Part I FCA preparation
Anatomical & physiological changes
in pregnancy
Body composition
• ↑ metabolic rate
• ± 12 kg weight gain (T1 1-2kg; T2&T3 5-6kg each)
- uterus, 1 kg;
- amniotic fluid, 1 kg;
- fetus and placenta, 4 kg;
- blood volume & interstitial fluid (approximately 2 kg
each);
- new fat & protein (approximately 4 kg)
• DEPRESSING FACT: The OR for CS are 1.46, 2.05, and 2.89 for
overweight, obese, and severely obese women, respectively,
compared with pregnant women of normal weight.
Endocrine function
• Principal hormone is progesterone
- initially, placental production of β-hCG sustains the corpus
luteum, enabling it to produce progesterone
- from 6-8 weeks, the placenta takes over
progesterone production
• Human placental lactogen is produced by the placenta
- similar effects to growth hormone; may be the cause of
maternal insulin resistance
- may be cause of acromegalic-like changes in pregnancy
• Thyroid gland hypertrophy
Endocrine
functionthyroid
• ↑ T3 and T4
• ↑ TBG production
free hormone
levels unaltered
• ↓ PTH levels
• ↓ serum calcium level
• constant ionized Ca levels due to
changes in serum albumin
Endocrine function- pancreas
•
Hypertrophy and hyperplasia of the B cells
•
Fasting associated with accelerated starvation
– maternal hypoglycemia, hypoinsulinemia and hyperketonemia
– due to diffusion of glucose by the fetoplacental unit
•
Feeding response
– hyperglycemia, hyperinsulinemia, hypertriglyceridemia and reduced
tissue sensitivity to insulin
– glucose response greater during pregnancy
– peripheral resistance to insulin: diabetogenic effect of pregnancy.
• hPL and cortisol mediated
• greater insulin resistance as the pregnancy advances
•
Fetus primarily depends on glucose
– Facilitated diffusion (carrier-mediated but not energy dependent
process)
Respiratory system
• Major changes- hormonal & mechanical factors
• Difficult intubation much more common at term- bigger
breasts, airway mucosal oedema, need for smaller ETT, nasal congestion
with epistaxis risk
• Hyperventilation due to increased VT (40%) and lesser
increase in respiratory rate (15%)  slight drop in PaCO2 
mild, partially-compensated respiratory alkalosis
• Heightened oxygen consumption (up to 60% during labour)
• FRC decrease by 20% (and even more when supine!)
- After midgestation, the supine position frequently results in a PaO2
less than 13.2 kPa.
Why? The FRC may be less than closing capacity, resulting in
closure of small airways during normal tidal volume ventilation.
Respiratory system: Mechanics
• Configuration of thoracic cage changes early on
- increase in subcostal angle, transverse diameter and
circumference of chest
• With advancing gestation, the level of diaphragm is pushed
up by 4 cm
So…. Inspiration at term is almost totally attributable to
diaphragmatic excursion.
Why? Because of a greater descent of the diaphragm from its elevated resting
position and limitation of thoracic cage expansion because of its expanded resting
position.
Effects of pregnancy on respiratory mechanics
•
•
Both large- and small-airway function are minimally altered during pregnancy.
The shape of flow-volume loops, the absolute flow rates at normal lung volumes, FEV1,
and the FEV1/FVC ratio are unchanged during pregnancy, as is closing capacity.
Lung volumes and capacities
•
•
•
FRC falls from the fifth month and is decreased to 80% of the
prepregnancy capacity by term.
Diaphragm elevation  25% ↓ in ERV and a 15% reduction in RV,
accounts for the change.
Assumption of the supine position causes FRC to decrease further
to 70% of the prepregnancy volume.
The ABG in pregnancy
Non-pregnant
T1
T2
T3
pH
7.40
7.44
7.44
7.44
pCO2 (kPa)
5.26
3.95
3.95
3.95
pO2 (kPa)
13.16
14.08
13.82
13.55
HCO3 (mEq/L)
24
21
20
20
Ventilation & blood gases
• ↑ minute ventilation – due to progesterone & 30% ↑ CO2 production
• CO2 response: progesterone  ↑CO2 chemosensitivity  steeper
slope & leftward shift of the CO2 ventilatory response curve; early
change
- PaCO2 ↓ to 4 kPa by 12/40; thereafter ≈
• Hypoxic ventilatory response: ↑ two-fold by oestrogen and
progesterone , despite blood and cerebrospinal fluid (CSF) alkalosis.
• PaO2 ↑ to 13.2 – 13.8 kPa as a result of greater alveolar ventilation.
• As pregnancy progresses, oxygen consumption continues to increase,
and cardiac output increases to a lesser extent  reduced mixed
venous oxygen content and increased arteriovenous oxygen difference.
Blood volume changes
•
•
Plasma volume expands by about 50% from 6/40 to 34/40; thereafter stable.
Increased volume of distribution results in a prolonged elimination half life for
many drugs
•
Red blood cell volume falls in the first 8 weeks, returns to the prepregnancy
level by 16 weeks, and then rises to 30% above the prepregnancy volume at
term.
•
The plasma volume expansion increase exceeds that of the red blood cell
volume increase, resulting in the physiologic anaemia of pregnancy.
•
Why? Facilitated delivery of nutrients to the fetus, maternal protection from
hypotension, reduced risks associated with haemorrhage at delivery.
Decreased blood viscosity  lower resistance to blood flow, which helps
maintain the patency of the uteroplacental vascular bed; also reduced cardiac
work.
•
Plasma volume expansion mediated by: oestrogen, progesterone, fetal
dehydroepiandrosterone, adrenomedullin
Cardiac structural changes
• Eccentric LVH (like in exercise!) seen from 12/40; LV mass
increases by 23% from T1 to T3.
• Increase in size of pre-existing cardiomyocytes rather than in the
number of cells.
• Cardiac dilatation causes significantly-increased annular
diameters of the mitral, tricuspid, and pulmonic valves; 94% of
term pregnant women exhibit TR and PR, and 27% exhibit MR.
The aortic annulus is not dilated
Cardiac output
•
•
•
Measurable ↑ by 5/40 due to ↑ HR; 35-40% ↑ by the end of T1
↑ through T2 to ± 50% above non-pregnant values
Maximum of 6 L/min peaks at 18-24/40; then sustained through T3
How is the ↑ CO achieved?
• Heart rate ↑ 15% to 25% over baseline by the end of T1 and does not change
during T3.
• Stroke volume ↑ ± 20% between 5-8/40, and by 25% to 30% by the end of T2,
then sustained until term. Mediated by oestrogen
•
•
Normal diastolic ventricular function
Supranormal systolic function in T2  ↑EF
Cardiac output
• ↑ CO → ↑ perfusion to the uterus, kidneys, and
extremities.
• Blood flow to the brain and liver do not change.
• Uterine blood flow increases from around 50 mL/min
to 700 to 900 mL/min at term; 90% to IVS and 10% to
myometrium
• Cutaneous blood flow increases to approximately three
to four times the nonpregnant level, resulting in higher
skin temperature.
• Renal plasma flow is increased by 80% at 16 to 26
weeks’ gestation but declines to 50% above the
nonpregnant baseline at term
Blood pressure & vascular resistance
• Development of a low-resistance vascular bed (the intervillous space)
as well as vasodilation caused by prostacyclin, estrogen, and
progesterone → ↓ SVR
• SVR ↓ in early gestation, lowest value at 20/40 (35% decline), and rises
during late gestation to ± 20% below the nonpregnant level at term.
• SBP, DBP and MAP decrease during mid-pregnancy and return toward
baseline as the pregnancy approaches term.
• DBP falls more than SBP, with early to mid-gestational decreases of
approximately 20%.
Aortocaval compression
•
•
Caval compression
- evident in supine position from 13-16/40
-venous blood diverted via collaterals, particularly via the
vertebral venous plexus which drains into the azygous system
- at term, caval compression almost complete; collateral VR
reduced → ↓ RAP → 10-20% decrease in SV and CO
Aortic compression
- Angiography in supine pregnant women shows partial aortic
obstruction at the level of the lumbar lordosis and enhanced
compression during periods of maternal hypotension
Up to 15% of women at term experience bradycardia and a substantial
drop in blood pressure when supine, the so-called supine hypotension
syndrome. It may take several minutes for the bradycardia and hypotension
to develop, and the bradycardia is usually preceded by a period of
tachycardia.
Labour & postpartum cardiac physiology
•
Cardiac output during labour increases from prelabour measurements:
10% in the early first stage
25% in the late first stage
between contractions
40% in the second stage
•
With contractions: 300-500 mL of blood autotransfused from the intervillous space via the
ovarian veins into the central circulation
•
In the immediate postpartum period, cardiac output rises by another 10-20% and may be as
much as 75% above pre-delivery measurements.
Why? Increase in stroke volume- due to relief of vena caval compression, diminished lower
extremity venous pressure, and a reduction of maternal vascular capacitance, as well as
alterations in sympathetic nervous system activity.
•
•
24 hours postpartum: CO back to prelabour measurements
Back to pre-pregnancy levels between 12 and 24 weeks postpartum
•
Heart rate falls rapidly after delivery, reaches the pre-pregnancy rate by 2 weeks postpartum,
and is slightly below the pre-pregnancy rate for the next several months.
•
Other anatomic and functional changes of the heart are also fully reversible.
Haematology: plasma proteins
• ↑ plasma volume  reduced plasma protein concentration from
approximately 7.8 to 7.0 g/dL. The pharmacokinetics of protein
bound drugs are affected.
• Albumin levels drop to about 35 g/dl.
• Colloid oncotic pressure ↓ by 5 mm Hg (explains the oedema
seen in pregnancy).
• The plasma cholinesterase levels decrease by about 25%
reaching their nadir post-partum. Therefore, suxamethonium
may have a slightly prolonged duration of action.
Haematology: coagulation
•
Enhanced platelet turnover, clotting, and fibrinolysis – represents
activation of the clotting system; seen on TEG
•
Platelet aggregation is increased. So-called gestational thrombocytopenia
appears to be an exaggerated normal response.
•
The concentrations of most coagulation factors, including fibrinogen (factor
I), factor VII, factor VIII, factor IX, factor X, and factor XII, rise during
pregnancy, in some by over 100%
Prothrombin (factor II) and factor V concentrations ↔
Factor XI and fibrin-stabilizing factor (factor XIII) concentrations ↓
•
•
•
↑ fibrin degradation products & the marked rise in the plasminogen
concentration indicate enhanced fibrinolysis.
Immune function
• Significant ↓ serum [IgM & IgG] from 10/40; nadir at 30/40, then
plateaus
• Reduced effectiveness of NK-cell activity
• Normal T-cell function and activity
• More prone to infection, hence flu vaccine recommended
• LEUKOCYTES
– Peripheral WBC rises progressively during pregnancy
•
1st ∆ – mean 9500/mm3 (3000-15,000)
•
2nd and 3rd ∆ – mean 10,500 (6000-16,000)
•
Labour – may rise to 20-30,000
– Rise is due to increase in PMNLs (demargination)
Renal adaptation
RENAL HAEMODYNAMICS
Effective renal plasma flow (ERPF) and GFR increase: ↑ RPF ˃ ↑ GFR
 filtration fraction falls, but returns to normal by late T3
Creatinine clearance increases to 150-200 ml/min, beginning by 5/40
Increased GFR decline in serum urea and creatinine
Kidney enlargement
- increased renal vascular and interstitial volume, R>L
Ureteral and renal pelvis dilatation by 8 weeks, R>L
mechanical compression by uterus and ovarian venous plexus
smooth muscle relaxation by progesterone
Renal adaptation
•
•
SALT AND WATER METABOLISM
– Plasma osmolality begins to decline by 2 weeks after conception
• reduction in serum sodium and other anions
– Sodium loss during pregnancy
• 50% rise in GFR
• Progesterone: natriuresis
– Renal tubular reabsorption of Na+ increases (aldosterone, estrogen and
deoxycorticosterone)
– Sodium homeostasis: net Na+ accumulation of 900 – 1000 mEq
NUTRIENT EXCRETION
– Increase in glucose excretion
• 1-10 g glucose excretion per day
– Due to 50% increase in GFR, reabsorption rate unchanged
– Increase in amino acid excretion during gestation
• no increased protein loss (100-300 mg/24 hr)
– Increased urinary loss of folate and vitamin B12
Gastrointestinal physiology
• Oesophageal peristalsis and intestinal transit are slowed during
pregnancy.
• Oesophageal barrier function is impaired: displacement of the intraabdominal segment of the lower esophagus into the thorax 
reduction in tone of the lower esophageal high-pressure zone (LEHPZ),
plus progesterone-induced relaxation of the LEHPZ.
• In T2 and T3, LEHPZ pressure gradually falls to approximately 50% of
basal levels, reaching a nadir at 36 weeks’ gestation and returning to
prepregnancy levels at 1 to 4 weeks postpartum
• Gastric emptying only slows during labour, when gastric volumes
increase (and pH increases- less acid!)
• Gastric emptying is delayed during the early postpartum period but
returns to prepregnancy measurements by 18 hours postpartum.
Liver
•
•
•
•
Liver does not enlarge
Hepatic blood flow remains unchanged
– CO to the liver decreases by ~35%
Spider angiomata and palmar erythema
– elevated estrogen levels
Lab data
– Drop in serum albumin
– Rise in serum alkaline phosphatase
• placental production and some hepatic production
– Rise in serum cholesterol, fibrinogen, caeruloplasmin,
binding proteins for corticosteroids, sex steroids, thyroid
hormones, and vitamin D
– Slight increase in LDH, AST, ALT ; serum bilirubin
unchanged
– 30% reduction in plasma cholinesterase levels
Nervous system
•
•
•
•
•
Decreased LA requirements
– increased nerve sensitivity, decreased epidural & subarachnoid volumes,
exaggerated lumbar lordosis, acid-base changes in CSF and reduced CSF
specific gravity
CSF pressure increased- about 28 mm Hg between contractions; up to 70 mm
Hg during contractions
Epidural plexus engorgement  increased risk of intravascular “epidural”
catheter placement
MAC reduction ±40%, BUT ↑ risk of awareness!!!
– ? progesterone effect, ? pregnancy-induced activation of β-endorphins
Sympathetic nervous system: ↑ing reliance on heightened SNS activity to
maintain of hemodynamic stability; chief effect is on the venous capacitance
system of the lower extremities, which counteracts the adverse effects of
uterine compression of the inferior vena cava on venous return. The
dependence on SNS activity returns to that of the nonpregnant state by 36 to
48 hours postpartum.
Musculoskeletal system
•
•
•
Total serum calcium declines throughout pregnancy until 34-36 weeks
– due to the fall in serum albumin
Serum ionized calcium is constant and unchanged
– “Physiologic hyperparathyroidism”
• increased gut absorption
• decreased renal losses
• no bone loss seen in bone density studies
– preservation due to calcitonin?
Rate of bone turnover and remodeling increases throughout pregnancy
– twice as great at term
•
The placenta produces relaxin, a hormone that causes widespread relaxation of
ligaments.
•
Due to the enlarging uterus, there is a compensatory increase in the lumbar lordosis.
Does all this have a bearing on my GA technique for
caesarean section?
1. Careful airway assessment; be prepared to deal with a potentially difficult airway
2. Use either a left tilt of between 15 – 30 degrees on the table or a wedge under the right
buttock to minimize aorto-caval compression.
3. Venous access if often easier due to engorgement of the venous system.
4. Pre oxygenation is essential and should be with a tight fitting mask for at least 3 minutes.
5. Rapid sequence induction with the application of cricoid pressure is mandatory. The trained
anaesthetic assistant should be careful when placing cricoid pressure if there is left tilt on the
operating table as the temptation is to place the cricoid pressure straight down thus distorting
the view at laryngoscopy.
6. Once the airway is secured, ventilation should be aimed to keep the PCO2 in the normal
range for pregnancy.
7. The MAC of volatile anaesthetic is slightly reduced.
8. Volatile agents cause relaxation of the uterus (uterine atony) and may result in
haemorrhage after delivery of the fetus.
9. There is decreased sensitivity to endogenous and exogenous catecholamines and so if
vasopressors are required to maintain adequate blood pressure, the amounts needed may be
greater.
10. Extubation should be done with the patient awake and on their side to reduce the risk of
aspiration of gastric contents.
When does it all revert to normal?
• Immediate rise in cardiac output immediately after birth; CO
normalises at about 4/52 postpartum
• FRC and RV rapidly return to normal
• Alveolar ventilation returns to normal by 4/52 pp, with ↑pCO2
as progesterone level drops
• Haematocrit normalises within 4 weeks due to pp diuresis; urea,
creat & GFR normal within 3/52
• Mechanical effects of gravid uterus on GIT resolve within 2-3
days pp; however, as serum progesterone levels stay high for a
few weeks, “full stomach” precautions may still be prudent
True or false? Do these occur in normal pregnancy…..
1. A decrease in red cell mass causing a fall in the haematocrit
2. Increased oxygen carrying capacity of blood
3. Increased oxygen delivery
4. Decreased fibrinolysis and decreased level of coagulation factors
5. Decreased cardiac output in the third trimester
6. Slightly increased cardiac output during labour
7. Unchanged diastolic blood pressure
8. Decreased peripheral vascular resistance
9. Increased myocardial contractility
10. There is a marked respiratory alkalosis
11. There is a fall in arterial PCO2
12. Arterial PO2 is increased
13. Minute ventilation is increased
14. Tidal volume is decreased
15. Vital capacity is increased
16. The respiratory quotient is increased
17. Arterial bicarbonate concentration is increased
18. Increased glucose filtration into glomerular fluid