Maternal Physiology Flashcards

1
Q

Generally speaking, how is maternal physiology different than normal physiology

A
  • physiology different from baseline and continues to change through pregnancy
  • differential diagnosis may be different
  • lab value ranges may be different
  • choice of radiologic studies may be affected
  • 2nd patient to consider
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2
Q

Total body water metabolism in pregnancy

A
  • increase from 6.5-8L = 2 kg (expanded plasma by ~50%, more RBC by 20-30%, additional extravascular and intracellular fluid in uterus/breasts)
  • chronic volume overload with active Na and water retention (changes in osmoregulation/RAAS)
  • Total body water increases relate to weight gain, hemodilution, physiologic anemia of pregnancy, elevated cardiac output
  • impaired volume expansion linked to increased risk of pre-eclampsia and impaired fetal growth/fetal growth restriction
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3
Q

Osmoregulation in Pregnancy

A
  • early alteration of arginine vasopressin secretion (plasma AVP unchanged due to placental inactivation)
  • increased water retention > sodium retention. Additional 900 mEq Na retained but serum sodium drops 3-4mmol/l. Osmolarity decreases. These changes take place by 10 weeks gestation through 2-3 weeks post-partum
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4
Q

RAAS system during pregnancy

A

(Renin-Angiotensin-Aldosterone system)

  • Marked Increases in all components
  • Early pregnancy changes cause decreased MAP, which triggers activation of plasma renin, angiotensinogen, angiotensin–all 4-5x higher than nonpregnant
  • 2x inrease in aldosterone – increased Na retention and prevent loss
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5
Q

Atrial Natriuretic Peptides/Brain Natriuretic peptides in pregnancy

A
  • These are released by myocardium to maintain vascular hemostasis
  • Both are elevated in physiologic/path stages of volume overload–can be used to screen for CHF outside pregnancy in symptomatic pts
  • Many physiologic complaints of pregnancy mimic heart disease (i.e. dyspnea)
  • ANP changes unclear–likely increases but still within nl range
  • BNP increases mostly in 3rd trimester; highest in pregnancies with preeclampsia but to levels less than used to screen for CHF
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6
Q

Cardiac changes

A
  • increased plasma volume by 50%~ 1.2-1.3L, RBC mass by 20-30% –dilutional anemia
  • BP progressively decreases until 22-24 weeks and returns to baseline at 36 weeks
  • Decreased systemic vascular resistance– progesterone effect on smooth muscle and increased NO production
  • Increased CO: mainly due to increase in stroke volume since HR only goes up 10-20 bpm in 3rd trimester
  • Decreased Vascular resistance/BP: 2nd trimester. CO impacted by position. Greatest in left lateral position, avoid supine >20-24 weeks for IVC compression
  • ventricular Hypertrophy/muscle mass
  • increased preload due to increased venous return
  • decreased afterload due to decreased vascular resistance
  • Elevated: cardiac compliance, contractility, EDV (NO change in ESV),
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7
Q

What is the association between pregant women who do prolonged standing work

A

Decreased birthweight–decreased CO while standing may be physiologic basis for this

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8
Q

Regionalization of CO

A

increased CO not distributed evenly

  • no change in brain/liver
  • 50% increase in renal perfusion
  • increased perfusion to: breasts, skin, uterus. flow to uterus about 740 ml/min at term (15% CO compared to 2%)

** increases in venous pressure and pressure on vena cava contribute to edema, varicose veins, hemorrhoids, and increased risk for DVT

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9
Q

Cardiac assessment in pregnancy

A

PE:

  • nl sinus rhythm; HR >100 may be abnl (mild tachy may not be path; 39% pregnant women tachy at rest vs 58% for obese)
  • PMI displaced to left
  • systolic ejection murmur on LSB in up to 96%
  • Exaggerated aplit S1, less so with S2
  • S3 common in ?; S4 rare

CXR:

  • cardiothoracic ratio unchanged
  • left heart border more straight
  • heart position may be horizontal
  • prominent pulmonary vasculature

EKG:

  • mild left axis deviation
  • non-specific ST-T wave changes; small Q and negative P in lead III
  • increased premature atrial/ventricular contractions
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10
Q

Clinical s/sx mimicking heart dz in pregnancy

A

Sxs:

  • Dyspena
  • Decreased exercise tolerance
  • fatigue
  • occasional orthopnea, syncope and chest discomfort

Signs:

  • peripheral edema
  • mild tachycardia
  • JVD after midpregnancy
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11
Q

Arrhythmias in pregnancy

A
  • due to anatomic changes, heart closer to chest wall so more likely to notice palpitations
  • increased premature atrial and ventricular beats
  • if monitored in labor, almost all will have some type of arrhythmia (premature A/V/nodal complex, SA arrest, wandering atrial pacemaker, paroxysmal ventricular tachy, sinus tachy)
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12
Q

Cardio changes during labor

A
  • further increase in CO; highest 10-30 min after delivery
  • due to pain (increased sympathetic stimmulation) and uterine autotransfusion (300-500 cc forced from uterus in each contraction, so increases venous return/preload/CO)
  • valsalva in pushing creates wide fluctuation in BP and HR
  • pts with significant cardiac dz should have careful hydration/fluid balance, early epidural to decrease pain and epi’s effects on BP/CO, assisted 2nd stage to shorten dangerous pd that can tip them into heart failure or arrhytmias
  • For Cesarean delivery– major surgery, so significant fluid shifts and increased blood loss compared to vaginal delivery
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13
Q

Postpartum CV changes

A
  • acute increase in CO first hr due to decreased venocaval obstruction, autotransfusion from uterine circulation, mobilization of extra fluid
  • acute loss of up to 500-1000 cc blood with nl delivery (Vaginal: nl EBL up to 500cc; Cesarean: nl EBL up to 1000 cc)
  • anatomic/physiologic changes return to prepregnant baseline over weeks-months
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14
Q

Considerations for valvular heart dz

A
  • regurgitant lesions better tolerated than stenotic lesions during pregnancy
  • many valvular dz pts will have deterioration in NYHA functional class, some will develop CHF, some will have adverse pregnancy outcomes like preterm birth/IUGR, stillbirth)
  • women with AS- fixed SV and CO variation determined by HR. Bradycardia can cause hypotension, and excessive tachy can cause hypotension, syncope, and risk of MI due to decreased filling time. Severity defined by valve area and/or peak gradient (Mild: less than 36)
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15
Q

Aortic stenosis in pregnancy

A
  • at baseline keep preload adequate for CO
  • in pregnancy, decreased afterload may lead to progression of disease
  • avoid vasodilators
  • 15-20% mortality in critical AS pts (CHF, syncope, cardiac arrest)
  • If decompensation, consider early delivery

DURING LABOR:

  • careful hydration/fluid balance
  • early epidural
  • assisted 2nd stage to shorten dangerous pd that can tip into HF or arrhythmia
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16
Q

Pre-eclampsia

A

New HTN and proteinuria, edema

17
Q

Preexisting hypertension

A
  • intrauterine growth retardation–will perform several fetal US to check growth
  • ## pre-eclampsia superimposed upon chronic HTN: obtain baseline 24 hr urine protein for creatinine clearance/total protein with first prenatal visits and evaluate BP and dipstick proteinuria at each visit
18
Q

Pulmonary Changes in Pregnancy

A

VENTILATION

  • RR: unchanged
  • Tidal volume: increases 25-40% at expense to expiratory reserve (falls 15-20%)
  • minute volume (RR xTV): increased
  • O2 uptake: increase
  • Vital capacity: unchanged
  • Inspiratory reserve volume: unchanged
  • *Progesterone affects sensitivity of respiratory center to CO2– hyperventilation
  • decreased functional residual volume (from elevated diaphragm)
  • PaCO2: arterial and alveolar CO2 decreases 2nd half of pregnancy to facilitate CO2 transfer back to mom

Oxygenation:
- O2 consumption and PaO2 increases

Acid-base balance:

  • pH increases/no change
  • serum HCO3 decreases (18-21); attributed to progesterone effect - increased respiratory center sensitivity to CO2)
  • 7.4-7.45 due to increased bicarb secretion
  • *STATE OF PRIMARY RESPIRATORY ALKALOSIS w/COMPENSATORY METABOLIC ACIDOSIS
  • Changes to thoracic cage (increased subcostal angle/AP diameter/chest circumference)

LATER IN PREGNANCY

  • diaphragm pushed up 4 cm- decrease TLC and RV, so functional residual capacity reduced
  • FEV1 and FEV1/FVC unchanged – implies no change in large airway function; some studies indicate DECREASED airway resistance
  • diaphragmatic excursion not impeded by pregnancy–actual increases 1-2cm
  • breathing more diaphragmatic than costal
19
Q

Dyspnea in pregnancy

A
  • common complaing: 60-70% nl pregnancies by 3rd trimester
  • usually beginning in late 1st/early 2nd trimester
  • mild; doesn’t interfere with daily activities/occur at rest
  • Probably from reduced PaCO2, awareness of increased TV of nl pregnancy, increased ventilation-perfusion mismatch (shunting in nl pregnancy 5-15%, which is associated with SOB in nonpregnant ppl)
20
Q

Asthma management in pregnancy

A
  • 3% of reproductive aged women
  • asthma may improve from increased serum cortisol
  • key to keep pO2 WNL

common safe medical therapies:

  • inhaled beta agonists, steroids, cromolyn
  • oral steroids
  • certain antibiotics to treat infection (penicillins, cephalosporins, macrolides)
21
Q

Acute asthma attack in pregnancy

A
  • presentation similar to nonpregnant woman

- ABG crucial; PCO2 of 40 a sign of impending respiratory failure and O2 sat

22
Q

Renal changes

A

-Kidneys enlarge: increased vasculature, interstitial volume, urinary dead space (dilation of renal pelvis, calyces, uterters)

  • increased GFR, and Creatinine clearance, renal plasma flow but DECREASED filtration fraction (RPF increased more than GFR)–relaxin and NO implicated
  • will get lower urea and Cr levels
  • relative hydronephrosis (R>L) 2nd month and max by mid-2nd trimester; due to mechanical compression with enlarging uterus and smooth muscle relaxation from progesterone; resolves by 6 wk postpartum

HARD TO INTERPRET URINARY IMAGING STUDIES FOR OBSTRUCTION/NEPHROLITHIASIS

23
Q

urinary tract

A
  • increased risk of pyelonephritis due to urinary stasis/asymptomatic bacteriuria (R >L), so get culture at beginning of pregnancy. Treat asymptomatic lower UTI to prevent pyelo
  • Pyelonephritis has increased risks of complications like respiratory compromise/ARDS adn dvpt preterm labor
  • decreased bladder capacity but increased urine volume; increased nocturia; increased microhematuria from increased vascular supply
24
Q

Renal dz risks and implications

A
  • at risk for worsening dz, preeclampsia, IUGR, PTB and permanent worsening of renal fxn as result of pregnancy (33% of pts)
  • concomitant illness like chronic HTN multiplicatively increases complications

**Severe renal insufficiency causes healthy obstetric outcome likelihood to drop to 51% and medical complications to increase to 53%!!

  • want to get baseline CrCl/protein and subsequently evaluate with spot protein/creatinine ratio, treat underlying dz, US to assess fetal growth, fetal monitoring/nonstress tests at 32 weeks, close observation for preeclampsia
25
Q

Hematologic changes

A
  • plasma volume increases 50%, RBC mass by 20-30%. Since volume increases more than plasma, have hemodilultion– physiologic anemia.
  • may see thrombocytopenia 100k-150k in 9-15% vs only
26
Q

Immune system and leukocytes

A

Fetus= semi allograft; suffessful pregnancy depends on evasion of immune surveillance or suppression of maternal adaptive response

  • peripheral WBC increase, even more in labor (20-30,000) but returns to nl in 1st week postpartum. Most of increase attributed to increased volume of circulating segmented neutrophils or granulocytes. Maybe contribution from estrogen and cortisol?
  • immune tolerance to developing fetus: maternal non-reactivity to paternal antigens in fetus
  • altered immune function rather than relative immunodeficiency (protec fetus from cytotoxic response and TH1 cells move away from cell-mediated and more towards humoral response. However may increase susceptibility to certain intracellular pathogens. (increased TH2, fewer TH1, NK cells–preserved or enhanced humoral immunity)
27
Q

Coagulation system in pregnancy

A
  • want to decrease hemorrhage, so increased total amounts of clotting factors. No evidence of increased coagulability due to clotting factors as measured by clotting times
  • increased risk of DVT/PE in pregnancy (significant increased venous pressure)

MARKED increase in procoagulants

  • factors I (fibrinogen), VII, VIII, IX, X
  • minimal increase in II, V
28
Q

Thromboembolic dz

A
  • Increased DVT/PE due to increased risk for stasis/coagulation, increased risk for DVT/PE, anatomic factors (L sided DVT > R)
  • PE one of leading causes of maternal mortality in US
  • Same standards for diagnosis as nonpregnant; spiral CT has replaced combo of ventilation/perfusion scan and pulmonary arteriogram
  • DVT and PE prophylaxis and tx during pregnancy (Past = unfractionated heparin, but NO: LMWH due to longer half life and consistent levels through dosing interval). often switch to unfractionated heparin at 36 weeks

COUMADIN CONTRAINDICATED– nasal hypoplasia, stippling of fetal bones, bradydactyly

Postpartum: Rx coumadin 6-12 weeks

29
Q

FUCKING SUMMARY

A
  • pregno = unique physiologic state
  • need to understand physiology changes for treatment of medical conditions in pregnancy
  • manage pts either by an experienced perinatologist/maternal fetal medicine specialist or an OB in conjunction with medical specialist important when chronic disease present
30
Q

GI tract in pregnancy

A
  • Increased caloric intake for net weight gain of 25-35 lbs in nl sized ppl
  • Ptyalism (increased saliva) in women with nausea/vomiting/hyperemesis in early pregnancy (increased production vs lower ability to swallow)
31
Q

Stomach changes

A
  • Decreased tone/motility 2nd to progesterone; decreased motilin
  • mixed evidence re decreased gastric emptying but seen in laboring women
  • lower PUD risk due to increased mucin/lower acid, increased placental histaminase and lower histamine, enhanced immune tolerance to H pylori
  • Increased GERD 30-50%: esophageal mdysmotility, decreased LES tone (prog), gastric compression from enlarging uterus
  • Early satiety (3rd trimester)
32
Q

Intestinal Changes

A
  • increased constipation or diarrhea due to enlarging uterus compressing rectum and Fe often taken for anemia
  • Reduced motility (progesterone was implicated but newer studies say estrogen; also NO from nerves relax muscles))
  • Large intestines: increased water/Na absorption –contributes to constipation
  • Superior displacement of intestines due to uterus enlargement; contributes to rising appendix position–important in dx of appendicitis in pregnancy
  • increased portal venous pressure causes increased hemorrhoidal vein size
33
Q

Gallbladder in pregnancy

A
  • after 1st trimester, fasting/residual volumes doubled
  • empties more slowly/incompletely
  • increased cholesterol saturation with decreased biliary chenodeoxycholic acid promotes gallstone formation and biliary sludge

Treat gallstones: low fat diet and maybe
elective cholecystectomy
- consider surgery after 1st trimester when cholecystitis has occurred or sxs persist
- laparoscopic approach before 3rd trimester
- surgery associated with less days in hospital/less preterm birth compared to those not having surgery

34
Q

Liver in pregnancy

A
  • size not changed
  • clinical and lab signs of liver dz may be present as NL finding in pregnancy
    (spider angioma/palmar erythema from estrogen, lower albumin/total protein, increased Alk phos 2-4x from placental isoenzymes production, increased TOTAL protein concentrations (fibrinogen, transferrin, thyroid hormones, vit D, drug concentrations–measure free levels)
  • besides alk phos, other LFTs WNL

CHOLESTASIS

  • most common induced liver disorder/ Itching over palms/soles then generalized itching WITHOUT RASH; assd with Hep C/multiple gestation
  • more common in S. america/europe
  • elevated bile acids
  • some have jaundice/mild transaminitis (monitor LFTs and PT/PTT)
  • fat malabsorption can cause vit K deficiency and prolonged PTT–supplement around34-36wks
  • monitor fetus–increased stillborn risk
  • treat itching w/antipruritics; ursodiol also effective
35
Q

Nausea/vomiting in pregnancy

A
  • complicates 70% pregnancies
  • usually begins 4-8 weeks and resolves by 14-16, correlating with betaHCG levels and increases with multiple gestations
  • usually not serious/requireing hostpialization
  • Supportive therapy with frequent small meals, avoid trigger foods, many meds/alternative therapies available –B6 +/- doxylamine)
  • hyperemesis gravidarum in 1-3%
    refractory n/v associated with weight loss, dehydration, electrolyte imbalance and ketonemia– may need hospitalization or IV therapy at home and antiemetics/bowel rest.
  • assd w/increased HCG (multiple gestation/molar pregnancy) and hyperthyroid); rule out other causes
36
Q

Physiologic skin changes

A
  • hyperpigmentation in 90% (areola, nipples, genital skin, axillae, darkened linea nigra, melasma)
  • HCG stimulates melanocyte stimulating hormone
  • vascular/connective tissue changes
  • increased blood flow to skin (increased 4-16x): spider angiomata, palmar erythema, gum hyperemia, leg varicosities
  • striae gravidarum (90% caucasians; less in AA, Asians; often associated with pruritis)