Exam 1 drugs Flashcards
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
2
Q
GOALS OF SEDATION
A
- Old Term - Obtundation
- New Documentation – “Sleepy but arousable”
- Almost always a combination of anxiolytics and analgesics
3
Q
SEDATION MONITORING
A
- Light sedation when appropriate
* Richmond Agitation Sedation Scale (RASS)
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
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
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
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
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??
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.
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
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
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
13
Q
ANALGESICS
A
- Relieve Pain
- Opioids
- Non-opiods
- Can be given PRN but not consistent
- Continuous infusion is associated with sedation
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
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
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 & 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
DOPAMINE INOTROPIN
- 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
DOBUTAMINE DOBUTREX
• 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
PHOSPHODIESTERASE (PDE) INHIBITORS
* 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
NOREPINEPHRINE (LEVOPHED)
* 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
EPINEPHRINE
* 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
PHENYLEPHRINE (NEOSYNEPHRINE)
* 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
VASOPRESSIN
* Vasoconstrictor that may be useful in septic shock.
| * Use evolving to parallel hormone replacement therapy. • 0.4 units/min
32
NITROGLYCERINE TRIDIL
* 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
NITROPRUSSIDE NIPRIDE
• 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
ANTIARRYTHMICS
* AMIODARONE
* CARDIZEM
* ADENOCARD/ADENOSINE
* LIDOCAINE
35
AMIODARONE
* 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
Cardizem (antiarrhythmic)
• 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
ADENOSINE (antiarrhythmia)
* 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
Lidocaine
- 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
