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Obstetric Physiology

Dr Maddi Anupindi February 28, 2020 72


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Outline the cardiovascular, respiratory, haematological and genitourinary changes that occur during pregnancy

Cardiovascular: these include effects on cardiac output and mechanical effects

  • Cardiac output
    • Stroke volume:  increases by 20-30%, mainly in the first trimester
    • Heart rate: increases as early as 4 weeks after conception and increases by 17% at the end of first trimester and 25% by the middle of the third trimester with no further subsequent increase.
    • Preload: Increase in plasma and blood volume mainly occurs during the 1st and 2nd trimester. The ECF increases by 45% due to sodium and water retention as a result of increased oestrogen and activation of the renin-angiotensin system. Blood volume begins to increase in the first trimester and increases by about 35-40% by the end of pregnancy.
    • Afterload: Total peripheral resistance decreases by 30% at the end of the first trimester and 35% by the 20th week and remains at 30% below non-pregnant values due to the effect of increased progesterone and prostaglandins causing vasodilatation and smooth muscle relaxation. This results in decreased blood pressure with systolic and diastolic pressures decreased by about 10% and reaching their lowest values at about 20 weeks. The vascular system also becomes more refractory to the effects of vasoconstrictors.
    • As a result of the above factors cardiac output increases during pregnancy to 40-45% greater by 12-28 weeks and a peak of 50% during weeks 32-36 followed by a slight decrease to 47% greater at term. This is mainly due to increased venous return secondary to venodilatation and increased vascular volume. A large proportion of this increased cardiac output is directed to the uteroplacental circulation which receives up to 10 times increased blood flow to about 750ml/min at term.
  • Mechanical effects:
    • The heart is more rotated to the left and can result in q waves and TWI in the inferior leads on ECG.
    • Oedema occurs due to a 14% decrease in colloid oncotic pressure and the mechanical effects of the enlarging uterus compressing lymphatics
    • The uterus can also cause aortocaval compression when the patient is lying on her back resulting in hypotension and nausea.

Respiratory: these include changes to the airways, changes to ventilation, changes to lung volumes and changes in respiratory mechanics

  • Airway
    • Hyperaemia and oedema of the mucosal surfaces in the airway which can result in difficult intubation
    • Dilatation of the large airways which decreases airway resistance by about 35%
    • Anatomical dead space increases by 45%
  • Ventilation
    • Minute ventilation increases by 20 – 50% at due to an increase in respiratory rate and increase in tidal volume due to the effects of progesterone which stimulates the respiratory centre. This results in chronic respiratory alkalosis on ABG with a baseline pH of 7.47 a paco2 of 30 – 32 and renal compensation with a HCO3 of 18-21
    • Oxygen consumption increases by about 20%
  • Lung volumes
    • Tidal volume increases in the first trimester and rises to about 30% at term
    • Functional residual capacity decreases by 20% due to the elevation of the diaphragm and increase in pulmonary blood volume. In the supine position at term the FRC decreases to 70% of the FRC in the sitting position.
    • Inspiratory capacity increases by 10% at term while the expiratory capacity decreases by 5%
    • Total lung capacity decreases by approximately 5%
  • Respiratory mechanics
    • Diaphragm is pushed upwards by about 4cm by end of term
    • Chest wall compliance decreases whilst lung compliance does not change
    • AP and transverse diameters of thoracic cage increase 2-3%, lower ribs flare out, subcostal angle increases
    • Circumference of thoracic cage increased by 5-7cm due to the effects of relaxin produced by the corpus luteum

Haematological: include changes to coagulation and changes to full blood count

  • Coagulation factors
    • Significant increase in factors 5, 7, 8, 9, 10, 12, von Willebrand factor and fibrinogen
    • Decrease in factor XI to 60-70% of non-pregnant value
    • Protein S levels decrease during pregnancy
    • Plasminogen markedly raised. This is offset by plasminogen activator inhibitors produced by placenta
  • Full blood count
    • Physiological anaemia of pregnancy due to dilutional decrease in Hb
    • Relative leukocytosis
    • Greater platelet production but overall platelet count slightly reduced due to increased destruction in the uteroplacental circulation
    • RBC volume increases by 20% due to increased erythropoietin. However, there is a slower rate of rise in red cell mass compared with plasma volume resulting in a decreased haematocrit 

Genitourinary: mechanical changes and changes to blood flow

  • Mechanical
    • At 12/40 bladder becomes an abdominal structure and compression by the enlarging uterus can result in urinary frequency
    • Dilatation of renal pelvis, calcyces and ureters begin within 2-3 months resulting in physiological hydronephrosis
  • Blood flow
    • Gfr increases by up to 80% resulting in decreased urea and creatinine
    • Renal blood flow increases by 80% during first trimester and there is decreased tubular resorption of urate and glucose

List the functions of the placenta

The placenta is a fetomaternal organ which consists of the fetal part that develops from the chorionic sac and the maternal part which develops from the decidua basalis of the endometrium. It connects the developing fetus to the uterine wall. Placental development begins at 6 weeks and is completed by the 12th week. The placenta has four main functions; transport, immunological, metabolic and endocrinological.

  • Transport: this is one of the main functions of the placenta. It transports the following substances
    • Gases: delivers oxygen to the fetus and removes carbon dioxide from the fetal circulation
    • Nutrition: delivers water and nutrients including glucose, amino acids, fatty acids, calcium, iron, folate and vitamins A and C.
    • Drugs
    • Heat
    • Removes waste products such as urea and bilirubin
  • Immunological
    • Provides passive immunity to the fetus as the placenta is selectively permeable to IgG, but not IgA or IgM
    • Provides a barrier between the fetal blood in the chorionic villi and the maternal blood in the intervillous spaces. There is little HLA and blood group antigens on the trophoblast surface so there is poor antigenic stimulus.
    • Protects fetus from some substances: those with large molecular weight or size such as heparin are not transferred
  • Metabolic:
    • Synthesis of glycogen from maternal glucose and then stored
    • Synthesis of cholesterol which is a precursor to placental progesterone and estrogen
    • Synthesis of protein: up to 7.5g/day
    • Synthesis of fatty acids
  • Endocrine
    • Synthesis of multiple hormones including:
      • BHCG: a glycoprotein which supports the corpus luteum in the first 10 weeks of pregnancy. It also suppresses maternal immune function.
      • Oestrogens: has multiple effects including stimulation of growth of the myometrium and mammary gland development. It also suppresses gonadotropin secretion from the maternal pituitary gland.
      • Progesterone: supports the endometrium and suppresses uterine contractility. Both oestrogen and progesterone are responsible for the majority of the maternal changes in pregnancy.
      • Human placental lactogen: involved in regulation of nutrient supply to the fetus. It inhibits gluconeogenesis, is lipolytic thus increases free fatty acids, promotes growth and has a lactogenic effect. It is structurally similar to growth hormone
      • Hypothalamic and pituitary like hormones: include chorionic thyrotropin, chorionic adenocorticotropin, gonadotrophin releasing hormone,
      • Others such as inhibin, relaxin, beta endorphins

Outline the determinants of placental blood flow

Placental blood flow consists of a maternal and fetal part.

Maternal or utero-placental circulation:

The maternal blood supply to the uterus is via the uterine and ovarian arteries which then form the arcuate arteries from which radial arteries divide and penetrate the myometrium. The radial arteries then divide into spiral arteries which supply the intervillous space.

Fetal-placental circulation:

The basic structural unit of the placenta is the choronic villus which are vascular projections of fetal tissue surrounded by chorion. The chorion is composed of an outer syncytiotrophoblast in direct contact with maternal blood within the intervillous space, and the inner cytotrophoblast. The villous capillaries are branches of the chorionic arteries which are branches of the two umbilical arteries which bring blood from the fetus to the placenta. Oxygenated blood then leaves the placenta via the umbilical vein.

Determinants of utero-placental circulation:

  • Blood pressure: Flow is passive and pressure dependent not auto-regulated: pressure is about 80-100mmHg in uterine arteries, 70mmHg in spiral arteries and just 10mmHg within the intervillous space. This low-resistance and pressure gradient allows efficient maternal blood perfusion. Consequently, hypotension will decrease the utero-placental circulation
  • Vasoconstrictors: utero-placental circulation exist in a state of vasodilatation so vasodilator stimuli have minimal effect. Vasoconstrictors such as alpha adrenergic stimuli, sympathomimetic agents and severe hypoxemia can reduce placental blood flow
  • Myometrial contraction: decreases placental blood flow as the intervillous space lies within the uterine cavity and contraction will result in increased pressure within this space and therefore decreased perfusion pressure.

Determinants of fetal-placental circulation:

  • Gestational age: umbilical blood flow increases as the fetus grows
  • Umbilical blood flow is increased during fetal movements
  • Placental vascular resistance: increased vascular resistance decreases blood flow therefore vasoconstrictors can decrease placental blood flow
  • Fetal cardiac output

List the mechanisms of transport across the placenta

Mechanism of transport across placenta:

  • Diffusion
    • Governed by Fick’s law of diffusion where rate of diffusion is proportional to surface area and concentration gradient and inversely proportional to membrane thickness
    • Examples include water, electrolytes and gases
  • Facilitated diffusion
    • Transport by specific carriers down a concentration gradient and does not require energy expenditure – glucose is transported in this manner via hexose transporters.
  • Active transport
    • Mediated by specific protein carrier, occurs against a concentration or electrochemical gradient, involves energy expenditure
    • Examples include amino acids, calcium and iron
  • Piniocytosis
    • Only way to transport molecules which are large, non-lipid soluble and/or do not have a carrier. The substance becomes completely enveloped into invaginations of the membrane and is then released on the other side of the cell.
    • Examples include globulins, phospholipids, lipoproteins, IgG antibodies

What is the Double Bohr and Double Haldane effect?

Oxygen transfer from the maternal to the fetal circulation is via simple diffusion down a partial pressure gradient of 30mmHg. This oxygen transfer is facilitated by fetal haemoglobin which has a higher affinity for oxygen compared to adult haemoglobin and has a left shifted oxygen haemoglobin dissociation curve. Furthermore, the haemoglobin concentration of fetal blood is approximately 50% greater than that of maternal blood, thus increasing oxygen transport. The Bohr effect states that increases in the partial pressure of carbon dioxide of blood or a decrease in pH will lead to a rightward shift of the oxygen-haemoglobin dissociation curve thus decreasing the affinity of haemoglobin for oxygen. The Double Bohr effect describes this happening in opposite directions in the maternal and fetal circulations. Within the feto-placental circulation, blood is releasing co2 down its concentration gradient from fetal to maternal blood. The fetal blood is thus becoming more alkaline leading to a leftward shift in the o2-hb dissociation curve and increasing the fetal haemoglobin’s affinity for oxygen. Conversely, within the utero-placental circulation the maternal blood is gaining co2 leading to a right shift of the o2-hb curve and encouraging oxygen release from maternal haemoglobin.

The Haldane effect describes the effect of oxygen on co2 carriage with deoxygenated haemoglobin having a greater affinity for carbon dioxide. The Double Haldane effect refers to the fact this happens in opposite directions within the fetal and maternal interface. Within the utero-placental circulation oxygen is lost thus increasing haemoglobin’s affinity for carbon dioxide. Conversely within the feto-placental circulation, oxygen is gained thus decreasing haemoglobin’s affinity for c02.

List the differences in the respiratory system between newborns and adults

The differences can be divided into anatomical, lung mechanics, lung volumes and respiratory control.

Anatomical: can be sub-divided into upper and lower airways.

Upper airways:

  • Narrow nasal passage
  • Large tongue
  • Obligate nasal breathers à obstruction can cause respiratory distress
  • Epiglottis is stiff, relatively larger, U shaped and angled back at about 45 degrees – C1 in children C3 in adults
  • Glottis is high: C3-4 (C5-6 in adults) with anterior angulation
  • Cricoid is usually narrowest part until age 8 (then becomes vocal cords) – subglottic oedema can cause severe respiratory distress
  • Cricoid opposite C4 (C6 in adults)
  • Thyroid cartilage flat and overlying cricoid cartilage and hyoid bone overlies it à space difficult to discern

Lower airway

  • Trachea is short 4-5cm (12cm in adults), diameter 6mm (2cm in adults)
  • Right main bronchus is more directly in line with trachea than left side à increased risk of right main intubation
  • Peripheral airways with diameter less than 2mm contribute 50% of airway resistance (contribute only 20% in adults) à can cause severe resp distress in disease
  • Less bronchial muscle present à bronchospasm is uncommon

Lung mechanics:

  • Chest wall is highly compliant (necessary to allow passage through birth canal) à ribs and sternum primarily cartilage so poor chest wall stabilisation
  • Ribs are horizontal – no bucket handle/pump movements during breathing à minimal thoracic component to breathing
  • Breathing is largely diaphragmatic but horizontal insertion of diaphragm and low proportion of high oxidative capacity fibres mean it is susceptible to fatigue à abdominal distension causes resp distress
  • Alveolar ventilation is 120-140ml/kg/min (twice that of adult) and have short time constants – work of breathing is thus minimised at high respiratory rates rather than large tidal volumes
  • Ratio of inspiration: expiration is 1:1

Lung volumes and gas exchange:

  • FRC is 30ml/kg (same as adult) – but less stable and more prone to atelectasis
  • FRC is less than closing capacity – gas trapping due to closure of small airways occurs during normal ventilation à alveolar-arterial po2 gradient is increased (30mmHg compared to 5mmHg) due to venous admixture
  • Oxygen consumption is higher on weight basis 6-7ml/kg/min compared to 3-3.5m/kg/min in adults à increased metabolic rate and consequent increased o2 demand is aided by high alveolar ventilation, high cardiac output and distribution of high percent of CO to metabolically active tissues

Respiratory control:

  • Less developed especially in premature babies
  • Periodic respirations are common – pauses 5-10 seconds during sleep up to 6x/night normal

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