UNIT 11 Across the Lifespan Flashcards
Pregnancy increases MV, Vt, RR change by % from what hormone?
Respiratory changes in pregnancy:
progesterone is a respiratory stimulant.
- MV increases by 50%
- Vt increases by 40%
- RR increases by 10%
Ph, vital capacity, closing capacity are unchanged in OB
how does pregnancy affect the mother’s ABG? What does NOT change?
progesterone is a respiratory stimulant, increasing MV up to 50%. In consequence, mom’s PaCO2 falls and she develops a respiratory alkalosis. Renal compensation eliminates bicarb to normalize blood pH.
increased PaO2 d/t reduction in physiologic shunt that increases driving pressure of oxygen across the fetoplacental interface + improves fetal gas exchange
pH = no change
PaO2 = 104-109
PaCO2 = 28-32
HCO3- = 20
how does pregnancy affect the oxyHgb dissociation curve?
R shift, facilitates O2 unloading to the fetus
how does pregnancy affect the lung volumes and capacities?
FRC is reduced as a function of a decrease in ERV and RV
(ERV decreases more than RV) if you see this on a question and there’s no FRC option choose this!
increased O2 consumption paired w/ decreased FRC hastens the onset of hypoxemia.
CV changes in pregnancy:
How does CO change during pregnancy and delivery? What about in a twin pregnancy?
- CO increases 40%
- uterus receives 10% of CO, uterine contraction causes autotransfusion = increased preload
- HR increases 15%
- SV increases 30%
- CO returns to pre-LABOR values in 24-48hrs
- CO returns to pre-PREGNANCY values in approx 2 weeks
- twins cause CO to increase 20% above a single fetus pregnancy
- Heart is pushed up and left axis
how do BP, SV,HR, SVR change during pregnancy?
- Diastolic blood pressure is decreased
- Stroke volume increases due to increased intravascular volume
- Heart rate is increased to satisfy higher metabolic demand.
Progesterone causes increased NO (vasodilation) and decreased response to angiotensin and NE
- SVR decreases 15%
- PVR decreases 30%
who is at risk for aortocaval compression and how do you treat it?
in the supine position, the gravid uterus compresses the vena cava and the aorta –> decreased venous return + decreased arterial flow
- compromised fetal perfusion and can also cause the mother to lose consciousness
- Left uterine displacement of 15-30 degrees by putting a wedge under the right side
- Should be used for anyone in 2nd or 3rd trimester.
how does the intravascular fluid volume change during pregnancy?
increases 35% (prepares mom for hemorrhage w/ labor)
plasma volume increase 45%
erythrocyte volume increase 20%
- creates dilutional anemia
what hematologic changes accompany pregnancy? What increases? What decreases?
- Increase in factors: 1, 7, 8, 9, 10, 12 = hypercoaguable state
- Increase in fibrin breakdown
- Decrease in protein S
- Decrease in antithrombin, platelets
- Decrease in factor 11 & 13 and PTT
- No change in protein C, sometimes platelets (can also be decreased)
how does MAC change during pregnancy?
decreased by 30-40% d/t increased progesterone
how does pregnancy affect gastric pH and volume? Which hormone is involved?
increase volume, decreases pH. due to gastrin
18-20 weeks considered a full stomach!
how does pregnancy affect gastric emptying?
before onset of labor = no change
after onset of labor = delayed
How does pregnancy affect uterine blood flow at term? How ml does it change? What % of CO?
At term, UBF increases to 500-700mL/min
Uterine blood flow receives 10% of cardiac output
It is not autoregulated, it relies on material MAP, cardiac output, and uterine vascular resistance
what conditions can reduce uterine blood flow?
uterine blood flow does NOT autoregulate –> therefore, it is dependent on MAP, CO, and uterine vascular resistance
UBF = (uterine artery pressure - uterine venous pressure)/uterine vascular resistance
causes of decreased UBF:
- decreased perfusion: maternal hypotension
- increased resistance: uterine contraction or maternal hypertension
discuss the use of phenylephrine and ephedrine in the laboring patient.
classic teaching = phenylephrine increases uterine vascular resistance and reduces placental perfusion
new evidence = phenylephrine is as efficacious as ephedrine in maintaining placental perfusion and fetal pH.
which law determines which drugs will pass through the placenta?
Fick
rate of diffusion = (diffusion coefficientsurface areaconcentration gradient)/ membrane thickness
drugs that favor placental transfer:
- low molecular weight
- high lipid solubility
- unionized
- nonpolar
define the 3 stages of labor
1 = beginning of regular contractions to full cervical dilation (10cm) 2 = full dilation to delivery of fetus (pain in the perineum begins during stage 2) 3 = delivery of the placenta
how does uncontrolled labor pain affect the fetus? What does it reduce?
uncontrolled pain may result in: reduced UBF and O2 delivery to fetus
- increased maternal catechols –> HTN –> reduced UBF
- maternal hyperventilation –> L shift of oxyHgb curve –> reduced delivery of O2 to fetus
compare and contrast the pain that results from the first and second stages of labor.
first
- Afferent pathway: Visceral C fibers hypogastric plexus
- pain begins in the lower uterine segment and the cervix
- origin: T10-L1 posterior nerve roots
second
- Afferent pathway: Punendal nerve, somatic pain
- adds in pain impulses from the vagina, perineum, and pelvic floor
- origin: S2-S4 posterior nerve roots
compare and contrast regional anesthetic techniques that can be used for first and second stage labor pain
1st stage (T10-L1), 2nd stage (S2-4)
uterus and cervix (diffuse, dull, cramping pain)
- neuraxial
- paracervical nerve block
- paravertebral lumbar sympathetic block
perineum (well localized, sharp pain)
- neuraxial
- pudendal nerve block
describe the “needle through needle” technique for CSE
- epidural space is ID-ed w/ the epidural needle
- spinal needle is placed through the epidural needle, LA injected into intrathecal space
- spinal needle is removed
- epidural catheter is threaded through epidural needle
- you’re able to add a smaller dose of local now
compare and contrast bupivacaine and ropivacaine for labor.
Read over this:
bupi: amide, long DOA
- racemic mixture
- minimal tachyphylaxis
- low placental transfer (high PB, ionization)
- sensory >motor block
- cardiac toxicity (before seizure)
- 0.75% contraindicated via epidural d/t risk of toxicity w/ IV injection
Ropivacaine: amide, long DOA
- S- isomer of bupi w/ propyl group substituation
- decreased risk of CV toxicity
- decreased potency c/w bupi
- decreased motor block
discuss the use of 2-chloroprocaine for labor
- useful for emergency c/s when epidural already in place (d/t fast onset)
- metabolized by plasma pseudocholinesterase (minimal placental transfer)
- antagonizes opioid receptors (reduces efficacy of epidural morphine)
- risk of arachnoiditis w/ intrathecal injection d/t preservatives
- those w/out methylparaben, metabisulfite don’t cause neurotoxicity
discuss the consequences of an epidural that is placed in the subdural space.
w/in 10-25mins after dosing, pt will experience symptoms of excessive cephalad spread
- subdural space is a potential space; holds very low volume –> block will go high quicker
what is the treatment for a total spinal?
vasopressors IVF LUD elevation of the legs intubation if LOC
discuss the fetal heart rate.
surrogate measure of overall fetal wellbeing (fetal hypoxia and acidosis)
normal 110-160
- intact CNS, ANS + normal pH
- normal uteroplacental perfusion
bradycardia <110
- asphyxia, acidosis
- hypoxemia, drugs that decrease uteroplacental perfusion
tachycardia >160
- hypoxemia, arrhythmias
- fever, chorioamnionitis, atropine, ephedrine, terbutaline
what type of fetal decelerations are unremarkable? which cause concern?
early decels (head compression) don’t present a risk of fetal hypoxemia, while late and variable decels require urgent assessment of fetal status.
what are the common causes of fetal deceleration patterns?
VEAL CHOP
Variable: Cord compression
Early: Head compression
Accels: OK (or give O2)
Late: Placental insufficiency
- A deceleration is described as a temporary decline in fetal heart monitoring, with a drop of > 15 beats/min for a maximum of 2 minutes related to uterine contractions.
- If a deceleration lasts 2-10 minutes, it is considered a prolonged deceleration caused by severe uteroplacental insufficiency.
define premature delivery, and list the potential complications from its occurrence.
delivery <37 weeks gestation
- leading cause of perinatal M&M
- risk is even higher w/ newborns <1500g
- increases with multiple gestations and premature rupture of membrane
complications:
- respiratory distress
- intraventricular hemorrhage
- NEC
- hypoglycemia
- hypocalcemia
- hyperbilirubinemia
discuss the use of steroids and tocolytic agents in the prevention of premature delivery
corticosteroids (betamethasone) hasten fetal lung maturity
- begin to take effect w/in 18hrs
- peak benefit 48hrs
tocolytic agents stop labor approx 24-48hrs
- provide a bridge that allows the corticosteroids time to work
- abx prophylaxis for chorio is also given at this time
neither of these are often given after 33 weeks gestation
what are the side effects of B2 agonists when used for tocolysis?
(terbutaline, ritodrine)
- hypokalemia
- cross placenta, may increase FHR
- hyperglycemia d/t glycogenolysis in the liver
- newborn of hyperglycemia mother is at risk for post-delivery hypoglycemia
how does the serum magnesium level correspond w/ its clinical effects?
Hypomag: hypokalemia and hypocalcemia
what are the side effects of magnesium?
pulmonary edema hypotension skeletal m weakness CNS depression reduced responsiveness to ephedrine/phenylephrine
what is the treatment for hypermagnesemia?
supportive measures
diuretics
IV calcium
how can oxytocin be administered? what are the potential side effects?
synthesized by suproptic and paraventricular nuclei of the hypothalamus, released from posterior pituitary
give it IV (diluted), or it can be injected directly into the uterus
side effects:
- water retention
- hyponatremia
- hypotension
- reflex tachycardia
- coronary vasoconstriction
how can methergine be administered?
ergot alkaloid
0.2mg IM (NOT IV)
IV administration = significant vasoconstriction, hypertension, and cerebral hemorrhage
what are the pros and cons of GA for c/s?
mortality is 17x higher w/ GA
- failure of successful a/w securement is the most common cause
benefits
- speed of onset
- secured airway
- greater hemodynamic stability
drawbacks
- difficult BMV, DL, intubation
- risk of aspiration
- potential MH
- absence of maternal awareness
- neonatal respiratory, CNS depression
describe aspiration prophylaxis for the patient scheduled for a c/s
triple prophylaxis against aspiration:
- sodium citrate
- H2 receptor antagonist
- gastrokinetic agent
when is the pregnant patient who presents for non-obstetric surgery at risk for aspiration?
What are some risks for GA?
if mom is >14 weeks gestation
- administer antacid w/in 30mins of induction
- H2 blocker 1hr pre-induction
- reglan +/-
if mom is >14 weeks gestation, use RSI + 6.0-7.0 ETT
what is the risk of NSAIDs when used in the pregnant patient?
Read over this:
avoid after the first trimester, as they may close the ductus arteriosus!
compare and contrast the diagnostic criteria for gestational HTN, preeclampsia, and eclampsia.
gest HTN
- HTN after 20 weeks
preeclampsia
- HTN after 20 weeks
- proteinuria
- edema
- HELLP
eclampsia
- HTN after 20 weeks
- proteinuria
- edema
- seizures
(edema is no longer a requirement for diagnosis)
discuss the balance of prostacyclin and thromboxane in the patient w/ preeclampsia
the healthy placenta produces thomboxane and prostacyclin in equal amounts
however, the pt w/ preeclampsia produces up to 7x more thromboxane than prostacyclin
–> favors vasoconstriction, platelet aggregation, and reduced placental blood flow
compare and contrast mild and severe preeclampsia.
Proteinuria is not a requirement for diagnosis
mild
- <160/<110
- <5g proteinuria/24hrs
- 24 UOP >500mL
- generalized edema w/out pulmonary edema, cyanosis, HA, visual impairments, epigastric pain
severe
- > 160/>110
- > 5g proteinuria/24hrs
- generalized edema + pulmonary edema
- cyanosis
- HA + visual impairment
- epigastric pain
- HELLP
discuss the use of magnesium for preeclampsia
the presence of seizures differentiates b/n preeclampsia and eclampsia.
sz prophylaxis w/ mg sulfate
- load: 4g over 10min
- gtt: 1-2g/hr
- tx for mag toxicity: 10mL of 10% calcium gluconate IVP
detail the anesthetic management for the patient w/ preeclampsia.
- balanced fluid management
- Risk of thrombocytopenia
- higher incidence of difficult intubation d/t a/w swelling
- exaggerated response to sympathomimetics + methergine
- if on mag they will have an increased NMB sensitivity
- mag also relaxes uterus = increased risk of postpartum hemorrhage
what is HELLP syndrome? what is the definitive treatment?
HELLP: hemolysis, elevated liver enzymes, low platelet count
- s/s: epigastric pain and upper abdominal tenderness
definitive tx = deliver the baby!
discuss the anesthetic considerations for maternal cocaine abuse.
- CV risks: tachycardia, dysrhtyhmias, MI
- acute intoxication increases MAC, chronic decreases
- OB risks: spontaneous abortion, premature labor, placental abruption, low APGAR scores
- HTN treated w/ vasodilators
- BB can cause HF since SVR is elevated but if you have to choose a BB. Labetolol is the preferred choice
- hypotension may not respond to ephedrine (d/t catechol depletion); use phenylephrine
- chronic cocaine abuse is associated w/ thrombocytopenia
what is the difference b/n placenta accreta, increta, and percreta? What is the major risk that these complications present?
accreta: placenta attaches to the surface of the myometrium
increta: invades the myometrium
percreta: extends beyond the uterus
uterine contraction is impaired and there is potential for tremendous blood loss, GA is preferred (though RA is safe)
what conditions increase the risk of abnormal placental implantation
placenta previa & previous c/s
what is placenta previa? How does it present?
when the placenta attaches to the lower uterine segment
- partially or completely covers the cervical os
- associated w/ painless vaginal bleeding
- potential for hemorrhage
- from multiple c/s and births
what are the risk factors for placental abruption? how does it present?
partial or complete separation of the placenta from the uterine wall prior to delivery. results in hemorrhage and fetal hypoxia
risks:
- PIH
- preeclampsia
- chronic HTN
- cocaine use
- smoking
- excessive EtOH
presents w/ painful vaginal bleeding; pain may be so severe as to cause breakthrough even w/ epidural placement
Associated with DIC!
what is the most common cause of postpartum hemorrhage? What are the risk factors?
uterine atony is the most common cause. Increased by:
- multiparity
- multiple gestations
- polyhydramnios
- prolonged oxytocin infusion prior to surgery
a patient suffers from retained placental fragments. What IV medication can you give to help w/ the extraction?
IV NTG for uterine relaxation
what are the treatment options for uterine atony?
uterine massage
oxytocin
ergot alkaloids (methergine)
intrauterine balloon
what does the APGAR score mean?
used to assess the newborn and guide resuscitative efforts. Five parameters are evaluated at 1 and 5 minutes after delivery.
1 min score correlates w/ fetal acid-base status
5min score may be predictive of neurologic outcome
normal 8-10
moderate distress 4-7
impending demise 0-3
know how to calculate the apgar score
what is the best indicator of ventilation during neonatal resuscitation?
resolution of bradycardia
SpO2 should rise in 10 minutes after delivery
how do you dose epi and fluids during neonatal resuscitation?
epi 1:10,000
- 10-30mcg/kg IV
- 0.05-0.1mg/kg intratracheal
PRBCs, NS, LR
- 10mL/kg over 5-10mins
what are the normal VS for a newborn? How do they trend as the child ages?
newborn
- 70/40
- HR 140
- rr 40-60
1yr
- 95/60
- HR 120
- rr 40
3yr
- 100/65
- HR 100
- rr 30
12yr
- 110/70
- HR 80
- rr 20
why is the neonates minute ventilation higher than the adult?
O2 consumption and CO2 production are twice those of an adult (ventilation increases accordingly)
it is metabolically more efficient to increase the rr than it is to increase the Tv (explains why rr increases, but Tv/weight is the same)
what is the primary determinant of BP in the neonate?
HR
BP = HRSVSVR
neonatal myocardium lacks the contractile elements to significantly adjust contractility or SV; the ventricle is noncompliant. Furthermore, the frank-starling relationship is underdeveloped (but not entirely absent) in the newborn
describe the autonomic influence on the newborns heart.
immature at birth, with the SNS being less mature than the PNS.
stressful situations (DL, sxning, etc.) may cause bradycardia, consider atropine pre-induction
baroreceptor reflex is poorly developed so the reflex fails to increase HR in the setting of hypovolemia. If they are hypovolemic their HR may not increase. You would see hypotension without tachycardia
contrast the breathing pattern in adults and infants.
adult: mouth or nose
infant: preferential nose breather up to 5 months of age
- most convert to oral breathing if the nasal passages are obstructed
- bilat choanal atresia may require emergency airway management if the infant is unable to mouth breathe.
contrast the relative size of the tongue in adults and infants.
adult: small relative to oral volume
infant: large relative to oral volume
- tongue is closer to the soft palate, which makes it more likely to obstruct the upper airway
- more difficult to displace during DL
contrast the relative neck length in adults and infants.
adult = longer
infant = shorter
- more acute angle required to visualize the glottis
contrast the epiglottis shape in adults and infants
adults: leaf (C-shaped), floppier, shorter
infant: U (omega shape), stiffer, longer
- makes it more difficult to displace during DL
contrast the vocal cord position in adults and infants
adult = peripendicular to trachea
infant = anterior slant
- visualization and passage of ETT may be more difficult
- ETT may get stuck in the anterior commissure
contrast the laryngeal position in adults and infants.
adults C5-6
infants C3-4
- larynx more superior/cephalad/rostral but NOT anterior. The only time the infants airway is more “anterior” is during neck flexion
- same position as the adult at age 5-6yrs
contrast the narrowest point of the airway in adults and infants
adult = glottis (VC)
infant = cricoid or glottis
- resistance to ETT insertion beyond the VC is likely at the cricoid ring
- cricoid tissue is prone to inflammation and edema formation –> stridor or obstruction
- Poiseuille’s law: small changes in radius can significantly increase resistance to airflow
Why is the “narrowest region of the infant airway” controversial?
classic teaching = infant’s airway is narrowest at cricoid ring and funnel shaped ariway
current evidence to support that the classic teaching may not be entirely accurate. New insight suggests that pediatric airway is likely more cylindrical than previously believed, and in the paralyzed child the VC is the narrowest point
contrast the orientation of the R mainstem bronchus in adults and infants.
adult = more vertical
infant = less vertical
- up to age 3, both bronchi take off at 55 degrees
- in the adult, the R bronchus takes off at 25 and the L at 45
contrast the optimal intubation position for adults and infants.
adult = sniffing position
infant = head on bed w/ shoulder roll
- infant has large occiput
- sniffing position will place the glottic opening in more anterior position
contrast the oxygen consumption, alveolar ventilation, respiratory rate, and tidal volume in neonates and adults?
bc neonatal alveolar surface area is only 1/3 of the adult and oxygen consumption is twice that of an adult, the neonate must increase alveolar ventilation in order to sustain normal arterial gas tensions.
It is metabolically more efficient to increase respiratory rate than it is to increase Tv.
oxygen consumption:
-6mL/kg/min neonate
-3 mL/kg/min adult
Tv same! 6mL/kg for both
why do neonates desaturate faster than adults?
they have:
- increased O2 consumption to support metabolic demand
- increased alveolar ventilation to increase O2 supply
- slightly decreased FRC reflecting a decreased O2 reserve
the net result = increased ratio of alveolar ventilation relative to FRC size. A faster gas turnover means that the O2 supply in the FRC is quickly exhausted during apnea.
why is inhalation induction faster w/ a neonate than w/ an adult?
increased ratio of alveolar ventilation to FRC
faster FRC turnover (fewer alveoli are needed to achieve steady state) allows for a speedier development of anesthetic partial pressure inside the alveoli and consequently a more rapid change in the anesthetic partial pressure inside the brain and SC
what is the difference b/n fast and slow twitch muscle fibers? how does this relate to neonatal pulmonary mechanics?
the diaphragm and intercostal muscles are composed to two types of muscle fibers:
Type 1 = slow twitch (endurance, fatigue-resistance)
Type 2 = fast twitch (fast, tire easy)
Neonates have more type 2 55% > than type 1 = risk of resp. Distress
compare and contrast neonates to adults in terms of: FRC, VC, TLC, RV, CC, and Vt.
Neonate respiratory changes
Increased residual volume and closing capacity
how does the newborn’s ABG change from delivery to the first 24hrs of life?
mother at term:
7.40 pH, PaO2 90, PaCO2 30
umbilical vein (placenta to fetus) 7.35/30/40
umbilical artery (fetus to placenta) 7.30/20/50
newborn at time after delivery:
10min: 7.20/50/50
1hr: 7.35/60/30
24hr: 7.35/70/30
how does hypoxemia affect ventilation in the newborn?
respiratory control doesn’t mature until 42-44 weeks
- before maturation: hypoxemia depresses ventilation
- after maturation: hypoxemia stimulates ventilation.
what is the P50 of fetal hemoglobin? Why is this important?
P50 = 19mmHg
Hgb shifts the curve to the L (L=love)
it benefits the fetus by creating an O2 partial pressure gradient across the uteeroplacental membrane that facilitates the passage of O2 from the mother to the fetus
Why does HgbF have a higher affinity for O2?
- adult hgb (hgbA) consists of 2 alpha and 2 beta chains, while hgbF contains 2 alpha and 2 gamma chains
- 2,3 DPG only has a binding site on the beta chain
- therefore, HgbF doesn’t bind 2,3 DPG, shifting the curve to the L and creating a higher affinity for O2 in the HgbF
- Purpose of fetal hgb = facilitates O2 passage from mother to the fetus. It’s completely replaced by Hgb A at 6 months!!!!!
discuss the physiologic anemia of the infant.
in the first 2 months of life, erythrocytes containing HgbF are replaced by those that produce HgbA.
After about 6 months, HgbF has been completely replaced by HgbA (P50 is now the same as the adult)
birth: Hgb = 17g/dL
2months: RBC production begins to shift to HgbA
2-3months: Hgb = 10g/dL
4months: erythropoiesis increases and Hgb rises
4-6months: HgbA has completely replaced HgbF and P50 is adult level
what is the dose for PRBC transfusion in the neonate? How much will this increase Hgb?
10-15mL/kg
10mL/kg will raise Hgb by 1-2g/dL
what are the indications for FFP transfusion in the neonate?
- emergency reversal of warfarin
- correction of coagulopathic bleeding w/ increase PT >1.5 or increased PTT
- correction of coagulopathic bleeding if >1 blood volume has been replaced and coagulation studies aren’t easily obtained.
FFP is NOT indicated for expansion of intravascular volume
what is the dose for FFP transfusion in the neonate?
10-20mL/kg
when is platelet transfusion indicated in the neonate? What is the dose?
invasive procedures to maintain platelet count > 50K!!!!
dose if obtained from apheresis: 5mL/kg
dose if pooled from platelet concentrate: 1 pack/10kg NEED TO KNOW THIS!!!
describe the physiologic changes that occur as a result of massive transfusion.
massive transfusion is associated with:
- acidosis (inadequate oxygenation and increased lactate)
- alkalosis (citrate metabolism to bicarb in the liver)
- hypothermia
- hyperglycemia (dextrose additive)
- hypocalcemia (citrate binding)
- hyperkalemia (administration of older blood d/t dysfunctional cell membrane. Risk is decreased is <7 day old blood)
what is the normal H&H at birth, 3 months, and 6-12months?
newborn: 14-20/45-65%
3months: 10-14/31-41%
6-12months: 11-15/33-42%
adult
female 12-16/37-47
male 14-18/42-50
Honestly idk this just transfuse if hgb < 10 or 13 in Neonate?
what is the estimated blood volume in the premature neonate, term neonate, infant, and child >1yr?
EBV:
Premie/neonate: 90mL/kg
Infant 75mL/kg
Child 75mL/kg
a 3kg term neonate requires emergency ex lap for necrotizing enterocolitis. Her pre-op Hct is 50%. What is the maximum ABL to maintain Hct of 40%?
ABL = EBV*(Hct-Hct target)/Hct
EBV = 3kg*(80 to 100mL/kg)
= 240-300mL
ABL = 300(50-40)/50 = 60mL
when do GFR and renal tubular function achieve full maturation?
Normal GFR is reached at 8-24months of age
- before maturation, neonates do a poor job of conserving water, so they are intolerant of fluid restriction. On the flip side, they are unable to excrete large volumes of water, so they don’t do well w/ fluid overload either
Normal tubular function is reached at 2yrs of age, in the first few days of life, they are an obligate sodium loser.
- After that, they’re better able to retain Na+ than excrete it.
- They also have a tendency to lose glucose in the urine.
compare and contrast the distribution of body water in premature neonate, child, and adult.
premature:
TBW 85%: ECF 60%, ICF 25%
neonate
TBW 75%: ECF 40%, ICF 35%
child & adult
TBW 50%: ECF 20%, ICF 40%
describe the 4:2:1 rule of fluid management.
0-10kg: 4mL/kg/hr
10-20kg: add 2mL/kg/hr to previous total
>20kg: add 1mL/kg/hr to previous total
what ratio should be used to replace blood loss w/ crystalloid, colloid, and blood?
What number is a sign of Hypoglycemia?
crystalloid 3:1 ratio
colloid 1:1 ratio
blood 1:1 ratio
which pediatric patient populations should receive an IVF that contains glucose?
infants and children that are at risk of hypoglycemia:
- prematurity
- newborns of diabetic mothers
- those w/ diabetes who received insulin on day of surgery
- those who received glucose based parental nutrition
- blood sugar < 40
At how many months in an infant are there lower concentrations of albumin ain’t alpha 1 acid glycoprotein?
What does highly protein drugs do?
- <6months, there are lower concentrations of albumin and alpha1 acid glycoprotein
- highly protein bound drugs = higher free drug levels, increased toxicity risk
discuss MAC in children. Does this rule apply to all volatile anesthetics?
- Premie: MAC is lower than neonate
- Neonate 0- 30 days: MAC is lower than infant
( Basically premie and neonate’s MAC is lower than infant)
- Infant 1-6months: MAC higher than adult MAC
- 2-3months: MAC peaks
But with Sevo it’s different 0 days- 6months it’s higher 3.2%
how do you dose IV succinylcholine in the neonate?
2mg/kg
- largely d/t a relatively higher ECF (Vd is higher)
how do you dose NDMR in the neonate? Why?
same as adult on a mg/kg basis.
- although ECF is larger, the NMJ is highly sensitive to the effects of NDMR. These things cancel each other out.
describe the 5 types of tracheoesophageal atresia. Which is the most common?
- most common congenital defect of the esophagus
- most of these children also have a tracheoesophageal fistula
A: “missing” piece of esophagus (two blind pouches), no tracheal involvement
B: upper esophagus communicates w/ trachea, lower esophagus not connected
C: upper esophagus blind pouch, lower esophagus communicates w/ trachea
D: both upper and lower esophagus communicate w/ trachea, not each other
E: communicating esophagus w/ tracheoesophageal fistula
Type C accounts for approx 90% of all TEFs
a patient has a hernia at the foramen of Bochdalek. Which congenital condition does this patient have?
= congenital diaphragmatic hernia allows the abdominal contents to enter the thoracic cavity
- Keep PIP less than 25-30
- foramen of Bochdalek is the most common site (usually on L)
- other sites: foramen of Morgagni and around the esophagus
- Increases PVR, pulmonary hypertension
describe the anesthetic concerns for a patient w/ omphalocele or gastroschisis.
- gastroschisis: abdominal contents in bag after delivery to minimize water/heat loss
- monitor PIP, keep <25-30
- closure may increase intraabdominal pressure and decrease systemic perfusion
- place SpO2 on LE
- avoid N2O
- expect major fluid/e-lyte shifts
describe the anesthetic management of the pt w/ pyloric stenosis.
- not surgical emergency (optimize fluids/pH/e-lytes first) THIS IS ONLY A MEDICAL EMERGENCY! NOT SURGICAL
- anticipate full stomach (OGT pre-induction) + RSI
- liberal hydration +/- glucose supplementation
- post-op apnea is common possibly d/t residual alkalotic CSF
Late complication is metabolic acidosis
give the name, location, and function of the 3 fetal shunts.
1) ductus venosus
- umbilical vein –> IVC.
- Bypasses liver
2) foramen ovale
- Right atrium –> Left atrium.
- Bypasses lungs
3) ductus arteriosus
- Pulmnary artery to-> aorta.
- Bypasses lungs
when does each fetal shunt close? what is the adult remnant of each?
ductus venosus closes w/ clamping of umbilical cord
- remnant: ligementum venosus
foramen ovale closes in 3 days
- remnant: fossa ovalis
ductus arteriosus closes several weeks after birth
- remnant: ligamentum arteriosum
what is an intracardiac shunt?
describes an abnormal blood flow pattern that occurs from an abnormal communication b/n the pulmonary and systemic circulations
what are the hemodynamic goals for the patient w/ a R-L shunt?
patho: decreased pulmonary blood flow results in:
- hypoxemia
- LV volume overload
- LV dysfunction
hemodynamic goals:
- maintain SVR
- decrease PVR: hyperoxia, hyperventilation, avoid lung hyperinflation
what are the hemodynamic goals for a patient w/ a L-R shunt?
patho: decreased systemic blood flow (low CO, hypotension) and increased pulmonary blood flow (pHTN, RVH)
goals:
- avoid increase SVR
- avoid decrease PVR (decrease FiO2 though, hypoventilation)
what is coarctation of the aorta? which syndrome is highly associated w/ this anomaly?
- narrowing of the thoracic aorta in the vicinity of the ductus arteriosus
- typically just after or before the ductus arteriosus
- Turner syndrome is highly associated w/ coarctation of the aorta
- Prostaglandin E can keep it OPEN till surgery
Place blood pressure on the RIGHT ARM here!
Preductal- RUE
Post ductal- Lower extremity
what is truncus arteriosus?
characterized by a single artery that gives rise to the pulmonary, systemic, and coronary circulations.
w/ only one artery, no specific pathway for blood to enter the pulmonary circulation before being pumped systemically
- usually a VSD is present as well
- decreasing PVR or increasing pulmonary blood flow steals from systemic and coronary circulations
discuss the typical ages affected and speed of onset for epiglottitis and croup.
epiglottitis
- bacterial (H.influenza, group A strep, pneumococci, staph)
- 2-6yrs
- rapid onset (<24hrs)
croup (laryngotracheobronchitis)
- viral (influenza viruses), bacterial is rare (mycoplasma)
- <2yrs
- gradual onset (24-72hrs)
Review normal vital signs for peds
SBP < 60 is hypotension for newborn
How many weeks post conceptual age should infant be admitted after receiving anesthesia?
Read through all of this
Neonate respiratory changes
FRC: decreased
VC: decreased
TLC: decreased
RV: increased
CC: increased
Lung compliance: decreased
Chest wall: increased (flimsy)
Respiratory changes in pregnancy:
FRC:
TV:
IRV, ERV:
RV:
VC:
CC:
FRC: decreased
TV: increased
IRV, ERV: decreased
RV: decreased
VC: no change
CC: no change
Sinusoidal pattern and absent baseline variability
Identify each FHT
1st- late decals
2nd- variable
3rd- early decels
Prostaglandin F2
250 mcg I.M. Avoid in asthmatics
Neonate SBP < 60 = hypotension
Neonates have increased alveolar ventilation to FRC ratio
Neonate’s O2 consumption is 2x the adult
Neonate O2 consumption is 6ml/kg while adults 3ml/kg
The newborn’s kidney tends to:
excrete sodium.
reabsorb sodium.
reabsorb water.
reabsorb glucose.
excrete sodium
Newborn’s kidney has an immature concentrating mechanism, so it tends to excrete sodium - it is a sodium loser
For the same reason, it partially lacks the ability to retain water and glucose.
They also lose a lot of body of water through evaporation. Surface area to body weight is 4x more than adult and immature skin is more permeable to water.
Why are neonates more sensitive to hypnotics?
They have an immature BBB
What does NOT reduce the risk of respiratory issues if a pediatric patient has a recent upper respiratory infection?
What are some things that CAN help?
Preoperative Albuterol does NOT help
Things that can help: prophylactic decadron 0.25mg/kg IV, use Sevo it’s least pungent
