Mod 7 + 8 Flashcards
Can pregnant women take asthma medications?
Yes
_________ does not commonly involve wheezing and coughing while asthma does
Dyspnea
Risks associated with_______:
FGR
SGA
PTB
Asthma
Pregnancy causes ___% of cases to improve, ____% of cases to unchange, ____% of cases will worsen
33%, 33%, 33%
first test to order when PE is suspected
CXR
pregnant women are in stable respiratory:
alkalosis
progesterone causes decreased ___________ and _____________
airway conduction and pulmonary resistance
elevated diaphragm causes ___________ and ___________
functional residual capacity and residual air volume
GERD can make asthma:
worse
Asthma Severity: symptom frequency: 2 days per week or less night waking: 2x/month or less NO intereference with normal activity PFR > 80% of personal best
Intermittent
Asthma Severity:
symptom frequency: >2 days per week but not daily
night waking: >2x/month
Intereference with normal activity: minor
PFR > 80% of personal best
Mild Persistent
Asthma Severity: symptom frequency: daily night waking: >1x/week Intereference with normal activity: some limitation PFR 60-80% of personal best
Moderate Persistent
Asthma Severity: symptom frequency: throughout day night waking: 4x/week or more Intereference with normal activity: extreme limitation PFR <60% of personal best
Severe Persistent
Treatment for _________ Asthma:
No daily meds
Albuterol PRN
Mild Intermittent
Treatment for _________ Asthma:
Preferred: Low-dose inhaled corticosteroids
Alternative: Cromolyn, Leukotriene Receptor Antagonist, Theophylline
Mild Persistent
Treatment for _________ Asthma:
Preferred: Low-dose inhaled corticosteroids AND Salmeterol or Medium-dose inhaled corticosteroids
Alternative: Low-dose or Medium-dose inhaled corticosteroids AND Leukotriene Receptor Antagonist or Theophylline
Moderate Persistent
Treatment for _________ Asthma:
Preferred: High-dose inhaled corticosteroids AND Salmeterol AND oral corticosteroid (if needed)
Alternative: High-dose inhaled corticosteroids AND Theophylline AND oral corticosteroid (if needed)
Severe Persistent
Maternal Implications of \_\_\_\_\_\_\_\_\_: Variable - 23% improve, 30% worsen Need monitoring w/ PEFR and FEV1 testing + tracking symptoms throughout pregnancy LBW Prematurity Susceptibility to hypoxia and hypoxemia Slight increase (studies not consistent): -stillbirth -preeclampsia -PTL -FGR -perinatal mortality -abruption -previa -PROM -GDM Morbidity (severe disease, poor control, or both) **Otherwise usually good outcomes Status asthmaticus can → morbidity, muscle fatigue, resp arrest, pneumothorax, pneumomediastinum, acute cor pulmonale, cardiac arrhythmias
Asthma
**Fetal Implications of \_\_\_\_\_\_\_\_\_: Fairly uncommon--If any risk it is slight and studies are not consistent** SAB PTL/PTB FGR (with increased severity) Abruption/Previa PROM Fetal response to maternal hypoxemia → ↓umbilical blood flow, ↑systemic and pulmonary vascular resistance, ↓cardiac output Possible teratogenic or adverse effects of Meds Slight risk for abnormalities: -Cleft lip and palate -Autism spectrum disorders
Asthma
Differential Dx for \_\_\_\_\_\_\_\_: Dyspnea of pregnancy GERD Chronic cough from postnasal drip Bronchitis
Asthma
Collaborate or refer for ANY level of _______ asthma
persistent
Avoid ______ corticosteroid in ____ trimester
oral in 1st
Give stress dose of corticosteroids to women in labor that have used ___________ in the past 4 weeks
oral steroids
med that is possibly teratogenic or may have adverse fetal effects - several reports show slightly higher risk for abnormalities such as cleft lip/palate and autism spectrum
oral steroids
ICS usually bumped up to q__-__ hours to reduce need for extra SABAs in persistent asthma
3-4
Interventions for Asthma during __________:
Keep rescue inhaler at bedside
Continue ICS
Labor
Avoid nubain during:
acute asthma attack
Labetolol and Hemabate - not first line for:
asthmatics
If patient also allergic to ASA, DO NOT give ____________ during labor, consult physician
corticosteroids
Medication for all severities of asthma
SABAs
Add __________ to SABA for Mild Persistent Asthma
Low-dose ICS
Add __________ to SABA for Moderate Persistent Asthma
Low-dose ICS + LABA
Add __________ to SABA for Severe Persistent Asthma
High-dose ICS + LABA
Add __________ to SABA for VERY Severe Persistent Asthma
High-dose ICS + LABA + PO corticosteroids
Do not _______ asthma medications DURING pregnancy
step-down
What to assess if asthma symptoms ___________:
medication technique, adherence, and environmental control
not controlled
Nonpharmacologic Interventions for \_\_\_\_\_\_\_\_: Control of triggers Herbal remedies (NOT in place of meds!) Licorice, Ginkgo Biloba, Coltsfoot, Hops Fish Oil, Vitamin C Yoga, acupuncture, biofeedback
Asthma
Causes increased risk for __________ in pregnancy:
decreased venous outflow
hypercoagulable state
damage to venous lining
VTE
V I R C H ow's Triad
Vascular Injury
Reduced blood flow (venous stasis)
HyperCoaguability
pauses in respiratory movements greater than 20 sec that is common in preterm infants…involves changes in HR (often <80 bpm)
apnea
apnea with no breathing effort and no airflow
central apnea
apnea with breathing effort but no airflow
obstructive apnea
apnea that begins with no breathing effort then once breathing effort starts, there is no airflow
mixed apnea
venous stasis, hypercoagulable state, vascular trauma
Virchow’s
Venous wall relaxation due progesterone and venous pressure due to gravid uterus
venous stasis
DVT is usually in _______ left leg– ileal femoral veins
proximal
Pathophysiology of ____________:
the placenta experiences ischemia because the spiral arteries of the uterus fail to reshape and increase in diameter
preeclampsia
Preeclampsia: ___creased serum creatinine
increased
Preeclampsia: ___creased creatinin clearance
decreased
Preeclampsia: ___creased liver enzymes
increased
Preeclampsia: ___creased Lactate Dehydrogenase (LDH)
increased
level that indicates proteinuria in 24-hour urine
> 300
Risk Factors for \_\_\_\_\_\_\_\_\_\_: Obesity (BMI>30) Smoking Age>35 Hx thrombosis Inherited thrombophilias Antiphospholipid antibody syndrome Sickle cell disease Heart disease Diabetes Immobility (paraplegia) [Due to Pregnancy:] Hypercoagulable state Venous stasis Multiple pregnancy Preeclampsia [Due to Labor and Birth:] Operative vaginal birth C/S Infection Vascular trauma Immobilization PPH Preterm birth Stillbirth
DVT
LOOK AT ACOG Chronic HTN & Gestational HTN tables that explain difference b/t severe and nonsevere features
!!!!!!!!
LOOK AT CLINICAL RISK FACTORS FOR ASPIRIN USE IN PREGNANCY
!!!!!!!!!
Management of ____________:
**Immediate referral
Thrombophilia testing first if indicated
Anticoagulation w/ unfractionated heparin (UFH) or low-molecular-weight heparin (LMWH)
PP: simultaneously start warfarin (safe during lactation)
Anticoagulation continues for 6 months minimum
Limited activity, leg rest, elevation
Over several days leg pain should subside
After symptoms pass - graded ambulation started, fit elastic stockings, continue anticoagulation
Graduated compression stockings are worn for 2 yrs to prevent post-thrombotic syndrome
DVT
Recovery of DVT is usually __-___ days
7-10
PE incidence: 1 in _______
7,000
Symptoms of \_\_\_\_\_\_\_: Dyspnea Chest pain Cough Syncope Hemoptysis Tachypnea Apprehension Tachycardia Pulmonic closure sound Rales Friction rub Deceptively nonspecific - s/s and lab testing
PE
Diagnostics for _______:
ECG (right axis deviation + T wave inversion)
CXR (results normal 40% of the time, otherwise may have atelectasis, infiltrate, cardiomegaly, or effusion)
Most hypoxemic–Normal arterial blood glass does not exclude
⅓ have PO2 value of >80mmHg
Alveolar-arterial oxygen tension difference more useful indicator - 86% have alveolar-arterial difference >20mmHg
PE
Gestational HTN will deliver @ ___ weeks
37
Risk Factors for __________:
Rapid labor
MSAF
Tears into uterine/other large pelvic veins (permits fluid exchange b/w mother & fetus)
AMA Post-term pregnancy Labor induction or augmentation Eclampsia Cesarean, forceps, or vacuum delivery Abruption or previa Hydramnios
AFE
Risk Factors for __________:
Rapid labor
MSAF
Tears into uterine/other large pelvic veins (permits fluid exchange b/w mother & fetus)
AMA Post-term pregnancy Labor induction or augmentation Eclampsia Cesarean, forceps, or vacuum delivery Abruption or previa Hydramnios
Male gender fetus
Fetal distress
PROM
IUFD
AMA >35
Multiparity
Diabetes
C/S
cervical laceration
Uterine rupture
Uterine Hypertonus - likely effect rather than cause, hypertonus from oxytocin not implicated
AFE
Symptoms of __________:
Classic triad:
hemodynamic compromise, respiratory compromise, DIC
Classic example:
dramatic behavior
late stages of labor immediately postpartum
gasping for air
Seizures or cardiorespiratory arrest rapidly follows w/ massive hemorrhage from consumptive coagulopathy
Manifestations can be variable
AFE
Management for \_\_\_\_\_\_\_\_\_\_\_: Protect airway 2 large-bore IVs Type+Cross Consider vasopressors Contact OR Emergent C/S ICU Volume resuscitation serial ACT/ABG/VBG PRBC/FFP/platelets
AFE
Most efficient way for NB to temporarily increase ventilation and compensate for hypoxia and hypercarbia
tachypnea
developmental deficiency in surfactant synthesis accompanied by lung immaturity and hypoperfusion
Neonatal Respiratory Distress
Do NOT give ___________ to protect against infections from MVP (mitral valve prolapse)
prophylactic abx
Causes of ___________:
Prematurity and exacerbated by asphyxia
Impaired or delayed surfactant synthesis
Neonatal Respiratory Distress
Risk Factors for ____________:
Fetal - Prematurity, asphyxia, anemia
Maternal - poorly controlled GDM
Pregnancy- polyhydramnios, oligohydramnios
Intrapartum - previa, abruption, MSAF
Risk decreases w/ higher gestational age
Neonatal Respiratory Distress
Risk Factors for \_\_\_\_\_\_\_\_\_\_: Male gender Maternal GDM Perinatal asphyxia Hypothermia Multiple gestations
Respiratory Distress Syndrome
NB’s most efficient way to temporarily increase ventilation and compensate for hypoxia and hypercarbia
tachypnea
sound created by exhaling against a partially closed glottis in an attempt to increase functional residual capacity in lungs and stabilize (stint) alveoli
helps keep the lungs expanded and preserves oxygen
grunting
attempt to decrease resistance to airflow by increasing the size of nostrils that results from increased inspiratory pressure
this decrease in resistance will decrease total work of breathing
nasal flaring
Attempt to increase lung compliance and assist the diaphragm as it mechanically expands the lung during inspiration
occurs with airway obstruction
retractions
apparent when 5 g/100 mL of hemoglobin is unsaturated and SpO2 decreases to 80-85%
central cyanosis
developmental deficiency in surfactant synthesis accompanied by lung immaturity and hypoperfusion
caused by prematurity and exacerbated by asphyxia
or impaired/delayed surfactant synthesis
neonatal respiratory distress
Risk Factors for \_\_\_\_\_\_\_\_\_\_\_\_: Fetal - Male gender Prematurity Asphyxia Anemia Hypothermia Multiple gestations
Maternal -
Poorly controlled diabetes
Pregnancy-
Polyhydramnios
Oligohydramnios
Intrapartum- Previa Abruption MSAF **Risk decreases w/ increased gestational age
neonatal respiratory distress
NB Respiratory Problem:
Begins early
and Increases in severity over the first 72 hours
neonatal respiratory distress
results in poor compliance, rapid, shallow breathing
surfactant deficiency
results in slower deep breathing
increased airway resistance
Symptoms of _________________:
Tachypnea
Grunting
Pitting edema
Cyanosis
Diminished breath sounds
Retractions
Isolated tachypnea w/ congenital heart disease
Temp instability (infection?)
Tachycardia (hypovolemia?)
Scaphoid abdomen (congenital diaphragmatic hernia?)
Asymmetric chest movement/ breath sounds
Tension pneumothorax possible
Stridor (possible subglottic stenosis in previously intubated)
neonatal respiratory distress
Diagnostics for \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_: Follow NRP guidelines until infant is stable then... -Chest x-ray -ABG -CBC w/diff -Blood cultures -Review maternal/fetal history
neonatal respiratory distress
Inadequate or delayed clearance of lung liquid leading to transient pulmonary edema
Transient Tachypnea of the Newborn
Caused by fluid in lungs increasing inspiratory activity, RR, and grunting
- Possibly from alteration in permeability of pulmonary capillary vessels, aspiration of amniotic fluid during in uterine gasping efforts or decreased vaginal thoracic squeeze
- Immaturity leads to slower lung fluid removal
- Delayed respiratory transition w/ increase in diffusion distance
- Increased risk of V/Q mismatching
Transient Tachypnea of the Newborn
Risk Factors for \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_: Cesarean birth before labor onset Perinatal hypoxic stress event Precipitous labor Male gender infant Genetic change in alveoli 𝛃-adrenergic receptor expression
Transient Tachypnea of the Newborn
Uncommon in preterm infants born by C/S possibly due to increased interstitial tissue and smaller gas exchange areas that decrease movement of lung fluid from the interstitial space back into the airway
Transient Tachypnea of the Newborn
No transition after birth with symptoms resolving usually in 48-72 hours
Transient Tachypnea of the Newborn
Symptoms of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_: Tachypnea (up to 120-140 bpm) Mild to moderate retractions Grunting Cyanosis (usually not prominent) Breath sounds may be initially moist but clear quickly
Transient Tachypnea of the Newborn
Diagnostics for _______________:
CBC + blood cultures (Rule Out sepsis)
Chest X-ray (vascular engorgement, moderate cardiomegaly, occasional air bronchogram, hyperaeration)
ABG (may indicate respiratory acidosis)
Transient Tachypnea of the Newborn
Management of \_\_\_\_\_\_\_\_\_\_\_\_\_\_: Supportive based on symptoms Rule out sepsis O2 required (usually needs to be >40%) **Not a severe respiratory problem
Transient Tachypnea of the Newborn
breathing alternating w/ a pause of up to 20 seconds which may be induced by hypoxemia and respiratory depression that is more common in preterm infants
*can be relieved by respiratory stimulants like caffiene
periodic breathing
lapse of 20 seconds or more in breathing that occurs w/ color changes or bradycardia (often < 80 bpm) that is common in preterm infants and more frequent for infants w/ chronic lung disease or other respiratory problems
*Abnormal finding in full-term infants - may indicate an underlying problem, like sepsis, hypoglycemia, CNS injury or abnormality, seizures, or maternal drug use
apnea
type of apnea with no airflow or breathing efforts
central apnea
type of apnea where there is no airflow WITH breathing efforts
obstructive apnea
apnea that begins as central and becomes obstructive
mixed apnea
this is caused, in theory, by vagal stimulation from common, transient umbilical corn entrapment resulting in bowel peristalsis
MSAF
Risks correlated with \_\_\_\_\_\_\_\_\_\_\_\_: C/S Forceps Intrapartum FHR abnormalities Low APGARs Need for assisted ventilation at delivery
Meconium aspiration
inactivates surfactant and activates complement cascade causing inflammation and vasoconstriciton of the pulmonary veins
Meconium Aspiration
Current belief is that this occurs when infant is compromised by a chronic event like chronic metabolic acidosis, infection, or other comorbidities rather than only an acute event in labor
Meconium Aspiration
Induces hypoxia via 4 major pulmonary effects: Airway obstruction Surfactant dysfunction Chemical pneumonitis Pulmonary hypertension
Meconium Aspiration
increases risk for intrauterine infection
MSAF
Symptoms of \_\_\_\_\_\_\_\_\_\_\_\_: Death (thick) Long term neurological sequelae Barrel chest Crackles and Rhonchi on auscultation Associated complication - Pulmonary Hypertension
MAS
Risk Factos for ____________:
Postterm
FGR
*due to decreased amniotic fluid + cord compression or uteroplacental insufficiency
MAS
Management of \_\_\_\_\_\_\_\_\_\_\_\_: Ventilatory support Intubation as needed CXR (varies w/ severity, areas of patchy atelectasis, areas of overinflation) Surfactant replacement Inhaled corticosteroids
MAS
M R S O P A
Mask adjustment Reposition airway Suction (mouth + nose) Open mouth Pressure increase Alternative airway
Start NRP with PIP of:
20-25
Start NRP with PEEP of:
5
chest compressions are necessary when the baby’s HR is below ____ after at least ___ seconds of PPV
below 60 after at least 30 seconds of PPV
chest compression should be pressure applied to the _________ of the sternum
lower 1/3
Arterial: Low pH High PCO2 Normal HCO3 Normal Base Deficit
Respiratory Acidosis
Arterial: Low pH Normal PCO2 Low HCO3 High Base Deficit
Metabolic Acidosis
Arterial: low pH High PCO2 Low HCO3 High Base Deficit
Mixed Acidosis
Arterial Normal pH
7.26 +/- 0.07
Arterial Normal PCO2
53 +/- 10
Arterial Normal HCO3
22 +/- 3.6
Arterial Normal Base Deficit
4 +/- 3
Venous: Low or Normal pH High or Normal PCO2 Normal HCO3 Normal Base Deficit
Respiratory Acidosis
Venous:
Normal pH (short duration) or Low pH (long duration)
Normal PCO2
Normal HCO3 (short duration) or Low HCO3 (long duration)
Normal Base Deficit (short duration) or Low Base Deficit (long duration)
Metabolic Acidosis
Venous: Low or Normal pH High or Normal PCO2 Low or Normal HCO3 High or Normal Base Deficit
Mixed Acidosis
Arterial Normal PO2
18 +/- 6.2
Venous Normal pH
7.35 +/- 0.05
Venous Normal PCO2
38 +/- 5.6
Venous Normal PO2
29 +/- 5.9
Venous Normal HCO3
20 +/- 2.1
Venous Normal Base Deficit
4 +/- 2
Typically within a 20-30 minute period, if placental perfusion disruption is not corrected and anaerobic metabolism continues, the respiratory component will dissipate, and organic acid levels will continue to increase causing bicarbonate and serum pH levels to drop further. This is now a:
metabolic acidemia
Target rectal temp during HIE:
32.5-34 C
Requirements for ___________:
- Greater than 35 weeks gestation
- Birth weight >/= 1.8 kg
- Less than 6 hours since insult
- One or more of the following predictors:
pH = 7.0 + Base Deficit >/= 16 on arterial cord gases
pH 7.01–7.15 + Base Deficit 10–15.9 with acute perinatal event AND 10 min APGAR = 5 AND/OR Assisted ventilation at birth required for 10 or more minutes
5. Seizures OR 3 of the following: Lethargy / Stupor / Coma Decreased or NO Activity Distal flexion/ Complete Extension/ Decerebrate Posturing Hypotonia or Flaccid Tone Weak/ Absent Suck Incomplete/ Absent Moro Reflex Constricted/ Dilated/ Deviated/ Non-reactive Pupils Bradycardic or Variable HR Periodic Breathing or Apnea
HIE
usually begins 6-12 hours or more after the initial insult and is characterized by hyperexcitability, cytotoxic edema, and damage from the release of free oxygen radicals and Nitrous Oxide, inflammatory changes and imbalances in inhibitory and excitatory neurotransmitters
Reperfusion Phase after HIE
cerebral palsy caused by HIW is more common in _______ infants
preterm
_____ infants with moderate to severe HIE have a higher mortality rate, as well as long term cognitive and motor problems
Term
in preparation for cooling, take rectal temp q ___ minutes
15
Causes for _____________:
Primary intracranial process: Meningitis Ischemic stroke Encephalitis Intracranial hemorrhage Tumor Malformation
Systemic problem: Hypoxia-ischemia Hypoglycemia Hypocalcemia Hyponatremia Other disorders of metabolism
Electrolyte imbalances: (calcium, potassium, magnesium, sodium) Acidosis Hyperbilirubinemia Viruses (CMV) Sepsis
NB Seizures
Symptoms of __________ Seizures:
Eyes: staring, deviation, blinking, fluttering, fixed open stare
Oral: chewing, sucking, lip-smacking, tongue thrusting
Limbs: cycling, swimming, rowing, boxing, pedalling
Systemic: apnea, tachycardia, blood pressure alterations
Subtle
Symptoms of \_\_\_\_\_\_\_\_\_\_ Seizures: Usually, involve one limb or one side of the body jerking rhythmically at 1-4 times per second. Consciousness usually preserved Multifocal, simultaneous or sequential Non-ordered/nonJacksonian migration
Clonic
Symptoms of ___________ Seizures:
Generalized and rapid isolated jerking of muscles
May be focal or multifocal
Usually Conscious.
Myoclonic
seizures that primarily occur in preterm infants
Clonic
seizures that primarily occur in term infants
Myoclonic
seizures that occur in preterm and term infants
Subtle
Symptoms of ___________ Seizures:
Rare
Sustained posturing of the limbs or trunk or deviation of the head
Generalized extensions of upper and lower limbs accompanied by pronation of arms and clenching of fists
Focal: sustained posturing of limb (rare)
May mimic decerebrate or decorticate posturing
Only 30% have EEG correlation
Difficult to treat with anticonvulsants
Tonic
type of seizure seen in drug withdrawal (especially opiates)
- If it occurs during sleep then it is probably ‘benign neonatal sleep myoclonus’
- Can also occur in a very severe form of encephalopathy
Myoclonic
type of seizure that may be due to an underlying focal neuropathology such as haemorrhage or cerebral infarction
Clonic
seizures that arise from the basal ganglia as a result of diminished cortical inhibition so further depression of the cortex with anticonvulsants may not alter these seizures
Subtle
% of NB that develop normally after hypoxia-ischemia seizures develop normally
50%
\_\_\_\_\_\_\_\_\_\_\_\_ causes for Seizures: Prenatal: Toxemia Fetal distress Abruptio placentae Cord compression)
Perinatal:
Iatrogenic
Maternal haemorrhage
Fetal distress
Postnatal:
Cardio-respiratory (hyaline membrane disease)
Ccongenital heart disease
Pulmonary hypertension
Hypoxia-Ischemia
_________ causes for Seizures:
Intraventricular and Periventricular Infarction (mainly preterm neonates)
Intracerebral infarction (spontaneous, traumatic)
Subarachnoid hemorrhage
Subdural hematoma
Cerebral artery and Vein infarction
Hemorrhage/Infarction
__________ causes for Seizures:
Intracranial haemorrhage
Cortical vein thrombosis
Trauma
\_\_\_\_\_\_\_\_\_\_\_ causes for Seizures: Hypoglycemia (BG <20 in preterm or <30 in term infants) GDM Maternal Toxemia Pancreatic disease Glycogen storage disease (idiopathic) Hypocalcaemia Hypomagnesemia (may accompany or occur independently of Hypocalcemia) Maternal Hyperparathyroidism DiGeorge’s syndrome Hyponatraemia Hypernatraemia Inborn errors of metabolism (amino acid and organic acid disorders, hyperammonemia; they usually manifest with peculiar odours, protein intolerance, acidosis, alkalosis, lethargy, or stupor) Pyridoxine dependency
Metabolic
NB seizures caused by intraventricular hemorrhage have a:
high morbidity rate
Earlier onset of idiopathic or malformation seizures is associated with:
worse outcomes
Labs to order for \_\_\_\_\_\_\_\_\_\_\_ HTN: Baseline labs: CBC LFTs CMP 24 hr urine Serum creatinine PCR (evaluate for kidney function) EKG (screening purposes) Platelets Early GDM screening
Chronic HTN
Fetal Surveillance for ____________:
Anatomy/Growth scan 16-20 wks gestation (20 wks better)
Repeat growth US @ 30-32 wks, then every 3-4 wks
Biweekly NST & BPP (full or modified)
Chronic HTN
Chronic HTN BP should be kept within this range:
Systolic:
Diastolic:
120-160
80-105
Complications of \_\_\_\_\_\_\_\_\_\_\_\_: Abruption Superimposed Pre-E PTB FGR
Chronic HTN
Chronic HTN patients should limit salt intake to:
2.4 g/day
Chronic HTN patients should be induced at _____ weeks but may be monitored until ____ weeks if low-risk
38 weeks; 40 weeks
Risk Factors for \_\_\_\_\_\_\_\_\_\_\_: African American race Obesity Smoking AMA HTN for 4 years or more Diastolic BP > 100 mmHg at baseline Hx Preeclampsia Hx Diabetes Hx Obesity
Superimposed Pre-E
Diagnostic Criteria for \_\_\_\_\_\_\_\_\_\_\_: Worsening HTN w/ new development of: Proteinuria Elevated liver enzymes Thrombocytopenia Pulmonary edema Cerebral or visual disturbances Renal insufficiency
Superimposed Pre-E
Medications for \_\_\_\_\_\_\_\_\_\_\_\_\_: low dose ASA 81 mg starting @ 12 weeks Calcium if dietary intake < 600 mg/day Anti-HTN medication: labetalol, nifedipine, or methyldopa
Chronic HTN
Risk Factors for \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_: 1st pregnancy Multiple gestation Molar pregnancy GDM pregestational DM Renal dx CVD Genetic predisposition to HTN developing in pregnancy Hx PreE cHTN Thrombophilia SLE Prepregnancy BMI >30 Antiphospholipid antibody syndrome AMA Assisted reproductive technology Obstructive sleep apnea
Gestational HTN
progression of gestational HTN to Pre-E is more likely if it occurs prior to ___ weeks
32
Management of ___________:
BP monitoring (home once/week, in-office once/week)
weekly or twice weekly visits
Decrease activity level (no working)
Lying left lateral multiple times per day
**IOL usually @ 37-38 weeks
Gestational HTN
Fetal Surveillance for ____________:
NST or modified BPP 2 x/week switching between full BPP
Growth US every 3-4 wks
Fetal kick counts daily @ home
Gestational HTN
Risk Factors for \_\_\_\_\_\_\_\_\_\_\_\_\_: High Risk: Autoimmune disease (SLE, APA) Chronic HTN Hx of Pre-e (especially if adverse outcome) Multifetal gestation Renal disease Type 1 or 2 DM
Moderate Risk: AMA BMI >/= 30 Family Hx of Pre-e in mother or sister Nulliparity Hx LBW, SGA, previous adverse pregnancy outcome, >10 yr pregnancy interval African American race Low SES
Preeclampsia
A multisystem disorder that begins early in pregnancy
where placental tissue is key (placental tissue must be present but fetus doesn’t need to be)
Characterized by abnormal placentation and failed remodeling of the spiral arteries, which usually occurs early in gestation in two distinct phases
Preeclampsia
Phase 1 of ____________:
failure of the process of spiral placental arteries becoming larger to accomodate increased blood flow causing hypoperfusion, hypoxia, and ischemia within the developing placenta
Preeclampsia
Phase 2 of _____________:
the maternal inflammatory response to the initial abnormal placentation and subsequent placental hypoxia that causes endothelial cell dysfunction in the maternal arteries, the release of cytokines which leads to systemic inflammation, vascular endothelial dysfunction, and prothrombotic condition
*Manifests at HTN and in severe cases, liver, kidney and brain damage
Preeclampsia
symptom of Pre-E that is thought to be due to periportal and focal parenchymal necrosis, hepatic cell edema, or Glisson’s capsule distension, or a combination
RUQ or epigastric pain
FGR or new-onset proteinuria in the 2nd half of pregnancy without ___________ may precede development of diagnostic criteria for Pre-E
HTN
Labs for \_\_\_\_\_\_\_\_\_\_\_: UA Urine dipstick LFTs CBC with diff (PLTs)
Preeclampsia
PLT count less than 100K
Thrombocytopenia
Diagnostic Criteria for \_\_\_\_\_\_\_\_\_\_\_\_: New onset HTN + proteinuria *If no proteinuria, must have: -Thrombocytopenia -Impaired Liver function -Renal insufficiency -Pulmonary edema -Cerebral or visual disturbances
Preeclampsia
Proteinuria: Protein >\_\_\_\_\_ mg/ per 24 hr urine collection or PCR > \_\_\_\_\_\_ mg/dL or Urine dipstick > \_\_\_\_\_ protein
300 mg/ 24 hr urine
PCR > 0.3 mg/dL
dipstick > 1+
Renal insufficiency: > ____ mg/dL creatinine
or doubling creatinine
1.1
Impaired Liver Function: Elevated ___________ to twice normal
Liver Enzymes (transaminases)
Complications of \_\_\_\_\_\_\_\_\_\_\_\_: Abruption Pregnancy loss Stroke Organ failure Maternal death Preterm birth FGR Stillbirth Neonatal death Twice the risk for cardiovascular disease and mortality from ischemic heart disease, HF or stroke HTN after perinatal period
Preeclampsia
______________ medication not recommended for Pre-E unless severe features present
Antihypertensive
Mild Preeclampsia: IOL by ____ weeks
37
Severe Preeclampsia: IOL by ____ weeks
34
first line agents to keep BP after Mag
Hydralazine, labetalol, and nifedipine
H
EL
LP Syndrome
Hemolysis
Elevated Liver enzymes
Low Plateletss
Rapid progression to HELLP or eclampsia is more likely to occur when onset of preeclampsia is prior to ___ weeks gestation
34
Symptoms of \_\_\_\_\_\_\_\_\_\_: Triad: Platelets < 100K Serum AST ≥ 70 or 2 x baseline levels Elevated LDH > 600 \+ Elevated indirect bili (usually just use total bili)
HELLP
Treating thrombocytopenia in HELLP syndrome with _______________is not supported by evidence
corticosteroids
Type of seizure in eclampsia
Grand mal/ tonic-clonic
Risk Factors for \_\_\_\_\_\_\_\_\_\_\_: chronic HTN Uteroplacental insufficiency without definitive cause, PP hemorrhage NSAID use? (possible in ACOG statement) Cardiovascular disease Gestational HTN
PP Preeclampsia
immune maladaptation, very low-density lipoprotein toxicity, genetic imprinting, increased trophoblast apoptosis or necrosis, and an exaggerated maternal inflammatory response to deported trophoblasts
PP Preeclampsia
AST and ALT ________ in Pre-E
elevated
H+H ________ in Pre-E
elevated or decreased
LDH ________ in Pre-E indicating tissue damage and hemolysis
elevated
Bili ________ in Pre-E
elevated
Fibrinogen __________ in Pre-E
decreased
PT/PTT ____________ in Pre-E
decreased
Risk for Mag toxicity is greater with a ____ GFR
low
Signs of \_\_\_\_\_\_\_\_\_\_\_: Hypotension Resp depression Decreased DTRs EKG changes Oliguria SOB/chest pain
Mag toxicity
Antidote for Mag toxicity
Calcium Gluconate Calcium Chloride IV
SE of ___________:
flushing
decreased FHR variability
Mag
_________ IV drops BP quickly while ____________ IV drops BP more slowly
Hydralazine fast
Labetolol slow
a combined alpha & beta-blocking agent that decreases BP by dilating arterioles and decreasing HR
Should not be given to those with
Asthma, Cocaine or Amphetamine Use
Labetolol
reduces BP by dilating arteries
S/E - tachycardia, HA, delayed maternal hypotension, fetal bradycardia, rarely upper abdominal pain
Hydralazine
PP women with persistent BPs over ___/___ on 2 occasions at least __-__ hours apart should receive anti-hypertensive meds
150/100
4-6 hours apart
In Pre-E with BP over 160/110, anti-hypertensive meds should be started with ___ minutes
30
LR fluid should be given to Pre-E patients @ __-__ mL/hr
SLOW 60-125
__________ is a risk in Pre-E due to renal/HTN sequelae oliguria w/ severe pre-e.
ARDS and pulmonary edema
In Preeclampsia w/o severe features and severe Pre-e: Sum of oral and IV fluid should be ≤ _____ ml/hr unless there are other clinical circumstances that dictate a different management plan
125
Eclamptic seizure meds that are justified only in the context of antiepileptic treatment or when mag is contraindicated or unavailable.
Benzos and phenytoin
Immediate Management of Eclamptic Seizure:
___-___ grams Mag over 15-20 min (loading dose)
4-6 grams
If seizure continues despite Mag:
Give additional loading dose of ___ mg IV over 5 min
2 grams
Second-line anti-seizure medications for uncontrolled eclamptic seizures
IV barbituates, Clonazepam, Diazepam, Midazolam or Lorazepam
Symptoms of \_\_\_\_\_\_\_\_\_\_\_\_\_\_: Most are asymptomatic Anxiety Palpitations Atypical chest pain Syncope Dyspnea w/ exertion INCREASED risk of sudden death Infective endocarditis
Mitral Valve Prolapse
Mitral Valve Prolapse Antibiotics?
No longer recommended for dental work or childbirth
If MVP patient develops infective endocarditis, give:
Pen G IV with Gentamycin x 2 weeks
Increases risk for congenital complete AV block
Maternal Lupus
Drugs. Alcohol, anticonvulsants, lithium, retinoic acid, thalidomide, warfarin, amphetamines increase risk of NB heart:
murmur
\_\_\_\_\_\_\_\_\_\_\_ CHD: PDA Atrial Septic Defect Ventricular Septal Defect (most common) Pulmonary Stenosis Aortic Stenosis Coarctation of the Aorta
Acyanotic
should be used to maintain patency of the ductus arteriosus once it is established that a ductal dependent lesion exists.
Prostaglandin E1
Symptoms of \_\_\_\_\_\_\_\_\_\_\_\_: Many asymptomatic Frequent respiratory or lung infections Difficulty breathing Tiring when feeding (infants) Shortness of breath when being active or exercising Skipped heartbeats Palpitations Heart murmur Swelling of legs, feet, or stomach area Stroke
Atrial Septal Defect
Symptoms of \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_: Some Asymptomatic Shortness of breath, Fast or heavy breathing, Sweating, Tiredness while feeding, or Poor weight gain. Heart murmur
Ventral Septal Defect
PDA normally functionally closes at ____-____
24-48 hours
PDA patency is abnormal at ____-____
2-3 months
PDA, VSD, ASD causes ____ to _____ shunting
left to right
Symptoms of _______________:
Typically Asymptomatic
May report decrased exercise tolerance or pulmonary congestion in conjunction with a murmur.
3-6-week-old infants can present with:
Tachypnea
Diaphoresis
Inability or difficulty with feeding
Weight loss or no weight gain.
With a moderate-to-large left-to-right shunt may be associated with a hoarse cry, cough, lower respiratory tract infections, atelectasis, or pneumonia
With large defects, may have a history of feeding difficulties and poor growth during infancy, described as failure to thrive (FTT).
Frank symptoms of congestive heart failure (CHF) are rare.
Adults who go undiagnosed may present with s/s of heart failure, atrial arrhythmia, or even differential cyanosis limited to the lower extremities
PDA
pumonary stenosis, aortic stenosis, and coarctation of the aorta cause ___________ obstruction
outflow
