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
Norketamine has ___-___% the activity of ketamine
20-30%
Ketamine CNS effects—airway reflexes maintain ___; ___ (increase/decrease) in salivary gland secretions; ___ (increase/decrease) in skeletal muscle tone; ___ (increase/decrease) in CBF, CMRO2, ICP; causes ___ waves on EEG
Airway reflexes maintain intact; increase in salivary gland secretions (give glycopyrrolate); increase in skeletal muscle tone (may have no purposeful movements); increase in CBF, CMRO2, ICP (give with a GABA agonist to counterract…i.e.: propofol, etomidate); causes theta waves on EEG
Ketamine CV effects—indirect ___mimetic—use with caution in patients where an increase in ___ could be detrimental; ___ (increase/decrease) in myocardial contractility, may ___ (increase/decrease) myocardial oxygen consumption; ___ (increase/decrease) in BP, HR, CO, CVP
Indirect sympathomimetic—use with caution in patients where an increase in HR could be detrimental; increase in myocardial contractility, may increase myocardial oxygen consumption; increase in BP, HR, CO, CVP
Benefits of ketamine—___ properties; potent ___
Analgesic properties; potent bronchodilator
Side effects of ketamine—emergence ___; night___; ___ations
Emergence delirium, nightmares, hallucinations
Caution using ketamine in patients with ___tension, ___ heart failure, and ___ ICP—the benefits of a stable hemodynamic profile may be outweighed by the potential for overstimulation of ___ release/___ (increase/decrease) in myocardial oxygen consumption
Caution using ketamine in patients with hypertension, congestive heart failure, and increased ICP—the benefits of a stable hemodynamic profile may be outweighed by the potential for overstimulation of catecholamine release/increase in myocardial oxygen consumption
Ketamine is usually used in CV cases as an adjunct for multimodal analgesia, but not as a primary induction agent—T/F?
True
Dexmedetomidine MOA—alpha 2 receptor ___ (agonist/antagonist)
Agonist
Precedex dose—infusion loading dose of ___mcg/kg over ___ minutes; infusion ___-___ mcg/kg/hr
Loading dose of 1 mcg/kg over 10 minutes; infusion 0.2-1.5 mcg/kg/hr
In CABG, precedex loading dose ___ (is/is not) used
Is not used—precedex is often just an adjunct sedative for time on bypass/transport to ICU at a drip rate of 0.4 mcg/kg/hr
Precedex metabolism—extensive ___ metabolism
Hepatic
Precedex CNS effects—dose-dependent sedation that resembles natural ___; ___ (does/does not) cause respiratory depression; ___ (does/does not) interfere with EEG monitoring; ___ (does/does not) change CMRO2; ___ (increase/decrease) in CBF d/t cerebral vaso___
Dose-dependent sedation that resembles natural sleep; does not cause respiratory depression; does not interfere with EEG monitoring; does not change CMRO2; decrease in CBF d/t cerebral vasoconstriction
Precedex CV effects—___tension and ___cardia —> result of alpha 2 ___ and systemic vaso___; can occasionally see transient ___tension with loading dose/___ (low/high) maintenance rate (rare to see); no direct effect on myocardial ___
Hypotension and bradycardia —> result of alpha 2 stimulation and systemic vasodilation; can occasionally see transient hypertension with loading dose/high maintenance rate (rare to see); no direct effect on myocardial contractility
Fentanyl MOA—___ agonist
Opioid
Fentanyl dose—dependent on technique—standard ___-___ mcg/kg; can give doses up to ___ mcg/kg for induction
Standard 5-10 mcg/kg; can give doses up to 100 mcg/kg for induction
Fentanyl metabolism—___ metabolism into ___ (active/inactive) metabolites
Hepatic metabolism into inactive metabolites
Fentanyl CNS effects—___ and ___ properties; ___gesia; can cause ___ (increased/decreased) ICP if respiratory depression induced ___carbia occurs
Sedative and euphoric properties; analgesia; can cause increased ICP if respiratory depression induced hypercarbia occurs
Fentanyl CV effects—___cardia; ___ effect on blood pressure; ___ (does/does not) affect myocardial contractility or baroreceptor function; these traits are why a high dose fentanyl induction can be useful for CABG patients where the need for rapid extubation postoperatively is not an issue—very stable cardiac profile
Bradycardia; no effect on BP; does not affect myocardial contractility or baroreceptor function
Tabletop rescue drugs—phenylephrine MOA—direct acting alpha ___ agonist; virtually no ___ stimulation
Direct acting alpha 1 agonist; virtually no beta stimulation
Phenylephrine—unopposed alpha stimulation can elicit a ___ reflex, causing reflex ___cardia with administration; useful for patients in which an increase in ___ is not desired, but an increase in ___ is necessary
Unopposed alpha stimulation can elicit a baroreceptor reflex, causing reflex bradycardia with administration; useful for patients in which an increase in heart rate is not desired, but an increase in BP is necessary
Phenylephrine dose—syringes come in ___ mcg/ml; administer ___-___ mcg intervals to treat BP
Syringes come in 80 mcg/ml; administer 80-160 mcg intervals to treat BP
Phenylephrine infusion—usually comes ___mg/___ml (peripheral strength concentration—a heavier concentration may be used via central line in ICU, so always check the bag)—start infusion at ___mcg/kg/min
Usually comes 20 mg/250 ml—start infusion at 0.02mcg/kg/min
Tabletop rescue drugs—ephedrine MOA—synthetic non___ ___mimetic; stimulates ___ and ___ receptors directly; indirectly causes a release of endogenous ___
Synthetic noncatecholamine sympathomimetic; stimulates alpha and beta receptors directly; indirectly causes a release of endogenous catecholamines
Ephedrine—causes dose dependent ___ (increase/decrease) in BP, cardiac output, HR, and SVR; acts in a similar manner to ___, only carries a ___ (shorter/longer) duration of action and ___ (does/does not) increase glucose levels like ___ can
Causes dose dependent increase in BP, cardiac output, HR, and SVR; acts in a similar manner to epi, only carries a longer duration of action and does not increase glucose levels like epi can
Ephedrine dosing—comes in vials of ___mg/ml —> mix 1 ml of ephedrine with ___ ml of NS for a concentration of ___mg/ml; dose in ___-___mg increments IV
Comes in vials of 50 mg/ml —> mix 1 ml of ephedrine with 9 ml of NS for a concentration of 5 mg/ml; dose in 5-10 mg increments IV
Ephedrine—can see ___phylaxis with subsequent dosing due to depletion of ___ stores
Can see tachyphylaxis (diminished response to successive doses of a drug) with subsequent dosing due to depletion of catecholamine stores
You will see an increase in effectiveness of ephedrine over time—T/F?
False—you will see a decrease in effectiveness of ephedrine over time
Tabletop rescue drugs—epinephrine—MOA—strong alpha ___ sympathomimetic catecholamine; dose dependent stimulation of ___ and ___ receptors
Strong alpha 1 sympathomimetic catecholamine; dose dependent stimulation of B1 and B2 receptors
Epinephrine is used to treat patients in ___ states where there is poor tissue oxygen ___ and ___tension
Used to treat patients in shock states where there is poor tissue oxygen delivery and hypotension
Epinephrine is used when patients are unresponsive to ___ (direct/indirect) acting sympathomimetics
Indirect acting sympathomimetics
Epinephrine causes marked increase in ___tropy, heart ___, and conduction ___
Marked increase in inotropy, heart rate, and conduction velocity
Epinephrine also increases myocardial oxygen ___
Consumption—need to watch your oxygen supply/demand balance
Epi is rarely used in CV anesthesia outside of an arrest situation, but it is important to always have readily available for a patient who may be hypotensive and unresponsive to other tabletop rescue drugs—T/F?
True
Epi comes in ___mg/ml vial doses
1 mg/ml vial
Epi heavy concentration = ___mcg/ml
100 mcg/ml—mix 1 ml vial of epi in 9 ml of NS dilutent
Epi lite concentration = ___mcg/ml
10 mcg/ml—mix 1 ml of epi “heavy” mixture in 9 ml of NS dilutent
Tabletop rescue drugs—vasopressin—MOA—endogenous hormone produced in the ___, stored in the ___ pituitary gland; release is stimulated by ___ (increased/decreased) osmolality and ___volemia
Endogenous hormone produced in the hypothalamus, stored in the posterior pituitary gland; release is stimulated by increased osmolality and hypovolemia
Vasopressin is also known as ___
ADH
Vasopressin is a potent ___
Vasoconstrictor—second line usage after catecholamine vasopressors
Vasopressin dosing—comes in vials ___ units/ml
20 units/ml
Mix 1 ml with 19 ml NS for a concentration of 1 unit/ml
Vasopressin dosing—dose in increments of ___ unit at a time
1 unit at a time
Vasopressin infusion dose—___units/min
0.04 units/min
Vasopressin complications—___ ischemia, ___ (increased/decreased) cardiac output, digital ___, cardiac ___ at elevated doses
GI ischemia, decreased cardiac output, digital necrosis, cardiac arrest at elevated doses
Tabletop rescue drugs—esmolol—MOA—beta ___ selective ___onist
Beta 1 selective antagonist
Esmolol metabolism—___
Nonspecific plasma esterases
Esmolol has an extremely ___ (slow/quick) onset and ___ (short/long) half-life
Extremely quick (2 min or less) onset and short half-life
^^^ this is d/t its metabolism but nonspecific plasma esterases
Esmolol is useful to transiently treat ___ heart rate without carrying lasting effects that may cause subsequent ___ BP
Useful to transiently treat elevated heart rate without carrying lasting effects that may cause subsequent low BP
Esmolol is often used alongside induction agents to prevent an increase in ___ during laryngoscopy
Prevent an increase in HR
Esmolol concentration—___mg/ml in a ___ ml vial
10 mg/ml in a 10 ml vial (so total of 100 mg in the vial)
Esmolol dosing—administer in increments of ___-___mg at a time
Administer in increments of 10-30 mg at a time
Tabletop rescue drugs—nitroglycerin—MOA—direct vaso___, venous ___ (more/less than) arterial; caused by an induced release of vascular ___
Direct vasodilator, venous more than arterial; caused by an induced release of vascular nitric oxide
Nitroglycerin causes veno___; used to treat elevated ___, prevent ___, and treat ___ during anesthesia
Venodilation; used to treat elevated BP, prevent angina, and treat ischemia during anesthesia
Nitroglycerin decreases myocardial wall ___, cardiac ___ pressures, ___load, and myocardial ___ requirements
Decreases myocardial wall tension, cardiac filling pressures, preload, and myocardial oxygen requirements
Nitroglycerin concentration—nitro “lite” vials obtained from pharmacy come ___mcg/ml in a ___ ml vial—dose in increments of ___ mcg at a time
40mcg/ml in a 10 ml vial (so 400 mcg in whole vial)—dose in increments of 40 mcg at a time
Nitroglycerin infusion—UPMC Hamot infusion is 400 mcg/ml in a 250 ml bottle—infusion rate is typically started at ___mcg/min in a heart room
5 mcg/min
Rescue infusions—norepinephrine MOA—potent alpha ___ sympathomimetic; little activity on ___ receptor at low doses (this increases some with higher doses)
Potent alpha 1 sympathomimetic; little activity on B1 receptor at low doses
Norepinephrine infusion—causes ___ (increased/decreased) coronary artery perfusion pressure d/t increase in ___ BP; vaso___ causes a ___ (increase/decrease) in preload; ___ (increases/decreases) SVR
Causes increased coronary artery perfusion pressure d/t increase in diastolic BP; vasoconstriction causes an increase in preload; increases SVR
___ is a first line choice for infusion when a vasopressor is indicated in a cardiac case
Norepinephrine
Norepinephrine infusion concentration—___mg/250 ml; titration of infusion starting at ___ mcg/kg/min
16 mg/250 ml; titration of infusion starting at 0.02 mcg/kg/min
Rescue infusions—dobutamine MOA—synthetic sympathomimetic ___; primarily a ___ agonist with some ___ effects
Synthetic sympathomimetic amine; primarily a beta 1 agonist with some B2 effects
Dobutamine increases ___tropy, cardiac ___; BP may slightly increase or remain the same; decreases ___ d/t peripheral vaso___, decreases ___ pressure
Dobutamine increases inotropy, cardiac output; BP may slightly increase or remain the same; decreases SVR d/t peripheral vasodilation, decreases pulmonary artery pressure
Dobutamine infusion dosing—___-___ mcg/kg/min
0.5-20 mcg/kg/min
Rescue infusions—milrinone MOA—___ inhibitor; prevents the breakdown of ___
Phosphodiesterase 3 inhibitor; prevents the breakdown of cAMP
Milrinone causes ___ (positive/negative) inotropic action and vaso___ without producing ___cardia
Positive inotropic action and vasodilation without producing tachycardia
Vasodilation occurs within milrinone because in the smooth muscle, cAMP causes an efflux of ___ which results in ___ of the muscle
Efflux of calcium which results in relaxation of the muscle
Milrinone ___ (increases/decreases) preload and afterload
Decreases
Milrinone causes pulmonary vaso___
Vasodilation
Milrinone improves ___ function; causes acceleration of ___ uptake by the sarcoplasmic reticulum
Improves LV function; causes acceleration of calcium uptake by the sarcoplasmic reticulum
Milrinone is eliminated via the ___; caution in patients with ___ disease; buildup may cause ___
Via the kidneys; caution in patients with kidney disease; buildup may cause arrhythmias
Milrinone infusion dosing—start infusion at ___mcg/min up to ___mcg/min
0.375 mcg/min up to 0.75 mcg/min
