Anesthetics Flashcards
What are the five primary effects of anesthetics?
- Loss of consciousness
- Amnesia
- Analgesia
- Inhibition of autonomic reflexes
- Skeletal muscle relaxation
Note: No single drug produces all five effects
Describe how alveolar ventilation, inspired partial pressure, and solubility affect the pharmacokinetics of inspired anesthesia.
Alveolar concentration is increased by increases in partial pressure and alveolar ventilation.
Solubility in blood determines the onset of action: low solubility (nitrous oxide) is fast, while high solubility (halothane) is slow. All agents are more soluble in the brain than the blood.
How does cardiac function impact the onset of action of inspired anesthesia?
Increased cardiac output increases the disbursement to all tissues –> slower onset of action
Describe elimination of inspired anesthesia.
Elimination occurs in reverse of absorption. Less soluble substances will be eliminated faster. Hyperventilation is the only way to speed recovery.
What is the significant of MAC?
Minimum alveolar concentration - the concentration required to prevent a patient’s response to surgical incision.
1.0 MAC = the concentration required to eliminate response in 50% of patients.
MAC is additive across agents (i.e. 0.5 MAC + 0.5 MAC = 1.0 MAC)
What are the four stages of anesthesia?
Stage 1 - Analgesia (may have amnesia in late stage)
Stage 2 - Excitability (increased HR, RR, and BP)
Stage 3 - Surgical anesthesia (no response to trapezius squeeze)
Stage 4 - Medullary Depression
Describe the MOA and effects (CNS, CV, and resp) of propofol.
MOA - potentiates GABA-A receptors
CNS - depressant; no analgesia, but neuroprotective in neurosurgery d/t EEG burst suppression
CV - hypotension
Resp - depressant
Name two barbituates used for anesthesia. Describe their MOA and effects on CNS and respiratory systems.
Drugs - thiopental and methohexital
CNS - depressant; suppress EEG activity, beneficial as anti-convulsant (not methohexital)
Resp - depressent
What is the suffix of benzodiazepines? Describe their MOA and effects on CNS and respiratory systems.
Suffixes - azolam and azepam
MOA - GABA-A agonist; enhances GABA-A sensitivity
CNS - depressant; potent anticonvulsants
Resp - Severe depression with opiods
Describe the MOA and effects (CNS, CV, and endocrine systems) of etomidate.
MOA - GABA like; potentiates GABA-A
CNS - cerebral vasoconstriction; decreases blood flow and ICP
CV - minimal
Endo - adrenocortical suppression
Describe the MOA and effects (CNS and CV systems) of ketamine.
MOA - NMDA antagonist
CNS - cerebral vasodilator; emergence reactions (hallucinations and out-of-body experiences); Dissociative anesthesia (opens eys with nystagmic gaze)
CV - Central SANS stimulant (increases HR, BP; direct myocardial depressant (overridden)
Describe the MOA and effects (CNS and CV systems) of dexmedetomidine.
MOA - alpha-2 agonist
CNS - hypnosis (locus ceruleus); analgesia (spinal cord); sedation (activates sleep pathways)
CV - decreases heart rate and systemic resistance
Describe the MOA of local anesthetics.
Inhibit impulse propagation and generation through blockage of voltage-gated sodium channels
Describe the absorption, distribution, and metabolism of local anesthetics.
Local anesthetics consists of lipophilic groups combined with either an amide or ester group.
Lipophilicity allows higher potency, longer duration, and longer onset.
Amides are metabolized in the liver, while esters are metabolized in the blood by butrylcholinesterase. All are cleared in the urine.
Name the amide and ester local anesthetics.
Amide - lidocaine, bupivacaine, ropivacaine
Esters - cocaine, procaine, tetracaine, and benzocaine
