Physiology Of Pregnancy Flashcards
Effect of pregnancy on cardiac output
Effect during labour
Why?
Rises to 150% of normal by end of second trimester - increased HR, SV and reduced SVR
Transient rises in cardiac output of further 45-60% during contractions
Transient rise in cardiac output of further 80% immediate post delivery phase as a result of uteroplacenal transfusion of 300-500ml.
Effect of pregnancy on hr and sv
Hr increases 15% by end of first trimester and 25% by end of second
Sv increased 20% by end of first trimester and 30% by end of second
Both increase further in labour and on delivery.
How would the lithotomy position effect pregnant cardiac output vs supine?
What about left lateral
Lithotomy decreases by 17% vs supine
Left lateral increases by 13.5% vs supine
However note left lateral still causes some decrease overall vs non pregnant person
SVR in pregnancy and in non pregnancy
Pregnancy - 980 dyne.s.cm-5
Non pregnancy 1150 dyne.s.cm-5
Why does SVR decrease in pregnancy
Development of low resistance vascular bed and vasodilation from oestrogens, prostacyclin and progesterone
What is uterine blood flow at term
500-700ml/min
Pattern of systolic blood pressure during pregnancy
Effect of lying flat
Decreases during early / mid gestation retuning to non pregnant level at term
70% of mothers drop Bp by 10% lying flat
10% drop by 50%
What factors influence aortocaval compression in pregnancy
Position
Gestation
Systolic Bp
Presence of sympathetic block
How does blood bypass the aortocaval obstruction when lying supine
Vertebral venous plexuses emptying into azygos vein.
Why might aortocaval compression lead to fetal compromise
Vena cava compression reducing venous return lowering Bp and thus placenta perfusion
Aortic compression reducing aortic blood flow to placenta
ECG changes in pregnancy
Sinus tachycardia
Short pr and qt
Left axis deviation
St depression
T wave flattening
Echo changes in pregnancy
Left ventricular hypertrophy
50% increase lv mass at term
Increased tricuspid, pulmonary and mitral valve diameter
Tricuspid and pulmonary regurgitation
27% mitral regurgitation
Pericardial effusion
How do heart sounds change in pregnancy
Loud and sometimes spilt first heart sound
Third heart sound common
16% have fourth heart sound
Common mid systolic murmur
What factors can increase CVP in labour
Contractions - about 5cmH2O
Expulsion effort of the second stage - about 50cmH20
I’ve ergometrine - about 8cmH20
Change in plasma volume and cellular composition in pregnancy
Change in total blood volume over three trimesters
Plasma volume increases 50%
Red cell volume increases 18% following an initial dip
Results in 15% drop in Hb and HCT
Total blood volume increases 10-30-45% over each trimester
What happens to plasma volume post delivery
Implication
Sharp rise by 1 litre in 24hrs post delivery
Important in those with cardiac disease such as fixed cardiac output
Effect of pregnancy on immune system?
WBC rise (mainly neutrophils)
Overall however depressed immunity due to decreased reduced leukocyte function and increased adherence of neutrophils.
Effect of pregnancy on platelets
Enhanced platelet turnover
Thrombocytopenia in 1%
Platelet function normal
Effect of pregnancy on coagulation factors
All increase except XI and XIII which drop and II and V which stay the same
Especially high increase in I, VII, VIII, IX
What happens to plasma proteins during pregnancy
Consequences
Decrease in albumin concentration
Overall decrease in colloid osmotic pressure, increased ECF volume and oedema
Drug binding altered
Plasma cholinesterase concentration decrease 25%
Effect of pregnancy on bleeding pt and APTT
Decreases 20%
Anatomical changes to the respiratory system in pregnancy
Capillary engorgement of the mucosa in the nasal cavity, pharynx and larynx
Increased thoracic cage circumference due to flaring of ribs.
Upward displacement of diaphragm
Changes to lung mechanics during pregnancy
Decreased movement of chest wall, increased dependence on diaphragmatic movement
Bronchial smooth muscle relaxation reducing resistance
Changes to lung volumes during pregnancy
Tidal volume increases 45%
FRC decreases 20-30% due to decreased ERV and RV
Dead space increases
Closing capacity increases to near FRC increasing v/q mismatch
IRV increases
Change in minute ventilation in pregnancy
What drives this
Increases by 50% due to tidal volumes, rr remains same
Increased progesterone and co2 production
Effect of pregnancy on DLCO (diffusing capacity of lungs for carbon monoxide)
Increases first trimester then decreases then normal
Effect of pregnancy on blood gases
Co2 decreases
Bicarb excretion increases to maintain pH dropping BE
Slight elevation of pH as compensation not complete
Slight increase in PaO2
What causes dysponea in pregnancy?
Prevelance
Likely due to low co2
60%
What is the change in oxygen consumption during pregnancy
Increase 30-60%
Why do pregnant women become hypoxic on induction
Reduced FRC
Increased metabolic demand
Why are pregnant women more at risk of aspiration
Decreased barrier pressure at LOS due to increased intragastric pressure and lower LOS pressure, displaced intraabdominal oesophagus, relaxation from progesterone
Lower ph in stomach
Increased gastric volume
Decreased gastric emptying during labour (due to analgesia!)
Changes to the CNS during pregnancy
Increased venous pressure below gravid uterus diverted through vertebral plexus in epidural space - epidural volume reduced
Epidural pressure slightly positive, during contraction rises to 2-8cmH2O, and during expulsion between 20-60 cmH2O
CSF pressure increases due to aortocaval compression and with contractions/expulsion
Increased SNS tone
MAC is reduced by around 40%
Clinical considerations for anaesthesia during pregnancy due to neurological changes of pregnancy
Epidural and spinal anaesthetics will spread further thus less needed for same level of block
Sympathetic block will have greater relative effect thus sudden drop in BP due to increased baseline tone
Less inhalational agent needed.
Endocrine changes during pregnancy
Increased melanocyte stimulating hormone causing pigmentation
Increased thyroid gland size and production but also increased thyroid binding globulin so thyroid levels actually remain the same
Increased corticosteroid production and prolonged cortisol half life
Increased size of adrenal cortex zona fasciculata
Increased size and weight of pituitary
Increased pancreatic beta islets and increased number of receptor sites for insulin however resistance to insulin due to lactogen, prolactin etc and raised BM due to cortisol etc.
Why are pregnant women more at risk of sheehans syndrome
Increased size and weight of pituitary makes it more at risk of ischaemia and necrosis on haemorrhage - the portal circulation means it operates at a lower pressure than systemic so generally vulnerable.
Renal changes in pregnancy
Increase GFR
Decreased reabsorbative capacity due to increased volume of urine
RAAS increases leading to na and water retention
Progesterone triggers smooth muscle relaxation leading to urinary stasis and dilated collecting system
Increased renal bicarb excretion to counter resp alkalosis
Liver and biliary system changes in pregnancy
Minor changes to liver enzymes ( increase in alp)
Progesterone decreases Ckk release so less gall bladder contraction and more gallstones
Decreased plasma cholinesterases
Msk changes in pregnancy
Relaxin simulates ligamental relaxation
Widens pubis symphysis and increases sacroiliac and sacrococcygeal joints mobility
Enhanced lumbar lordosis to maintain centre of gravity with gravid uterus
Half of pregnant women experience lower back pain as a result of above
Rough weight gain in pregnancy
What proportion is due to fetus, amniotic fluid placenta and uterus?
10kg
40%
Formation of the placenta
Trophoblast of blastocyst infiltrates into endometrium
Differentiates into syncytiotrophoblast and cytotrophoblast
The cytotrophoblast cells covered in syncytiotrophoblast extend out into lacunae of maternal blood in the endometrial decidua
Cytotrophoblastic cells grow into maternal spiral vessels destroying surrounding smooth muscle tissue reducing their ability to vasoconstrict and decreases distance between maternal and fetal blood.
What causes pre eclampsia
Failure of cytotrophoblast cells to destroy spiral artery smooth muscle so they still respond to vasoconstriction
How does maternal blood flow through the placenta?
Uterine blood vessels
Spiral arteries (open ended)
Intravillous space (past the villous trees of fetal circulation)
Collecting veins
Uterine blood vessels
Flow of fetal circulation through the placenta
Internal iliac arteries
Umbilical arteries x2 (deoxygenated blood)
Chorionic arteries
Villous tree
Chorionic vein
Umbilical vein (oxygenated)
Formula for uterine blood flow
UBF = (uterine artery pressure - uterine venous pressure)/uterine vascular resistance
Factors that decrease uterine artery pressure
Hypovolaemia
Aortocaval compression
Sympathetic block
Factors that increase uterine venous pressure
Contractions
Aortocaval compresssion
Valsalva maneuver
Factors that increase uterine vascular resistance
Maternal htn
Preeclampsia
Vasoconstrictors
PO2 in fetal artery and vein
Fetal artery 2.0
Fetal vein 3.9
PCO2 in fetal artery and vein
Artery 5.9
Vein 4.7
What drives transfer of O2 from mother to fetus across the placenta?
High maternofetal oxygen concentration gradient
Left shift of fetal ODC
Bohr effect causing further left shift of ODC in fetal blood and right shift in maternal
High fetal hb concentration
How is co2 carried in fetal blood with percentages? Which state crosses the placenta readily
Dissolved 8% -crosses readily
Bicarbonate 62%
Carbamino haemoglobin 30%
Fractions of carbonic acid and carbonate
How does oxygen transfer effect co2 diffusion across the placenta?
Haldane effect
Fetal o2 rises reducing fetal hb affinity for co2 releasing it
Maternal o2 falls increasing maternal hb affinity for co2 absorbing it
How do nutrients cross the placenta
Glucose - facilitated transport - steriospecific for d isomer
Amino acids - secondary active transport usually with na
Fatty acids - diffuse across
Which Ig crosses the placenta? How?
IgG by Pinocytosis
Hormones released by the placenta
Human chorionic gonadotropin
Human placental lactogen
Hypothalamic releasing factor
Hypothalamic inhibitory factor
Oestrogen
Progesterone
Thyroid stimulating hormone
Prostaglandins
What are the main hormonal changes in pregnancy
Rapid rise in HCG stimulating corpus luteum to secrete progesterone maintaining viability of pregnancy. This role is taken over by the placenta by week 8.
Human placental lactogen is released by the plea beta causing lipolysis, gluconeogenesis and anti insulin effects
Oestrogen is secreted by the placenta stimulating uterine expansion
Factors which could effect fetal maternal drug concentration ratios
Site of fetal sampling
Time between administration and sampling
Bolus or infusion of drug
Factors effecting placental drug transfer
Lipid solubility - more lipid soluble more easily transferred
Degree of ionisation - non-ionised fraction can cross, ionised not
pH of maternal blood - effects degree of ionisation and protein binding
Protein binding - diffusion of protein bound drugs negligible
Molecular weight of drug - <600daltons readily diffuse
Maternal fetal concentration gradient
Placental blood flow
Do muscle relaxants cross the placenta? Why
No, highly ionised
Which drugs will placental blood flow have a larger impact on for transfer to fetus
Highly diffusible ones - less diffusible ones there is very little change on placental transit so flow doesn’t matter, but Highly diffusible drugs drop in concentration on transit so faster flow has bigger effect
What law determines diffusion of drug across placenta by concentration gradient
Ficks law
Q = kA.([m]-[f])/D
Rate = constant.area.(maternal conc - fetal conc)/diffusion difference
How readily do opioids cross the placenta?
F/M ratios for pethadine, morphine, fentanyl, alfentanyl
In significant amounts
Pethadine 1
Morphine 0.61
Fentanyl 0.37-0.57
Alfentanyl 0.3
Why is alfentanyls F/M ratio so low
Highly protein bound
How does pethadine behave across the placenta when administered in labour
Rapidly metabolised in mother (t1/2 4hrs) but readily crosses placenta with F/M ratio of 1 and due to decreased metabolism in fetus has t1/2 of 19 hrs and it’s active metabolite norpethidine 62hrs!
Why do local anaesthetics readily cross the placenta
What is the issue when in the fetus
Low molecular weight (around 240-280 daltons), highly lipophilic and low degree of ionisation in maternal circulation.
When in fetal circulation more acidic conditions so more ionisation of the local anaesthetic so doesn’t diffuse back thus accumulates
Which local anaesthetics diffuse across the placenta more than others? Why?
Lidocaine, mepivicaine more so than bupivicaine due to less protein binding.
How easily do inhalational anaesthetics travel across the placenta
What can this cause
Rapidly as highly lipid soluble.
Diffusion hypoxia before delivery
F/M ratios of induction agents
Thiopental - 0.4 - 1.1
Ketamine 1.3
Propofol 0.65-1.15
What effects propofols F/M ratio specifically
Maternal protein concentration as it is highly protein bound.
How readily do atropine and glycopyrronium travel across the placenta
Atropine - readily
Glycopyrronium - poorly
F/M ratio of ephedrine
0.7
How readily do benzodiazepines cross the placenta
Diazepam readily (fm ratio of 2 within 2hrs!)
Midazolam less so fm ratio of 0.76
