Shannon-Induction Of Anesthesia For The CV Patient Flashcards
(94 cards)
Patients with ___tension display an exaggerated response to induction agents and laryngoscopy —> more extreme ___tension to laryngeal stimulation, but also an increased ___tensive reaction to induction agents
Patients with hypertension display an exaggerated response to induction agents and laryngoscopy —> more extreme hypertension to laryngeal stimulation, but also an increased hypotensive reaction to induction agents
Administering ___ or arterial ___ (i.e.: nitroprusside) can decrease the hyperdynamic sympathetic response to laryngoscopy
Administering beta blockers or arterial dilators (i.e.: nitroprusside) can decrease the hyperdynamic sympathetic response to laryngoscopy
Use of ___ IV prior to intubation blunts the laryngeal reflex with intubation
Lidocaine IV
Propofol MOA—direct ___ agonist
GABA-A
Propofol induction dose ___-___ mg/kg in healthy patient; often much ___ (lower/higher) for CV patients
1-2 mg/kg in healthy patient; often much lower for CV patients
Two compartment model for propofol distribution in the body—propofol rapidly distributes to ___ and highly ___ areas following IV injection in one circulation time; propofol rapidly redistributes into ___ compartments, circulates to less perfused areas, concentration ___ (increases/decreases) and ___ (slow/rapid) awakening occurs
Propofol rapidly distributes to brain and highly perfused areas following IV injection in one circulation time; propofol rapidly redistributes into peripheral compartments, circulates to less perfused areas, concentration decreases and rapid awakening occurs
Propofol is rapidly metabolized in the ___
Liver
Metabolism of propofol—extrahepatic metabolism sites (due to metabolism exceeding hepatic blood flow) results in tissue uptake of Propofol into areas including possibly the ___; need your patient to be ___ to metabolize this out!
Possibly the lungs; need your patient to be breathing to metabolize this out!
Benefits of propofol—___ (slow/fast) onset; relatively ___ (short/long) half life; mild anti___ effects; very few serious ___ effects
Fast onset; relatively short half life; mild antiemetic effects; very few serious side effects
Propofol CNS effects—___ (increases/decreases) cerebral blood flow, CMRO2
Decreases cerebral blood flow, CMRO2
Propofol CV effects—___ (increases/decreases) BP, cardiac output, SVR; dose dependent ___ (increase/decrease) in BP within ___ minutes after induction
Decreases BP, cardiac output, SVR; dose dependent decrease in BP within 10 minutes after induction
Etomidate MOA—___ agonist
GABA
Etomidate induction dose = ___-___mg/kg
0.2-0.3 mg/kg
Metabolism of etomidate = ___ hydrolysis
Ester hydrolysis—this is why the duration of action is so short
Etomidate CV effects—hemodynamic ___ is achieved—___ (changes/no changes) in HR, pulmonary artery pressure, SVR, CO, and BP; acts as an alpha 2B adrenoreceptor agonist, which leads to a ___ (increase/decrease) in BP; no significant ___mias associated with etomidate
HD stability is achieved—no significant changes in HR, PA pressure, SVR, CO, and BP; acts as an alpha 2B adrenoreceptor agonist, which leads to an increase in BP; no significant arrhythmias associated with etomidate
Etomidate CNS effects—dose dependent ___ (increase/decrease) in cerebral blood flow and CMRO2
Decrease
Etomidate CNS effects—awakening occurs ___-___ minutes after administration
5-15 minutes
Etomidate side effects—___ on injection; ___ and ___; thrombo___; myoclonia may resemble ___ like activity, but does not cause them; ___ suppression
Pain on injection; nausea and vomiting; thrombophlebitis; myoclonia may resemble seizure like activity, but does not cause seizures; adrenocortical suppression
Etomidate side effects—adrenocortical suppression—inhibits 11B-___, which is essential in the body’s production of ___steroids and ___corticoids; the effects of a single etomidate dose can last for ___ hours; can cause increases in morbidity and mortality in patients on prior ___ therapy and/or patients in a ___ state
Inhibits 11B-hydroxylase, which is essential in the body’s production of corticosteroids and mineralocorticoids; the effects of a single etomidate dose can last for 72 hours; can cause increases in morbidity and mortality in patients on prior steroid therapy and/or patients in a septic state
Ketamine MOA—noncompetitive ___ antagonist; inhibits ___; depressant effect on ___ nuclei, which blocks afferent signals of pain perception to the ___ and ___
Noncompetitive NMDA antagonist; inhibits glutamate; depressant effect on thalami nuclei, which blocks afferent signals of pain perception to the thalamus and cortex
Ketamine causes a ___ state where the patient feels separated from the ___
Catatonic state where the patient feels separated from the environment
Ketamine has ___ and ___ effects
Amnesic and analgesic effects
Ketamine inhibits ___ factor alpha—may be responsible for its anti___ and anti___analgesic effects
Inhibits tumor necrosis factor alpha—may be responsible for its anti-inflammatory and antihyperanalgesic effects
Metabolism of ketamine = ___ metabolizes ketamine into ___
Liver metabolizes ketamine into norketamine metabolite