Anesthesia & Pharmacology Flashcards
Cormack-Lehane Classification
- Grade 1: Full view of glottis
- Grade 2a: Partial view of glottis
- Grade 2b: Only posterior extremity of glottis seen or only arytenoid cartilages
- Grade 3: Only epiglottis seen, none of glottis seen
- Grade 4: Neither glottis nor epiglottis seen
Difficult intubation
= LEMON = Look externally / Evaluate 3-3-2 rule / Mallampati score / Obstruction / Neck Mobility
Difficult BVM
= BONES = Beard / Obese / No teeth / Elderly / Sleep Apnea / Snoring
Difficult surgical airway
= SHORT = Surgery / Hematoma / Obesity / Radiation distortion or deformity / Tumor
- Propofol - Receptors and Dose
GABA + NMDA + Mu + Histamine + Serotonin
dose: 2-4mg/kg induction then 50 mcg/kg/min
ketamine dosage
- dose: 1-2mg/kg induction (dose comes in 50mg vial) 0.1-5 mcg/kg/min maintenance
Fentanyl dosage
- dose: 1 to 2 mcg/kg (25 to 100 mcg)
Morphine Dose
- Dose: 2-5mcg/kg induction & 50-100mcg/hr maintenance
Midaz Dose
- Dose: 0.2mg/kg induction loading; 0.01 to 0.05 mg/kg Δ(0.5 to 4 mg) / infusion 0.02 to 0.1 mg/kg/hour infusion (2 to 8 mg/hour)
succ contraindications
- Malignant hyperthermia history (personal or family)
- myopathic metabolic disorder = sympathetic hyperactivity, muscular rigidity, acidosis, & hyperthermia
- Neuromuscular disease involving denervation (note SCh is safe in myasthenia gravis)
- Muscular dystrophy
- Stroke over 72 hours old
- Rhabdomyolysis
- Burn over 72 hours old
- Significant hyperkalemia
roc dose + mechanism
- 0.8-1.2 mg/kg onset <1 min - dur 45min
ACh antagonists - competitive blocker - non-depolarizing
succ dose
ACh agonists - depolarizing
- 1.5mg/kg duration 8 min
Vasopressors and Doses
- Phenylephrine 20-200mcg/min 50-100mcg push
- Norepinephrine 0-20mcg/min
- Vasopressin 0.01-0.04 units/min
Inotropes and Doses
- Epinephrine 0-20mcg/min
- Milrinone 0.125-1.0mcg/kg/min
- Dopamine 0-10mcg/kg/min
- Dobutamine 0-20mcg/min
MOI of
- Dopamine
- Vasopressin
- Milrinone
Dopamine = ↑norepinephrine release = ↑cAMP = vasoconstrictor
- Vasopressin = V1 receptor on smooth muscles = vasoconstrictor
- Milrinone = inhibits PDE3 = ↑cAMP = ↑ Ca2+ = ↑cardiac muscle contractility + ↑smooth muscles relaxation in vasculature = ↓SVR
- cAMP = ↑ Ca2+
- PDE breaks down cAMP into AMP
Midaz advantages and disadvantages
- Advantage: A potent amnestic and anxiolytic agent with an immediate onset of action and a short duration of effect when administered shortterm (<48 hours)
- Disadvantages: Hepatically metabolized by CYP3A4 to active metabolites that may accumulate and cause prolonged sedation if delivered longterm. Halflife may be prolonged in critically ill patients with hepatic or renal impairment. Risk of delirium. Also, it interacts with drugs used in the ICU (eg, some antiretrovirals, azole antifungals) that alter CYP metabolism such that excess sedation can occur with concomitant use of midazolam and drugs metabolized by CYP3A4.
Midaz MOI
- GABA - inhibitory terminals produce GABA (G-aminobutyric acid) - ↓ Ca influx during AP invasion of presynaptic axon = blocks transmitter release from terminal = presynaptic inhibition (inhibitory neurotrasmitters cause HYPERpolarization via transient ↑ permeability to Cl (moves in) or K (moves out) = moves away from threshold
- Cortex & RAS
- Anterograde NOT retrograde amnesia
- PARADOXICAL responce - they are disinhibited = can be restless and more agitated
- benzo’s can worsen long term cognitive function in elderly - i.e. dumbdumbs for the next 6 months
Ketamine Advantages and Disadvantages
- Advantages: A potent dissociative sedativeanesthetic with marked analgesia that maintains cardiac output and mean arterial pressure without inhibition of respiratory drive. Doesnot inhibit protective reflexes.
- Disadvantages: Sympathetic stimulation (ie, increased heart rate and myocardial oxygen demand, elevated intracranial pressure and systemic blood pressure), hallucinations, delirium upon withdrawal, tonicclonic movements, dissociative experiences, unpleasant recall, hypersalivation, nausea, and vomiting.
Ketamine MOI
- “short-acting non-barbiturate anaesthetic” = NMDA Uncompetitive Antagonist
- NMDA (N-methyl-D-asparate) receptor ANTAGONISM + CNS sympathetic outflow stimulation
- NMDA = cerebrum/cortex/thalami/brainstem = excitatory receptor = must remain open to transmit signals from spinal column into brain (usually open w Glutamate) = closed to pain sensation in dorsal horn neurons
Propofol Advantages and Disadvantages
- advantages: potent sedativehypnotic associated with an immediate onset and rapid awakening upon discontinuation when administered for shortterm use. Metabolism is reportedly unaltered in hepatic or renal impairment and subject to few significant drug interactions. Infusion is readily titratable to desired depth of sedation, minimizing risk of oversedation. Propofol effectively decreases intracranial pressure, lowers cerebral metabolism, controls intractable seizures
- disadvantages: hypotension, bradycardia, respiratory depression, decreased myocardial contractility, elevated triglycerides, and rarely propofol infusion syndrome, potential allergens (egg, soy, peanut). No analgesic effects.