EXAM#4 Review Flashcards
CYP 450 Isoenzymes ________= Ultra
CYP2D6 Rapid metabolization
With the CYP2D6 what happens to morphine
Codeine is broken down into greater quantities of morphine than normal
Genetic variability in _________may increase formation of active
UGT2B7; morphine-6- glucuronide
Changes at β2-adrenergic receptor →
alter tocolysis, require less ephedrine
What is responsible for the mophine-6-glucuronide formation?
UGT2B7
Activities of enzymes can be increased:• CYP450 isoenzymes
CYP3A4
CYP2D6
CYP2C9
Activities of enzymes can be increased:•UGT
(UGT) isoenzymes UGT1A4 and UGT2B7
Which enzyme can increase metabolism of drugs phenytoin?
CYP2C9
Which enzyme can increase metabolism of drug: midazolam
CYP3A4
Which enzyme can increase metabolism of drug: morphine ?
UGT2B7
Anesthetics and lactations
There are generally no concerns regarding anesthetic drugs and perioperative medicines in the breast milk of women who require an anesthetic
NSAIDS and lactation
No harmful effects of acetaminophen or NSAIDs have been noted except for aspirin
FDA has singled out ketorolac with a “black box” warning that it is
“contraindicated in nursing mothers because of the potential adverse effects of prostaglandin-inhibiting drugs on neonates”
• Normal maternal doses ,NAME 4 DRUGS that DO NOT
have obvious adverse effects on most nursing infants
codeine, morphine, tramadol, and meperidine
Neonates are particularly vulnerable because their drug
metabolism and elimination are poorly developed
Infants of breast-feeding mothers taking codeine
may have CNS depression
CYP2D6 and concentration of breastmilk?
ultra-rapid metabolization to morphine → high concentration in breast milk
Ultra-rapid metabolism has been reported as a problem for breast-feeding
only with codeine, although the FDA suggested that “it has the potential to affect other opioids”
Maternal oxycodone for postpartum analgesia has been associated with
neonatal depression
If a sedative must be used in a lactating woman, what kind of drug should be used?
a relatively short-acting agent with inactive metabolites,
Short acting benzo that can be used on pregnant women are, is recommended (MOLA)
midazolam
oxazepam
lorazepam
alprazolam
Atenolol has 10% protein binding and is 85% renally excreted =
bad choice!
Associated c/neonatal cyanosis and bradycardia
Beta-blockers and transfer
relatively higher transfer to breast milk
Which beta blocker which one more likely to accumulate in the neonate?
Those renally excreted more likely to accumulate in neonate
Amiodarone and breast milk
Very long half-life and still EXCRETED in breast milk weeks after d/c meds
ACE inhibitors and antihypertensives are considered
safe
Salbutamol, terbutaline, and salmeterol inhalers are considered
compatible with breast-feeding
Histamine type 2 (H2)-receptor antagonists theoretically
could suppress gastric acidity or cause CNS stimulation in the infant
Heparin and milk?
does not cross significantly into breast milk and is not active when administered orally
Pregnancy and vaccination in general
Generally appropriate to administer vaccinations during pregnancy
No evidence exists of risk to fetus from vaccinating pregnant women with (safe ones)
inactivated virus or bacterial vaccines or toxoids
Contraindicated vaccines for pregnancy are (VMTB)
Live vaccines attenuated virus Varicella Measles-mumps-rubella[MMR]) Tuberculosis Bacillus Calmette Guérin [BCG]) are contraindicated
For pregnant women Influenza vaccination is recommended with the
inactivated virus preparation
Best time to do surgery during pregnancy
2nd Trimester
All-or-nothing phenomenon
Exposure in 1st 2 weeks after conception(i.e., having either no effect or resulting in spontaneous fetal loss
What is the classic period of susceptibility during period of organogenesis?
2½ to 8 weeks after conception
Each organ system has __________of
sensitivity and there may significant differences in effect
different critical periods
Thalidomide @ 35-37 days’ gestation
ear malformations
Thalidomide @ 41-44 days’ gestation
amelia or phocomelia
After 8 weeks what is development or growth?
Growth.
Classic Teratogenic
31 days - 71 days
31 days two organs
Heart and CNS
71 days two organs
Palate ear
CNS development goes up to
16 weeks
Heart development goes up to
6 1/2 weeks for major
9 weeks total
________exposure during 2nd trimester results in uterine anomalies, fetal alcohol syndrome may occur with chronic exposure to alcohol during pregnancy
diethylstilbestrol
Upper limbs development
6-8 weeks
Not susceptible to teratogens
Week 1 and 2
Eyes development goes up to
8 1/2 weeks
Ear development goes up to
9 1/2 weeks
Fetal anticonvulsant syndrome
Orofacial
CV
Digital malformations
Fetal hydantoin syndrome
Constellation of minor anomalies, such as craniofacial abnormalities and limb anomalies
PH4EN Mnemonic
P Cleft plage, cleft lip
H Small head, hypoplastic face, hirsutism, heart defects
E Embryopathy, Antiepileptic use
N Hypoplastic nails and digits, neurologic deficits
Fetal carbamazepine syndrome closely resembles the malformations seen in
cases of fetal hydantoin syndrome
Fetal phenobarbital syndrome
Minor dysmorphic features similar to those seen with fetal hydantoin syndrome
Fetal valproate syndrome
DES-HFL- MUT- DTH
Dysmorphic features Epicanthal folds Shallow orbits \_\_\_\_\_\_\_\_\_\_\_\_ Hypertelorism Low-set ears Flat nasal bridge \_\_\_\_\_\_\_\_\_\_\_\_ Upturned nasal tip Microcephaly Thin vermillion borders \_\_\_\_\_\_\_\_\_\_\_\_\_ Downturned mouth Thin overlapping fingers and toes Hyperconvex fingernails
Fetal warfarin syndrome consists of (NDS-NMG)
Nasal hypoplasia Depressed nasal Stippled epiphyses Nail hypoplasia Mental retardation Growth restriction
Typically absent in less than 20 weeks gestation
Hemoconcentraton, Thrombocytopenia, Proteinuria
Chronic hypertension absent symptoms
Severity? when ?
Mild or severe
<20 weeks of gestation
Proteinuria
Uric acid RARE
Hemoconcentration
Thrombocytopenia
Gestational HTN absent symptoms
Severity? when ?
Mild
Typically in third trimester
Proteinuria
Uric acid RARE
Hemoconcentration
Thrombocytopenia
Pre-Eclampsia
Severity and when?
> 20 weeks
Pre-Eclampsia What is present in ALMOST ALL CASES
Serum uric acid > 5.5
Pre-Eclampsia what is present in SEVERE DISEASE
Hemoconcentration
Thrombocytopenia
Pre-eclampsia what is typically present
Proteinuria.
Diagnostic Criteria for Preeclampsia : Preeclampsia WITHOUT severe features (BPP 1E)
BP ≥ 140/90mmHg after 20 weeks gestation Proteinuria ≥ 300mg/24h Protein-Creatinine ratio ≥0.3 1+ on urine dipstick specimen Edema
Diagnostic Criteria for Preeclampsia : SEVERE Pre-eclampsia (BTSPNI)
BP ≥ 160/110 mmHg Thrombocytopenia (plt count < 100,000) Serum Cr > 1.1mg/dl OR 2 times the baseline Cr. Pulmonary Edema New onset CEREBRAL+ Visual disturbances Impaired liver function (HELLP)
Can you have proteinuria w/o Eclampsia?
Yes
HTN
the answer is NITRO
Nitroglycerin Pertinent information
Venous > arterial relaxation ↓preload > afterload, very rapid onset (HoTN), UteroPlacental Blood Flow preserved but crosses UP/FP
Most common used antihypertensive
Hydralazine
Hydralazine effects (RDN)
Relaxes arterioles
Decrease SVR, BP and may Increase HR
NO effect on UP/FP BF
2nd most common use antihypertensive (LADA)
Labetalol
Alpha:beta 1:7
Decrease SVR with Increase HR
AVoid in asthmatic /liver dysfunction , crosses the placenta
Treatment goals BP
DBP 90-105mmHg
MAP 105-125 mmHg
ESMOLOL characteristics
IV bolus for sympathetic block during intubation.
Nifedipine characteristics (AC)
Arterial dilator with little cardiodepresion
Can exaggerate HoTN if receiving MgSO4
Nitroprusside characteristics (PDC)
Powerful Vadodilator arterial>venous Decrease Afterload Crosses Placenta (worry about cyanide toxicity)
HELLP stands for
Hemolysis, Elevated Liver Enzymes, Low Platelets
What is HELLP a complication of
Severe form of preeclampsia
HELLLP occurs due to
Occurs d/t unknown insult
→intravascular plt activation & microvascular endothelial damage
What is the hallmark of HELLP?
Hemolysis
All abnormal labs in HELLP
ALT
- Abnormal peripheral blood smear + ↑bilirubin level (> 1.2mg/dL)
- ↑liver enzymes AST (SGOT) > 70, LDH > 600
- Thrombocytopenia < 100,000
• Nonspecific initial complaints of HELLP
(malaise, AB pain, N/V)
Maternal complications of HELLP
Maternal complications
• CVA, CV arrest, DIC, placental abruption,
• ALL patients show some evidence of compensated DIC
• Postpartum onset (hrs to 6 days after delivery) → ↑risk of ARF and pulmonar
edema
Maternal complications of HELLP
Maternal complications
• CVA, CV arrest, DIC, ARF placental abruption,
ALL patients in HELLP show some evidence of
compensated DIC
• Postpartum onset of HELLLP can occur __________And increase risk for → ↑risk of ARF and pulmonary edema
hrs to 6 days after delivery ;ARF and pulmonary edema
Postpartum onset of HELLLP can occur __________And increase risk for → ↑risk of ARF and pulmonary edema
hrs to 6 days after delivery ;ARF and pulmonary edema
HELLP check for retained products with
US
Tx meds for HELLP
Decadron
Common occurrence during C-section and vaginal delivery
VAE
Subclinical VAE occurs in both GA and
Spinal
VAE occurs less with regional
Because they are spontaneously breathing
VAE may account for common symptoms during C-section: (DASHA)
Dyspnea Angina ↓SaO2 HoTN Arrhythmias
M&M of VAE is r/t volume/rate of air infusion into :
central circulation and site of embolization
VAE: Pathophysiology
Pressure gradient as small as -5 cmH2O between surgical field and heart allows venous air entrainment
What is associated with INCREASED VENOUS AIR? (SU)
Steep Trendelenburg position
Uterine exteriorization during C-section
VAE Large air volumes is fatal
> 3 mL/kg
VAE Small air volumes: VHAH
V/Q mismatch
Hypoxemia
Arrhythmia
HoTN
VAE Presentation
50% angina
25% Decrease SaO2
>20% drop in BP (2%)
Resuscitation of patient with massive venous air embolism
PDS -CEIP
Prevent air entrapment (change position, flood surgical
field)
Discontinue Nitrous give 100% oxygen
Support ventilation and circulation
Central venous catheter to aspirate air
Expedite delivery
Imaging to rule out intercerebral air.
Paradoxical cerebral artery gas may benefit from
Hyperbaric oxygen therapyRisk factors of Eclampsia (FMMN-PPRST)
First pregnancy Multiple Gestation Molar Pregnancy Triploidy Preexisting HTN Renal diseas Non-immune hydrops fetalis SLE Previous hx of preeclampsia/eclampsia
Risk Factors of Preeclampsia: Demographic factors (ABH)
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
Risk Factors of Preeclampsia: Demographic factors (ABH)
Advanced maternal age > 35 years
Black race
Hispanic ethnicity
Risk Factors of Preeclampsia: Genetic Factors (HFHP)
History of Preeclampsia in previous pregnancy
Family Hx of Preeclampsia
History of Placental Abruption, Fetal growth restriction, or fetal death (PFD)
Partner who fathered a preeclamptic pregnancy pregnancy in another woman (through fetal genes)
Risk Factors of Preeclampsia: Medical Conditions (CODCAS)
Chronic HTN Obesity Diabetes Mellitus Chronic Renal Disease Antiphospholipid antibody syndrome Systemic Lupus Erythematus
Risk Factors of Preeclampsia:Obstetric conditions
Multiple Gestation
Hydatidiform mole
Risk Factors of Preeclampsia: Behavioral factor
Cigarette smoking (risk reduction)
Risk Factors of Preeclampsia: Partner related risk factors
Nulliparity
LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM
All risk factors for Preeclampsia together
Advanced maternal age > 35 years Black race Hispanic ethnicity History of Preeclampsia in previous pregnancy Family Hx of Preeclampsia History of Placental Abruption, Fetal growth restriction, or fetal death (PFD) Partner who fathered a preeclamptic pregnancy pregnancy in another woman (through fetal genes) Chronic HTN Obesity Diabetes Mellitus Chronic Renal Disease Antiphospholipid antibody syndrome Systemic Lupus Erythematus Multiple Gestation Hydatidiform mole Cigarette smoking (risk reduction) Nulliparity LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM
Postparthum hemorrhage : Etiology (4) Ts
Tone
Tissue
Trauma
Thrombin
Tissue cause of PPH
Retained products of conception
Trauma cause of PPH
Genitral tract trauma
Thrombin cause of PPH
Coagulation abnormalities.
Take home message for PPH
Do not go over 1 MAC of anesthesia with FURTHER DECREASE UTERINE TONE
Causes of Pregnancy Related hemorrhage
ALUCPUR
Abruptio Placenta Laceration /uterine rupture Uterine atony Coagulopathies Placenta previa--> accreta, increta, percreta Uterine bleeding Retained placenta
4 main causes of Antepartum hemorrhage
PPUV
Placenta Previa
Placenta Abruptio
Uterine Rupture
Vasa Previa
4 types of Placenta Previa
TPML
Total
Partial
Marginal
Low-lying placenta
What is a TOTAL placenta previa?
Internal cervical OS covered completed by placenta
What is a PARTIAL placenta previa>?
Internal cervical OS partially covered by placenta
What is a MARGINAL placenta previa?
Edge of placenta at margin of internal os
What is a low lying placenta?
Placenta is implanted in lower uterine segment –> Placental edge does not actually reach internal os but in close proximity to it
What are the 3 types of placenta accreta
Accreta vera
Placenta increta
Placenta percreta
Placenta Accreta vera is
Adherence of basal plate of placenta directly to uterine myometrium without penetrating the decidua layer
Placenta Accreta increta is
Chorionic villi invade myometrium
Placenta accreta percreta is
Invasion through MYOMETRIUM into SEROSA and even adjacent ORGANS (bladder)
VASA Previa is
rare condition where fetal vessels from placenta cross entrance of birth canal
3 typical causes of Vasa previa
Bi-lobed placenta
Velamentous insertion of umbilicord
Succenturiate (accessory lobe)
Placenta Previa symptoms Hallmark
Painless hemorrhage
Placenta Previa risk Factors AMMPPS
Advanced Maternal Age >35 Multiparity Multifetal gestations Prior C-section Smoking Prior Placenta previa
Placenta abruption factors
External hemorrhage
Concealed (internal hemorrhage)
Total
Partial
Hallmark of Placenta Abruption
Bleeding with PAIN varying from mild cramping to severe
Placenta abruption signs and symptoms uterus
Firm , tender uterus with INCREASE FUNDUS HEIGH
Placenta Abruption risk factors
PPP CCC HIUEM
Prior abruption
Pre-eclampsia
PROM
Chronic HTN
CIgarette smoking
Cocaine use
Hydramnios Increage age and parity Uterine Leiomyoma Multiple gestation External Trauma
Risk factors of VASA PREVIA (LAMPP)
Abnormal placenta morphology Low lying Multiple gestation Pregnancies resulting from IVF Palpate vessel on vaginal exam
Uterine rupture most common with
VBAC
Uterine rupture classic presentation
VAPCLEP
Vaginal bleeding
Absence/deterioration of FHR
Pain
Cessation of contraction
Loss of station of the fetal head from birth canal
Easily palpate fetal parts
Profound Maternal TACHYCARDIA and HYPOTENSION
Risk factors for Uterine Rupture
PPP TEMFS
Prior rupture Previous uterine sx Previous C section Trauma Excessive uterine stimulation Multiparity Forceps delivery Shoulder distocia
Contraindications for uterotonic agents: Oxytocin
Hypersensitivity to drug
Contraindications for uterotonic agents: Methergine
HTN, hypers.
Contraindications for uterotonic agents: Carboprost
Heart, PULMONARY, RENAL, hepatic disease
Contraindications for uterotonic agents: Vasopressin
CAD
Minimize risk of aspiration
Small volumes (150 mL; 5.7 fluid ounces) of fluid other than milk and pulp containing juices consumed up to 2 hours before elective
Minimizing Risk: H-2 Receptor
Antagonists
• Cimetidine, Ranitidine, Nizatidine, Famotidine
H2 Receptor antagonists Reduces gastric acidity significantly approximately 30 min after IV
administration, maximal effect @ 60-90 min how?
• Block histamine receptors on oxyntic cell → ↓diminish gastric acid production → leading to a slight ↓ in gastric volume in fasting patient
•Guidelines for perinatal care (American College of
Obstetrics & Gynecology, American Academy of
Pediatrics) for aspiration risk
“Patients in active labor should avoid
oral ingestion of anything excepts sips of clear
liquids, occasional ice chips, or moistening of
mouth/lips” Because Some clear liquids are highly acidic (e.g., cranberry juice)n
Normal laboring patients should not receive
aspiration prophylaxis unless
They are high risk for C-section
PPI minimize risk for aspiration
Inhibit the H+ pump on gastric surface of oxyntic cell
Non particulate antacid:
30 mL Na citrate [Bicitra] can neutralize 255 mL of hydrochloric acid with a PH of 1.0
Particulate antacids
(e.g.. Maalox, Mylanta)
When aspirated causes serious pneumonitis?
Particulate antacids (e.g.. Maalox, Mylanta)
When should non particulate antacid be administered?
Should be administered within 20 minutes of induction
of GETA
What is short definition of action of H2 blockers
Keeps from making more acid
Prior administration of what may antagonize metoclopramide action?
Prior administration of opioid and atropine
How much acid is produced per day by the stomach
•
Up to 1500 ml highly acidic fluid
Pyloric glands
Chief cells secrete pepsinogen →pepsin
Oxyntic glands
Oxyntic cells secrete HCl (pH 0.8)
This is where PPIs work
Oxyntic cells oxyntic glands
Vagus stimulates
G cells to secrete gastrin →bind to oxyntic cells and
stimulates HCl secretion
Ach binds
to muscarinic receptors and ↑Ca2+
H-2 receptors ↑cAMP →
dramatic ↑ acid production (also increase calcium)
Histamine potentiates both
gastrin and acetylcholine
Acid is secreted at a low basal rate of approximately ________ even whenty
10% of maximal output; stomach is empty
• Diurnal variation:
lowest in morning, highest in evening
Increase dramatically with ingestion
• ↑ dramatically with ingestion
No significant differences in __________________
were seen between pregnant and nonpregnant women
basal gastric acid secretion
Cephalic phase:s
chewing, smelling, or tasting without significant
ingestion ↑ vagal stimulation
What happens to gastric acid during the cephalic phase?
Gastric acid output ↑ to 55% of peak levels
Gastric phase:
entry into stomach of ingested contents, acid output
peak
When does gastric acid output peak ?
Gastric phase
Intestinal phase begins
begins with movement of food into small intestine
Gastrin role
Increase gastric acid secretion
Pathophysiology of Aspiration Pneumonitis: Acidic Liquid
Acidic liquid aspiration injures alveolar epithelium
→ alveolar exudate (edema, albumin, fibrin, cellular
debris, and RBCs)
In pathophysiology of Aspiration Pneumonitis what does Alveolar exudate/pulmonary edema leads to:
- ↓ in lung compliance
- Loss of lung volume
- Intrapulmonary shunting of blood
- Bronchial obstruction/ bronchospasm
Aspirates with a ph lower than 2.5 cause
a granulocytic reaction
General rule for aspiration pneumonitis
ph<2.5, gastric volume >25 Aspiration pneumonitis
Pathophysiology: Particle Aspiration
• Direct airway obstruction from larger particles
atelectasis; Obstructing large airways
In pathophysiology of Smaller particles: similar response as
with acidic liquid
In pathophysiology of Smaller particles causes
exudative neutrophilic response at levels of bronchioles and alveolar ducts
• Aspiration pneumonitits = Is is an injury from _______
What does basic aspirate do?
• Cellular debris and bronchial denuding = bronchial obstruction
• Exudative pulmonary edema, bronchial obstruction, ↓ lung
compliance, and shunting → hypoxemia, ↑ pulmonary vascular
resistance, and increased work of breathing.
chemical injury from sterile acid gastric contents
• Basic aspirate ↓ surfactant levels
• MOA of Aspiration Pneumonitis:
↑ intraalveolar water and protein content and a loss of lung volume leading ↓ in pulmonary compliance and intrapulmonary shunting of blood
After direct acid-mediated injury of respiratory tract,
• Amplification of these inflammatory processes may result in development of
acute lung injury or acute respiratory distress syndrome (ARDS)
an intense inflammatory response ensues from macrophage activation and secretion of cytokines, interleukins and tumor necrosis factor-alpha (MSIT)
In Aspiration pneumonitis, After direct acid-mediated injury of respiratory tract, and activation of MSIT what does it lead do ? CAUA
Leads to :
Chemotaxis
Accumulation and activation of neutrophils in alveolar
exudate,
Up-regulation of adhesion molecules within pulmonary
vasculature and
Activation of the complement pathways
In Aspiration Pneumonitis Neutrophils release OPLO
oxidants, proteases, leukotrienes, and other proinflammatory molecules
In aspiration pneumonitis: Cellular debris and bronchial denuding.
bronchial obstruction
In aspiration pneumonitis, Exudative pulmonary edema –>
BDPI
What happens to lung compliance? PVR , WOB
bronchial obstruction
↓ lung compliance, and shunting → hypoxemia,
↑ pulmonary vascular resistance
Increased work of breathing
Most common site of aspiration and why?
RLL; d/t large size of right mainstem bronchus
Aspiration pneumonitis: Recovery involves proliferation and differentiation of
surviving type II pneumocytes in alveolar epithelial cells
• Actively transport Na+ out of alveolus, water follows
Recovery aspiration pneumonitis: Soluble proteins are removed by
paracellular diffusion and endocytosis
Recovery of Insoluble proteins are removed by
macrophages.
Neutrophils are removed by
programmed cell death and phagocytosis by
macrophages
Aspiration pneumonitis Type II
Type II pneumocytes gradually restore normal composition of surfactant
DIC Results from an
abnormal activation of the coagulation system
Abnormal activation of the coagulation system DIC leads to : (FDAH)
Formation of large amount of thrombin
Depletion of coagulation factors
Activation of fibrinolytic system
Hemorrhage
If severe enough DIC leads to
diffuse microvascular thrombosis → end-organ injury
DIC depletion of platelet
Intravascular deposition of fibrin –>Thrombosis of small and midsize vessels and organ failure
Depletion of platelets and anticoagualtion factors-> Bleeding
Obstetric triggers of DIC
include entry of procoagulant tissue extracts into the blood which interact with factor VII and activate the extrinsic coagulation pathway
DIC and dead tissue
dead tissue and amniotic fluid contains thromboplastic substances that trigger coagulation
What really activate the cascade?
Endothelial injury.
What is the hallmark of DIC
Elevated D-dimer, Fibrin and Fibrin Degradation Products (FDPs)
Other proteins Depleted in DIC
Antithrobin 3, Fibronectin, Plasminogen
Decreased labs in DIC
Platelet count, Fibrinogen, and antithrombin III concentrates.
DIC : There is Variable Increase in
PT, aPTT, and thrombin and Reptilase times
Reptilase time is
Detect abnormalities in Fibrinogen
In DIC Endothelial cells –> Plasminogen activator–>
Plasminogen –> Plasmin
In DIC platelets
Platelets –> thrombin–> Activated platelets.
DIC Pathophysiology: Intravascular
Fibrin Formation
• Formation of small strands/microclots of fibrin is the immediate result of DIC (may lead to obstruction of pulmonary vessels)
• Fibrinolysis present in
•
every patient with DIC
• Fibrin degradation products (FDP) are Protein fragments that (APID)
Act as antithrombins (↑ bleeding)
Produce defective fibrin polymer (↑ bleeding)
Impair platelet clearance
Directly damage pulmonary vasculature (ARDS!
Tx for preeclampsia High MAG
Calcium gluconate and Furosemide
33 weeks scheduled for procedure, which drug to avoid
Ketorolac (NSAIDS)
33 weeks scheduled for procedure, which drug to avoid
Ketorolac (NSAIDS) (can close the ducturs arteriosus)
Consistent with Preeclamspia?
Proteinuria Increased thromboxane Decreased Prostacyclin Vasoconstriction Enhanced Platelet aggregation
How does Nitroglycerin help
Provide uterine relaxation
IF the patient has DIC no
spinal anesthesia
Alternative GA
Late severe DIC
Rule out severe liver disease (elevated platelets, elevated PT)
DIC Active bleeding or invasive procedure is required,
transfuse: FFP how much and why?
• Ventilation, multiorgan system support
(15 to 30 mL/kg) to maintain the PT and aPTT within
1.5 times normal values
DIC and Cryoprecipitate or fibrinogen concentrate
to maintain fibrinogen concentration above 150 to 200 mg/dL
DIC and Platelets to
maintain a platelet count above 50,000/mm3
Normally, avoid neuraxial anesthesia with
coagulation disorders
In selected circumstances, neuraxial anesthesia can be offered to a patient with an
Isolated laboratory abnormality and no clinical evidence of coagulopathy.
With patient with coagulopathy , Frequent neurologic examinations are performed to
Facilitate the early detection of an “epidural hematoma” during the postpartum
MAP 1st formula
MAP = (CO x SVR) + CVP
MAP 2nd formula
1/3 (systolic pressure – diastolic pressure) + diastolic pressure
Possibility of high spinal block if
too much LA administered
High spinal can lead do =
respiratory paralysis
Absolute Neuraxial CONTRAINDICATIONS
PUCISH
• Pt refusal • Uncorrected hypovolemia • Clinical coagulopathy • Infection at injection site • Severe preeclampsia • Hx thrombocytopenia and labs have not resulted yet
Can help c/maintaining hemodynamics during modest hemorrhage
Ketamine
Preventing Sympathectomy
from Becoming a Problem
- Phenylephrine OK but go slow
* 50 mcg until BP remains stable (SBP > 100)
What gauge needle to Insert for Subarachnoid space:
25g spinal needle to subarachnoid space
Spinal Needles: Cutting-bevel needles (Quincke) =
rarely used due to unacceptably ↑risk of PDPH
Still used in elderly population
Non-cutting needles (Whitacre, Sprotte) preferred
• “Pencil-point needles” causes what?
Causes more trauma to dura → more intense
inflammatory response → more rapid closure of
dural defect
• “Pencil-point needles”
Non-cutting needles (Whitacre, Sprotte)
Needles that are preferred are
Non-cutting needles (Whitacre, Sprotte) preferred
Bigger gauge needle advantages
More control, more resistant to bending/shearing from hitting bones
Smaller spinal needles risk?
↓PDPH risk, harder to control
Emergencies usually necessitate what kind of needles?
larger gauge needles
Awareness during GETA
• High incidence between______and _______
• 50% N2O /O2
administered c/following agents ↓awareness to <1%
• 0.6% Isoflurane
• 1% Sevoflurane
• 3% Desflurane
induction of anesthesia and delivery of fetus
What leads to maternal Awareness.?
Administration of only 50% N2O with O2 without other agents resulted in maternal awareness in 12-26% of cases
What medication help prevent Awareness during GETA
Ketamine on induction can help
To help prevent awareness minimize
Minimize time from induction to delivery
50% N2O /O2 administered c/following agents ↓awareness to <1%
- 0.6% Isoflurane
- 1% Sevoflurane
- 3% Desflurane
____are now considered the preferred anesthetic
• SAB
Preventing Sympathectomy from Becoming a Problem
• ↑SVR c/pressors - Phenylephrine
How to Treat HoTN from Sympathectomy
• Arteriolar constrictors (pressors)
- LUD
- Proper fluid loading
- Preload alone might not prevent hypothermia
Treating HoTN
• 500mL hetastarch can be better than 1500mL
crystalloid
For C/S If tachycardic, use
phenylephrine
For Hemodynamic stability in C/S If bradycardic,
use ephedrine
Atropine if severe (glycopyrrolate works too slow)
For Hemodynamic stability in C/S Bradycardia can occur with
generous phenylephrine boluses (HTN)
If SBP < 110, pretreat with some
ephedrine (50mg IM, or 25 mg into skin local you are going to use)
C/S meds to be available to maintain
- Ketamine should be available
* Ephedrine and Phenylephrine should already be diluted
