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Critical Care Nursing > Exam 1 drugs > Flashcards

Exam 1 drugs Flashcards

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1
Q 
SEDATION
• Decrease?
• May prolong?
• Alters?
• Do not forget to address?
A
  • Decrease anxiety and agitation, provide amnesia, reduce patient-ventilator dysynchrony, decrease respiratory muscle oxygen consumption, facilitate nursing care.
  • May prolong mechanical ventilation and increase costs.
  • Alters neuro assessment
  • Do not forget to address pain while on sedation
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2
Q

GOALS OF SEDATION

A
  • Old Term - Obtundation
  • New Documentation – “Sleepy but arousable”
  • Almost always a combination of anxiolytics and analgesics
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3
Q

SEDATION MONITORING

A
  • Light sedation when appropriate

* Richmond Agitation Sedation Scale (RASS)

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4
Q

BUTYROPHENONES

A 
• Haloperidol (Haldol)
• Treatment of choice for hospital acquired delirium 
• Anti-psychotic tranquilizer
• Slow onset
• No respiratory depression or hypotension
- Side effects
• QT prolongation
• Extrapyramidal side effects
• Neuroleptic malignant syndrome
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5
Q

CENTRAL ALPHA-2 ADRENERGIC AGONIST

A
  • Dexmedetomidine (Precedex)
  • Light sedation
  • Mild analgesic effect
  • Not associated with respiratory depression (unlike propofol)
  • Used in ETOH withdrawal without associated intubation
  • Enhances effect of beta blockers
  • Newest sedation medication approved 1999
  • Expensive
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6
Q

BENZODIAZEPINES (what are they)

A
  • Act as sedative, hypnotic, amnestic, anticonvulsant, anxiolytic.
  • No analgesia.
  • Develop tolerance.
  • Synergistic effect with opiates.
  • Lipid soluble, metabolized in the liver
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7
Q

BENZODIAZEPINES

A
  • Diazepam (Valium)
    • Repeated dosing leads to accumulation
    • Difficult to use in continuous infusion
  • Lorazepam (Ativan)
    • Slowest onset, longest acting
    • Metabolism not affected by liver disease
  • Midazolam (Versed)
    • Fast onset, short duration
    • Accumulates when given in infusion >48 hours
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8
Q

BENZODIAZEPINES SIDE- EFFECTS

A
  • Hypotension
    • Bradycardia
    • Respiratory depression
    • Confusion
    • Worsens hospital acquired delirium
    • Associated with ICU post-traumatic stress disorder (PTSD)
    • What is the reversal agent for benzos??
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9
Q

PROPOFOL

A
  • Sedative, anesthetic, amnestic, anticonvulsant
  • Respiratory and CV depression
  • Obtain lipid panel- highly lipid soluble
  • Rapid onset, short duration
  • Clearance not changed in liver or kidney disease.
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10
Q

PROPOFOL SIDE EFFECTS

A
  • Unpredictable respiratory depression
  • Use only in mechanically ventilated patients
  • Hypotension
  • First described in post-op cardiac patients
  • Increased triglycerides
  • 1% solution of 10% intralipids
  • Daily tubing changes, dedicated port
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11
Q

CLINICAL APPLICATION for propofol

A
  • Propofol is preferred over midazolam for neurologic patient because propofol allows for quicker arousal
  • Daily interruption of sedation/“sedation vacation” to ensure the patient is on the lowest sedation needed
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12
Q

MONITORING SEDATION

A
  • Many scoring systems, none are validated.
  • Ramsey
  • 1: Anxious, agitated, restless
  • 2: Cooperative, oriented, tranquil
  • 3: Responds to commands
  • 4: Asleep, brisk response to loud sounds
  • 5: Asleep, slow response to loud sounds
  • 6: No response
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13
Q

ANALGESICS

A
  • Relieve Pain
  • Opioids
  • Non-opiods
  • Can be given PRN but not consistent
  • Continuous infusion is associated with sedation
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14
Q

OPIOIDS

A 
1) Morphine
• Hypotension
• Greatest pruritis risk
2) Dilaudid
• 4 times stronger than morphine 
• hypotension
• Decreased itching
3) Fentanyl
• Higher potency of morphine
• Lowest risk of hypotension
• Slowed breathing
• Decreased histamine release 
• Decreased itching
4) Demerol
• Hallucinations, metabolites build up and can lead to seizures
• Not used frequently
• Used for chills in oncology patients
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15
Q

Non-Opiods

A

1) Ketamine
• Analog of phencyclidine, sedative and anesthetic, dissociative anesthesia.
• Hypertension, hypertonicity, hallucinations, nightmares.
• Potent bronchodilator
2) Ketorolac (Toradol)
• NSAID
• Limited efficacy (post-op ortho)
• Synergistic with opiodes
• No respiratory depression
• Increased side effects in the critically ill
• Renal failure, thrombocytopenia, gastritis

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16
Q

PARALYTICS

A
  • Paralyze skeletal muscle at the neuromuscular junction.
  • They do not provide any analgesia or sedation.
  • Sedate and treat for pain prior to using paralytic
  • Think about it—what if you could hear and feel everything but couldn’t move?!?
  • Prevent examination of the central nervous system
  • Increase risks of DVT & pressure ulcers
17
Q

USE OF PARALYTICS

A
  • Intubation
  • Facilitation of mechanical ventilation
  • Preventing increases in ICP
  • Decreasing metabolic demands (shivering)
  • Used for patient with increased intracranial pressure or status epilepticus
18
Q

PARALYTICS

A
  • Depolarizing agents - Succinylcholine
  • Non-depolarizing agents
  • Pancuronium
  • Vecuronium
  • Atracurium
19
Q

COMPLICATIONS OF PARALYSIS

A

• Persistent neuromuscular blockade
- Drug accumulation in critically ill patients
- Renal failure and >48 hr infusions raise risk
• Hypokalaemia, hyperkalaemia, hypophosphataemia and drugs may enhance paralysis
• In patients given neuromuscular blockers for >24 hours, there is a 5-10% incidence of prolonged muscle weakness (post-paralytic syndrome)

20
Q

COMPLICATION OF PARALYSIS

A

• Persistent neuromuscular blockade
- Drug accumulation in critically ill patients
- Renal failure and >48 hr infusions raise risk
• In patients given neuromuscular blockers for >24 hours, there is a 5-10% incidence of prolonged muscle weakness (post-paralytic syndrome).

21
Q

MONITORING PARALYSIS

A
  • Observe for movement

* Twitch monitoring, train of four, peripheral nerve stimulation

22
Q

PRESSORS

A
  • Vasopressors are class of drugs that elevate Mean Arterial Pressure (MAP) by inducing vasoconstriction.
  • Inotropes increase cardiac contractility.
  • Many drugs have both vasopressor and inotropic effects.
  • Vasopressors are indicated for a decrease of >30 mmHg from baseline systolic blood pressure or MAP <60 mmHg, when either condition results in end-organ dysfunction secondary to hypoperfusion
23
Q 
RECEPTOR PHYSIOLOGY
1) Alpha-1 Adrenergic
2) Beta Adrenergic: Beta 1 &amp; Beta 2
3) Dopamine
Location and effect
A

1) Alpha-1 Adrenergic
- Location: Vascular wall> Effect: Vasoconstriction
- Location: Heart> Effect: Increase duration of contraction without increased chronotropy
2) Beta Adrenergic: Beta 1 & Beta 2
- Location Beta 1: Heart> Effect: ↑Inotropy and chronotropy
- Location Beta 2: Blood vessels> Effect: Vasodilation
3) Dopamine
- Location: Renal> Effect: Vasodilation
- Location: Splanchnic (mesenteric)> Effect: Vasodilation
- Location: Coronary> Effect: Vasodilation
- Location: Cerebral> Effect: Vasodilation
- Subtype
- Effect: Vasoconstriction

24
Q

DOPAMINE

A
  • More potential for arrhythmias/increased heart rate
  • May increase both blood pressures and flow; may be best used in patient with low heart rate and inadequate fluid resuscitation
25
Q

DOPAMINE INOTROPIN

A
  • Renal (2-4 mcg/kg/min)- increase in mesenteric blood flow
  • b (5-10 mcg/kg/min)- modest positive ionotrope
  • a (10-20 mcg/kg/min) vasoconstriction
  • “Renal dose” dopamine probably only transiently increases u/o without changing clearance.
  • There are better b and a agents
  • Adverse effects- tachyarrhythmias
26
Q

DOBUTAMINE DOBUTREX

A

• Primarily b1, mild b2.
• Dose dependent increase in stroke volume, accompanied by
decreased filling pressures.
• SVR may decrease, baroreceptor mediated in response to  SV.
• BP may or may not change, depending on disease state.
• Useful in right and left heart failure.
• May be useful in septic shock.
• Dose- 5-15 mcg/kg/min.
• Adverse effects- tachyarrhythmias.

27
Q

PHOSPHODIESTERASE (PDE) INHIBITORS

A
  • Amrinone/Inamrinone (Inocor), Milrinone (Primacor)
  • Positive ionotrope and vasodilator
  • Little effect on heart rate
  • Uses- CHF
  • Adverse Effects - arrhythmogenic, thrombocytopenia
  • Milrinone dosing- 50mcg/kg bolus, 0.375-0.5 mcg/kg/min infusion
28
Q

NOREPINEPHRINE (LEVOPHED)

A
  • Potent a agent, some b
  • Vasoconstriction (that tends to spare the brain and heart).
  • Good agent to increase SVR in high output shock.
  • Dose 1-12 mcg/min
  • Can cause reflex bradycardia (vagal).
29
Q

EPINEPHRINE

A
  • b at very low doses, a at higher doses.
  • Very potent agent.
  • Some effects on metabolic rate, inflammation.
  • Useful in anaphylaxis.
  • AE- Arrhythmogenic, coronary ischemia, renal vasoconstriction, increase metabolic rate.
30
Q

PHENYLEPHRINE (NEOSYNEPHRINE)

A
  • Strong, pure a agent.
  • Vasoconstriction with minimal increase in heart rate or contractility. • Does not spare the heart or brain.
  • BP at the expense of perfusion.
31
Q

VASOPRESSIN

A
  • Vasoconstrictor that may be useful in septic shock.

* Use evolving to parallel hormone replacement therapy. • 0.4 units/min

32
Q

NITROGLYCERINE TRIDIL

A
  • Vasodilators at low doses (<40mcg/min)
  • Arteriolar dilation at high doses (>200 mcg/min)
  • Rapid onset, short duration, tolerance.
  • AE- inhibits platelet aggregation, increase ICP, headache.
33
Q

NITROPRUSSIDE NIPRIDE

A

• Balancedvasodilator
• Rapidonset,shorteliminationtime
• Useful in hypertensive emergency, severe CHF, aortic dissection
• Accumulatesinrenalandliverdysfunction.
Toxicity= CN poisoning (decreased CO, lactic acidosis, seizures).
• Dosing-0.2-10mcg/kg/min
• OtherAE-increase ICP

34
Q

ANTIARRYTHMICS

A
  • AMIODARONE
  • CARDIZEM
  • ADENOCARD/ADENOSINE
  • LIDOCAINE
35
Q

AMIODARONE

A
  • Only for treatment of the following documented life- threatening recurrent ventriculararrhythmias that do not respond to other antiarrhythmics or when alternative agents are not tolerated: Recurrent ventricular fibrillation, recurrent hemodynamically unstable ventricular tachycardia. Serious and even fatal toxicity has been reported with this drug; use alternative agents first; very closely monitor patient receiving this drug
  • 1,000 mg IV over 24 hr—150 mg loading dose over 10 min, followed by 360 mg over 6 hr at rate of 1 mg/min. For maintenance infusion, 540 mg at 0.5 mg/min over 18 hr. May be continued up to 96 hr or until rhythm is stable. Switch to oral form as soon as possible
36
Q

Cardizem (antiarrhythmic)

A

• Decrease in BP.
• Decrease in frequency and severity of anginal attacks.
• Decrease in need for nitrate therapy.
• Increase in activity tolerance and sense of well-being.
• Suppression and prevention of tachy arrhythmias.
• V Push: Diluent: Administer bolus dose undiluted. Concentration: 5
mg/mL.
• Rate: Administer over 2 min.
• Continuous Infusion: Diluent: Dilute 125 mg in 100 mL, 250 mg in 250 mL, or 250 mg in 500 mL of 0.9% NaCl, D5W, or D5/0.45% NaCl. Infusion is stable for 24 hr at room temperature or if
refrigerated. Concentration: 125 mg/125 mL (1 mg/mL), 250 mg/300 mL (0.83 mg/mL), 250 mg/550 mL (0.45 mg/mL)

37
Q

ADENOSINE (antiarrhythmia)

A
  • Paroxysmal Supraventricular Tachycardia
  • Indicated for conversion to sinus rhythm of paroxysmal supraventricular tachycardia (PSVT), including that associated with accessory bypass tracts (Wolff-Parkinson-White Syndrome)
  • Adenocard: 6 mg IVP over 1-3 seconds (maybe given IO) followed by rapid flush with 20 mL NS, if no conversion within 1-2 minutes give 12 mg IVP, repeat a second time if necessary (30 mg total)
  • Dosingconsiderations
  • WhenclinicallyadvisableforPSVT,appropriatevagalmaneuvers (eg, Valsalva maneuver), should be attempted prior to adenosine administration
38
Q

Lidocaine

A
  • Indications: V Fib, VT, stable wide complex TC ? type, ventricular ectopy
  • Loading Dose: 1.0-1.5 mg/kg IVP and repeat 0.5-1.5 mg/kg IVP q 3-5 min until converted or to a total of 30 mg/kg
  • Maintenance Dose: 2-4 mg/min (2 gms/500cc at 30 cc/hr = 2 mg/min)
  • Complications: CNS depression, drowsiness, unconsciousness, apprehension, change in vision, vomiting, bradycardia, hypotension, seizures, AV block

Critical Care Nursing (15 decks)

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