Anesthesia Pharm Final Flashcards
1
Q
parenteral routes of drugs
A
IV, IM, SC,etc
2
Q
volatile anesthetics: cerebral blood flow
A
increase vasodilation, decrease vasc resistance, increase CBF, increase ICP
3
Q
opioids: metabolism
A
fentanyl 75% lungs, remi=plasma/tissue, morphine= gluc acid hepatic/renal, meperidine 90% hepatic
4
Q
midazolam: first pass metabolism
A
50% first pass
5
Q
local anesthetics: target channels
A
Na channels
6
Q
volatile anesthetics: coronary blood flow
A
iso is a potent coronary vasodilator
7
Q
desflurane and CO2 absorber
A
carbon monoxide, from dry dessicated absorber
8
Q
bupivicaine toxicity
A
lower dose of bupivicaine will produce Cardiovascular collapse then lidocaine, pregnant patients may be more sensitive, cardiac resuscitation is more difficult after bupivacaine, cardiotoxicity potentiated by acidosis and hypoxia
9
Q
uptake and distribution: alveolar PP
A
uptake = solubility x CO x (PA-PV)
10
Q
opioids: side effects
A
pruritis, N/V, urinary retention, vent despression
11
Q
local anesthetics: metabolism
A
amides: liver CYP450, esters- cholinesterase enzymes
12
Q
opioids:best for neurological assessment post-op
A
remifentanyl
13
Q
inhaled agents: pharmacokinetics
A
highly soluble=less uptake=faster induction
14
Q
desflurane and heart rate
A
increased due to SNS stimulation
15
Q
local anesthetics: nodes of ranvier
A
2-3 blocked will stop the action potential
16
Q
compound A formation
A
sevo interation with CO2 absorbers, higher levels seen in Baralym vs soda lime, nephrotixin in rates, use flows higher than 2
17
Q
EMLA components
A
5% lidocaine, 5% prilocaine
18
Q
Induction drugs: hiccups
A
methohexital
19
Q
benzodiazepine-ion channel effect
A
hyperpolarization
20
Q
induction drugs: cortisol secretion
A
etomidate
21
Q
inhaled agents: bone marrow suppression
A
nitrous oxide
22
Q
Induction drugs: propofol method of action
A
decrease GABA dissociation
23
Q
opioids: histamine release
A
morphine, meperidine
24
Q
opioids: potency
A
MMHAFRS
25
opioids: remi metabolism
plasma cholinesterase
26
opioids: seizure
meperidine or normeperidine with renal failure
27
local anesthetics: cardiotoxicity
circumoral numbness, tinitus
28
dibucaine number
80
29
propofol: additives
glycerol burns, disodium edetate is bacteriostatic
30
opioid: side effects, glucagon
tx biliary coloc 2mg IV
31
ketamine: tx for emergence delirium
benzos
32
thiopental redistribution
effects 5-10 minutes bc of redistribution
33
benzodiazepine: clinical effect
20%: anxiolytic, 30% sedation, amnestic 60% unconscious
34
opioid: dynorphon receptors
kappa
35
inhaled agents: metabolism
exhalation, biotransformation, transcutaneous loss(hal - sevo - iso - des - n20)
36
opioids: renal failure
alfentanyl
37
dose of etomidate
0.2-0.3mg/kg
38
induction drugs: causes analgesia
ketamine
39
duration of naloxone
30-45 minutes
40
local anesthetic: effect of epinephrine
increase duration due to vasoconstriction
41
inhaled anesthetics: MH
don't use
42
local anesthetics: cauda equina syndrome
serious potential complication of spinal anesthesia
43
local anesthetics: methemoglobemia
benzocaine/prilocaine (ortholuidine is the metabolite that causes methemoglobinemia); decreases oxygen carrying capacity of hemoglobin, oxidation of hemoglobin to methemoglobibemia, neonates at higher risk, normal metHbB is less than 1%, pulse ox will read 85, treat with methylene blue 1-2 mg/kg
44
induction drugs: effect of ICP
thio and etom decrease ICP, prop and ketamine increase ICP
45
chloroprocraine: contraindicated in
spinal
46
premedication in children
0.5mg/kg versed PO
47
midazolam: drug interactions
synergistic with opioids
48
induction drugs: myoclonus
etomidate
49
volatile anesthetics: preservatives
halothane has thymol
50
volatile anesthetics: reactive airway
don_t use des, use sevo
51
maximum dose of bupivacaine
225mg with epi, 175 mg w/out epi
52
flumazenil metabolism
quick, doesn_t last = resedation, hepatic enzymes
53
mechanism of action for barbiturates
decrease GABA dissociation
54
propofol CV effects
decrease BP and increase HR
55
alpha 1 glyco protein (protein binding)
basic
56
benzodiazepine: contraindications
PO no grapefruit, pregnancy
57
division of CO
75% VRG (10% of body mass), 19% muscle (50% of body mass) 6% fat (20% body mass) 0% VPG (20% body mass)
58
isoflurane CV effects
decrease SVR, increase HR, no effect of CO, coronary steal
59
desflurane, physical properties
liquid at room temp
60
iso and des
increase heart rate
61
inhaled anethetics: cerebral metabolic rate of oxygen
decrease CMRO2
62
MAC additive properties
MACs are additive
63
thiopental pH
10.5
64
induction drugs: does not interact with GABA
ketamine
65
thiopental concentration
2.50%
66
inhaled anesthetic: analgesic properties
NO only
67
propfol in ICU
3 days then hyper lipidemia
68
routes of administration: onset times
IV, intraosseous, endotracheal, inhalational, sublingual, IM
69
indirect agonist definition
acting receptor agonist _ drug that produces its physiologic response by increasing the concentration of ENDOGENOUS substrate (neurotransmitter or hormone) at receptor site
70
local anesthetics: ion trapping
refers to a phenomenon that occurs when a difference on pH exists in two body compartments. The more acidotic the pH, the greater the fraction of local, which is a basic compound, that ionizes. Ionized compounds are water soluble and cannot easily pass biologic membrands. when a local becomes more ionized and water soluble it becomes less able to leave the body compartment. If a patient who has CNS toxicity due to local overdose, is improperly managed, and becomes hypoxic with accompanying acidosis, the local becomes trapped in the CNS worsening the toxicity. Can also occur in pregnant patients because fetal pH is lower than maternal pH.
71
racemic mixture
50-50 entantiomers
72
CPP=
CPP = MAP - ICP
73
propofol metabolism
hepatic metabolism, glucuronidation is the major pathway
74
propoful IV sedation dose
25-100 mcg/kg/min
75
propofol GA TIVA dose
100-200 mcg/kg/min
76
solubility definition
_Relative affinity of an anesthetic for two phases and therefore the partitioning of that anesthetic between the two phases at equilibrium
77
inhaled anesthetics: what is equilibrium
no difference in partial pressure exists
78
partial pressure
the pressure which is the pressure the gas would have if it alone occcupied the volume
79
two ways to increase initial concentration of gas and the uptake
concentration effect, 2nd gas effect
80
effect of solubility on gas uptake
decreased solubility increases PA/PI so induction is quicker, increased solubility slows induction time
81
inhaled anesthetics: CO effect
increased CO means increased solubility and slower induction
82
what changes pharmacokinetics?
age, lean muscle, body fat, hepatic fxn, pulmonary gas exchange, CO
83
What do we want GA to do?
Minimize deleterious direct and indirect effects of agents, Sustain physiologic homeostasis during procedure, Improve postop outcomes
84
what MAC prevents mvmt in 95%
1.3
85
MAC and hypothermia
For each decrease in core temp 1 degree C_MAC is decreased by 5%
86
MAC and chronic alcohol abuse
MAC unaltered
87
MAC and acute alcohol intox
MAC decreased
88
Agents that decrease myocardial contractility and CO
halothane and enflurane
89
Which agents decrease SVR?
iso, des, sevo
90
Which agents decrease PVR?
all, blunt hypoxic pulmonary vasoconstriction response, (N2O known to increase PVR in pts with hypertension)
91
Inhaled agents and arrythmias
halothane desensitizes the myocardium to catecholamines, exogenous epi can cause vtach and pvc, sinus brady and av rhythms bc of direct depressive effect on SA node / halo, iso, des and sevo prolong QT interval
92
Inhaled agents and MV
increase RR decrease TV, rapid shallow breathing which causes and increase in PaCO2, drugs probably inhibit medullary vent center. Des and Sevo produce apnea around 1.5, 2 mac (decrease in vent response to hypoxemia, decrease in airway resistance, except for des, decrease in FRC)
93
inhaled anesthetics and renal effects
decrease renal blood flow, decrease GFR, decrease urine output, nephrotoxicity
94
inhaled anesthetics and hepatic effects
decrease hepatic blood flow, decrease hepatic clearance, hepatic toxicity
95
inhaled anesthetics in vitro
can cross placenta, baby usually ok until 1 mac
96
inhaled anesthetics and skeletal muscle
ether derived produce more relaxation than halothane, NO does not produce relaxation and may produce rigidity
97
opioid agonist/antagonist
nalbuphine- used for people who are narcotic dependent or weaning off opioids (agonist at kappa, antagonist at mu)
98
opioid: mechanism of action
Bind specific G protein-coupled receptors that are located in brain and spinal cord regions involved in the transmission and modulation of pain
99
opioid receptors: Mu1
analgesia, euphoria, N/V, pruritis, low abuse potential, bradycardia
100
opioid receptors: Mu2
(spinal) hypoventilation, analgesia, euphoria, sdeation, physical dependence, constipation
101
opioid receptors: kappa
(supraspinal, spinal) analgesia, respiratory depression
102
opioid receptors: delta
(supraspinal, spinal) analgesia, resp despression, physical dependence, urinary retention, enkaphalins
103
opioid overdose triad
respiratory depression, CNS depression, pin point pupils
104
opioid miosos
edinger-westphal nucleua of the oculomotor nerve, toolerance does not develop
105
opioid withdrawal
chills, gooseflesh, hyperventialtion, hyperthermia, vomiting, diarrhea, hostility
106
morphine
potency 1, onset 15-30 minutes, 2-10mg, peak effect 45-90 minutes, duration 3-4 hours, metabolized bia conjuction with glucuronic acid, metabolite morphine 6-glucaronide (accumulation in kidney failure pts can lead to prolonged narcosis and vent depression), histamine realease
107
meperidine (demerol)
0.1 potency of morphine, peak effect 5-7 minutes, duration 2-4 hours, local/atropine side effects (block Na channels, tachycardia, dry mouth, mydriasis), 90% hepatic metabolism to normeperidine which is renally eliminated, tx for post-op shivering
108
fentanyl
75-125 more potent than morphine, peak effect 3-5 minutes, duration 30-50, 75% undergoes 1st pass pulmonary uptake, highly lipid soluble and protein bound, hemodynamic stability,
109
induction dose of fentanyl
2-6 mcg/kg with a sedative hypnotic
110
sufentanil
5-10x as potent as fentanyl, 1000x more potent than morphine, greater affinity for opioid receptor, peak 3-5 minutes, duration 30-60 (dosing 0.3-1.omcg/kg 1-3 minutes before DL)
111
alfentanyl
1/5 to 1/10 as potent as fentanyl, duration 10-20 minutes, peak 1.5-2 minutes, renal failure doesn_t alter clearance, rapid on/off, good for RBB, DL, 5-10mcg/kg
112
remifentanyl
similar potency to fentanyl, peak effect 1.5-2 minutes, duration 6-12 minutes, metabolized by plasma and tissure esterases, good for RBB, continuous gtt, MAC vs general, quick recovery cases (0.5-1mcg/kg + propofol for FL then 0.25-.5mcg/kg/min)
113
codeine
antitussive, analgesia for mild to moderate pain
114
methadone
long term relief of chronic pain and opioid withdrawal
115
hydromorphone
8x as potent as morphine but shorter acting
116
pentazocine, butorphanol, nalbuphine
partial agonist and or comp antagonist, produce analgesia with limited resp depression, ceiling effect
117
local anesthetics
bind Na channels in activated state, rate of depolarization is decreased, resting potential and threshold are not altered, blockade of Na channels prevent achievement of the threshold potential; action potential is not progagated
118
lipophilic groups have a
benzene ring
119
hydrophilic groups hav a
tertiary amine
120
what effects potency of local
fiber size, type, myelination, pH, frequency of stimulation
121
metabolites of esters
para-aminobenzoic acid (PABA) **allergies
122
local inj sites and vascularity
IV>tracheal>intercostal>caudal>paracervical>epidural>BP>sciatic>subcutaneous
123
toxicity dosages of locals
bupi is 2.5, lido is 5, lido with epi is 7
124
CV effects of systemic toxicity
hypotension, decreased cardiac conduction, ventricular arrythmias
125
dose of intralipid
1.5mg/kg iv over 10 minutes
126
brain stem anesthesia
Accidental injection into the CSF can occur during the block due to perforation of the meningeal sheaths that surround the optic nerve. The patient may experience disorientation, aphasia, hemiplegia, unconsciousness, convulsions, and respiratory or cardiac arrest. The incidence of this is estimated in studies to be 0.13%. Direct injection intravascularly via the optic nerve sheath or local anesthesia carried by the ophthalmic and internal carotid artery by retrograde flow to the thalamus and midbrain can also present the same way. This situation requires prompt recognition and treatment (including airway control, respiratory support, possible cardiac intervention, etc.)
127
drugs used for topical anesthesia
tetracaine, cocaine, lidocaine (with oxymetazoline)
128
anticholinergic overdose
physostigmine?
129
name Beta-1 agonists
norepi
130
metoclopramide, contraindications
Parkinson's and GI obstruction
131
diuretics- hyperglycemia
HCTZ
132
Reye Syndromw with aspirin
kids with flu treated with tylenol not ASA
133
metformin- renal excretion
100% unchanged by kidneys
134
zofran, ped dose
0.1mg/kg
135
metoclopramide, side effects
Prolong QT, dty mouth, ab cramping, extrapyramidal effect (dysphoria, agitation, sedation) RARE side effects: hirsuitism, maculopapular rash Prolactin side effects: breast enlargement, menstrual irregularities FETAL effects = doesn_t cross, no effects on baby
136
cardiac arrhyhmias with lasix
hypo K and hypo Mg, increased risk of digitalis toxicity and ventricular arrhythmias
137
H2 blockers as premed
˙ˇ pepcid can be used as a premedication. It will decrease hydrogen ion secretion, so the gastric contents in the future hours may be less acidic. However, H2 blockers will not decrease the acidity of what is already in the stomach. Pepcid premed = 20 mg IV, 30 minutes prior.
138
bicitra beneficial preop effects
˙ˇ 30 ml cup of nonparticulate antacid. Neutralizes the pH of the stomach contents. If the patient does aspirate it will be a higher pH, but possible more volume (weigh the risks vs. benefits).
139
decadron, peds dose
0.1mg/kg
140
droperidol contra
dopamine antagonists. 0.625 mg dose. Significant decrease in PONV. Black box warning = Increases QT interval, so contraindicated in patient_s with prolonged QT intervals already. Also contraindicated in parkinson_s disease.
141
amiodorone side effects
pulmonary fibrosis
142
side effect of 2nd generation H1 antagonists
prolong QT
143
histamine antagonists, mechanism of action
competitive inhibition
144
zofran mechanism of action
serotonin 5HT3 receptor antagonist
145
Histamine
autocoid = naturally occurring endogenous amine. Histamine is a chemical mediator in inflammation. Histamine increases acid production. It is released from mast cells (skin, lungs, GI tract, basophils). Histamine DOES NOT cross the BBB, but some H2 blockers do cross the BBB. Histamine is involved in the antigen-antibody response.
146
H1 receptor
respiratory and GI smooth muscle contraction, pruritis and sneezing, nitric oxide release by vascular smooth muscle_ vasodilation_ hypotension.
147
H2 receptor
increased GI secretion of H+, increased HR/contractility
148
H3 receptor
presynaptic receptors = decreased histamine synthesis and release
149
Generalized effects of histamine
dilation of arterioles and capillaries due to NO release, flushing (red/hives), decreased systemic vascular resistance, decreased blood pressure, increased capillary permeability.
150
H1 activation
oˇˇ occurs at lower concentrations of histamine than activation of H2 receptors. Decreased AV node conduction, coronary artery vasoconstriction, bronchial smooth muscle constriction.
151
H2 activation
oˇˇ CV effects (increased myocardial contractility, increased HR), catecholamine release, coronary artery vasoDILATION. increased gastric hydrogen ion secretion.
152
skin response
dilated capillaries in affected area, edema due to increased capillary permability, _wheal_ = dilated arterioles around edema.
153
allergic rxn
histamine is one of several chemical mediators released. Histamine antagonists will block edema and pruritis but WILL NOT block hypotension.
154
H1 blocker
˙ˇ first generation H1 blockers also activate muscarinic cholinergic, serotonin and alpha receptors and cause significant SEDATION. Second generation H1 blockers only bind to H1 receptors and they are non-competitive at higher doses and they cause much LESS SEDATION.
155
1st generation H1 blocker
oˇˇ diphenhydramine (benadyrl) and Dramamine; ˇ Side effects: somnolence, decreased alertness, slowed reaction time, dry mouth, blurred vision, urinary retention, impotence, tachycardia, dysrhythmias. Benadryl inhibits alcohol dehydrogenase
156
2nd generation H1 blocker
loratadine (claratin), fexofenadine (allegra); _ Side effects: QT prolongation (at high doses), limited side effects.
157
clinical uses of H1 blockers
rhinoconjunctivitis, bronchospasm, anaphylactoid/anaphylactic reactions (most allergic reactions in anesthesia are due to muscle relaxants _ give Benadryl 25 mg), motion sickness.
158
H2 blockers
inhibit gastric acid secretion, doesn_t affect what is already in the gut
159
Potency of H2 blockers
Cimetidine (tagamet) =1; Ranitidine (zantac) =10; Nizatidine (axid)=10; Famotidine (Pepcid)=50 Iv dose 20mg
160
Pharmacokinetics of H2 blockers
rapid oral absorption, extensive 1st pass metabolism, cross BBB and placenta (usually no effects on baby), avoid in patients with renal dysfunction/increased age = decreased elimination time and prolonged effects. Decrease the dose in renal dysfunction and elderly patients.
161
Clincal uses of H2 blockers
˙ˇ treatment of duodenal ulcers, active reflux/GERD, allergy prophylaxis (block histamine receptors), preop med (decrease gastric acid secretion, but will not decrease the H+ ions already in the gut). Keep taking H2 blockers up till am of surgery because if they are discontinued there can be a hypersecretion of gasric acid in the stomach.
162
Side effects of h2 blockers
˙ˇ diarrhea, headaches. Side effects are usually only present in patients with renal/hepatic dysfunction. Prolonged use may weaken the barrier to bacteria.
163
H2 blockers with drug interactions
cimetidine is the most common. Hepatic metabolism of other drugs is affected. Cytochrome P450 system is inhibitedÖ leads to prolonged duration of drugs that are metabolized by P450 enzymes (valium, propanolol). Other H2 blockers (other than cimetidine) do not bind P450 enzymes. Also there is a delayed lidocaine metabolism = increased risk of lidocaine toxicity.
164
Histamine blockers and CYTP450
cimetidine (tagamet). Cytochrome P450 system is inhibitedÖ leads to prolonged duration of drugs that are metabolized by P450 enzymes (valium, propanolol). Other H2 blockers (other than cimetidine) do not bind P450 enzymes
165
cromolyn
inhibits antigen-induced release of histamine from mast cells (pulmonary mast cells). Administered by inhalation. Used as prophylaxis for bronchial asthma. Patients on cromolyn can actually become allergic to it.
166
proton pump inhibitors
˙ˇ prazoles_. They have longer durations than H2 blockers. PPI prolong the inhibition of gastric acid secretion up to 24 hours. Better results that H2 blockers because they increase the gastric pH and decrease the volume of the gastric contents. If a patient is on PPIs, then they probably have GERD and are considered an aspiration risk.
167
PPIs as premed
can increase gastric fluid pH if given early enough, can decrease gastric fluid volume, MUST BE GIVEN >3 HOURS PRIOR TO SURGERY
168
Serotonin and 5-HT3 receptor antagonists
autocoid Ö cerebral, coronary, and pulmonary vasoconstriction. Oxidized by the liver and lungs and taken up by platelets (stored inactivated in platelets). Many subtypes with greatly varying actions. NT in the CNS. 90% found in enterochromaffin cells of GI tract and the rest are in CNS and platelets.
169
Serotonin and 5-HT3 receptor antagonists; sites of action
GI tract, platelets, vascular system (vasoconstriction), CNS (15 sub-types = sleep, cognition, sensory perception, motor activity, temp regulation, nociception, appetite, sexual behavior, hormone secretion.
170
5HT1
5 subtypes = cerebral vasoconstriction; _ Agonist: Sumatriptan (imitrex) reverses middle cerebral artery vasodilation to improve migraines and cluster headaches.
171
5HT2
3 subtypes, coronary artery and pulmonary vessels, _ Antagonist: Ketanserin attenuates vasoconstriction, bronchoconstriction, platelet aggregation and also acts as an alpha blocker.
172
5HT3
nausea and vomiting, appetite, addiction, pain and anxiety. These receptors are predominantly in the chemotaxic center in the brain that causes N/V./ ondansetron (zofran), tropisetron, dolasetron (12.5 mg dose; 0.035 mg/kg), granisetron (0.01 mg/kg).
173
Sumatriptan and receptor interaction
˙ˇ 5HT1 receptor agonist. Reverse cerebral artery vasodilation = vasoconstriction.
174
Ondansetron
structurally related to serotonin. Therapeutic effects include decreased PONV in susceptible patients _ used prophylactically. Side effects include: headache, diarrhea, increased liver enzymes with chronic use.
175
Antacids
tums. Neutralize the acid that is already in the stomach. Antacids are usually a salt and they combine with HCl to neutralize it. As the pH in the gut increases, the gastric emptying also increases. Why use themÖ inexpensive, promote healing (due to increased pH and less reflux), work quickly.
176
Sodium bicarbonate (tums)
highly soluble, rapid action in stomach, brief duration, can cause alkalosis. May increase Na+ levels = bad for patients with bad hearts.
177
Magnesium hydroxide (milk of magnesia)
oˇˇ no acid rebound when discontinued, laxative effect (osmotic diarrhea), beware of HIGH doses Ö hypermagnesemia can lead to renal dysfunction and neurological/neuromuscular effects.
178
calcium carbonate
rapid absorption, metabolic alkalosis with chronic use, hypercalcemia, acid _rebound_.
179
Aluminum hydroxide
minimal absorption, phosphate depletion, decreased gastric emptying = constipation.
180
antacid drug interactions
˙ˇ increased delivery of PO medications because of the increased gastric pH. Decreased bioavailability of medications due to increased gut pH
181
Preop use of antacids
anecdotal (no real evidence to support/not support). Antacids have no effect on regurgitation and aspirationÖ just make the patient aspirate a higher pH. Non-particulate (sodium bicitrate) is better to use preop than particulate antacids (such as tums).
182
Sucralfate
coats ulcerated lesions so the stomach acid doesn_t irritate the lesion. Viscous suspension. Used to treat duodenal and gastric ulcers.
183
Prokinetics
˙ˇ increase gastric emptying by increasing peristalsis. Clinically useful prokinetics include metoclopramide, cisapride, domperidone, erythromycin.
184
Metoclopramide
dopamine antagonist. Increases gastric emptying, increases lower esophageal tone (decreased aspiration risk), relaxes pylorus and duodenum when the stomach contracts.
185
Who gets metoclopramide?
oˇˇ ll stomach, trauma, obese, diabetics, parturient (women at full term). 10mg IV or 0.15mg/kg
186
Domperidone (motilyium)
not really used much in anesthesia. Dopamine antagonist. Effects = stimulates peristalsis, increases LES tone, increases gatric emptying. NO cholinergic activity. NO central effects.
187
Cisapride (propulsin)
GI prokinetic. Increases ACh and ACh binds to parasympathetic receptors to increase gastric emptying. Treatment of opioid induced gastroparesis.
188
alpha-glucosidase inhibitors, side effects
˙ˇ acarbose. Slows digestion and absorption of carbohydrates. Does not induce hypoglycemia. Side effects: flatulence, abdominal cramping and diarrhea.
189
Graniestron dose
0.01mg/kg
190
scopolamine patch
patch behind the ear. Must go on at least 1 hour preop, but preferably the night before surgery. Antimuscarinic effects. Crosses the BBB = sedation.
191
dolasetron dose
12.5mg (o,o35mg/kg)
192
Metoclopramide dose
10mg (0.15mg/kg)
193
Decadron dose
4-10mg
194
antihypertensives, sites of action
Arterioles (resistance), Venules (capacitance), Heart (cardiac output), Kidneys (volume).
195
calcium channel blockers
selectively inhibit L-type (slow) calcium channels in the heart. Mechanism of action = decrease phase 4 and depress AV node conduction. Inhibit the flux of calcium across the slow channels of cardiac muscles resulting in decreased rate of spontaneous phase 4 depolarization.
196
types of calcium channel blockers
phenylalkylamines, dihydropyridines, benzothiazepines
197
phenylalkylamines
intracellular pore blocking of channel at binding site , verapamil
198
Dihydropyridines
extracellular allosteric modulation of channel at binding site, "pines"
199
Pharmacological effects of calcium channel blockers
decrease contractility, decrease heart rate, decrease SA node activity, decrease AV node conduction, decrease systemic BP (secondary vascular smooth muscle relaxation) / o CLINICAL USES_ coronary artery spasm, stable angina, cerebral vasospasm (after stroke of SAH), HTN (usually in combination with beta blockers or nitrates; CCB+nitrates = synergistic effect for dilating the coronaries).
200
CCB, vasodilation
nicardipine has the most, it has no SA/AV node effect, NO mycardial depression, used intraop to treat HTN
201
Tx of cerebral artery vasospasm
nimodipine crosses BBB so it is used to treat - verapamil may be used in IR bc it is injected into cerebral arteries
202
antihypertensives and local anesthetic toxicity
verapamil has effects on fast Na channels so can get prolonged LA effects
203
effects of verapamil
AV node depression, SA node negative chronotrope, negative ionotrope, some vasodilation
204
CCB and drug interations
exaggerated response to volatiles (greater decrease in MAP), impaired NMB reversal, increase risk of LA toxicity (verpamil), decrease platelet function, increase plasma concentration of digoxin, CCB + dantrolene = increase K+ and prolonged effect, hyperkalemic effects when used with K+ containing solutions.
205
CCBS in a nutshell
___pines_ DILATE, nimodipine = _nimoTOP_ it goes to the head and crosses the BBB, Diltiazem = _CARDIzem_ AV node conduction with little cardiac depression (good for heart failure patients).
206
Peripheral vasodilators
sodium nitroprusside, nitroglycerin, hydralizine, papavarine, trimethaphan
207
when to use peripheral vasodilators
treat HTN crisis, maintain controlled hypotension ((surgery, ICU post-heart surgery to keep a decreased afterload and give the heart time to recover), improve LV stroke volume for CHF patients or regurgitant valves.
208
how do peripheral vasodilators work?
DECREASE SYSTEM BLOOD PRESSURE by decreasing SVR (vasodilation), decrease RA filling (decreased preload), and increase Nitric Oxide production (increased NO = increased cGMP production = vasodilation).
209
nitric oxide
NO is an endogenous gas that acts as a chemical messenger. It helps maintain CV tone and CNS signaling (excitatory transmission). NO inhibits platelet aggregation. NO aids in GI relaxation and immune functions.
210
duration of nitric oxide
5 seconds
211
pathophysiology related to NO
essential HTN is caused due to decreased NO production
212
hypotension and septic shock
are caused by increased NO production. Atherosclerosis is due to decreased NO production and thus increased platelet aggregation. Vasospams after SAH is due to not enough production of NO.
213
anesthesia mechanism of action
˙ˇ nitric oxide is involved in the excitatory transmission in the CNS. NO is produced by NO synthase. Anesthetic agents may decrease NO synthase Ö decreased excitatory pathway in the brain and increase the inhibitory pathway so that GABA (inhibitory NT) will predominate. Inhibiting nitric oxide may be involved in global suppression.
214
clinical uses of nitric oxide
inhaled NO can be used to treat pulmonary HTN (vasodilate the pulmonary vasculature specifically) and to treat ARDS. o Dosing: 1-100 ppm dose. NEED HIGH FGF. The FGF must = Minute ventilation. o Toxicity: NO + O2 _ NO2. Toxicity occurs when NO2 builds up.
215
papaverine, vasodilation
from poppy (opium) plant. Used by surgeons to keep the mammary vessels open. There may be a systemic decrease in the BP. Very short half life so the systemic decrease in BP is only transient.
216
Thiocyanate toxicity treatment
dialysis
217
Antihypertensives and methemoglobinemia_
sodium nitroprusside
218
Treatment of methemoglobinemia
sodium nitroprusside
219
Nitroglycerin mechanism of action
requires a _thio_ substance to interact with. Increases NO release = increased cGMP = vasodilation (principally a venous dilator).
220
Angiotensin-Converting Enzyme Inhibitors
__prils_. Block the coversion of angiotensin IÖ angiotensin II. Prevent angiotensin II vasoconstriction and stimulation of sympathetic system = vasodilation. Angiotensin II is responsible for the secretion of aldosterone, thus ACE-I decrease aldosteroneÖ less vasoconstriction.
221
ACE inhibitor side effects
no CNS side effects. COUGH, angioedema, contraindicated in patients with renal artery stenosis because these patients are dependent on Angiotensin II for renal blood flow.
222
angiotensin receptor blockers
"sartans" Prevent angiotensin II from binding to its receptor. Clinical uses include: essential HTN and CHF. Side effects: no cough like ace, dizzy from vasodilation, no profound hypotension with GA, losartan
223
labetalol
Alpha 1 and nonselective beta 1 and beta 2 antagonist. Beta:alpha is 3:1 oral and 7:1 IV. Works in 5-10 min.
224
beta blockers overdose
glucagon
225
nitroprusside cGMP
upregulates
226
alpha antagonist, tx of BPH
tamulosin (flomax)
227
beta blockers, effects on ECG
sotalol - long QT
228
isoproterenol, receptor effects
B2
229
beta blocker metabolism
liver all but esmolol
230
beta blockers, airway resistance
atenalol least likely bc beta 1 specific
231
lab value and ketorolac
creatinine
232
toradol IV and morphine doses
30 mg toradol = 10mg morhphine
233
diuretic for IOP
mannitol
234
hirudin, mechanism of action
direct thrombin inhibitor
235
inhaled nitric oxide and fresh gas flows
fresh gas flows must be greater than MV
236
naloxone, duration
30-60 minutes
237
antidysrhyhthmic, class II mechanism
blockade of sympathetic activity, decrease rate of phase 4 depolarization, decreased rate of SA node discharge
238
beta blocker for glaucoma
timolol
239
antimicrobial prophylaxis, 2006 medical letter guidelines for bowel procedures
cefoxitin
240
thrombolytics
-ases break up all clots
241
action of transexamic acid
antifibrinolytic agent
242
antidysrhyhthmic, class IV mechanism
CCB
243
sulfonylurea mechanism of action
promote insulin secretion
244
bupivicaine toxic dose
2.5mg/kg
245
ACT normal range
90-100
246
vitamin k dependent coag factors
2+7,9,10
247
amiodarone infusion rate
150mg/10 min then 1mg/min
248
contraindications for acute intermitteny porphyria
thiopental
249
gabapentinoids
affect Ca channels, do not act on gaba, provides sedation 600-900mg (15mg/kg) , reduction in pain and opoiod use, does help in chronic pain
250
nmda receptor antagonists
glutamate-acticated Ca channels, inplicated in neural changes asoociated wth chronic or sustrained pain
251
drugs that block nmda receptors
ketamine, memantine hcl, dextrorphan (entantiomer of codeine)
252
ketamine
related to PCP, direct inhibition of nmda receptors, augmentation of noradrenergic output from locus ceruleus, weak opoiod receptor agonist, inhibits production of inflamm cytokines; alpha, beta waves predominant; decrease NV, decreases opoiod consumption
253
magnesium
competitive antagonist of nmda, clinically significant reduction on pain
254
dexmedetomidine
fxns centrally in locus ceruleus, inhibition of descending spinal cord projections likely the mechanism by which drug inhibies nociception, sedation very similar to natural sleep; reduces need for post op opoiods, decreases pain, decrease NV (prob from less opoids) MORE bradycadia and hypotension!
255
uses for precedex
tonsilectomy: most widely used pt population, 1mcg/kg over 15 minutes, faster wakeup
256
clonidine in caudals
prolongs duration of analgesia
257
precedex and spinal, peripheral nerve blocks
prolongs sensory block but 3.7x in bradycardia
258
clonidine as premed for kids
improved post-op pain contrl and reduced emergence delirium
259
precedex pharmacokinetics
must be started earlier, need loading dose but there are hemodynamic consequences, doesn’t reach peak as fast
260
decadron
4mg for PONV, high doses show pain reduction, decrease in bleeding
261
toradol
bleeding effects exaggerated / transient reduction in GFR,no sig change in creatinine
262
acetaminophen (paracetamol)
antipyretic effect, analgesua, weak peripheral anti-inflamm, must be given prophylatically- about 30 minutes before wakeup
263
acetaminophen, metabolism
glucuronidation, sulfation, oxidation to NAPQI (NAPQI is hepatatoxic)
