TL block 4 Flashcards
1
Q
Benefits of prone positioning
A
-improved ventilation perfusion matching enter
– improved functional residual capacity
– Improve drainage of secretions
2
Q
What are electrolytes does a trade affect?
A
Calcium and magnesium
3
Q
What blood products contain the highest amount of citrate
A
FFP and platelets
4
Q
How is citrate metabolize?
A
By the liver
5
Q
What increases the likelihood of citrate toxicity?
A
– Hypothermia
– Liver disease, or transplant
– Hyperventilation
– Pediatric patients
(decrease metabolism of citrate)
6
Q
Most common cause of acute liver failure
A
Acetaminophen overdose
7
Q
Pathophysiology as to why there is liver failure with acetaminophen overdose
A
Acetaminophen overdose causes increased, ammonia levels, excess ammonia, combines with glutamate to form glutamine -> glutamine acts as an osmotic agent, causing swelling of astrocytes and cerebral edema
– Elevated ammonia levels are toxic to the brain -> cereal, edema, third vision, vomiting, asterixis , seizures
8
Q
How does lactulose decrease ammonia levels?
A
Causes a decrease in intestinal pH -> traps ammonia as ammonium ion -> Can no longer cross intestinal membrane and can’t be absorbed
9
Q
Grades of hepatic encephalopathy
A
I: short, attention, span, minor, lack of awareness, and disordered sleep
II: asterixis, lethargy, and behavioral change
III: confusion, disorientation bizarre behavior, and tiredness
IV: coma
10
Q
What should be screened for preoperatively and Duchenne and Becker muscular dystrophy?
A
Heart, commonly associated with dilated cardiomyopathy
11
Q
Why do patients with the Shane and Beck are muscular dystrophy get hyper kalemia?
A
No association with malignant hyperthermia, but when exposed to volatile anesthetics and succinylcholine, can get hyperkalemia from rhabdomyolysis -> cardiac arrhythmias and arrest
12
Q
Treatment for hyperkalemia
A
Calcium, hyperventilation, insulin, bicarb, and albuterol
13
Q
Why do patients with spinal cord injury get succinylcholine induced hyperkalemia
A
Extra junctional acetylcholine receptors
14
Q
Where is the mutation in hyperkalemic periodic paralysis?
A
Sodium channel mutations
15
Q
Where is the mutation and hypokalemic periodic paralysis?
A
Calcium channels
16
Q
Why do you get bradycardia with carotid, stent application?
A
Afferent limb of carotid sinus baroreceptor reflex disease (glossopharyngeal) -> stimulation of the nucleus tractus solitarius in medulla -> vagal nuclei activation -> bradycardia and hypotension
17
Q
Carotid body chemoreceptors
A
Monitors partial pressure of oxygen, secondarily monitors pH and PaCO2
** after carotid endarterectomy chemoreceptors lose innervation, and have a decreased response to hypoxia **
18
Q
Alveolar partial pressure of O2
A
PAO2 = FiO2 * (Patm - PH2O) - (PaCO2/.8)
FiO2 is % at ambient air
19
Q
Risk factors for the development of postherpetic neuralgia
A
– Older age
– Female gender
– Increased pain or sensory abnormalities during acute phase
– Severe skin lesion
-Presence of prodrome
20
Q
How to decrease incidence of postherpetic neuralgia
A
Vaccines
21
Q
Where does herpes zoster remain after primary infection to cause shingles?
A
Dorsal root ganglia
22
Q
Contraindications to shockwave lithotripsy
A
– Pregnancy
– Anticoagulation
– Uncorrected bleeding disorders
– Large abdominal aortic aneurysm
23
Q
Shunt fraction equation
A
Qs/Qt = (1-SaO2)/ (1-SvO2)
24
Q
Ex of anatomical shunts
A
thebesian veins (valveless veins in walls of cardiac chambers that drain directly into cardiac chambers they are on)
bronchial veins (into pulm veins)
25
Normal shunt
5% in healthy pts
26
Def of oliguria
< 0.5 cc/kg/hr in adults
27
ADH and surgery
inc in surgical stress -> inc ADH -> contributes to postop oliguria
28
hemodynamic changes in ECT
parasym immediately -> sympathetic lasts for 10 minutes
29
Absolute CI to ECT
pheochromocytoma
MI w/i 4-6 weeks
stroke < 3 months
intracranial surgery < 3 months
Intracranial mass lesion
Unstable cervical spine
30
Why is intracranial mass lesion a CI for ECT?
CBF inc 100-400% in ECT due to inc CMR and in BP -> inc ICP -> at risk for stroke or herniation
31
MCC of maternal death in pts with preeclampsia
Hemorrhagic stroke
-commonly postpartum
-best predictor: high systolic pressure
32
preeclampsia w /severe features
plts < 100
Cr > 1.1
baseline Cr x2
LFTs x2
pulm edema
cerebral or visual symp
33
Leading cause of maternal death in USA
cardiac dx
34
Leading cause of maternal death worldwide
PPH
35
Goal for BP dec in preeclampsia
< 160 systolic, and if dec no more than 15-25%
36
1 noncoronary cusp
2 L coronary cusp
3. R coronary cusp
4. RA
5. RV
6. LA
**noncoronary cusp at interatrial septum
37
How does uremia affect plt aggregation?
1. interferes w/ vWF formation and release (impaired plt activation at injury site)
2. function of glycoprotein IIb-IIIa abnormal
3. prostacyclin and nirtic oxide synthesis inc (plt inhibitory effects)
4. dec factor III activity (can't bind to factor VII to activate factor X)
38
what does vWF do?
subendothelial vWF binds plts, activates plts and helps plts aggregate
39
what does glycoprotein IIb-IIIa do?
on surface of plts -> receptor for fibrinogen, fibronectin, vWF
-helps w/ plt activation and aggregation
40
acid-base status hyperparathyroidism
-prevents reabsorption of bicarb -> non-AG metabolic acidosis
-inhibits Na-Cl cotransporter in DCT -> hyperCl
**same as excessive NS admin in OR
41
RV appears large on echo w small lLV, cause? shock
PE, obstructive shock
42
small RV and LV, dilated IVC, dx? shock
cardiac tamponade, obstructive
43
dilated ventricles and dec contractility, shock?
cardiogenic
44
normal ventricular sizes, tachycardia inc contractility, shock?
distributive sepsis
45
small LV and RV, contracility inc, shock?
hypovolemic
46
MOA MH
d/o ryanodine receptor -> uncontrolled release of Ca -> sustained m contraction, hypermetabolic state, hyperthermia -> myoglobinuria, rhabdo, organ failure cardiac arrest
47
acid-base MH
mixed resp and metabolic acidosis
48
bolus dose of acute MH
Dantrolene 2.5 mg/kg
49
maintenance dose of dantrolene
1 mg/kg every 6 hours for 24-48 hours
50
Monitoring for MH
CK (peak 12-24 hrs later)
Liver enzymes
Coag studies (monitor for DIC)
Blood gas (looking for resolution of acidosis)
Electrolytes (esp K)
51
MC SE dantrolene
skeletal m weakness > thrombophlebitis > GI upset
52
earliest symp of MH in peds
tachycardia and rapid inc in EtO2
53
Dantrolene MOA
muscle relaxant restores Ca homeostasis
54
Lab monitoring for long term use of dantrolene
LFTs
55
What pain medication works through the inhibitors of VG Ca channels?
gabapentin and pregabalin
56
MOA inhaled nitric oxide
inc cGMP prod -> selective pulm vasodilator -> dec pulm artery pressures and red RV afterload
**primarily arterial dialtor
57
Nitric oxide function in body
-nitric oxide prod by vascular endothelium: is a neurotransmitter, prevents plt aggregation, and smooth m relaxant (vasodilatory)
58
Nitric oxide and tissue damage
tissue damage, less nitric oxide -> plt aggregation at damaged tissue, vasoconstriction/spasm to dec bleeding and start coag cascade
59
Why does inhaled nitric oxide not have systemic effects?
erythrocytes w/i pulm circulation rapidly inactivate the gas
60
Max dose of lidocaine w/ epi
7 mg/kg
61
Max lidocaine dose w/o epi
5 mg/kg
62
Max bupi dose
2.5 mg/kg
63
Max bupi dose w/ epi
3
64
Max mepivacaine dose
5 mg/kg
65
Max mepivacaine dose w/ epi
7 mg/kg
66
Max dose of ropi
3 mg/kg
67
Max dose of ropi w/ epi
3.5 mg/kg
68
CI to sugammadex
hypersensitivity to cyclodextrins
69
What NMB can be reversed by sugammadex
roc and vecuronium
70
What is incompatible w/ sugammadexx?
Ondansetron and Verapamil
**flush adequately b/w admin
71
increase in K after succ in healthy pts
0.5 mEq/L
72
How long after burns, trauma, denervation should you avoid succ?
after 24 hours no succ!
73
How is sugammadex dosed? Actual, lean, or ideal body weight?
ACTUAL
74
Triad of sodium nitroprusside toxicity
CN toxicity
elevated mixed venous O2, sodium nitroprusside tachyphylaxis, and metabolic acidosis, flushing
75
types of toxicity with sodium nitroprusside
CN and thiocyanate
76
Increased risk of toxicity w/ sodium nitroprusside
renal failure
diets low in sulfur or Vit B12
77
sodium nitroprusside after: hypoxia, nausea, tinnitus, m spasm, disorientation, psychosis
thiocyanate toxicity (usually several days after SNP)
levels 5-10 mg/dL
78
When does CN toxicity w/ sodium nitroprusside occur?
blood levels > 100 mg/dL
SNP > 1mg/kg in less than 2 hours
> 0.5 mg/kg over 24 hours
79
Antidote for cyanide poisoning
Amyl nitrite
-converts Hg to met-Hg -> binds CN -> nontoxic cyanometHg
80
How is vecuronium metabolized?
hepatically then renally cleared
81
succ dosing in infants
increased compared to kids due to increased volume of distribution
82
Bioavailability
IV > subq > IM > sublingual/buccal > intranasal > rectal > oral
83
Phases of liver transplant
preanhepatic
anhepatic
neohepatic
84
What is the preanhepatic phase liver transplant?
incision to cross clamping of the major vessels of the liver
85
What is the anhepatic phase? liver transplant
starts w/ cross clamping and continues until anastomosis made and perfusion restarts
86
What is the neohepatic phase? liver transplant
unclamping of portal vein when reperfusion starts until abd closure
87
postreperfusion syndrome (liver transplant)
systemic hypoTN
pulm HTN
possible emboli
88
What causes postreperfusion syndrome?
Build up of K, lactate, H+ into circulation -> lack of ATP and glycogen -> Na/K pump stops working -> extracellular Na moves into cells causing swelling
-vascular permeability also inc due to lack of ATP
89
Metabolism of chloroprocaine
plasma cholinesterase
**b/c ester local anesthetic, same as all esters!
90
Metabolism of amide local anesthetics
hepatic metabolism
91
Why chloroprocaine for OB emergency sections?
-metabolized by plasma cholinesterase, little availabily to cross placenta
-does not participate in ion trapping, so useful w/ acidotic in distress fetus
-fast onset
92
What local anesthetics most likely to cross placenta?
Lidocaine! less protein bound
-Bupi and Ropi more protein bound, so harder
-Amides more likely than esters (Chloroprocaine least likely)
93
What dx associated w/ MH?
Central core dx
Multiminicore Dx
King Denborough Syndrome
Hyper/hypokalemic periodic paralysis
94
Central core dx
Auto Dom mutation in ryanodine receptor
-spine and pelvic weakness w/ foot deformities
**assoc w/ MH!
95
Duchenne muscular dystrophy
X linked recessive, dystrophin gene
-hyperK to succ
-rhabdo w/ volatile anesthetics
**no MH assoc
96
Treatment of neuroleptic malignant syndrome
bromocriptine (DA agonist)
97
Diagnostic test for MH
caffeine halothane contracture test
98
tx for benzo OD
flumazenil
99
What OD: AMS, nausea, tachypnea, ringing in the ears
salicylate (ASA)
100
acid-case for salicylate OD
combined anion gap metabolic acidosis and resp alk
-salicylates act on resp drive in medulla to inc RR
101
Treatment of salicylate toxicity
1. supportive (ABCs)
2. activated charcoal and/or gastric lavage if recent
3. dextrose to avoid CSF hypoglycemia
4. IV fluids to replace losses from tachypnea and vomiting
5. Bicarb: inc pH to dec tissue distribtuion and raises urine pH to inc renal clearance
**if severe symptoms: HEMODIALYSIS
102
OD: abd pain, N/V, sweating
Acetaminophen tox
liver failure
**don't show many symptoms in first 24 hours, but have worse liver failure
103
tx for acetaminophen OD
N-acetylcysteine
104
What pressor should not be given IM?
Norepi
105
Tx for area of necrosis caused by Norepi in a PIV?
Phentolamine
106
Best lab test to determine if someone in end stage liver failure is in DIC
***factor VII! b/c inc/normal in end stage liver dx, but dec in DIC
-in endstage liver dx, fibrinogen will already be dec, so will a lot of other factors, and if pt had surgery d-dimer will be inc
107
Primary signs of acute liver failure
inc in INR
encephalopathy
elevated AST/ALT
*no symp of portal HTN b/c rapid progression
108
What causes hepatic encephalopathy?
Ammonia!
-ammonia metabolized to glutamine by astrocytes in CNS -> swelling of astrocytes and cerebral edema
-untreated can cause inc ICP, herniation, death
109
postop shivering, then rigidity, hyperthermia, N/V, hyperreflexia, dx? tx?
Serotonin Syndrome
tx: Cyproheptadine (antihistamine)
110
Treatment of acute dystonia likely 2/2 antipsychotics
benztropine
diphenhydramine
benzos
111
AMS, hypthermia, rigitidity, dysautonomia w/ antipsychotics dx? tx?
NMS
tx: bromocriptine, amantadine, dantrolene
112
Methadone MOA
full agonist at mu receptors
NMDA antag
monoamine reuptake inh
113
Safest opioids in ESRD
fent
methadone (metabolites inactive, metabolized by liver cytochrome P450)
114
SE methadone
resp depression
QTc prolongation (caution if > 450, d/c if > 500)
N/V
constipation
biliary spasms*
115
What drugs increase conc of methadone?
Alcohol
Benzos
Ciprofloxacin
Fluconazole
Urinary alkalinizers
116
What drugs dec methadone conc?
Anti-retroviral therapy
Phenobarb
Phenytoin
Urinary acidifiers
117
Inhaled anesthetics QTc?
causes prolongation
118
tx of torsades de points
IV Mg
119
Metabolized by butylcholinesterase
succ
ester local anesthetics
heroin
cocaine
mivacurium
ASA
120
If information submitted to National Anesthesia Clinical Outcomes Registry, what other registry does the data go to?
Multicenter Perioperative outcomes Group
-both get data from AIMS: anesthesia information management systmes
121
Where does anesthesia closed claims project get its data?
case summaries submitted by ASA from malpractice insurance claim files -> goal of pt safety
122
where does society for thoracic surgery w/ society of cardiovascular anesthesiologist get its info?
it's own anesthesia module -> checkboxes to collect info about pts underoing cardiothoracic surgery -> research purpose
123
PCWP PE
deceased! b/c circulation to the L atrium is limited
124
PCWP tamponade
increased
125
PCWP tension PTX
increased
126
severe pulm HTN PCP
decreased
circulation to LA is limited
127
MC type of shock
distributive
128
What type of shock is neurogenic shock?
Distributive
-dec BP and dec HR -> discruption in CNS that regulate circulation
**SC injuries
129
Cardiac index for cardiogenic shock
< 2.2 L/min/m^2
130
def of shock
life-threatneing emergncy where tissues of body not getting adequate BF
131
Hemodynamics for cardiogenic shock
HypoTN for > 30 minutes w/ systolic < 90 (or decrease from baseline by 40)
-PCWP > 18
-CI < 2.2
132
Which measure of ABG is calculated not measured?
base excess
bicarbonate
SaO2
133
How is PCO2 measured ABG?
Severinghaus electrode
134
Blood PO2 measured how ABG?
Clark electrode
135
How is blood pH measured?
pH electrode, optical absorbance technique
-difference b/w known and measuring sample
136
What to do if d/c TPN?
start IV glucose and freq monitoring of blood glucose
-body inc insulin production during constant TPN
137
Who is more likley to get refeeding syndrome
pts who have had poor or no nutrition for >72-96 hours
-low levels of prealbumin (<10)
**hypophos severe
138
Septic shock pathophys
Exposure to certain microbial components -> activate cytokine cascade -> upregulation of tissue factor (prothrombotic state) -> release of TNF alpha from macrophages -> enhance release of other cytokins (interferon gamma, IL 1, 2, 6, 8, 10) and plt activating factor
-activation of complement -> promotes vascular permeability, leukocyte chemotaxis, inc inflammatory resp
139
Which NMB has the most potent metabolite?
Vecuronium 3-desacetyl vec is 90% as potentn -> can accumulate w/ infusions and in pts w/ renal failure
140
Difference between alpha and pH stat for CPB
in hypothermia w/ CPB -> total CO2 content the same, but partial pressure CO2 decreases
-pH corrects this and adds CO2 into the circuit to correct alkalosis
-alpha stat doesn't do this
141
Advantages of pH stat during CPB
-increased speed of homogenous cerebral cooling (cerebral vasodilation)
-inc cerebral blood flow
-improved O2 delivery (corrects alkalosis, counteracts L shift of oxy-Hg curve)
142
Disadvantages of pH stat
-inc delivery of embolic load to brain
-loss of cerebral autoregulation
143
Goals for brain dead organ donors
MAP 60-120
CVP 4-12
Na < 155
ideally low dose pressor
PaO2/FiO2 ratio > 300
pH 7.25-7.5
Glucose < 150
UOP .5-3 cc/kg/hr
LV EF > 50%
Hg > 10
144
for brain dead organ donors best pressor?
Vasopressin
-dec catecholamine req and effective for diabetes insipidus (80% of pts following brain death)
145
CVP tracing tamponade
exaggerated x descent (initial ventricular ejection and atrial relaxation)
146
normal CVP tracing
147
CVP pericartiditis
-change in compliance during diastole w/o inc pericardial pressure
148
hemodynamic goals for cardiac tamponade
tachycardia
hypervolemia
inv SVR
full, fast, strong
** cardiac output HR dept**
149
what blood test should be monitored w/ inhaled NO?
Met-Hg
150
tx for CN tox
amyl nitrite
151
what dyes cause a dec in SpO2?
methylene blue, indocyanine green, indigo carmine
152
what type of adrenal insuff w/ exogenous glucocorticoids?
tertiary
153
type of adrenal insuff in ICU
Functional
-inadequate synthesis of cortisol due to cellular dysfunction and change sin adrenal gland
-peripheral glucocorticoid resistance
-transport of cortisol to organs reduced
-resp to cortisol impaired
154
Hemodynamic changes in cirrhosis
build up of nitric oxide and carbon monoxide (vasodilators) -> dec SVR and decreased afterload -> increased cardiac output
-inc renin b/c kidneys see vasodilation as depleted state
-inc mixed venous O2 saturation due to inc cardiac output and arteriovenous collaterals
155
Platypnea
dyspnea and hypoxia while sitting that is relieved while laying flat
**hepatopulm syndrome
156
exposure to pt w/ unknown HIV status at low risk for HIV
no post exposure ppx
157
ppx if exposed to known HIV pt and exposure is superficial or exposure w/ solid needle
2 drug ppx
158
ppx if pt has HIV w/ high viral load or AIDS
3 drug ppx
159
It provider exposed to hep B and unvaccinated or vaccine nonresponder
Hepatitis B immunoglobulin
160
when to give hydrocortisone in pt w/ septic shock
unresponsive to fluids and vasopressors
161
How does hydrocortisone help w/ septic shock?
inhibits nitric oxide synthesis
162
intubated pt on TPN having difficulty vent weaning, how to fix?
increase percentage of lipid content in TPN
-lipid content has a lower resp quotient than protein or carbs -> limiting CO2 production
163
MC adverse event in peds propofol sedation
apnea or airway obstruction
164
how long after no PO should parenteral nutrition be started?
7 days
165
enteral vs parenteral nutrition
enteral helps to maintain gut integrity > prevents inc in gut permeability, provides nutrition support for lymphoid tissue
-dec risk of infxn, no IV needed
parenteral: inc infxn risk, cholestasis (no stimulus for GB contraction)
166
complications of enteral nutrition
inc risk of aspiration (esp if bed not above 30 degrees)
-sinusitis
-diarrhea
-hypophosphatemia
167
Normal mixed venous blood jugular bulb sat
55-75%
168
change in jugular bulb venous O2 saturation monitoring w/ stroke
none (only global, not focal)
169
change in jugular bulb venous O2 saturation monitoring w/ barbiturate infusion
increased!
dec CMRO2 -> dec O2 consumption
170
change in jugular bulb venous O2 saturation monitoring w/ severe anemia
dec b/c dec hgb -> dec O2 deliver
171
change in jugular bulb venous O2 saturation monitoring w/
increased b/c dec O2 extraction by cerebral tissue
(inc cardiac output)
172
oculogyric crisis
spasmodic movements of eyeballs into fixed upwardsposition
-acute dystonia
