well with elimination half-life becasue its dissociation from the dopamine receptor site is slow.

Question 10

By what mechanism of action does dexmedetomidine work?

Answer 10

An alpha-2 adrenergic agonist.

Similar to clonidine, dexmedetomidine has anxiolytic, sedative, and analgesic effects but has 8x higher affinity for the alpha-2 receptor.

Question 11

T or F: Dexmedetomidine is water soluble. How is dexmedetomidine metabolized? Excreted?

Answer 11

True. It is metabolized in the liver, and the metabolites are excreted via the kidney.

Question 12

T or F: when dexmedetomidine is abruptly discontinued after infusions of more than 24 hours, withdrawal symptoms may occur, including agitation, tachycardia, and hypertension.

Answer 12

True

Question 13

T or F: a transient phase of hypertension after the loading dose may be induced by the binding of dexmedetomidine to vascular alpha-2 receptors and seldom requires action.

Answer 13

True- a large bolus has been reported to cause vasoconstriction and hypertension, followed by progressive hypotension. Whether the patient develops hypertension or hypotension depends on the patient’s ability to mount a sympathetic response.

Dexmedetomidine is an alpha-2 agonist that binds to receptors in the locus ceruleus and spinal cord.

Question 14

T or F: dexmedetomidine is associated with reduced opioid and hypnotic agent requirements around anesthesia, without producing significant respiratory depression. Added benefits include short duration, lack of effect on gut motility, and absence of active metabolites. May have renoprotective effect and blunts postoperative catecholamine surge. May induce significant bradycardia (seen in patients with hypovolemia).

Answer 14

True- a bolus dose of 2 mcg/kg has resulted in profound sinus bradycardia and even sinus arrest. This can be treated effectively with administration of anticholinergics such as glycopyrrolate or atropine.

Question 15

T or F: tylenol has analgesic and anti-pyretic effects but minimal anti-inflammatory action.

Answer 15

True

Question 16

T or F: tylenol has virtually no antiplatelet or GI effects.

Answer 16

True

Question 17

T or F: hepatotoxicity from Tylenol occurs as a result of an accumulation of the toxic metabolite NAPQI, which ordinarily reacts with glutathione resulting in conjugates that can be renally excreted. When large amounts of Tylenol are ingested, glutathione becomes depeted and NAPQI accumulates, leading to hepatoxicity and hepatic necrosis.

Answer 17

IV acetylcysteine is the treatment of acetaminophen overdose.

When Tylenol is taken in large quantities, a minor metabolite called NAPQI accumulates. It is normally conjugated by glutathione, but when taken in excess, the body’s glutathione reserves are not sufficient to inactivate the toxic NAPQI. NAPQI then reacts with key hepatic enzymes, damaging hepatocytes, and leading to severe liver damage and even death by fulminant liver failure.

Acetylcysteine augments the glutathione reserves in the body and, together with glutathione, directly bind to toxic metabolites. These actions protect hepatocytes from NAPQI toxicity.

Question 18

T or F: ketorolac is an NSAID drug that is metabolized in the liver and excreted by the kidneys. Adverse effects include GI irritation, ulceration, bleeding. Effects on platelets is reversible. What is the half-life?

Answer 18

True- Half life is 5 hours

Question 19

T or F: Patients with asthma and chronic rhinitis are at increased risk of developing bronchospasm when given NSAIDs, particularly aspirin. Ketorolac should be withheld from patients with a history of NSAID-induced bronchospasm.

Answer 19

True

Question 20

T or F: onset of anticoagulation of heparin is established immediately after IV administration.

Answer 20

True

Question 21

T of F: heparin is eliminated via kidneys and hepatic metabolism. Monitoring of heparin should be via ACT. HIT is seen after repeated administration.

Answer 21

True

Question 22

What agent can be administered for the immediate reversal of heparin? What is the ratio of this agent to heparin?

Answer 22

Protamine- 1 mg of protamine inactivates 100 units of heparin.

Question 23

What are adverse effects associated with the administration of protamine?

Answer 23

Hypotension
noncardiogenic pulmonary edema
pulmonary vasoconstriction
right heart decompensation
cardiovascular collapse
hypersensitivity reaction
causes direct histamine release

Question 24

What is the mechanism of action of aspirin?

Answer 24

Irreversible inhibition of the production of thromboxane A2, which is an important factor involved in platelet aggregation and activation.

Question 25

How long do the effects of aspirin last?

Answer 25

7-10 days

Question 26

How many days before surgery should Plavix be discontinued?

Answer 26

7 days prior to surgery

Question 27

What is the duration of cocaine intoxication if administered via a) IV and smoking, b) snorting, and c) oral ingestion?

Answer 27

15-30 minutes after IV injection and smoking
+/- 1 hour after snorting
3 hours after oral ingestion

Question 28

What is the mechanism of action of cocaine?

Answer 28

Cocaine’s sympathicomimetic and vasoconstrictive properties are caused by presynaptic reuptake blockade of serotonin and catecholamines and peripheral alpha-adrenergic agonistic activity.

Cocaine is also a sodium channel blocker, which in severe overdoses may lead to QRS-complex prolongation and negative inotropy.

Question 29

T or F: Naloxone, succinylcholine, and beta blockers are contraindicated during cocaine intoxication. How does one manage cocaine intoxication therapy?

Answer 29

True- Supportive care, oxygen, benzodiazepines, and phentolamine are cornerstones of acute cocaine intoxication therapy.

Question 30

T or F: furosemide inhibits the Na/K/2Cl co-transporter in the loop of Henle, resulting in diuresis with loss of Na, K, Ca, and Mg.

Answer 30

True

Question 31

T or F: IV furosemide may elicit prerenal kidney failure in patients with pre-existing kidney disease.

Answer 31

True

Question 32

T or F: ototoxicity is seen at high doses of furosemide or with rapid administration, expecially when combined with aminoglycosides or in patients with kidney failure.

Answer 32

True

Question 33

Volatile anesthetic and chemotherapy contraindications:

Cyclophosphamide- halothane –> inhibits plasma cholinesterase, prolonging duration of action of Sch
Doxorubicin- cardiomyopathy
Methotrexate- nitrous oxide –> severe bone marrow suppression and mucositis

Answer 33

True

Question 34

T or F: metoclopramide has significant adverse effects, including sedation, extrapyrimidal symptoms, and tardive dyskinesia.

Answer 34

True

Question 35

T of F: metoclopramide is contraindicated in patients using levodopa and patients with epilepsy or pheochromocytoma. Reglan is not effective in paralytic ileus.

Answer 35

True

Question 36

T of F: reglan is eliminated renally.

Answer 36

True

Question 37

T or F: ketamine, in contrast to most other anesthetic drugs, is associated with a disorganized EEG pattern that is variable in all doses.

Answer 37

True

Question 38

T or F: electrocortical silence, or an isoelectric state, cannot occur with anesthetic doses of ketamine, even in patients who are deeply anesthetized.

Answer 38

True- in fact, ketamine is associated with increased epileptiform activity.

Question 39

T or F: opioids in general will cause a dose-related decrease in the frequency and an increase in the amplitude of the EEG waves.

Answer 39

True

Question 40

T or F: Neuromuscular blockers can lower the processed EEG values.

Answer 40

True

Question 41

T or F: barbiturates have been shown to lower ICP by inducing a dose-dependent reduction in CBF and CMRO2.

Answer 41

T- large doses of barbiturates casue the EEG to become isoelectric and the CMRO2 to be reduced by 45%.

Question 42

T or F: flumazenil is a competitive benzodiazepine antagonist that has high affinity and great specificyt for the benzodiazepine receptor.

Answer 42

T- has minimal intrinsic effect. Onset of action is 3 min and is cleared rapidly, more rapidly than all the benzos, so it is possible that resedation may occur.

Question 43

T or F: flumazenil reverse the hypnotic and respiratory effects of benzos more than the amnestic effects. HAs no negative side effects on the cardiovascular system.

Answer 43

True

Question 44

T or F: dexmedetomidine decreases both CBF and CMR. This may be beneficial for patients with ischemic neurological injury.

Answer 44

True

Question 45

When barbiturates are injected into the radial artery, what is the treatment?

Answer 45

The risk is prolonged vasoconstriction leading to gangrene. Treatment is stellate ganglion block.

Question 46

T or F: ketamine increases ICP, CMRO2, and CBF.

Answer 46

True- contraindicated in patients with already increased ICP

Question 47

T or F: metoclopramide can cause increased prolactin levels.

Answer 47

True- thus it must be avoided in patients in assisted reproductive therapy. Droperidol also causes increased prolactin levels.

Question 48

T or F: phenobarbital, primidone, phenytoin, and carbamazepine are potent hepatic enzyme inducers.

Answer 48

True- the most noticeable effect is the short duration of clinical effect with aminosteroid neuromuscular blocking agents.