maternal physiology Flashcards

1
Q

maternal total body water, plasma volume, RBC volume

A

Increase in TBW from 6.5 to 8.5 L = 2 kg. Expanded plasma volume by 1.2 – 1.3 liters (50%). Expanded RBC volume 0.3 – 0.4 liters (30%). Additional extravascular fluid & intracellular fluid in uterus and breasts. Chronic volume overload with active sodium & water retention

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2
Q

What conditions does increased maternal body water predispose to

A

Increased TBW can cause weight gain, hemodilution, anemia of pregnancy, elevated cardiac output. Impaired volume expansion has been linked to increased risk of preeclampsia, and impaired fetal growth

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3
Q

maternal changes in osmoregulation

A

From 10 weeks to 2 weeks postpartum: Placental release of NO and relaxin alters AVP secretion (but plasma AVP is unchanged due to placental inactivation by vasopressinase). Water and sodium retention occurs (water > sodium), plasma osmolality decreases.

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4
Q

Maternal renin-angiotensin-aldosterone system

A

Marked increases in all components of RAAS. Early pregnancy changes cause decreased MAP which triggers activation of renin-angiotensin (4-5X) and aldosterone (2X). Sodium retention occurs. Deoxycorticosterone and estrogen may contribute to increased tubular Na retention.

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5
Q

Maternal Potassium levels

A

Potassium is increased, but nost is stored in placenta and fetus. The kidney’s ability to conserve potassium has been attributed to increased progesterone levels.

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6
Q

Maternal ANP/ BNP

A

Myocardium releases these neuropeptides that maintain vascular hemostasis. ANP/BNP elevated in both physiologic and path states of volume overload; ANP most likely increases but remain within normal range. BNP increases mostly in 3rd trim; highest in pregnancies complicated by preeclampsia but to levels less than used to screen for CHF, so BNP can still be used to screen for CHF in pregnancy.

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7
Q

What causes increased intracellular volume in pregnancy

A

is increased levels of progesterone which lead to decreased smooth muscle tone and increased volume capacity

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8
Q

maternal BP

A

•Progressively decreases until 22-24 weeks; returns to baseline at 36 weeks. Diastolic is affected more than systolic. This is due to decreased systemic vascular resistance (progesterone effect on smooth muscle and increased Nitric oxide production)

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9
Q

How to measure maternal BP

A

take sitting using Korotkoff 5 , when diastolic sound disappears, not Korotkoff 4, when it becomes muffled.

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10
Q

maternal cardiovascular adaptations

A
  1. Cardiac output increases 40%: Mainly an increase in stroke volume. HR increases (3rd trimester). 2. Vascular resistance drops (Second trimester): BP > 140/90 mm Hg represents hypertension in pregnancy. Cardiac output is greatest in left lateral position. Uterus compresses the vena cava—avoid supine positioning > 20 weeks.
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11
Q

Changes to the maternal heart

A

Hypertrophy of ventricular muscle, Increase in preload (end diastolic volume) due to increased venous return, Decrease in afterload due to decreased vascular resistance, increased cardiac compliance, increased myocardial contractility

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12
Q

maternal cardiac output

A

Increased due to increased HR and stroke volume. Affected by position: Greatest in left lateral position and knee chest position, Uterus compresses the vena cava so lying supine can cause dizziness, nausea, syncope. CO lowest in supine/standing position

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13
Q

Changes in perfusion

A

No change to brain or liver, but 50% increase in renal perfusion and increased perfusion of breasts, skin, uterus

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14
Q

complications of increased venous presure

A

Increases in venous pressure & pressure on vena cava contribute to edema, varicose veins, hemorrhoids & increased risk for DVT

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15
Q

maternal cardiac exam

A

Snus rhythm, BPM < 100, PMI displaced to left, systolic ejection murmur along left sternal border in most (due to increased flow across pulmonary and aortic valves), split S1 (less so with S2), S3 common in third trimester (rapid diastolic filling). S4 rare.

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16
Q

maternal CXR

A

the apex is displaced laterally and increases in the pulmonary vasculature. Left heart border more straight. Heart more horizontal.

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17
Q

Maternal EKG

A

mild left axis deviation and nonspecific ST and T wave changes. Small Q wave and negative P wave in lead III. premature atrial and premature ventricular contractions may occur. Almost all women have an arrhythmia during labor.

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18
Q

List the maternal changes in HR, CO, SVR, CVP, PCWP, PAP and MAP

A

HR increases (20%), CO increases (1.5-2L), SVR decreases, CVP decreases, PCWP unchanged, PAP decreases, MAP decreases

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19
Q

Cardiac output during labor

A

Increases (most during second stage), highest right after delivery. This is due to Pain: increased sympathetic stimulation. Uterine autotransfusion: 300-500 cc of blood is forced from the uterus into the systemic circulation during each contraction.

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20
Q

physiology of 2nd stage of labor (cardio effects)

A

Straining phase: increased intrathoracic pressure causes decreased venous return to heart. This combined with elevated SVR causes a transiet reflex bradycardia and decreased CO. Sympathetic discharge causes increased HR and contractility, maintaining cardiac output

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21
Q

Physiology of relaxation phase of valsalva

A

decreased intrathoracic pressure > rapid increase in preload > increased MAP > reflex bradycardia

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22
Q

postpartum cardiovascular changes

A
  1. Acute increase in CO for first hour- Decreased venocaval obstruction, Autotransfusion from uterine circulation, Mobilization of extravascular fluid. 2. Acute loss of up to 500 (vaginal) or 1000 cc (C section) blood with normal delivery. 3. Changes return to prepregnant baseline over a period of wks-mos
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23
Q

Which heart diseases are tolerated better during pregnancy

A

Regurgitant lesions are better tolerated during pregnancy than stenotic lesions b/c regurgitatant lesions usually compensate by increasing volume anyways

24
Q

Aortic stenosis peak gradients

A

Mild < 36 mm Hg, Moderate 36-63 mm Hg, Severe > 63 mm Hg (Sometimes defined > 50)

25
Q

Aortic stenosis management in pregnancy

A

At baseline need to keep preload adequate for CO. Avoid vasodilators. Consider early delivery if pt decompensates. During labor- careful fluid balance, early epidural to decrease epi effects on BP/ CO. Assisted second stage to shorten this period which can tip them into heart failure or arrythmias

26
Q

pre-eclampsia

A

•new hypertension and proteinuria, edema

27
Q

complications of pre-existing HTN

A

•Intrauterine growth retardation.

28
Q

maternal ventilation

A

•Progesterone increases sensitivity of respiratory center to C02 resulting in hyperventilation. This is accomplished by increasing tidal volume, while the respiratory rate remains stable.

29
Q

maternal oxygenation

A

oxygen consumption increases, PaO2 increases

30
Q

maternal acid-base balance

A

pH increases (decreased CO2), serum bicarb decreases. Primary respiratory alkalosis with compensatory metabolic acidosis

31
Q

Maternal mechanical Respiratory Adaptations to Pregnancy

A

Early in pregnancy (before pressure from uterus): Subcostal angle increases, Chest AP diameter increases, Chest circumference increases. Later in pregnancy: Diaphragm pushed up by 4 cm, Diaphragmatic excursion increases 1-2 cm, Breathing becomes more diaphragmatic than costal

32
Q

maternal respiratory volume changes

A

Increased tidal volume (increased minute ventilation and O2 uptake). Forced vital capacity unchanged. Residual volume decreased (due to elevated diaphragm), expiratory reserve volume decreases, inspiratory reserve volume unchanged, functional residual capacity reduced. FEV1 and FVC are unchanged (implies no change in large airway function)

33
Q

What causes dyspnea during pregnancy

A

–Reduced PaCO2 levels, awarenes of increased TV, increased ventilation-perfusion mismatch (shunting)

34
Q

Which therapies for asthma are safe during pregnancy

A

Inhaled beta agonists, steroids, cromolyn. Oral steroids. Certain antibiotics to treat infections such as penicillins, cephalosporins, macrolides

35
Q

What are the values for pH, pO2, pCO2 and bicarb in pregnancy

A

pH: 7.4-7.45 (nl 7.4). pO2: 100-108 (nl 95-100). pCO2: 27-32 (nl 37-40). bicarb: 18-21 (nl 24-29)

36
Q

treatment for acute asthma attack during pregnancy

A

If pCO2 > 32mmHg consider albuterol nebulizor (can cause increased fetal heart rate) or steroid taper. May need IV steroids during labor due to adrenal suppression if given steroid taper

37
Q

kidneys during pregnancy

A

Enlarged - Increased vasculature, interstitial volume and urinary dead space (dilation of renal pelvis, calyces and ureters). Relative hydronephros of pregnancy is greater in right side and begins in 2nd month. Caused by mechanical compression of uterus plus smooth muscle relaxation triggered by progesterone. resolves by 6 weeks postpartum

38
Q

urinary tract during pregnancy

A

Increased risks of pyelonephritis during pregnancy due to urinary stasis and asymptomatic bacteriuria (right greater than left). Also decreased bladder capacity (uterus compression) but increased urine volume. Treat asymptomatic lower UTIs to prevent pyelo which has increased complications such as ARDS and preterm labor. Increased nocturia and microhematuria (increased vascular supply)

39
Q

how does renal physiology change with pregnancy

A

Increased GFR by 50%, increased renal plasma flow. Filtration fraction (GFR/ RPF) decreases. These changes are due to NO and relaxin. Increased GFR plus increased plasma volume leads to decreased serum Cr and BUN.

40
Q

Risk of pre-existing renal insufficiency during pregnancy

A

Risk of worsening renal dz, pre-eclampsia, intrauterine growth restriction, PTB

41
Q

treatment of renal insufficiency during pregnancy

A

Baseline 24 hr Cr and protein. Treat underlying condition. Serial ultrasounds to assess fetal growth. Start fetal monitoring at 32 weeks

42
Q

maternal platelets

A

hemodilution occurs- thrombocytopenia seen in small proportion.

43
Q

WBC changes during pregnancy

A

Increases- 8000 in first trimester, 8500 in second, upt to 30,000 during labor without evidence of infection. Returns ton ormal first week postpartum. Most of the increase is due to increased neutrophils

44
Q

maternal immune system changes

A

Altered immune function- Shift from TH1 towards TH2 to protect fetus from cytotoxic maternal immune response. This increases susceptibility to intracellular pathogens (CMV, herpes, varicella) and may improve conditions like RA. Lupus, TH2 related, flares during pregnancy.

45
Q

Maternal coagulation system

A

The coagulation factors are increased in total amounts, though the concentration in the serum is not dramatically affected. This increase is secondary to increased production in the liver secondary to stimulation by estrogen. Increased risk of DVT and PE. Factors I, VII, VIII, IX and X increase. II, V and XII stay same. Protein C stays Constant. Protein S sinks. Decrease in fibrinolytic system. PT/ PTT/ thrombin time drop within nl range. Whole blood clotting unchanged.

46
Q

Which side is more common to have a DVT during pregnancy

A

left- Right proximal common iliac artery overlies the bifurcation of the IVC and primarily compresses the left common iliac vein

47
Q

treatment/ prevention of DVT and PE during pregnancy

A

LMW heparin is standard. Switch to unfractionated heparin at 36 weeks. Coumadin contraindicated

48
Q

GI tract changes in pregnancy

A

Increased caloric intake, Ptyalism (increased saliva production) in women with nausea/vomiting/ hyperemesis in early pregnancy. No change in dental caries.

49
Q

stomach changes during pregnancy

A

Decreased tone and motility (progesterone and motilin mediated), decreased emptying during labor, decreased risk of peptic ulcer dz (Increased gastric mucin, decreased gastric acid, enhanced immune tolerance to H. pylori), increased risk of GERD (esophageal dysmotility, decreased tone of lower esophageal sphincter, gastric compression from uterus)

50
Q

Intestine changes during pregnancy

A

Constipation in some, diarrhea in others (uterus compresses rectum). Reduced small intestine motility (progesterone). Increased water/sodium absorption. Displacement of intestines superiorly 2o enlarging uterus contributes to rising position of appendix. Increased hemorrhoidal vein size (increased portal venous pressures)

51
Q

Gallbladder changes during pregnancy

A

GB size doubles and empties more slowly during first trimester. Increased biliary cholesterol saturation with decreased. Promotes formation of gallstones

52
Q

Treatment of gallstones

A

Low fat diet and possibly elective cholecystectomy. Surgery considered after 1st trimester when cholecystitis has occurred or symptoms persist

53
Q

Liver changes during pregnancy

A

liver size unchanged. Spider angioma and palmar erythema secondary to estrogen. Decreased serum albumin and total protein (hemodilution). Increased serum alk phosphatase (placental production). Other LFT WNL. Increased total concentration of fibrinogen, transferrin, thyroid hormones, Vit D, drugs

54
Q

nausea/vomiting during pregnancy

A

From week 4-16. Correlates with beta HCG levels and increases in multiple gestation. Supportiv therapy.

55
Q

Hyperemesis gravidarum

A

•Refractory nausea/vomiting associated with weight loss, dehydration, electrolyte imbalance and ketonemia. Caused by elevated HCG, also hyperthyroidism, pancreatitis, gallstones, hepatitis, psych illnesses

56
Q

Cholestasis of pregnancy

A

Itching over palms and soles then generalized itching without rash. Elevated serum bile acids, juandice in 20%. Malabsorption of fat may cause Vit K deficiency and prolonged PTT (supplement around 34-36 weeks). Increased risk of stillbirth.

57
Q

skin changes during pregnancy

A

hyperpigmentation of areolae, nipples, genital skin, axilla. Darkening of linea nigra. Melasma (mask of pregnancy). HCG stimulates melanocyte stimulating hormone. Increased blood flow to skin cn lead to spider angiomata, palmar erythema, leg varicosities, gum hyperemia.