TL round 2 Flashcards
How much of the cardiac output goes to uterus at full term?
20%
BF supply to uterus during pregnancy
85% uterine arteries
15% ovarian arteries
-> terminate as spiral arteries -> supply intervillous space
Which side of placental has villi?
Fetal side
Where does the umbilical artery originate off of?
fetal internal iliac arteries
-that’s why there’s two!
Best way to assist in proper positioning of thoracic aortic aneurysm stent?
- induced hypoTN (MAP goal 70-80) -> dec likelihood of migratation
- transient asystole (adenosine)
- rapid ventricular pacing (> 180)
When to have elective repair of TAA or AAA?
size > 5.5 cm or grows >1cm in 1 year
When to cautiously use adenosine?
Asthma, upper resp dx
***adenosine causes bronchoconstriction
which neuraxial opioids are lipophilic?
fentanyl and sufentanil (diffuse away faster)
Which epidural opioids cause more N/V?
Morphine
-hydrophilic opioids
which epidural opioids cause less pruritis?
fentanyl
-lipophilic opioids
Monitoring for OB hydrophilic epidural opioids?
hourly for 1st 12 hours
every 2 hours for next 12 hours
Klippel-Feil syndrome
-congenital condition assoc w/ fusion of the cervical spine
Klippel Feil Syndrome
congenital fusion of cervical spine
-limited neck motion
-difficult to intubate
-scoliosis, strabismus, or scapular defects
Trisomy 21 airway concerns
macroglossia
subglottic stenosis
atlanto-axial instability
**assoc w/ endocardial cushion defects
newborn hypoglycemia, macroglossia, organomegaly
Beckwith-Wiedemann Syndrome
-assoc w/ omphalocele
Pierre Robin sequence
micrognathia
macroglossia
severe upper airway obstruction
Confirm brain death cerebral angio results
-absence of intracerebral filling at level of carotid bifurcation or circle of Willis
-patency of external carotid circulation
-delayed filling of superior longitudinal sinus
Clinical criteria for dx brain death
-known cause and evidence of acute, catostrophic, irreversible brain injury
-reversible conditions must be excluded
-temp > 36C
-not have any chance of drug intoxication, NMB or shock
RF for developing fat emboli syndrome
closed long bone fx or pts undergoing intramedullary instrumentation (inside bone) during ortho procedures
Triad for fat embolic syndrome
petechiae (head, neck, axillae)
hypoxemia
neuro abnormalities (altered LOC, sz)
diagnosis of fat embolic syndrome
at least 1 major and 4 minor criteria
MAJOR: axillary/subconjuctival petechiae, hypoxemia (PaO2 < 60), CNS dep, pulm edema
MINOR
tachycardia, hyperthermia, retinal fat emboli
-urinary fat globules, dec plts/Hct, inc ESR, fat globules in sputum
how to prevent fat emobli syndrome
minimizing delay to reduction of long bone fx
treatment of fat emobli syndrome
aggressive resp support (high flow O2, PEEP)
-crystalloids and albumin (can bind fatty acids, dec lung injury and replace lost blood volume)
in recovery after c/s:
SpO2 dec to 85%, BP hypoTN, diffuse bleeding at surgical site
amniotic fluid embolism
criteria for amniotic fluid emoblism
- acute hypoTN or cardiac arrest
- acute hypoxia
- coagulopathy, or severe hemorrhage
2 phases of amniotic fluid emoblism
1st: amniotic fluid in maternal circulation -> release of inflammatory mediators -> coronary constriction, bronchoconstriction, pulm vasoconstriction -> pulm HTN and RV dyzfxn -> hypoxemia and hypoTN
-systemic vasodilation from inflammatory resp
2nd: LV fails b/c not filling and septal deviation -> hypoTN and inc pulm pressures -> pulm edema
-massive consumptive coag –> hemorrhage
tx of amniotic fluid embolism
resuscitative -> ETT, fluids, vasopressors/inotropes, blood products
Myasthenic syndrome
Lambert Eaton
-Ab to VG Ca channels
NMB and myasthenia gravis
inc succ needed
dec roc needed
Intraop mannitol and renal transplant
-shown to dec post-transplant kidney injury, but non effect on graft rejection
-***b/c renal vasodilation, renal PG release and scavenging of free radicals
Goals for renal transplant flluids
maintain intravascul volume!!
-hypovolemia and hypoTN -> impaired graft perfusion w/ injury
-mannitol dec incidence of post-transplant renal injury req HD
Normal Mg level
1.4-2
Mg 4-6
lethargy
drowsiness
flushing
N/V
diminished Deep tendon reflex
Mg 6-10
somnolence
loss of DTR at 10
hypoTN
ECG changes
HypoCa/hyperMg EKG
prolonged QT
lengthened ST
Mg 10-20
Resp arrest
AV conduction block
progressive QRS widening and bradycardia
Mg >25
cardiac arrest
Tx of hyperMg w/ hemodynamic collapse
Calciuim chloride/gluconate
HD is definitive tx, but may take a long time to make happen
Dialyzable toxins
Lithium
Toxic alcohols
Salicylates
Reasons for emergent dialysis
AEIOU
Acidosis: pH < 7.1
Electrolytes: K > 6.5
Ingestions (toxins)
Overload (fluid)
Uremia (pericarditis, encephalopathy, bleeding)
RF for post-cardiopulm bypass acute kidney inury
-preop Cr greater than 1.2
-combined valve, bypass procedures
-preop intraaortic balloon pump
minor: female, CHF, COPD, IDDM, dec LVEF
How kidneys and calcium
-kidney converts 25-hydroxycholecalciferol to 1,25-hydroxycholecalciferol
-1,25-hydroxycholecalciferol is resp for inc Ca absorption into GI tract
Changes in ESRD
Anemia
hypoCa
hyperK
hyperMg
hyperlipidemia
HTN
hyperphos
2ndary hyperparathyroidism
uremic bleeding diathesis
***can be hyper/hypoNa -> no definitive!
prealbumin pre and post HD
higher post due to concentration effects
electrolytes post HD
determined by the composition of the dialysate! which substances move
Endothelin
vasoconstrictor
-inc w/ damage to endothelial cells
Nephrotoxic substances and can cause ATN:
-Aminoglycosides
-hemoglobinuria
-myoglobinuria
-IV contrast
-hetastarch
-mannitol
Gold standard for differentiation b/w ATN and prerenal
response to fluid repletion
-Cr responds to baseline in 1-3 days if repletion adequate
-persistent AKI despite repletion = ATN
FeNa calculation
(UNaSCr)/ (UCrSNa) * 100
Intrarenal FENa
> 1%
Prerenal FENa
<1%
Prerenal UNa
< 20
Intrarenal UNa
> 40 b/c tubules can’t retain sodium
BUN to Cr ratio ATN
10:1 - 15:1
Urine specific gravity ATN
same as plasma b/c can’t conc
1.001-1.0035
Prerenal Urinen osmolality
> 500
intrarenal urine osm
< 350
prerenal specific gravity
1.015
Fractional excretion of urea prerenal
< 35%
fractional excretion of urea ATN
> 50%
urine to plasma osmolar ratio prerenal
> 1.5
-makes sense! urine is more concentrated than blood
Sodium deficit equation
Sodium deficit = (140 - serum Na) * total body water
total body water = kg * 0.6
When to use hypertonic saline
symptomatic pt w/ Na < 120
-stop Hypertoni when Na above 120
Concern w/ rapid inc in serum Na if hypoNa
central pontine myelinolysis
Oliguria
inadequate production of urine
<0.3 cc/kg/hr
in OR: < 0.5 cc/kg/hr
Prerenal oliguria causes
HypoTN
hypovolemia
inadeq circulating volume
renal artery/vein stenosis
intrarenal causes of oliguria
ATN
ischemia
nephrotoxins
inflammatory conditions: vasculitis, interstitial nephritis
Postrenal oliguria
occlusion or uterers, bladder, or urethra
Best way to differentiate b/w prerenal and intrarenal causes of oliguria in pts taking diuretics
fractional excretion of urea b/c diuretics will causes pt to have high excretion of sodium
What channel is mutated in hypoK periodic paralysis?
Na or Ca
pt presents w/ flaccid paralysis after carb heavy meal
hypoK periodic paralysis
Triggers for hypoK periodic paralysis
-high-salt containing meals
-strenuous activity
-stress
-hypothermia
-menstruation
-glucose-insulin infusions
K < 3
PPx for hypoK periodic paralysis
-prevention!
-ppx: acetazolamide and K sparing diuertics
anesthetic triggers for hypoK periodic paralysis
long-acting NMB assoc w/ attacks
Myotonia congenita
mutations in VG Chloride channels
-sustained muscle tensing, prevents m from relaxing normally
inheritance of hypoK periodic parlysis
Auto Dom w/ incomplete penetrance
MOA of hyperK periodic paralysis
Na channel mutation -> prolonged muscle membrane depolarization and flaccid paralysis
Triggers for hyperK periodic paralysis
K infusions
rest after exercise
metabolic acidosis
hypothermia
K > 5.5
What type of drugs cross placenta?
small (<500 Daltons)
lipophilic
nonionized at physiological pH
subendocardial ischemia
imbalance of myocardial O2 supply and demand
-more commonly seen b/c small capillaries and arterioles blocked by high intraventricular pressures
EKG subendocardial ischemia shown as
ST depressiosn
Acute transmural myocardial injury
STEMI
-suggests injury or infarction, not just ischemia
ST elevation criteria in women
New ST elevations in 2 contiguous points > 0.15 mV in women
ST elevation criteria in men
New ST elevation 2 contiguous leads
>0.2 mV in men > 40
>0.25 in men < 40
ST depression def
> 0.05 mV in 2 contiguous leads
T wave inversion def
> 0.1 mV in 2 contiguous leads
Dx of brugada syndrome
EKG abnormality: ST elevation >2mm followed by negative T wave
-VF or polymorphic V tach
-family hx of sudden cardiac death at < 45
-inducibility of VT w/ electrical stim
-syncope
-nocturnal agonal respiration
Tx for brugada syndrome
ICD
Tx for unstable SVT in transplanted heart
Synchronized cardioversion
Alveolar gas equation
PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2/0.8)
-room air FiO2 = 21 or 0.21
Normal alveolar-arterial gradient
< 10
How to get alveolar-arterial gradient
Calculate PAO2 using alveolar gas equation
PAO2 = (FiO2 * [Patm - PH2O]) - (PaCO2/0.8)
PH2O is water vapor pressure
Then do PAO2- PaO2, < 10 is normal
Infraorbital n block good for what type of surgery?
Cleft lip repair
Infraorbital n branch of
maxillary division of trigeminal nerve (CN V2)
Infraorbital n provides sensation to
skin and mucosa of lower eyelid, lateral nose, cheek, and upper lip
Infraorbital n block
-emerges from infraorbital foramen inferior to orbital rim
-extraoral: cover foramen w/ finger, superomedial orientation until bone, 1-3 cc
-intraoral: needle via buccal mucosa at level of upper canines w/ cephalad and lateral advancement