Term
| central venous pressure (CVP) |
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Definition
equivalent to right atrial pressure
indicates the VOLUME STATUS OF THE RIGHT VENTRICLE (right ventricular end diastolic pressure)
CVP can be inaccurate (falsely elevated) in patients:
with pulmonary or cardiac disease
on mechanical ventilation
normal value: 2-6 mmHg |
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Term
| pulmonary capillary wedge pressure (PCWP) |
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Definition
PCWP equilibrates with distal pressure on the left side
PCWP = left ventricular end diastolic pressure = left ventricular end diastolic volume
PCWP estimates PRELOAD
conditions that elevate PCWP (inaccurate prespresentation):
mitral stenosis
pulmonary veno-occlusive disease
high levels of positive end-expiratory pressure (PEEP) with mechanical ventilation)
normal value: 5-12 mmHg |
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Term
| systemic vascular resistance (SVR) |
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Definition
SVR = change in pressure/CO
estimates AFTERLOAD
increased SVR = vasoconstriction
decreased SVR = vasodilation |
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Term
| mixed venous oxygen saturation (SVO2, MVO2) |
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Definition
indicates TISSUE PERFUSION and can be used to calculate O2 consumpation
normal value ~70%
levels > 75-80% can indicate hyperdynamic states (i.e. sepsis, hyperhydroidims, alsohol withdrawl, etc.)
levels < 65% can indicate poor cardiac output states (i.e. cardiogenic shock, etc.)
ESTIMATES CARDIAC OUTPUT
decreased CO -> blood stays in the periphery longer -> tissues extract more O2 from the blood -> less O2 coming back to the heart -> decreased SVO2 |
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Term
| alpha 1 receptor stimulation |
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Definition
physiological effect:
vasoconstriction of arteries and veins
hemodynamic effect:
increased SVR
increased MAP |
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Term
| beta1 receptor stimulation |
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Definition
physiological effect:
increased contractility (inotropy); tachycardia
hemodynamic effect:
increased CO
increased HR |
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Term
| Beta2 receptor stimulation |
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Definition
physiological effect:
vasodilation of arteries and veins, bronchodilation
hemodynamic effect:
decreased SVR |
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Term
| dopamine receptor stimulation |
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Definition
physiological effect:
vasodilation
increased kidney perfusion
hemodynamic effect:
increased urine output (?) |
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Term
| vasopressin receptor stimulation |
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Definition
physiological effect:
vasoconstriction
increased urine output
hemodynamic effect:
increased SVR
increased urine output |
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Term
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Definition
dopamine
norepinephrine
epinephrine
phenylephrine
vasopressin |
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Term
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Definition
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Term
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Definition
supply does not equal demand
syndrome involving poor tissue perfusion
tissue perfusion determined by MAP
MAP dependent on CO and SVR
often accompanied by hypotension -> multiple organ system failure and death |
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Term
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Definition
etiology: reduction in intravascular volume
conditions causing intravascular volume depletion:
hemorrhagic - GI bleed, trauma, surgery, internal bleeding
non-hemorrhagic - dehydration (vomiting, diarrhea, diuretics), fluid shifting (ascites), cutaneous loss (burns, excessive perspiration, insensible water loss)
HEMODYNAMIC PARAMETERS:
DECREASED PCWP AND CVP due to decreased venous return (preload)
DECREASED CO due to decreased venous return (decreased stroke volume)
COMPENSATORY INCREASE IN SVR to maintain BP, however often inadequate compensation and hypotension and hypoperfusion prevail |
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Term
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Definition
etiology: abnormality in cardiac function
conditions that can precipitate cardiogenic shock:
non-mechanichal - acute MI (causing LV dysfunction), acute CHF exacerbation, cardiomyopathy (end stage)
mechanical - mitral or aortic valve insufficiency, severe aortic stenosis, septum or free wall rupture
HEMODYNAMMIC PARAMETERS:
DECREASED CO due to pump failure
COMPENSATORY INCREASED SVR to maintain BP
INCREASED PCWP OR CVP (especially in CFH) b/c heart cannot pump blood through circulation -> volume overload
overall decrease in arterial BP and hypoperfusion; can lead to ischemia in various organs |
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Term
| DISTRIBUTIVE (VASODILATORY) SHOCK |
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Definition
etiology: loss of vascular tone leading to hypotension and hypoperfusion
conditions causing distributive shock:
SEPTIC SHOCK - infection that causes systemic reaction; due to inflammation from sepsis the vessels dilate and become very leaky
ANAPHYLAXIS
neurogenic causes - spinal injury, cerebral damage, etc.
drug induced - anesthesia, overdose of opioids
acute adrenal insufficiency
HEMODYNAMIC PARAMETERS:
DECREASED SVR b/c no vasoconstriction
INCREASED CO to maintain organ profusion |
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Term
| systemic inflammatory response syndrome (SIRS) |
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Definition
body's response to a variety of clinical insults
must meet 2 OF THE 4 following criteria:
temperature: > 38C or < 36C
heart rate: > 90 beats/min
respiratory: > 20 breaths/min
WBC count: > 12,000 or < 4,000 or > 10% bands |
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Term
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Definition
| SIRS + suspected/documented infection |
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Term
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Definition
| sepsis + organ dysfunction, hypoperfusion, or hypotension (measured by MAP) |
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Term
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Definition
| severe sepsis + need for vasopressors |
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Term
| goals of therapy for early goal directed therapy |
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Definition
goals of therapy (within the initial 6 hours):
CVP 8-12
MAP > 65
urine output > 0.5 ml/kg/hr
central venous O2 sat (SVO2) > 70% or mixed venous O2 sat (MVO2) > 65% |
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Term
| implementation of early goal directed therapies |
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Definition
fluids, vasopressors, blood products, inotropes
INITIAL FLUID RESUSCITATION AND HEMODYNAMIC STABILITY: USE IF CVP < 8 AND MAP < 65
choice of fluids - crystalloid vs. colloid
crystalloids:
isotonic solution - 0.9% NaCl or LR
recommended initially to expant intravascular volume
cheaper and readily available
colloids:
albumin, hetastarch, dextran
expand intravascular space for longer duration than crystalloids
more expensive and more side effects
may be beneficial in patients with low albumin or patients not responding to cyrstalloids
SAFE - no difference in morbality between crystalloids or colloids for sepsis resuscitation
VISEP - hetastartch compared to LRs resulted in higher rates of acute renal failure in patients resuscitaed with heatstartch
VASOPRESSORS: USE IF MAP < 65
initiate if hemodynamic instability
MAP < 65 mmHg persists despite adequate fluid resuscitation (CVP 8-10 mmHg)
FIRST LINE AGENTS: NE or DA
refractory hypotension despite high doses NE consider adding vasopressin
BLOOD PRODUCT ADMINISTRATION: USE IF SVO2 < 70% AND HCT < 30%
transfuse to achieve a Hct of 30%
INOTROPIC THERAPY: USE IF SVO2 < 70% AND HCT > 30%
FIRST LINE AGENT - dobutamine
SUMMARY OF EGDT:
early initiation is KEY -> FIRST 6 HOURS
targeting specific GOALS OF THERAPY -> CVP + MAP + urine output + SVO2
FIRST LINE FLUIDS -> isotonic crystalloids
if UNRESPONSIVE TO FLUIDS (MAP < 65) -> dopamine or NE
if SVO2 < 70% -> transfuse PRBCs to Hct > 30%
if SVO2 < 70% AND HCT > 30% -> dobutamine |
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Term
| empiric antibiotics for a patient with sepsis/septic shock |
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Definition
obtain cultures prior to antibiotic therapy is started
ANTIBIOTICS SHOULD BE ADMINISTERED WITHIN 1 HOUR OF RECOGNIZING THE CLINICAL SYNDROME OF SEPSIS
choice of antibiotics should cover Pseudomonas from 2 different classes as well as MRSA coverage
recommended antibiotics:
antipseudomonal cephalosporin (ceftazedime, cefepime)
OR
antipseudomonal carbapenem (imipenem, meropenem, doripenem, ertapenem)
OR
beta-lactam/beta-lactamase inhibitor (piperacillin/tazobactam)
OR
aztreonam (if beta-lactam allergy)
PLUS
antipseudomonal fluoroquinolone (ciprofloxacin, levofloxacin 750 mg) OR minoglycoside (gentamicin, tobramycin, amikacin)
PLUS
MRSA coverage (vancomycin, linezolid, daptomycin, tigecycline)
initial choice is empiric in most cases - depends on several factors:
activity against presumed organisms
patient's history and antimicrobial history
penetration into suspected site of infection AND likely pathogens of suspected site of infection
patient medication allergies
local susceptibilities |
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Term
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Definition
all patients presenting with s/sx of sepsis should be evaluated for a source/site of infection
unable to identify via physical assessment -> x-ray/ultrasound/CT scan/MRI/etc.
focal source identified:
abscess - remove via drainage/debridement
wound - debridement of necrotic/infected tissue
medical device (intravascular catheters, urinary catheters, etc.) - removal of device if possible
evaluate risk vs. benefit of intervention for source removal
inability/failure to remove source of infection prolongs sepsis and leads to poor outcomes
duration of antimicrobial therapy:
7-10 days is recommended
should be dictated by patient response and site of infection
should treat for recommended duration for specific infection that caused sepsis (i.e. endocarditis 4-6 weeks; osteomyelitis 4-6 weeks) |
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Term
| hypercapnic respiratory failure |
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Definition
progressive increase in PaCO2 = respiratory acidosis
PaCO2 > 55 mmHg AND pH < 7.35 |
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Term
| hypoxic respiratory failure |
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Definition
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Term
| common etiologies for hypercapnic respiratory failure |
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Definition
INCREASED CO2 PRODUCTION
fever, seizures, sepsis
CAN'T BREATH
lung disease: COPD, asthma, cystic fibrosis, pulmonary fibrosis, obstructive sleep apnea, respiratory muscle fatigue
WON'T BREATH:
hypoventilation - meds or CNS
drug overdose (opioids, BZDs), CNS disorders, central sleep apnea |
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Term
| common etiologies of hypoxic respiratory failure |
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Definition
CARDIOGENIC
pulmonary edema, acute MI, CHF exacerbation, valve disorders
NON-CARDIOGENIC:
pneumonia (any fluid in the lung that prevents oxygen exchange)
acute respiratory distress syndrome
sepsis/septic shock
chemical aspiration
pulmonary embolism |
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Term
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Definition
the amount of air inhaled or exhaled with each normal breath
average healthy person (non-ventilated) = ~500 mL or 5-7 ml/kg (IBW) |
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Term
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Definition
number of breaths per minute
typical initial ventilatory rate 12-16 bpm
patients with restrictive lung disease may require higher initial respiratory rates (16-20 bpm)
increasing respiratory rate -> increased respiratory CO2 excretion -> decreased paCO2 |
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Term
| fraction of inspired oxygen (FiO2) |
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Definition
percentage of oxygen delivered to patient
room air = FiO2 21%
on mechanical ventilation - FiO2 can range from 21-100%
goal - to provide lowest FiO2 to maintain adequate PaO2 (>60 mmHg)
FiO2 is usually started at 100% and decreased to maintain an adequate PaO2 >60-70 mmHg
high FiO2 for long periods of time increases the risk of oxygen toxicity (direct lung injury, CNS effects, retinal effects) |
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Term
| positive end expiratory pressure (PEEP) |
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Definition
pressure held in the lungs during exhalation
helps to increase the surface area of the alveoli
prevents the alveoli from collapsing during exhalation
PEEP can help reduce oxygen requirements (by increasing PEEP can decrease FiO2 due to increased surface area of alveoli recruited for oxygenation)
typically PEEP < 5 cm H2O |
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Term
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Definition
amount of air inhaled or exhaled per one minute
VM (L/min) = [VT (ml/kg) x RR (breaths/min)]/1000
normal VM = 5-8 L/min
increased minute ventilation = increased respiratory CO2 excretion (i.e. hyperventilation) |
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Term
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Definition
PaCO2:
VT or RR (changes in minute ventilation)
decreased PaCO2 = increased RR or increased VT (increased minute ventilation)
increased PaCO2 = decreased RR or decreased VT (decreased minute ventilation)
PaO2:
PEEP or FiO2
increased PaO2 = increased PEEP or increased FiO2 |
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Term
| when is the patient improving? |
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Definition
minute ventilation decreasing back to patient's baseline
FiO2 and PEEP decreasing
pH within normal range on ventilator
patient able to sustain on pressure support breathing trial
patient awake and available to protect airway if tube is out |
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Term
| causes of agitation for ICU patients |
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Definition
PHYSICAL AND PSYCHOLOGICAL STRESS
non-life threatening:
uncomfortable body position
room temperature
fear/anxiety
pain
itching
fever
inability to communicate
sleep deprivation
uncomfortable catheters
dysynchrony with the ventilator
nicotine, drug, alcohol withdrawal
dry mouth
delirium
life threatening:
ventilator related - tube in wrong position, pneumothorax
gas exchange - hypoxia, hypercarbia
metabolic - hypoglycemia, acidosis
infection
ischemia - cardiac, intestinal, cerebral |
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Term
| patient factors that affect response to sedative and analgesic medications |
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Definition
advanced age
malnutrition
decreased protein binding
high total body water
increased volume of distribution
decreased fat or lean mass
altered liver or renal function
slowed metabolism
obesity
prior substance abuse
polypharmacy |
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Term
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Definition
PK/PD:
active metabolites
metabolized through the liver
onset: 30 minutes
duration: 120-240 minutes
ADRs: histamine release, hypotension, constipation, RESPIRATORY DEPRESSION
advantages: quick onset, longer acting than other IV agents
disadvantages: ACTIVE METABOLITES, hemodynamic changes, ACCUMULATION OF ACTIVE METABOLITE - ESPECIALLY WITH RENAL FAILURE, respiratory depression, longer half life |
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Term
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Definition
PK/PD:
no active metabolites
metabolized through the liver
onset: 5 minutes
duration: 120-240 minutes
ADRs: hypotension, constipation, RESPIRATORY DEPRESSION
advantages: quick onset, no active metabolites, moderate duration
disadvantages: hemodynamic changes, respiratory depression |
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Term
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Definition
PK/PD:
no active metabolites
metabolized through the liver
onset: 2-5 minutes
duration: 30-45 minutes
ADRs: rigidity with high doses, hypotension, constipation, RESPIRATORY DEPRESSION
advantages: quick onset, short duration, no active metabolites, good for continuous drips
disadvantages: hemodynamic changes, respiratory depression, short half life and duration makes it not a great agent for intermittent dosing |
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Term
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Definition
PK/PD:
active metabolites
metabolized through the liver
onset: 2-5 minutes
duration: 240 minutes
ADRs: phlebitis, hypotension, respiratory depression, DELIRIUM
advantages: quick onset with longer duration makes it good for one time dosing or intermittent dosing
disadvantages: ACTIVE METABOLITES, UNPREDICTABLE HALF LIFE, not great for continuous drips, good for one time dosing or intermittent dosing |
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Term
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Definition
PK/PD:
no active metabolites
metabolized through the liver
onset: 5-20 minutes
duration: 240-480 minutes
ADRs: SOLVENT RELATED ACIDOSIS/RENAL FAILURE AT HIGH DOSES, long duration and/or renal failure, hypotension, respiratory depression, DELIRIUM
advantages: no active metabolites, moderate duration, can be used effectively as either bolus or intermittent dosing
disadvantages: longer duration of onset, solvent related ADRs a risk, lipophilic |
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Term
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Definition
PK/PD:
active metabolite
metabolized by the liver
onset: 2-5 minutes
duration: 30-120 minutes
ADRs: hypotension, respiratory depression, DELIRIUM
advantages: quick onset with bolus dosing, can be used as either bolus or intermittent
disadvantages: active metabolites, shortest duration of activity for intermittent dosing, lipophilic |
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Term
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Definition
PK/PD:
no active metabolites
metabolized by the liver
onset: < 1-2 minutes
duration: 5-10 minutes
ADRs: hypotension, BRADYCARDIA, HYPERTRIGLYCERIDEMIA, PANCREATITIS, PROPOFOL-INFUSION SYNDROME, respiratory depression
advantages: QUICK ONSET - QUICK OFFSET, NO ACTIVE METABOLITES, predictable awakening time
disadvantages: hemodynamic changes - especially hypotension, risk of multiple ADRs, only continuous infusion |
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Term
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Definition
PK/PD:
no active metabolites
metaboliezed by the liver
onset: n/a
duration: n/a
ADRs: hypotension, BRADYCARDIA
advantages: NO RESPIRATORY DEPRESSION, arousable sedation, DECREASED DELIRIUM, advantage in patients with substance abuse
disadvantages: hemodynamic changes - bradycardia, FDA limitations on dosing, NOT FOR DEEP DESATION, NO BOLUS DOSING |
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Term
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Definition
PK/PD:
active metabolite
metabolized by the liver
onset: 3-10 minutes
duration: variable
ADRs: sedation, QTC PROLONGATION, EPS
advantages: NO RESPIRATORY DEPRESSION
disadvantages: ACTIVE METABOLITES, ADRs |
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